FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Surgucheva, I McMahan, B Ahmed, F Tomarev, S Wax, MB Surguchov, A AF Surgucheva, I McMahan, B Ahmed, F Tomarev, S Wax, MB Surguchov, A TI Synucleins in glaucoma: Implication of gamma-synuclein in glaucomatous alterations in the optic nerve SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE astrocytes; cell models; nucleus; centrosomes; optic nerve; gamma-synuclein ID MULTIPLE SYSTEM ATROPHY; ALPHA-SYNUCLEIN; PARKINSONS-DISEASE; LEWY BODIES; OXIDATIVE STRESS; EXPRESSION; GENE; PERSYN; FAMILY; DEMENTIA AB Synucleins are small proteins associated with neurodegenerative diseases and some forms of cancer. They are studied predominantly in the brain; information about their presence and functions in ocular tissues is scarce. Here we describe the localization of three members of the synuclein family in the optic nerve of donors with different types of-glaucoma compared with control samples from donors without ocular diseases. We did not find significant differences in the localization of alpha- and beta-synucleins in the optic nerve or retina of glaucoma patients compared with controls, whereas considerable redistribution of gamma-synuclein occurred in the glaucomatous optic nerve compared with control eye without glaucoma. In the optic nerve from control and glaucomatous individuals, nerve bundles are immunopositive for gamma-synuclein; however, a strong gamma-synuclein-immunopositive staining in a subset of glial cells was observed in the lamina and postlamina cribrosa regions of the optic nerve only in glaucoma patients. In the optic nerve of rats with episcleral vein cauterization used as an animal model of glaucoma, the quantity of both gamma-synuclein mRNA and protein was decreased compared with the optic nerves of control animals. Incubation of rat astrocyte culture at elevated hydrostatic pressure reduced the,amount of gamma-synuclein but did not affect the quantities of actin and glial fibrillary acidic protein. These data suggest that significant changes in the pattern of expression and/or localization occur in the glaucomatous optic nerve for gamma-synuclein but not for alpha- and beta-members of the synuclein family. (C) 2002 Wiley-Liss, Inc. C1 Washington Univ, Dept Ophthalmol & Visual Sci, St Louis, MO 63130 USA. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RP Surguchov, A (reprint author), Univ Kansas, 4004 Haworth Hall, Lawrence, KS 66045 USA. FU NEI NIH HHS [EY 13784] NR 45 TC 49 Z9 50 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR 1 PY 2002 VL 68 IS 1 BP 97 EP 106 DI 10.1002/jnr.10198 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 538AW UT WOS:000174792700012 PM 11933054 ER PT J AU Weil, RJ Vortmeyer, AO Zhuang, ZP Pack, SD Theodore, N Erickson, RK Oldfield, EH AF Weil, RJ Vortmeyer, AO Zhuang, ZP Pack, SD Theodore, N Erickson, RK Oldfield, EH TI Clinical and molecular analysis of disseminated hemangioblastomatosis of the central nervous system in patients without von Hippel-Lindau disease - Report of four cases SO JOURNAL OF NEUROSURGERY LA English DT Article DE von Hippel-Lindau disease; tumor suppressor gene; immunohistochemistry; fluorescence in situ hybridization; DNA methylation; comparative genomic hybridization ID TUMOR-SUPPRESSOR GENE; SPORADIC CEREBELLAR HEMANGIOBLASTOMAS; CPG ISLAND METHYLATION; SOMATIC MUTATIONS; RENAL-CARCINOMA; HUMAN CANCERS; CHROMOSOME; DELETIONS; DNA; MICRODISSECTION AB Hemangioblastomas of the central nervous system (CNS) may occur sporadically or in association with von Hippel-Lindau (VHL) syndrome. The authors present four patients with no family history or clinical evidence of VHL syndrome in whom extensive, progressive, en plaque coating of the brainstem and spinal cord with hemangioblastomas developed 1 to 8 years after complete resection of a solitary cerebellar hemangioblastoma. Analysis included detailed physical, biochemical, radiological, and pathological examinations in all four patients, combined with family pedigree analysis. In addition, a detailed investigation of the VHL gene was undertaken. Allelic loss, comparative genomic hybridization (CGH), single-stranded conformational polymorphism screening, CpG island methylation status, and X chromosome inactivation clonality analyses were performed. Although there was no evidence of germline alterations in the VHL gene on clinical and radiological examination or in the family history (all four patients) or analysis of peripheral blood (three patients), somatic deletion of one copy of the VHL gene occurred in these tumors. These findings indicate that the multiple, separate deposits of tumors were likely derived from a single clone. Results of CGH indicate that one or several additional genes are probably involved in the malignant behavior of the hemangioblastomas in these patients. Furthermore, the malignant biological and clinical behavior of these tumors, in which multiple sites of subarachnoid dissemination developed 1 to 8 years after initial complete resection, followed by progressive tumor growth and death of the patients, occurred despite a histological appearance typical of benign hemangioblastomas. Malignant hemangioblastomatosis developed 1 to 8 years after resection of an isolated cerebellar hemangioblastoma. Alterations of the VHL gene may be permissive in this setting, but other genes are likely to be the source of the novel biological and clinical presentation of the disseminated hemangioblastomas in these patients. This appears to represent a novel condition in which the product of one or more mutations in several genes permits malignant tumor behavior despite retention of a benign histological picture, a circumstance previously not recognized in CNS tumors. C1 NINCDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. Vanderbilt Univ, Sch Med, Dept Neurosurg, Nashville, TN 37212 USA. Univ Chicago, Dept Neurosurg, Chicago, IL 60637 USA. RP Oldfield, EH (reprint author), NINCDS, Surg Neurol Branch, NIH, Room 5D37,Bldg 10,9000 Rockville Pike, Bethesda, MD 20892 USA. RI Pack, Svetlana/C-2020-2014; OI Theodore, Nicholas/0000-0001-5355-2683 NR 47 TC 23 Z9 24 U1 0 U2 1 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 USA SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 2002 VL 96 IS 4 BP 775 EP 787 DI 10.3171/jns.2002.96.4.0775 PG 13 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 535UJ UT WOS:000174664500022 PM 11990821 ER PT J AU Weinstein, SJ Gridley, G Harty, LC Diehl, SR Brown, LM Winn, DM Bravo-Otero, E Hayes, RB AF Weinstein, SJ Gridley, G Harty, LC Diehl, SR Brown, LM Winn, DM Bravo-Otero, E Hayes, RB TI Folate intake, serum homocysteine and methylenetetrahydrofolate reductase (MTHFR) C677T genotype are not associated with oral cancer risk in Puerto Rico SO JOURNAL OF NUTRITION LA English DT Article DE folate; homocysteine; methylenetetrahydrofolate reductase; oral cancer; epidemiology ID METHIONINE SYNTHASE GENE; PHARYNGEAL CANCER; COLORECTAL-CANCER; PLASMA FOLATE; UNITED-STATES; FOOD GROUPS; POLYMORPHISM; DIET; VITAMIN-B-12; METABOLISM AB We examined the relationships between folate and methionine intake, serum homocysteine levels (as a biomarker for folate metabolism), and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism genotype and risk of oral cancer in a population-based, case-control study in Puerto Rico. Structured questionnaires were used to collect information on demographic factors, usual adult diet, and tobacco and alcohol use. Oral epithelial cells and blood samples were collected from a subset of subjects. Analyses were conducted by logistic regression, adjusting for age, sex, lifetime smoking and lifetime alcohol intake, with the following numbers of cases/controls, respectively: dietary data (341/521); MTHFR genotype (148/149); and homocysteine (60/90). Although increased folate intake was associated with decreased oral cancer risk [adjusted odds ratio (OR) in highest vs. lowest quartile = 0.6, 95% confidence interval (CI): 0.4, 1.0, P-trend = 0.05)], this finding was due almost entirely to folate intake from fruit (adjusted OR = 0.4, 95% Cl: 0.2, 0.6; P-trend = 0.0001), whereas other dietary folate sources showed no clear association. Methionine intake and serum homocysteine levels were not associated with oral cancer risk. Subjects with the MTHFR C677T homozygous variant (TT) genotype had a nonsignificantly lower risk, and risk patterns tended to differ by level of folate, methionine, alcohol intake and smoking, although the power to detect significant associations in subgroups of these variables was low. Risks for oral cancer are not folate specific; preventive recommendations for this disease should emphasize the importance of a healthy diet, including substantial intake of fruits. C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Craniofacial Epidemiol & Genet Branch, Bethesda, MD 20892 USA. NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. Univ Puerto Rico, Sch Dent, San Juan, PR 00936 USA. RP Weinstein, SJ (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NR 59 TC 45 Z9 48 U1 0 U2 1 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3166 J9 J NUTR JI J. Nutr. PD APR PY 2002 VL 132 IS 4 BP 762 EP 767 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 538ZG UT WOS:000174844500023 PM 11925474 ER PT J AU Bottone, FG Baek, SJ Nixon, JB Eling, TE AF Bottone, FG Baek, SJ Nixon, JB Eling, TE TI Diallyl disulfide (DADS) induces the antitumorigenic NSAID-activated gene (NAG-1) by a p53-dependent mechanism in human colorectal HCT 116 cells SO JOURNAL OF NUTRITION LA English DT Article DE apoptosis; colorectal cancer; diallyl disulfide (DADS); NAG-1; p53 ID TGF-BETA SUPERFAMILY; COLON-CANCER; TUMOR-CELLS; P53; APOPTOSIS; INDUCTION; GROWTH; PROLIFERATION; ANTIOXIDANTS; EXPRESSION AB Garlic is appealing as an anti-carcinogenic agent due to its ability to induce apoptosis in vitro and inhibit the formation and growth of tumors in animals in vivo. Diallyl disulfide (DADS) is a constituent of garlic that suppresses neoplastic cell growth and induces apoptosis. We examined the effects of DADS on various cancer cell lines to better understand its effect on apoptosis and apoptosis-related genes. The nonsteroidal anti-inflammatory drug (NSAID)-activated gene (NAG-1) has proapoptotic and antitumorigenic activities and is upregulated by anticancer agents such as NSAIDs. In this study, human colorectal HCT-116 (wild-type p53), HCT-15 (p53 mutant) and human prostate PC-3 (p53 mutant) cells were exposed to DADS. DADS inhibited cell proliferation in all cell lines albeit to a lesser extent in HCT-15 and PC-3 cells at 11.5 and 23 mumol/L. In HCT-116 cells, DADS induced p53 and NAG-1 in a dose-dependent manner and the induction of p53 preceded that of NAG-1. In HCT-116 cells, NAG-1 protein expression was increased 2.4-fold 0.6 at 4.6 mumol/L and 6.1-fold +/- 1.7 at 23 mumol/L DADS, whereas p53 was induced 1.5-fold +/- 0.1 and 2.3-fold +/- 0.4. DADS did not induce NAG-1 or p53 in p53 mutant cell lines; however, NAG-1 expression was induced by sulindac sulfide. HCT-116 cells treated with 4.6 and 23 mumol/L DADS resulted in a 1.9- and 2.9-fold increase in apoptosis, respectively. In contrast, 23 mumol/L DADS induced apoptosis only 1.8-fold in HCT-15 cells and not at all in PC-3 cells. Thus, DADS-induced apoptosis and NAG-1 protein expression appear to occur via p53. C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Eling, TE (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. OI Baek, Seung/0000-0001-7866-7778 NR 39 TC 87 Z9 91 U1 0 U2 0 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3166 J9 J NUTR JI J. Nutr. PD APR PY 2002 VL 132 IS 4 BP 773 EP 778 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 538ZG UT WOS:000174844500025 PM 11925476 ER PT J AU Kleinerman, RA Wang, ZY Wang, LD Metayer, C Zhang, SZ Brenner, AV Zhang, SR Xia, Y Shang, B Lubin, JH AF Kleinerman, RA Wang, ZY Wang, LD Metayer, C Zhang, SZ Brenner, AV Zhang, SR Xia, Y Shang, B Lubin, JH TI Lung cancer and indoor exposure to coal and biomass in rural China SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID AIR-POLLUTION; XUAN-WEI; DEVELOPING-COUNTRIES; NONSMOKING WOMEN; RISK-FACTORS; SHENYANG; FEMALES; HEALTH; SMOKE AB Incomplete combustion Of coal in homes has been linked with lung cancer in China. We report on a lung cancer case-control study in a rural area of China, where many residents live in underground dwellings and burn coal and unprocessed biomass (crop residues, wood, sticks, and twigs)for heating and cooking. We interviewed 846 patients with lung cancer (626 men, 220 women; aged 30 to 75 years) diagnosed between 1994 and 1998, and 1740 population-based controls. The odds ratio for lung cancer associated with coal use compared with that for biomass in the house of longest residence was 1.29 (95% confidence interval, 1.03 to 1.61), adjusted for smoking and socioeconomic status. The risk for lung cancer increased relative to the Percentage of time that coal was used over the past 30 years (P = 0.02). Our findings suggest that coal may contribute to the fish of lung cancer in this rural area of China. (J Occup Environ Med. 2002;44: 338-344). C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. Minist Publ Hlth, Lab Ind Hyg, Beijing, Peoples R China. Minist Hlth, Beijing, Peoples R China. RP Kleinerman, RA (reprint author), NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, 6120 Execut Blvd,EPS 7044,MSC 7238, Bethesda, MD 20892 USA. OI Kleinerman, Ruth/0000-0001-7415-2478 FU NCI NIH HHS [N02-CP-81121, N01-CP-50509] NR 30 TC 36 Z9 38 U1 0 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD APR PY 2002 VL 44 IS 4 BP 338 EP 344 DI 10.1097/00043764-200204000-00014 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 543MV UT WOS:000175106500015 PM 11977420 ER PT J AU Charmandari, E Johnston, A Honour, JW Brook, CGD Hindmarsh, PC AF Charmandari, E Johnston, A Honour, JW Brook, CGD Hindmarsh, PC TI Treatment with flutamide decreases cortisol clearance: Implications for therapy in congenital adrenal hyperplasia SO JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM LA English DT Article DE congenital adrenal hyperplasia; flutamide; cortisol clearance; cortisol half-life ID METABOLISM; CHILDREN AB Background. Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is characterized by a defect in cortisol and often aldosterone secretion, and adrenal hyperandrogenism. Current treatment is to provide adequate glucocorticoid and mineralocorticoid substitution to prevent adrenal crises and to suppress excess adrenocortical androgen secretion. Anti-androgen therapy with flutamide is an option that allows control of hyperandrogenism without recourse to supraphysiological doses of glucocorticoid. Methods: We examined the pharmacokinetic parameters of hydrocortisone administered i.v. as a bolus at a dose of 15 mg/m(2) in a 17.3 year-old female patient with classic CAH before and four weeks after institution of flutamide treatment by determining serum cortisol concentrations at 10 min intervals for 6 h following the i.v. bolus of hydrocortisone. Results: Treatment with flutamide resulted in a decrease in cortisol clearance from 420 ml/l to 305 ml/l (27% reduction), and a decrease in volume of distribution from 51.6 1 to 45 1 (12.9% reduction). The half-life of cortisol increased from 85.3 min to 102.1 min. Conclusions: Flutamide treatment decreases cortisol clearance, thereby prolonging its half-life. These findings indicate that a reduction in the daily dose of glucocorticoid replacement may need to be considered when flutamide is added to the treatment regimen of patients receiving hydrocortisone. C1 UCL, London Ctr Paediat Endocrinol, London, England. St Bartholomews & Royal London Sch Med & Dent, London, England. Middlesex Hosp, London, England. RP Charmandari, E (reprint author), NICHHD, NIH, 10 Ctr Dr,Bldg 10,Suite 9D42, Bethesda, MD 20892 USA. EM charmane@mail.nih.gov RI Hindmarsh, Peter/C-4964-2008; Charmandari, Evangelia/B-6701-2011 NR 11 TC 1 Z9 1 U1 0 U2 1 PU WALTER DE GRUYTER GMBH PI BERLIN PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY SN 0334-018X EI 2191-0251 J9 J PEDIATR ENDOCR MET JI J. Pediatr. Endocrinol. Metab. PD APR PY 2002 VL 15 IS 4 BP 435 EP 439 PG 5 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA 545JB UT WOS:000175212700012 PM 12008691 ER PT J AU Hagemann, D Naumann, E Thayer, JF Bartussek, D AF Hagemann, D Naumann, E Thayer, JF Bartussek, D TI Does resting electroencephalograph asymmetry reflect a trait? An application of latent state-trait theory SO JOURNAL OF PERSONALITY AND SOCIAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 40th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 18-22, 2000 CL SAN DIEGO, CALIFORNIA SP Soc Psychophysiol Res ID FRONTAL BRAIN ASYMMETRY; EEG ALPHA-ASYMMETRY; CEREBRAL ASYMMETRY; AFFECTIVE STYLE; INDIVIDUAL-DIFFERENCES; BIOLOGICAL SUBSTRATE; METHODOLOGICAL CONUNDRUMS; BEHAVIORAL ACTIVATION; AFFECTIVE RESPONSES; ELECTRICAL-ACTIVITY AB Recent research on brain asymmetry and emotion treated measures of resting electroencephalograph (EEG) asymmetry as genuine trait variables, but inconsistency in reported findings and modest retest correlations of baseline asymmetry are not consistent with this practice. The present study examined the alternative hypothesis that resting EEG asymmetry represents a superimposition of a traitlike activation asymmetry with substantial state-dependent fluctuations. Resting EEG was collected from 59 participants on 4 occasions of measurement, and data were analyzed in terms of latent state-trait theory. For most scalp regions, about 60% of the variance of the asymmetry measure was due to individual differences on a temporally stable latent trait. and 40% of the variance was due to occasion-specific fluctuations. but measurement errors were negligible. Further analyses indicated that these fluctuations might be efficiently reduced by aggregation across several occasions. C1 Univ Trier, Fachbereich Psychol 1, Dept Psychol, D-54286 Trier, Germany. NIA, Lab Personal & Cognit, NIH, Baltimore, MD 21224 USA. Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA. RP Hagemann, D (reprint author), Univ Trier, Fachbereich Psychol 1, Dept Psychol, Univ Ring 15, D-54286 Trier, Germany. NR 129 TC 91 Z9 91 U1 14 U2 29 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0022-3514 J9 J PERS SOC PSYCHOL JI J. Pers. Soc. Psychol. PD APR PY 2002 VL 82 IS 4 BP 619 EP 641 DI 10.1037//0022-3514.82.4.619 PG 23 WC Psychology, Social SC Psychology GA 540BP UT WOS:000174908600011 PM 11999928 ER PT J AU Igarashi, H Ito, T Hou, W Mantey, SA Pradhan, TK Ulrich, CD Hocart, SJ Coy, DH Jensen, RT AF Igarashi, H Ito, T Hou, W Mantey, SA Pradhan, TK Ulrich, CD Hocart, SJ Coy, DH Jensen, RT TI Elucidation of vasoactive intestinal peptide pharmacophore for VPAC(1) receptors in human, rat, and guinea pig SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CYCLASE-ACTIVATING POLYPEPTIDE; PANCREATIC ACINI; VIP RECEPTORS; HUMAN-LUNG; IN-VITRO; CELLS; ANALOG; CANCER; GROWTH; PACAP AB Vasoactive intestinal peptide (VIP) is a neurotransmitter involved in a number of pathological and physiological processes. VIP is rapidly degraded and simplified stable analogs are needed. VIP's action was extensively studied in rat and guinea pig. However, it is largely unknown whether its pharmacophore in these species resembles human. To address this issue we investigated the VIP pharmacophore for VPAC(1) (the predominant receptor subtype in cancers and widely distributed in normal tissues) by using alanine and D-amino acid scanning. Interaction with rat, guinea pig, and human VPAC(1) was assessed using transfected Chinese hamster ovary (CHO) and PANC1 cells and cells possessing native VPAC(1). Important species differences existed in the VIP pharmacophore. The human VPAC(1) expressed in CHO cells, which were used almost exclusively in previous studies, differed markedly from the native VPAC(1) in T47D cells. The most important amino acids for determining affinity are His(1), Asp(3), Phe(6), Arg(12), Arg(14), and Leu(23). Ser(2), Asp(8), Asn(9), Thr(11), Val(19), Asn(24), Ser(25), Leu(27), and Asn(28) are not essential for high-affinity interaction/activation. [Ala(2,8,9,11,19,24,25,27,28])VIP, which contained 11 alanines, was synthesized and it was equipotent to VIP at VPAC(1) receptors in all species and was metabolically stable. Our results show in any design of simplified VIP analogs for VPAC(1) it will be important to consider species differences and it is essential to use transfected systems that reflect the native receptor's pharmacophore. Last, with our results a simplified, metabolically stable VIP analog was identified that should be useful as a prototype for design of selective agonists/antagonists that could be useful therapeutically. C1 NIDDKD, NIH, Digest Dis Branch, Bethesda, MD 20892 USA. Univ Cincinnati, Med Ctr, Div Digest Dis, Cincinnati, OH 45267 USA. Tulane Univ, Dept Med, Hlth Sci Ctr, Peptide Res Labs, New Orleans, LA 70118 USA. RP NIDDKD, NIH, Digest Dis Branch, Bldg 10,Rm 9C-103,10 Ctr Dr,MSC 1804, Bethesda, MD 20892 USA. EM robertj@bdg10.niddk.nih.gov NR 40 TC 36 Z9 37 U1 0 U2 1 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA SN 0022-3565 EI 1521-0103 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 2002 VL 301 IS 1 BP 37 EP 50 AR UNSP 4617/972758 DI 10.1124/jpet.301.1.37 PG 14 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 536YV UT WOS:000174730200006 PM 11907155 ER PT J AU Leshner, AI AF Leshner, AI TI Ecstasy abuse and control: Hearing before the senate subcommittee on governmental affairs - July 30, 2001. Statement for the record SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Editorial Material C1 NIDA, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Leshner, AI (reprint author), NIDA, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAIGHT-ASHBURY PUBL PI SAN FRANCISCO PA 409 CLAYTON ST, SAN FRANCISCO, CA 94117 USA SN 0279-1072 J9 J PSYCHOACTIVE DRUGS JI J. Psychoact. Drugs PD APR-JUN PY 2002 VL 34 IS 2 BP 133 EP 135 PG 3 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA 574ET UT WOS:000176876000004 PM 12691202 ER PT J AU Trobst, KK Herbst, JH Masters, HL Costa, PT AF Trobst, KK Herbst, JH Masters, HL Costa, PT TI Personality pathways to unsafe sex: Personality, condom use, and HIV risk behaviors SO JOURNAL OF RESEARCH IN PERSONALITY LA English DT Article ID 5-FACTOR MODEL; SENSATION SEEKING; SUBSTANCE USE; AIDS; PREVENTION; MEN; PREDICTORS; INTERVENTIONS; INFECTION; VARIABLES AB Few studies have considered the importance of enduring personality characteristics in influencing health and HIV/AIDS risk behaviors. The current study examined relations between a comprehensive measure of personality, the Revised NEO Personality Inventory, and condom use and other HIV risk behaviors. The study sample consisted of 201 disadvantaged, primarily African American participants of an HIV risk reduction program in the Arkansas delta region. The sample was stratified into three risk groups. The low-risk group (n = 43) had 0% engaging in various risky sexual and substance use practices. Between 3% and 52% of the high-risk group (n = 62) engaged in these practices (e.g., shared needles, sex with partner who shoots drugs, received anal sex). The medium-risk group (n = 96) was intermediate. Results indicated that high Neuroticism, low Conscientiousness, and low Agreeableness are associated with HIV risk behaviors. Thus, high-risk behavior is associated with emotional distress, poor self-control, and hostile and antagonistic attitudes and behaviors. The high-risk group differed from the medium- and low-risk groups on the Neuroticism facet of Impulsiveness, indicating an inability to resist cravings and urges. The high-risk group also scored lower in Competence (i.e., feelings of self-efficacy), Self-Discipline (i.e., motivation to carry tasks through to completion), and Achievement Striving (i.e., aspiration levels). The current study, by identifying several personality traits that contribute to sexual risk behavior, raises important public health implications. Successful intervention in these AIDS-related behaviours may require interventions tailored to these basic tendencies. Such an approach may be a crucial element in attempts to lower HIV risk behaviour. (C) 2002 Elsevier Science (USA). C1 NIA, Lab Personal & Cognit, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Costa, PT (reprint author), NIA, Lab Personal & Cognit, NIH, Gerontol Res Ctr, 5600 Nathan Shock Dr,Box 03, Baltimore, MD 21224 USA. OI Costa, Paul/0000-0003-4375-1712 NR 62 TC 51 Z9 52 U1 6 U2 13 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0092-6566 J9 J RES PERS JI J. Res. Pers. PD APR PY 2002 VL 36 IS 2 BP 117 EP 133 DI 10.1006/jrpe.2001.2334 PG 17 WC Psychology, Social SC Psychology GA 537NN UT WOS:000174764900002 ER PT J AU Simpson, JK Brockow, K Turner, ML Akin, C Metcalfe, DD AF Simpson, JK Brockow, K Turner, ML Akin, C Metcalfe, DD TI Generalized erythematous macules and plaques associated with flushing, repeated syncope, and refractory anemia SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID STEM-CELL FACTOR; MASTOCYTOSIS; APOPTOSIS; RECEPTOR; LIGAND; LOCUS; MOUSE C1 NCI, Dermatol Branch, Bethesda, MD 20892 USA. NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA. RP Turner, ML (reprint author), NCI, Dermatol Branch, Bldg 10 Room 12N238,10 Ctr Dr,MSC 1908, Bethesda, MD 20892 USA. OI Akin, Cem/0000-0001-6301-4520 NR 13 TC 3 Z9 3 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 2002 VL 46 IS 4 BP 588 EP 590 DI 10.1067/mjd.2002.120446 PG 3 WC Dermatology SC Dermatology GA 581VB UT WOS:000177313600018 PM 11907513 ER PT J AU Lytle, LA Dixon, LB Cunningham-Sabo, L Evans, M Gittelsohn, J Hurley, J Snyder, P Stevens, J Weber, J Anliker, J Heller, K Story, M AF Lytle, LA Dixon, LB Cunningham-Sabo, L Evans, M Gittelsohn, J Hurley, J Snyder, P Stevens, J Weber, J Anliker, J Heller, K Story, M TI Dietary intakes of Native American children: Findings from the Pathways Feasibility Study SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID 24-HOUR RECALLS; NAVAJO; ADOLESCENTS C1 Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55454 USA. NYU, Dept Nutr & Food Studies, New York, NY USA. Univ New Mexico, Sch Med, Dept Pediat, Ctr Hlth Promot & Dis Prevent, Albuquerque, NM 87131 USA. Univ New Mexico, Coll Educ, Individual Family & Community Educ Program, Albuquerque, NM 87131 USA. NHLBI, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Int Hlth, Ctr Human Nutr, Div Human Nutr, Baltimore, MD USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. Gila River Indian Community, Dept Publ Hlth, Sacaton, AZ USA. Univ N Carolina, Dept Nutr, Chapel Hill, NC USA. Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA. Univ Arizona, Coll Med, Dept Physiol, Tucson, AZ 85724 USA. RP Lytle, LA (reprint author), Univ Minnesota, Sch Publ Hlth, Div Epidemiol, 1300 S 2nd St,Ste 300, Minneapolis, MN 55454 USA. NR 30 TC 26 Z9 26 U1 0 U2 1 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 USA SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD APR PY 2002 VL 102 IS 4 BP 555 EP 558 DI 10.1016/S0002-8223(02)90129-X PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 538YU UT WOS:000174843300028 PM 11985417 ER PT J AU Reuben, DB Cheh, AI Harris, TB Ferrucci, L Rowe, JW Tracy, RP Seeman, TE AF Reuben, DB Cheh, AI Harris, TB Ferrucci, L Rowe, JW Tracy, RP Seeman, TE TI Peripheral blood markers of inflammation predict mortality and functional decline in high-functioning community-dwelling older persons SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE IL-6; CRP; inflammation; older ID C-REACTIVE PROTEIN; CARDIOVASCULAR RISK-FACTORS; CORONARY HEART-DISEASE; BODY-MASS INDEX; SERUM-ALBUMIN; IL-6 LEVELS; INTERLEUKIN-6; ASSOCIATION; DISABILITY; ADULTS AB OBJECTIVES: Several peripheral blood markers of inflammation have demonstrated prognostic ability, but the value of combining multiple markers as a measure of inflammatory burden remains unknown. The objective of this study was to determine the prognostic value of combining four peripheral blood measures of inflammation in healthy older persons. DESIGN: Inception cohort study with 7 years of follow-up. SETTING: Three communities. PARTICIPANTS: Eight hundred seventy high-functioning subjects aged 70 to 79 who had serum albumin, cholesterol, interleukin (IL)-6, and C-reactive protein (CRP) levels measured at baseline. MEASUREMENTS: Three- and 7-year mortality and Rosow-Breslau functional decline. RESULTS: A summary score was created that assigned one point each for the following blood levels: albumin <3.8 g/dL, cholesterol <170 mg/dL (bottom decile), IL-6 >3.8 pg/mL (top tertile), and CRP >2.65 mg/L (top tertile). By 3 years, 6% of subjects had died, and, by 7 years, 23% had died. In subjects with three or four markers of inflammation, the adjusted odds ratios (AORs) for 3- and 7-year mortality were 6.6 and 3.2, respectively, compared with those who had no abnormal markers. Subjects with one or two markers were at more moderate and statistically, insignificant increased risk of 3- and 7-year mortality with AORs of 1.5 and 1.3, respectively. The risks for functional decline at 3- and 7-years were generally small (AOR 1.1-1.9) and not statistically significant. CONCLUSIONS: In high-functioning older persons, a measure of inflammation can identify those at a much higher risk of mortality and a possibly higher risk of functional decline. Whether therapies directed at reducing inflammation can attenuate such risk remains to be determined. C1 Univ Calif Los Angeles, Sch Med, Program Geriat Med & Gerontol, Los Angeles, CA 90095 USA. Natl Inst Aging, Epidemiol Demog & Biometry Program, Bethesda, MD USA. Italian Natl Res Council Aging, Florence, Italy. Mt Sinai Sch Med, New York, NY USA. Univ Vermont, Burlington, VT USA. RP Reuben, DB (reprint author), Univ Calif Los Angeles, Sch Med, Program Geriat Med & Gerontol, Multicampus 10945 Le Conte Ave Suite 2339, Los Angeles, CA 90095 USA. FU NIA NIH HHS [AG10415-01] NR 43 TC 173 Z9 174 U1 2 U2 8 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 BP 638 EP 644 DI 10.1046/j.1532-5415.2002.50157.x PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 541AT UT WOS:000174963600006 PM 11982663 ER PT J AU Leveille, SG Bean, J Bandeen-Roche, K Jones, R Hochberg, M Guralnik, JM AF Leveille, SG Bean, J Bandeen-Roche, K Jones, R Hochberg, M Guralnik, JM TI Musculoskeletal pain and risk for falls in older disabled women living in the community SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE pain; falls; osteoarthritis; fibromyalgia; aging; musculoskeletal; women ID OSTEOPOROTIC FRACTURES; RADIOGRAPHIC CHANGES; KNEE OSTEOARTHRITIS; OSTEO-ARTHRITIS; ELDERLY PERSONS; SELF-REPORT; HEALTH; ASSOCIATION; DISABILITY; HIP AB OBJECTIVES: To determine whether musculoskeletal pain increased risk for falls in older women with disabilities. DESIGN: Prospective population-based cohort study. SETTING: The city and county of the eastern area of Baltimore. PARTICIPANTS: One thousand two women aged 65 and older, participants in the Women's Health and Aging Study, representing the one-third of older women who were living at home with disabilities, followed semiannually for 3 years beginning in 1991. MEASUREMENTS: Pain was categorized into four groups according to severity and location. Widespread pain was defined as pain in the upper and lower extremities and in the axial skeletal region, with moderate to severe pain in at least one region ( greater than or equal to 4 on a 10-point numeric rating scale, 10 = excruciating pain). Moderate to severe lower extremity pain that did not meet criteria for widespread pain was the next category. The reference category was no pain or mild pain in one site. The additional category of "other pain" was pain that did not fit into the other three groups. The occurrence of falls and fall-related injuries were assessed at each interview. RESULTS: Of the 940 women who participated in at least one follow-up examination, 39% fell in first year; of the survivors, 36% fell in Year 2, and 39% in Year 3. After adjusting for several major risk factors for falls, women with widespread pain had an increased likelihood of falling during follow-up (adjusted odds ratio (AOR) = 1.66, 5% confidence interval (CI) = 1.25-2.21) compared with those with no or mild pain in only one musculoskeletal site. Women who had other musculoskeletal pain but not widespread pain or lower extremity pain also had an increased risk of falls (AOR = 1.36, 95% CI = 1.021.82). Among women with musculoskeletal pain, risk for falls was lower in those who used daily analgesic medication. Risk for recurrent falls and self-reported fractures due to falls was also elevated in women with musculoskeletal pain, most consistently in women with widespread pain. CONCLUSIONS: Musculoskeletal pain, particularly widespread pain, is a substantial risk factor for falls in older women with disabilities. These findings add an important dimension to our understanding of the multifactorial processes leading to falls in older persons. C1 Hebrew Rehabil Ctr Aged, Res & Training Inst, Boston, MA 02131 USA. Harvard Univ, Med Sch, Dept Phys Med & Rehabil, Spaulding Rehabil Hosp, Boston, MA USA. Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA. Univ Maryland, Dept Med, Baltimore, MD USA. Univ Maryland, Dept Epidemiol & Prevent Med, Baltimore, MD USA. Natl Inst Aging, Epidemiol Demog & Biometry Program, Bethesda, MD USA. RP Leveille, SG (reprint author), Hebrew Rehabil Ctr Aged, Res & Training Inst, 1200 Ctr St, Boston, MA 02131 USA. RI Jones, Richard/J-3488-2013; Bean, Jonathan/F-5798-2017 OI Jones, Richard/0000-0002-1049-218X; Bean, Jonathan/0000-0001-8385-8210 NR 50 TC 119 Z9 130 U1 0 U2 11 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 BP 671 EP 678 DI 10.1046/j.1532-5415.2002.50161.x PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 541AT UT WOS:000174963600010 PM 11982667 ER PT J AU Ostir, GV Goodwin, JS Markides, KS Ottenbacher, KJ Balfour, J Guralnik, JM AF Ostir, GV Goodwin, JS Markides, KS Ottenbacher, KJ Balfour, J Guralnik, JM TI Differential effects of premorbid physical and emotional health on recovery from acute events SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE depression; positive affect; older; heart attack; stroke; hip fracture ID NEW-HAVEN EPESE; HIP FRACTURE; STROKE REHABILITATION; SOCIAL NETWORKS; RISK-FACTORS; DEPRESSION; MORTALITY; DISABILITY; PREVALENCE; PREDICTORS AB OBJECTIVES: Emotional health may have an important effect on disease onset, but there has been little work evaluating premorbid emotional health on recovery from disability that results from acute medical events. The aim of this study is to determine whether premorbid emotional health is predictive of recovery in functional ability I year after reporting a stroke, heart attack, or hip fracture (event). DESIGN: A prospective cohort study of an older population-based sample from 1986 to 1992. SETTING: Data are from baseline and six annual follow-ups of the North Carolina Established Population for Epidemiological Study of the Elderly. PARTICIPANTS: Two hundred forty whites and blacks aged 65 and older who reported a stroke, heart attack, or hip fracture during one of the first five follow-up interviews and had an increased level of disability at that follow-up. MEASUREMENT: Improvement in disability in activities of daily living (ADLs) 1 year postevent. RESULTS: High depressive symptoms at baseline showed a significant association with poorer recovery in functional ability 1-year postevent after adjustments were made for sociodemographic characteristics, smoking status, ADLs at time of event, cognitive status, and prior history of disease. Compared with nondepresscd subjects, depressed subjects had an odds ratio (OR) of 0.38 (95% confidence interval (CI) = 0.16-0.94) for recovery I year after reporting a stroke, heart attack, or hip fracture. Additionally, among subjects who reported low depressive symptoms, high positive affect was significantly associated with increased odds of recovery (OR = 2.70, 95% CI 1.10-6.68), adjusting for the same variables. CONCLUSIONS: Emotional health, independent of other baseline measures, is associated with recovery in functional ability I year after a major health event. Our findings suggest that reducing premorbid levels of depressive symptoms or increasing positive affect may help the recovery process. C1 UTMB, Sealy Ctr Aging, Galveston, TX 77555 USA. UTMB, Dept Prevent Med & Community Hlth, Galveston, TX 77555 USA. UTMB, Dept Internal Med, Galveston, TX 77555 USA. Natl Inst Hlth, Natl Inst Aging, Epidemiol Demog & Biometry Program, Bethesda, MD USA. RP Ostir, GV (reprint author), UTMB, Sealy Ctr Aging, 301 Univ Blvd, Galveston, TX 77555 USA. FU NIA NIH HHS [P30 AG024832] NR 46 TC 50 Z9 52 U1 2 U2 5 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 BP 713 EP 718 DI 10.1046/j.1532-5415.2002.50167.x PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 541AT UT WOS:000174963600016 PM 11982673 ER PT J AU Boyd, CM Xue, Q Simpson, C Guralnik, JM Fried, LP AF Boyd, CM Xue, Q Simpson, C Guralnik, JM Fried, LP TI Hospitalization and incident walking and stair climbing disability in a cohort of disabled older women. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Johns Hopkins Univ, Baltimore, MD 21218 USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P423 BP S149 EP S149 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500468 ER PT J AU Cavazzini, C Bandinelli, S Benvenuti, E Lauretani, F Russo, CR Bartali, B Corsi, A Guralnik, JM Ferrucci, L AF Cavazzini, C Bandinelli, S Benvenuti, E Lauretani, F Russo, CR Bartali, B Corsi, A Guralnik, JM Ferrucci, L TI Clinical signs of neurogical dysfunction and walking limitations in older persons. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 INRCA, Lab Clin Epidemiol, Florence, Italy. NIA, Lab EDBP, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P376 BP S133 EP S134 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500421 ER PT J AU De Rekeneire, N Rooks, R Shorr, RI Kuller, LH Harris, TB AF De Rekeneire, N Rooks, R Shorr, RI Kuller, LH Harris, TB TI Racial differences in control of diabetes in healthier older diabetics: The Health, Aging and Body Composition Study. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 NIA, Epidemiol Lab, Bethesda, MD 20892 USA. Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA. Univ Pittsburgh, Div Geriatr Med, Pittsburgh, PA 15260 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA A37 BP S13 EP S13 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500038 ER PT J AU Harris, TB Visser, M Goodpaster, B Kritchevsky, S Newman, A Simonsick, E Pahor, M Nevitt, M Cummings, S Hubbard, V Everhart, J AF Harris, TB Visser, M Goodpaster, B Kritchevsky, S Newman, A Simonsick, E Pahor, M Nevitt, M Cummings, S Hubbard, V Everhart, J TI Muscle-marbling fat, a novel fat depot for aging: The health, aging and body composition (Health ABC) study. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands. Univ Pittsburgh, Pittsburgh, PA USA. Univ Tennessee, Memphis, TN USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P393 BP S139 EP S139 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500438 ER PT J AU Hu, P Reuben, DB Crimmins, EM Harris, TB Seeman, TE AF Hu, P Reuben, DB Crimmins, EM Harris, TB Seeman, TE TI The effects of serum beta-carotene and C-reactive protein levels on all-cause mortality in high-functioning older persons: Macarthur Studies of Successful Aging. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Sch Med, Div Geriatr Med, Los Angeles, CA 90024 USA. Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Los Angeles, CA 90089 USA. NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA A38 BP S13 EP S13 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500039 ER PT J AU Jones, H Onder, G Penninx, B Atkinson, HH Guralnik, JM Williamson, JD AF Jones, H Onder, G Penninx, B Atkinson, HH Guralnik, JM Williamson, JD TI Satisfaction with sexual activity and incident disability in community-dwelling older women. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P40 BP S28 EP S28 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500086 ER PT J AU Judd, L Reuben, DB Harris, TB Seeman, TE AF Judd, L Reuben, DB Harris, TB Seeman, TE TI Is physical activity associated with inflammatory markers in high functioning older persons? SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P37 BP S27 EP S27 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500083 ER PT J AU Newman, AB Visser, M Kupelian, V Kritchevsky, S Miles, T Rubin, S Simonsick, E Tylavsky, F Harris, T AF Newman, AB Visser, M Kupelian, V Kritchevsky, S Miles, T Rubin, S Simonsick, E Tylavsky, F Harris, T TI Defining sarcopenia in older adults: A comparison of two approaches. The Health Aging and Body Composition study. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA 15260 USA. VUMC, Amsterdam, Netherlands. Univ Tennessee, Memphis, TN USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX USA. NIA, EDB Lab, Baltimore, MD 21224 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P168 BP S68 EP S68 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500213 ER PT J AU Penninx, BW Guralnik, JM Wallace, R Pahor, M AF Penninx, BW Guralnik, JM Wallace, R Pahor, M TI Anemia is independent risk factor for physical performance decline in old age. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Wake Forest Univ, Sticht Ctr Aging, Winston Salem, NC 27109 USA. NIA, Bethesda, MD 20892 USA. Univ Iowa, Dept Prevent Med, Iowa City, IA 52242 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA A35 BP S12 EP S12 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500036 ER PT J AU Reuben, DB Keeler, E Seeman, TE Sewall, A Hirsch, SH Guralnik, JM AF Reuben, DB Keeler, E Seeman, TE Sewall, A Hirsch, SH Guralnik, JM TI Identification of risk for high hospital utilization: Cost-effectiveness of four strategies and performance across subgroups. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. RAND Corp, Santa Monica, CA USA. Sewall Inc, Bethesda, MD USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P461 BP S161 EP S161 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500506 ER PT J AU Reuben, DB Keeler, E Hayes, RP Bowman, L Seeman, TE Sewall, A Hirsch, SH Wallace, R Guralnik, JM AF Reuben, DB Keeler, E Hayes, RP Bowman, L Seeman, TE Sewall, A Hirsch, SH Wallace, R Guralnik, JM TI Refining the categorization or functional status: The added value of combining self-report and performance-based measures. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. RAND Corp, Santa Monica, CA USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Sewall Inc, Bethesda, MD USA. Univ Iowa, Iowa City, IA USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P416 BP S146 EP S147 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500461 ER PT J AU Reuben, DB Keeler, E Hayes, RP Bowman, L Seeman, TE Sewall, A Hirsch, SH Wallace, R Guralnik, JM AF Reuben, DB Keeler, E Hayes, RP Bowman, L Seeman, TE Sewall, A Hirsch, SH Wallace, R Guralnik, JM TI The costs of self-reported and perfomance-based functional impairment. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. RAND Corp, Santa Monica, CA USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Sewall Inc, Bethesda, MD USA. Univ Iowa, Iowa City, IA USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P415 BP S146 EP S146 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500460 ER PT J AU Simpson, C Boyd, C Guralnik, J Fried, LP AF Simpson, C Boyd, C Guralnik, J Fried, LP TI Does the validity of self-report of disease vary in disabled older women by number & type of disability? SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Johns Hopkins Univ, Ctr Aging, Baltimore, MD USA. Johns Hopkins Univ, Div Geriatr Med, Baltimore, MD USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA P299 BP S109 EP S109 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500344 ER PT J AU Volpato, S Ferrucci, L Blaum, C Fried, LP Guralnik, JM AF Volpato, S Ferrucci, L Blaum, C Fried, LP Guralnik, JM TI Progression of lower extremity disability in older women with diabetes: The women's health and aging study. SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Meeting Abstract C1 Univ Ferrara, Sect Internal Med 2, I-44100 Ferrara, Italy. NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA. I Fraticini Italian Natl Inst Res & Care Aging, Dept Geriatr, Florence, Italy. Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Epidemiol, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 2002 VL 50 IS 4 SU S MA A36 BP S12 EP S13 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 542EL UT WOS:000175030500037 ER PT J AU Biner, HL Arpin-Bott, MP Loffing, J Wang, XY Knepper, M Hebert, SC Kaissling, B AF Biner, HL Arpin-Bott, MP Loffing, J Wang, XY Knepper, M Hebert, SC Kaissling, B TI Human cortical distal nephron: Distribution of electrolyte and water transport pathways SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID EPITHELIAL SODIUM-CHANNEL; ACTIVE CALCIUM REABSORPTION; RENAL-CELL CARCINOMA; DIABETES-INSIPIDUS; RAT-KIDNEY; MEDIATED REGULATION; DIURETIC INFUSION; CONVOLUTED TUBULE; BLOOD-PRESSURE; ENTRY PATHWAYS AB The exact distributions of the different salt transport systems along the human cortical distal nephron are unknown. Immunohistochemistry was performed on serial cryostat sections of healthy parts of tumor nephrectomized human kidneys to study the distributions in the distal convolution of the thiazide-sensitive Na-Cl cotransporter (NCC), the beta subunit of the amiloride-sensitive epithelial Na channel (ENaC), the vasopressin-sensitive water channel aquaporin 2 (AQP2), and aquaporin 3 (AQP3), the H+ ATPase, the Na-Ca exchanger (NCX), plasma membrane calcium-ATPase, and calbindin-D28k (CaBP). The entire human distal convolution and the cortical collecting duct (CCD) display calbindin-D28k, although in variable amounts. Approximately 30% of the distal convolution profiles reveal NCC, characterizing the distal convoluted tubule. NCC overlaps with ENaC in a short portion at the end of the distal convoluted tubule. ENaC is displayed all along the connecting tubule (70% of the distal convolution) and the CCD. The major part of the connecting tubule and the CCD coexpress aquaporin 2 with ENaC. Intercalated cells, undetected in the first 20% of the distal convolution, were interspersed among the segment-specific cells of the remainder of the distal convolution, and of the CCD. The basolateral calcium extruding proteins, Na-Ca exchanger (NCX), and the plasma membrane Ca2+-ATPase were found all along the distal convolution, and, in contrast to other species, along the CCD, although in varying amounts. The knowledge regarding the precise distribution patterns of transport proteins in the human distal nephron and the knowledge regarding the differences from that in laboratory animals may be helpful for diagnostic purposes and may also help refine the therapeutic management of electrolyte disorders. C1 Univ Zurich, Inst Anat, Dept Anat, Div Vegetat Anat, CH-8057 Zurich, Switzerland. Univ Strasbourg 1, CNRS, UMR 7519, Strasbourg, France. NHLBI, Bethesda, MD 20892 USA. Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06510 USA. RP Kaissling, B (reprint author), Univ Zurich, Inst Anat, Dept Anat, Div Vegetat Anat, Winterthurerstr 190, CH-8057 Zurich, Switzerland. FU Intramural NIH HHS [Z99 HL999999, Z01 HL001285-21] NR 59 TC 88 Z9 89 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD APR PY 2002 VL 13 IS 4 AR UNSP 1046/6673/1304-0836 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA 535CM UT WOS:000174627700004 PM 11912242 ER PT J AU Schrump, DS Zhai, SP Nguyen, DM Weiser, TS Fisher, BA Terrill, RE Flynn, BM Duray, PH Figg, WD AF Schrump, DS Zhai, SP Nguyen, DM Weiser, TS Fisher, BA Terrill, RE Flynn, BM Duray, PH Figg, WD TI Pharmacokinetics of paclitaxel administered by hyperthermic retrograde isolated lung perfusion techniques SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID NONLINEAR PHARMACOKINETICS; PULMONARY METASTASES; CREMOPHOR EL; PHASE-II; DRUG; INFUSION; SARCOMA; CANCER; TAXOL; CELLS AB Objective: Although paclitaxel is widely used as a systemic agent for the treatment of solid tumors, limited information is available concerning administration of this taxane by regional techniques. The present study was undertaken to evaluate the pharmacokinetics and acute toxicity of paclitaxel administered by hyperthermic retrograde isolated lung perfusion techniques to ascertain its potential for the regional therapy of unresectable pulmonary neoplasms. Methods: Adult sheep underwent 90 minutes of retrograde isolated lung perfusion with escalating doses of paclitaxel and moderate hyperthermia using a protein-free, oxygenated extracorporeal circuit and a steady perfusion pressure of 14 to 16 mm Hg. An additional animal received paclitaxel by means of 1-hour central venous infusion. Paclitaxel concentrations in lung tissues, perfusates, and systemic circulation were determined by high-performance liquid chromotography techniques. Cytotoxicity of paclitaxel in cancer cells and in normal human bronchial epithelial cells was evaluated in vitro using 4, 5-dimethylthiazo-2-yl-25-dipagnyl tetrazolium bromide assays. Lung tissues were examined by hematoxylin-and-eosin techniques. Results: Paclitaxel concentrations (maximum concentration and area under the plasma concentration time curve) in perfused tissues increased with escalating perfusate doses. Uptake of drug into lung parenchyma appeared saturable at high paclitaxel exposure; a substantial pharmacokinetic advantage was observed. Paclitaxel concentrations in systemic circulation were undetectable or exceedingly low after perfusion. Histopathologic examination of lung tissues harvested 3 hours after completion of isolated lung perfusion revealed no immediate toxicity, even at a paclitaxel exposure 20-fold higher than that achievable after 1 hour of intravenous administration at the maximum tolerable dose in human subjects. Moderate hyperthermia enhanced paclitaxel-mediated cytotoxicity 5- to 100-fold in cultured cancer lines. No paclitaxel toxicity was observed in cultured normal human bronchial epithelial cells after exposure to paclitaxel under normothermic or hyperthermic conditions. Conclusions: These data support further evaluation of paclitaxel administered by hyperthermic retrograde isolated lung perfusion techniques for the treatment of unresectable malignant pulmonary tumors. C1 NCI, Thorac Oncol Sect, Surg Branch, NIH, Bethesda, MD 20892 USA. NCI, Clin Pharmacokinet Sect, Med Branch, NIH, Bethesda, MD 20892 USA. NCI, Anat Pathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA. NCI, Anim Sci Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Schrump, DS (reprint author), Bldg 10,Room 2B-07,10 Canc Dr, Bethesda, MD 20892 USA. RI Figg Sr, William/M-2411-2016 NR 41 TC 19 Z9 20 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD APR PY 2002 VL 123 IS 4 BP 686 EP 694 DI 10.1067/mtc.2002.120713 PG 9 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA 548QL UT WOS:000175400100012 PM 11986596 ER PT J AU Malone, FD Ball, RH Berkowitz, RL Bianchi, DW Carr, SR Comstock, CH Craigo, SD D'Alton, ME de la Cruz, F Dugoff, L Gross, SJ Hankins, GD Hobbins, JC Merkatz, IR Nyberg, DA Saade, GR Timor-Tritsch, IE Wolfe, HM AF Malone, FD Ball, RH Berkowitz, RL Bianchi, DW Carr, SR Comstock, CH Craigo, SD D'Alton, ME de la Cruz, F Dugoff, L Gross, SJ Hankins, GD Hobbins, JC Merkatz, IR Nyberg, DA Saade, GR Timor-Tritsch, IE Wolfe, HM CA FASTER Trial Res Consortium TI First-trimester nuchal translucency screening SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Letter C1 Columbia Presbyterian Med Ctr, New York, NY USA. Univ Utah Hosp, Salt Lake City, UT USA. Mt Sinai Med Ctr, New York, NY USA. Tufts Univ New England Med Ctr, Boston, MA USA. Women & Infants Hosp Rhode Isl, Providence, RI USA. William Beaumont Hosp, Royal Oak, MI USA. Tufts Univ New England Med Ctr, Boston, MA 02111 USA. Natl Inst Child Hlth & Human Dev, Bethesda, MD USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Albert Einstein Coll Med, Bronx, NY USA. Univ Texas, Med Branch, Galveston, TX USA. Swedish Med Ctr, Seattle, WA USA. Univ Texas, Med Branch, Galveston, TX 77550 USA. New York Univ, Med Ctr, New York, NY USA. Univ N Carolina, Chapel Hill, NC 27515 USA. RP Malone, FD (reprint author), Columbia Presbyterian Med Ctr, New York, NY USA. RI Malone, Fergal/D-6233-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 USA SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD APR PY 2002 VL 21 IS 4 BP 481 EP 483 PG 3 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA 534AP UT WOS:000174562700017 ER PT J AU Fletcher, DW Miller, DL Balter, S Taylor, MA AF Fletcher, DW Miller, DL Balter, S Taylor, MA TI Comparison of four techniques to estimate radiation dose to skin during angiographic and interventional radiology procedures SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE radiation dose; skin, effects of irradiation on ID FLUOROSCOPICALLY GUIDED PROCEDURES; AREA PRODUCT; CARDIAC-CATHETERIZATION; INJURIES; PATIENT; EXPOSURE; CARDIOLOGY AB PURPOSE: Four techniques used to estimate radiation risk were compared to determine whether commonly used dosimetry measurements permit reliable estimates of skin dose. Peak skin dose (PSD) is known to be the most reliable estimate of risk to skin. The purpose of this study is to determine peak skin dose with use of real-time software measurements and to correlate other measures of dose with PSD. MATERIALS AND METHODS: Two hundred twelve patients undergoing arch aortography and bilateral carotid arteriography (referred to as "carotid"), abdominal aortography and bilateral lower extremity runoff ("runoff"), or tunneled chest wall port placement ("port") were studied. Fluoroscopy time, dose-area product (DAP), and cumulative dose at the interventional reference point were recorded for all procedures; PSD was recorded for a subset of 105 procedures. The dose index, defined as the ratio between PSD and cumulative dose, was also determined. RESULTS: In general, correlation values for comparisons between fluoroscopy time and the other measures of dose (r = .29 to .78) were lower than values for comparisons among DAP, cumulative dose, and PSD (r = .52 to .94). For all procedures, pair-wise correlations between DAP, cumulative skin dose, and PSD were statistically significant (P < .01) The ratio between PSD and cumulative skin dose (dose index) was significantly different for ports versus other procedures (carotid, Z = 4.62, P < .001; runoff, Z = 4.52, P < .001), but carotid and runoff procedures did not differ significantly in this regard (Z = 0.746, P = .22). Within each individual procedure type, the range of values for the dose index varied 156.7-fold for carotid arteriography, 3.2-fold for chest ports, and 175-fold for aortography and runoff. CONCLUSION: Fluoroscopy time is a poor predictor of risk because it does not correlate well with PSD. Cumulative dose and DAP are not good analogues of PSD because of weak correlations for some procedures and because of wide variations in the dose index for all procedures. C1 Uniformed Serv Univ Hlth Sci, F Edward Hebert Sch Med, Dept Radiol & Nucl Med, Bethesda, MD 20814 USA. Natl Naval Med Res Inst, Dept Radiol, Bethesda, MD USA. NCI, Med Branch, Canc Res Ctr, Bethesda, MD 20892 USA. Lenox Hill Hosp, Dept Radiol, New York, NY 10021 USA. RP Fletcher, DW (reprint author), Uniformed Serv Univ Hlth Sci, Dept Radiol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA. EM dfletcher@usuhs.mil NR 26 TC 73 Z9 79 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1051-0443 J9 J VASC INTERV RADIOL JI J. Vasc. Interv. Radiol. PD APR PY 2002 VL 13 IS 4 BP 391 EP 397 DI 10.1016/S1051-0443(07)61742-4 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA 545GP UT WOS:000175209000007 PM 11932370 ER PT J AU Boyer, PL Sarafianos, SG Arnold, E Hughes, SH AF Boyer, PL Sarafianos, SG Arnold, E Hughes, SH TI The M184V mutation reduces the selective excision of zidovudine 5 '-monophosphate (AZTMP) by the reverse transcriptase of human immunodeficiency virus type 1 SO JOURNAL OF VIROLOGY LA English DT Article ID AMINO-ACID SUBSTITUTIONS; RESISTANCE MUTATIONS; COMBINATION THERAPY; HIV-1 RESISTANCE; DRUG-RESISTANCE; DNA-SYNTHESIS; INHIBITORS; MECHANISM; PROCESSIVITY; REPLICATION AB The M184V mutation in human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) causes resistance to lamivudine, bat it. also increases the sensitivity of the virus to zidovudine (3'-azido-3'-deoxythymidine; AZT). This sensitization to AZT is seen both in the presence and the absence of the mutations that confer resistance to AZT. AZT resistance is due to enhanced excision of AZT 5'-monophosphate (AZTMP) from the end of the primer by the RT of the resistant virus. Published data suggest that the excision reaction involves pyrophosphorolysis but that the likely in vivo pyrophosphate donor is not pyrophosphate but ATP. The mutations that lead to AZT resistance enhance ATP binding and, in so doing, enhance pyrophosphorolysis. The excision reaction is specific for AZT because HIV-1 RT, which can form a closed complex with a dideoxy-terminated primer and an incoming deoxynucleoside triphosphate (dNTP), does not form the closed complex with an AZTMP-terminated primer and an incoming dNTP. This means that an AZTMP-terminated primer has better access to the site where it can be excised. The M184V mutation alters the polymerase active site in a fashion that specifically interferes with ATP-mediated excision of AZTMP from the end of the primer strand. The M184V mutation does not affect the incorporation of AZT 5'-triphosphate (AZTTP), either in the presence or the absence of mutations that enhance AZTMP excision. However, in the presence of ATP, the M184V mutation does decrease the ability of HIV-1 RT to carry out AZTMP excision. Based on these results, and on the results of other excision experiments, we present a model to explain how the M184V mutation affects AZTMP excision. C1 NCI, FCRDC, HIV Drug Resistance Program, Frederick, MD 21702 USA. Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Chem, Piscataway, NJ 08854 USA. RP Hughes, SH (reprint author), NCI, FCRDC, HIV Drug Resistance Program, POB B,Bldg 539,Room 130A, Frederick, MD 21702 USA. OI Sarafianos, Stefan G/0000-0002-5840-154X FU NIAID NIH HHS [AI 27690, R37 AI027690]; NIGMS NIH HHS [GM 55609] NR 26 TC 71 Z9 74 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 2002 VL 76 IS 7 BP 3248 EP 3256 DI 10.1128/JVI.76.7.3248-3256.2002 PG 9 WC Virology SC Virology GA 529ZE UT WOS:000174330500017 PM 11884549 ER PT J AU Grundner, C Mirzabekov, T Sodroski, J Wyatt, R AF Grundner, C Mirzabekov, T Sodroski, J Wyatt, R TI Solid-phase proteoliposomes containing human immunodeficiency virus envelope glycoproteins SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN MONOCLONAL-ANTIBODY; CD4 BINDING-SITE; HIV-1 GP120; NEUTRALIZING ANTIBODY; ATOMIC-STRUCTURE; MEMBRANE-FUSION; TYPE-1; GP41; PROTEIN; INFECTION AB The human immunodeficiency virus type 1 (HIV-1) exterior envelope glycoprotein gp120 mediates receptor binding and is the major target for neutralizing antibodies. A broadly neutralizing antibody response is likely to be a critical component of the immune response against HIV-1. Although antibodies against monomeric gp120 are readily elicited in immunized individuals, these antibodies are inefficient in neutralizing primary HIV-1 isolates. As a chronic pathogen, HIV-1 has evolved to avoid an optimal host response by a number of immune escape mechanisms. Monomeric gp120 that has dissociated from the functional trimer presents irrelevant epitopes that are not accessible on functional trimeric envelope glycoproteins. The resulting low level of antigenic cross-reactivity between monomeric gp120 and the functional spike may contribute to the inability of monomeric gp120 to elicit broadly neutralizing antibodies. Attempts to generate native, trimeric envelope glycoproteins as immunogens have been frustrated by both the lability of the gp120-gp41 interaction and the weak association between gp120 subunits. Here, we present solid-phase HIV-1 gp160DeltaCT (cytoplasmic tail-deleted) proteoliposomes (PLs) containing native, trimeric envelope glycoproteins in a physiologic membrane setting. We present data that indicate that the gp160DeltaCT glycoproteins on PLs are trimers and are recognized by several relevant conformational ligands in a manner similar to that for gp160DeltaCT oligomers expressed on the cell surface. The PLs represent a significant advance over present envelope glycoprotein formulations as candidate immunogens for HIV vaccine design and development. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Div AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Wyatt, R (reprint author), NIH, Struct Virol Sect, Vaccine Res Ctr, 40 Convent Dr,Bldg 40,Room 4512, Bethesda, MD 20892 USA. FU NIAID NIH HHS [P30 AI028691, 1R21AI-44328-02, 5R21AI-44328-02, AI 31783, AI28691, R01 AI031783] NR 50 TC 77 Z9 79 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 2002 VL 76 IS 7 BP 3511 EP 3521 DI 10.1128/JVI.76.7.3511-3521.2002 PG 11 WC Virology SC Virology GA 529ZE UT WOS:000174330500043 PM 11884575 ER PT J AU Sato, H Pesnicak, L Cohen, JI AF Sato, H Pesnicak, L Cohen, JI TI Varicella-zoster virus open reading frame 2 encodes a membrane phosphoprotein that is dispensable for viral replication and for establishment of latency SO JOURNAL OF VIROLOGY LA English DT Article ID ORF47 PROTEIN-KINASE; DNA-SEQUENCE; TRIGEMINAL GANGLIA; IN-VITRO; VZV; INFECTION; TRANSCRIPTION; HERPESVIRUS-1; PARTICLES; HOMOLOG AB Varicella-zoster virus (VZV) encodes six genes that do not have homologs in herpes simplex virus. One of these genes, VZV open reading frame 2 (ORF2), was expressed as a 31-kDa phosphoprotein in the membranes of infected cells. Unlike equine and bovine herpesvirus type 1 ORF2 homologs that are associated with virions, VZV virions contained no detectable ORF2 protein. The ORF2 deletion mutant established a latent infection in cotton rats at a frequency and with a number of VZV genomes similar to that of the parental virus. ORF63 transcripts, a hallmark of latent infection, were present in ganglia latently infected with both the ORF2 deletion mutant and parental VZV. Thus, ORF2 is the first VZV gene shown to be dispensable for establishment of latent infection in an animal model. C1 NIAID, Med Virol Sect, Clin Invest Lab, NIH, Bethesda, MD 20892 USA. RP Cohen, JI (reprint author), NIAID, Med Virol Sect, Clin Invest Lab, NIH, Bldg 10,Rm 11N228,10 Ctr Dr, Bethesda, MD 20892 USA. NR 30 TC 35 Z9 37 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 2002 VL 76 IS 7 BP 3575 EP 3578 DI 10.1128/JVI.76.7.3575-3578.2002 PG 4 WC Virology SC Virology GA 529ZE UT WOS:000174330500051 PM 11884583 ER PT J AU Milner, JA AF Milner, JA TI Botanicals: The latest evidence-based finding SO JOURNAL OF WOMENS HEALTH & GENDER-BASED MEDICINE LA English DT Meeting Abstract C1 NCI, Div Canc Prevent, Nutrit Sci Res Grp, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1524-6094 J9 J WOMEN HEALTH GEN-B JI J. WOMENS HEALTH GENDER-BASED MED. PD APR PY 2002 VL 11 IS 3 MA S22 BP 315 EP 315 PG 1 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Obstetrics & Gynecology; Women's Studies SC Public, Environmental & Occupational Health; General & Internal Medicine; Obstetrics & Gynecology; Women's Studies GA 546YB UT WOS:000175303000036 ER PT J AU Picciano, MF AF Picciano, MF TI Vitamins and minerals in women's health - What you need to know about supplementation SO JOURNAL OF WOMENS HEALTH & GENDER-BASED MEDICINE LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1524-6094 J9 J WOMEN HEALTH GEN-B JI J. WOMENS HEALTH GENDER-BASED MED. PD APR PY 2002 VL 11 IS 3 MA S25 BP 315 EP 315 PG 1 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Obstetrics & Gynecology; Women's Studies SC Public, Environmental & Occupational Health; General & Internal Medicine; Obstetrics & Gynecology; Women's Studies GA 546YB UT WOS:000175303000039 ER PT J AU Perentes, Y Chan, CC Bovey, E Uffer, S Herbort, CP AF Perentes, Y Chan, CC Bovey, E Uffer, S Herbort, CP TI Massive vascular endothelium growth factor (VEGF) expression in Eales' disease SO KLINISCHE MONATSBLATTER FUR AUGENHEILKUNDE LA English DT Article DE Eales' disease; vascular endothelial growth factor (VEGF) ID MEMBRANES; CELLS AB Background: Eales' disease is an idiopathic retinal vasculitic and vaso-occlusive process complicated by extensive retinal neovascularisation and vitreous hemorrhages. The great propensity to produce retinal neovessels is one of the particular aspects of the disease that deserves to be further investigated. We report a case of Eales' disease having evolved over more than three decades, with a typical clinical presentation in one eye, while the other eye had to be enucleated because of a terminal neovascular glaucoma, thus allowing pathological examination. Methods: The functional right eye was treated by vitrectomy, cerclage, cryocoagulation and endolaser. The non-functional phthtic left eye was enucleated and submitted for histopathological and immunohistochemical examination using antibodies against vascular endothelial growth factor, T-cells, B-cells and Muller cells. Results: Evolution was favourable in the operated right eye, following management of the inflammatory reaction. The histopathological examination of the left eye revealed an occlusion of the anterior chamber angle by rubeosis iridis, tractional retinal detachments, pre-, intra- and sub-retinal neovascular membranes, and vitrous hemorrhages. Diffuse positive anti-VEGF immunostaining was found at the level of the retinal neovascular membranes. The retina exhibited prominent Muller cell immunostaining, indicating extensive gliosis, and predominantly B cell infiltrates were found in the eye. Conclusion: The present study indicates a close relationship between the prominent neovascular proliferation in Eales' disease and the intense expression of VEGF. The increased expression of VEGF, when compared to other conditions inducing neovascularisation, might explain the severity of neovascular growth and the propensity of repeated vitrous hemorrhages in Eales' disease. C1 La Source Eye Ctr, CH-1004 Lausanne, Switzerland. Univ Lausanne, Lausanne, Switzerland. NEI, Inst Hlth, Immunol Lab, Bethesda, MD 20892 USA. Univ Lausanne, Dept Ophthalmol, Lausanne, Switzerland. RP Herbort, CP (reprint author), La Source Eye Ctr, 2 Ave Bergieres, CH-1004 Lausanne, Switzerland. NR 11 TC 18 Z9 23 U1 1 U2 1 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0023-2165 J9 KLIN MONATSBL AUGENH JI Klinische Monatsblat. Augenheilkunde PD APR PY 2002 VL 219 IS 4 BP 311 EP 314 DI 10.1055/s-2002-30662 PG 4 WC Ophthalmology SC Ophthalmology GA 560UJ UT WOS:000176099500030 PM 12022026 ER PT J AU Blagosklonny, MV AF Blagosklonny, MV TI Hsp-90-associated oncoproteins: multiple targets of geldanamycin and its analogs SO LEUKEMIA LA English DT Review DE molecular therapeutics; geldanamycin; oncogenes; heat shock proteins ID BREAST-CANCER CELLS; CHRONIC MYELOID-LEUKEMIA; ANTICANCER DRUG TARGETS; HEAT-SHOCK PROTEINS; CHEMOTHERAPY-INDUCED APOPTOSIS; K562 ERYTHROLEUKEMIC CELLS; TYROSINE KINASE INHIBITOR; SCHEDULE-DEPENDENT MANNER; TUMOR BIOLOGY MATTERS; BCR-ABL AB Geldanamycin (GA), herbimycin A and radicicol bind heat-shock protein-90 (Hsp90) and destabilize its client proteins including v-Src, Bcr-Abl, Raf-1, ErbB2, some growth factor receptors and steroid receptors. Thus, Hsp90-active agents induce ubiquitination and proteasomal degradation of numerous oncoproteins, Depending on the cellular context, HSP90-active agents cause growth arrest, differentiation and apoptosis, or can prevent apoptosis. HSP-active agents are undergoing clinical trials. Like targets of most chemotherapeutics, Hsp90 is not a cancer-specific protein. By attacking a nonspecific target, HSP-90-active compounds still may preferentially kill certain tumor cells. How can this be achieved? How can therapeutic potentials be exploited? This article starts the discussion. C1 NIH, Bethesda, MD 20892 USA. New York Med Coll, Dept Med, Valhalla, NY 10595 USA. RP Blagosklonny, MV (reprint author), NIH, Bldg 10,R12 N226, Bethesda, MD 20892 USA. NR 116 TC 190 Z9 203 U1 1 U2 7 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 2002 VL 16 IS 4 BP 455 EP 462 DI 10.1038/sj/leu/2402415 PG 8 WC Oncology; Hematology SC Oncology; Hematology GA 545AA UT WOS:000175193000004 PM 11960322 ER PT J AU Monga, M Sausville, EA AF Monga, M Sausville, EA TI Developmental Therapeutics Program at the NCI: molecular target and drug discovery process SO LEUKEMIA LA English DT Review DE drug development; Developmental Therapeutics Program; drug discovery; molecular target ID CHRONIC LYMPHOCYTIC-LEUKEMIA; NATIONAL-CANCER-INSTITUTE; TUMOR-CELL-LINES; FLAVOPIRIDOL INDUCES APOPTOSIS; DEPENDENT KINASE INHIBITOR; PHASE-I TRIAL; REFRACTORY NEOPLASMS; VIVO; PHARMACOLOGY; SCREEN AB As the drug discovery and developmental arm of the National Cancer Institute (NCI), the Developmental Therapeutics Program (DTP) plans, conducts and facilitates development of therapeutic agents for cancer and AIDS. DTP's goal is to turn,molecules into medicine for the public health'. Areas of support by DTP are discovery, development and pathways to development for the intramural and the extramural community. The Developmental Therapeutics Program (DTP) operates a repository of synthetic and pure natural products, which are evaluated as potential anticancer agents. The repository derives from a historical database of greater than 600 000 compounds, which have been supplied to DTP from a variety of sources worldwide. The in vitro anti-cancer drug cell line screen established at DTP is unique in several respects. It has changed the NCI emphasis from a compound-oriented drug discovery effort to a disease-panel oriented exercise, emphasized human tumor cells derived from solid tumors, developed a high volume screening method that can adapt to processing of numerous chemical agents or natural source-derived extracts, that has minimized the use of animals, and saved on the amount of material required for the initial screening. The hallow fiber assay created at the DTP has demonstrated the ability to provide quantitative initial indices of in vivo drug efficacy, with minimum expenditures of time and materials and is currently being utilized as the initial in vivo experience for agents found to have reproducible activity in the in vitro anticancer drug screen. Drugs showing activity with unique mechanisms of actions are being further developed for treatment of hematopoietic neoplasms, prominent examples being flavopiridol, UCN-01 and depsipeptide among others. C1 NCI, Dev Therapeut Program, Div Canc Treatment & Diagnosis, NIH, Rockville, MD 20852 USA. RP Sausville, EA (reprint author), NCI, Dev Therapeut Program, Div Canc Treatment & Diagnosis, NIH, Execut Plaza N,Room 8018,6130 Execut Blvd, Rockville, MD 20852 USA. NR 30 TC 85 Z9 89 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 2002 VL 16 IS 4 BP 520 EP 526 DI 10.1038/sj/leu/2402464 PG 7 WC Oncology; Hematology SC Oncology; Hematology GA 545AA UT WOS:000175193000010 PM 11960328 ER PT J AU Blagosklonny, MV AF Blagosklonny, MV TI STI-571 must select for drug-resistant cells but 'no cell breathes fire out of its nostrils like a dragon' SO LEUKEMIA LA English DT Review DE STI-571; Bcr-Abl; leukemia; drug resistance; selective therapy ID ABL TYROSINE KINASE; CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; INHIBITOR STI571; PHILADELPHIA-CHROMOSOME; GENETIC INSTABILITY; AMPLIFICATION; GELDANAMYCIN; SENSITIVITY; DISEASE AB Seemingly disappointing, the Bcr-Abl kinase inhibitor STI-571 shares an 'unfortunate' characteristic with conventional cancer drugs: the development of drug resistance. I argue that the resistance must develop even faster to STI-571 than to conventional drugs, because STI-571 is so effective. This is predictable, but is it inevitable? And how do mechanisms of resistance in relapse depend on a degree of remission. In addition to mutation rate and number of tumor cells, one additional factor determines relapse vs 'extinction' of the leukemia cell population. C1 NCI, Med Branch, NIH, Bethesda, MD 20892 USA. New York Med Coll, Dept Med, Valhalla, NY 10595 USA. RP Blagosklonny, MV (reprint author), NCI, Med Branch, NIH, Bldg 10 Room 12 N 226, Bethesda, MD 20892 USA. NR 22 TC 28 Z9 30 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 2002 VL 16 IS 4 BP 570 EP 572 DI 10.1038/sj/leu/2402409 PG 3 WC Oncology; Hematology SC Oncology; Hematology GA 545AA UT WOS:000175193000016 PM 11960334 ER PT J AU Wells, RJ Arthur, DC Srivastava, A Heerema, NA Le Beau, M Alonzo, TA Buxton, AB Woods, WG Howells, WB Benjamin, DR Betcher, DL Buckley, JD Feig, SA Kim, T Odom, LF Ruymann, FB Smithson, WA Tannous, R Whitt, JK Wolff, L Tjoa, T Lampkin, BC AF Wells, RJ Arthur, DC Srivastava, A Heerema, NA Le Beau, M Alonzo, TA Buxton, AB Woods, WG Howells, WB Benjamin, DR Betcher, DL Buckley, JD Feig, SA Kim, T Odom, LF Ruymann, FB Smithson, WA Tannous, R Whitt, JK Wolff, L Tjoa, T Lampkin, BC TI Prognostic variables in newly diagnosed children and adolescents with acute myeloid leukemia: Children's Cancer Group Study 213 SO LEUKEMIA LA English DT Article DE childhood acute myeloid leukemia; prognostic factors ID ACUTE MYELOGENOUS LEUKEMIA; PEDIATRIC-ONCOLOGY-GROUP; ACUTE NONLYMPHOCYTIC LEUKEMIA; CHROMOSOMAL-ABNORMALITIES; DOWN-SYNDROME; THERAPY; REGRESSION; BIOLOGY; AML AB The objective of this study was to identify biologic parameters that were associated with either exceptionally good or poor outcome in childhood acute myeloid leukemia (AML). Among the children with AML who entered Children's Cancer Group trial 213, 498 patients without Down syndrome or acute promyelocytic leukemia (APL) comprise the basis for this report. Univariate comparisons of the proportion of patients attaining complete remission after induction (CR) indicate that, at diagnosis, male gender, low platelet count (less than or equal to20 000/mul), hepatomegaly, myelodysplastic syndrome (MDS), French-American-British (FAB) category M5, high (>15%) bone marrow BM blasts on day 14 of the first course of induction, and +8 are associated with lower CR rates, while abnormal 16 is associated with a higher CR rate. Multivariate analysis suggests high platelet count at diagnosis (>20 000/mul), absence of hepatomegaly, less than or equal to15% day 14 BM blast percentage, and abnormal 16 are independent prognostic factors associated with better CR. Univariate analysis demonstrated a significant favorable relationship between platelet count at diagnosis (>20 000/mul), absence of hepatomegaly, low percentage of BM blasts (less than or equal to15%), and abnormal 16 with overall survival. Absence of hepatomegaly, less than or equal to15% day 14 BM blast percentage, and abnormal 16 were determined to be independent prognostic factors associated with better survival. C1 Univ Cincinnati, Med Ctr, Childrens Hosp Res Fdn, Cincinnati, OH 45267 USA. NCI, Pathol Lab, Bethesda, MD 20892 USA. Univ Cincinnati, Ctr Med, Cincinnati, OH USA. Parker Hughes Inst, St Paul, MN USA. Univ Chicago, Chicago, IL 60637 USA. Univ S Carolina, S Carolina Canc Ctr, Columbia, SC 29208 USA. Univ So Calif, Keck Sch Med, Los Angeles, CA USA. Childrens Hosp, Med Ctr, Seattle, WA USA. Mayo Med Ctr, Rochester, MN USA. Univ Calif Los Angeles, Los Angeles, CA USA. Abbott NW Hosp, Virginia Piper Canc Inst, Minneapolis, MN 55407 USA. Univ Colorado, Ctr Canc, Denver, CO 80202 USA. Childrens Hosp, Denver, CO 80218 USA. Childrens Hosp Columbus, Columbus, OH USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Iowa, Iowa City, IA USA. Univ N Carolina, Chapel Hill, NC USA. Oregon Hlth Sci Univ, Doernbecher Childrens Hosp, Portland, OR 97201 USA. Childrens Oncol Grp, Operat Ctr, Arcadia, CA USA. RP Wells, RJ (reprint author), Childrens Oncol Grp, POB 60012, Arcadia, CA 91066 USA. FU NCI NIH HHS [CA36015, CA07306, CA03750, CA26270, CA02649, CA10198, CA11796, CA03888, CA13809, CA29013, CA28882, CA26126, CA03526, CA20320, CA2G044, CA05436, CA13539, CA10382, CA17829, CA29314, CA27678, CA14560, CA42764, CA02971, CA28851] NR 28 TC 27 Z9 29 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 2002 VL 16 IS 4 BP 601 EP 607 DI 10.1038/sj/leu/2402390 PG 7 WC Oncology; Hematology SC Oncology; Hematology GA 545AA UT WOS:000175193000021 PM 11960339 ER PT J AU Rojas, CV Greiner, RS Fuenzalida, LC Martinez, JI Salem, N Uauy, R AF Rojas, CV Greiner, RS Fuenzalida, LC Martinez, JI Salem, N Uauy, R TI Long-term n-3 FA deficiency modifies peroxisome proliferator-activated receptor beta mRNA abundance in rat ocular tissues SO LIPIDS LA English DT Article ID POLYUNSATURATED FATTY-ACIDS; RETINOID-X-RECEPTOR; GENE-EXPRESSION; DOCOSAHEXAENOIC ACID; ADIPOCYTE DIFFERENTIATION; PPAR-GAMMA; ARACHIDONIC-ACID; ADIPOSE-TISSUE; VISUAL-ACUITY; DIETARY-FAT AB Peroxisomal proliferator-activated receptors (PPAR) are a FA-response system involved in diverse cellular responses. FA regulate PPAR activity and modulate PPAR mRNA abundance. Increasing evidence indicates that PUFA are required for optimal neuronal development and function. To gain insight into the mechanism for nutrition-induced impairment of neuronal development and function we investigated the effect of chronic n-3 FA deficiency on PPAR mRNA levels in rat brain and ocular tissues. Rats were fed for three generations a diet designed to reduce DHA levels in tissues, and the abundance of PPARalpha and PPARbeta transcripts was measured by hybridization with specific probes. Chronic consumption of the alpha-linolenic acid (LNA)-insufficient diet caused a remarkable modification in DHA content in membrane phospholipids. The results reported here indicate that PPARalpha mRNA levels did not exhibit significant variation in ocular, hepatic, or nervous tissues from rats fed the experimental diet, In contrast, PPARbeta mRNA normalized to beta-actin mRNA was 21% higher in ocular tissue from F3 generation rats consuming the LNA-deficient diet but was independent of diet in hepatic and nervous tissues. The absolute abundance of PPARbeta transcripts shoved a 17% increase in ocular tissue from rats consuming the LNA-deficient diet (F3 generation). The biological significance of the reported changes in PPARbeta mRNA in ocular tissue remains to be determined. C1 Univ Chile, INTA, Santiago, Chile. NIAAA, Div Intramural Clin & Biol Res, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RP Rojas, CV (reprint author), Univ Chile, INTA, Casilla 138-11, Santiago, Chile. NR 60 TC 16 Z9 16 U1 0 U2 3 PU AMER OIL CHEMISTS SOC A O C S PRESS PI CHAMPAIGN PA 1608 BROADMOOR DRIVE, CHAMPAIGN, IL 61821-0489 USA SN 0024-4201 J9 LIPIDS JI Lipids PD APR PY 2002 VL 37 IS 4 BP 367 EP 374 DI 10.1007/s1145-002-0904-4 PG 8 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA 547CZ UT WOS:000175316600005 PM 12030317 ER PT J AU Casibang, M Moody, TW AF Casibang, M Moody, TW TI AH6809 antagonizes non-small cell lung cancer prostaglandin receptors SO LUNG CANCER LA English DT Article DE PGE(2); receptor binding; NSCLC; AH6809; proliferation ID AUTOCRINE GROWTH-FACTORS; BOMBESIN-LIKE PEPTIDES; PROSTANOID RECEPTORS; COLON CARCINOGENESIS; MESSENGER-RNAS; EP(2) SUBTYPE; EXPRESSION; CLONING; INHIBITION; MICE AB The effects of prostaglandin (PG)E-2 on lung cancer cells were investigated. H-3-PGE, bound with high affinity to membranes derived from small cell lung cancer (SCLC) and non-SCLC (NSCI-C) cell lines. Using NSCLC NCI-H1299 membranes, specific H-3-PGE, binding to NCI-H1299 membranes was inhibited with moderate affinity by PGE(2), PGE(1), PGF(2alpha) and 6-isopropoxy-9-xanthone-2-carboxylic acid (AH6809) but not PGD(2), LTB4 or 5-HETE. By RT-PCR, EP2 receptor PCR products were detected in extracts derived from lung cancer cells. PGE(2) caused cAMP elevation in a concentration-dependent manner using NCI-H1299 cells and the increase in cAMP caused by PGE(2) was antaconized by AH6809. PGE(2) had no effect on cytosolic Ca2+ but PGE(2) caused increased c-fos mRNA in NCI-H1299 cells. AH6809 inhibited the proliferation of NCI-H1299 cells using MTT and clonogenic assays. These results indicate that functional PG receptors are present on NSCLC cells which are antagonized by AH6809. Published by Elsevier Science Ireland Ltd. C1 NCI, Cell & Canc Biol Dept, Med Branch, Rockville, MD 20850 USA. RP Moody, TW (reprint author), NCI, Cell & Canc Biol Dept, Med Branch, Bldg KWC,Rm 300,9610 Med Ctr Dr, Rockville, MD 20850 USA. NR 40 TC 10 Z9 10 U1 1 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-5002 J9 LUNG CANCER-J IASLC JI Lung Cancer PD APR PY 2002 VL 36 IS 1 BP 33 EP 42 AR PII S0169-5002(01)00476-7 DI 10.1016/S0169-5002(01)00476-7 PG 10 WC Oncology; Respiratory System SC Oncology; Respiratory System GA 549QP UT WOS:000175456100007 PM 11891031 ER PT J AU Herzka, DA Kellman, P Aletras, AH Guttman, MA McVeigh, ER AF Herzka, DA Kellman, P Aletras, AH Guttman, MA McVeigh, ER TI Multishot EPI-SSFP in the heart SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE cardiac imaging; fast magnetic resonance imaging; SSFP; FISP; EPI; SENSE; ghost artifacts ID PULSE SEQUENCES; FREE-PRECESSION; ECHO; SIGNAL; IMAGES; NOISE; SENSITIVITY; ARTIFACTS; MRI AB Refocused steady-state free precession (SSFP), or fast imaging with steady precession (FISP or TrueFISP), has recently proven valuable for cardiac imaging because of its high signal-to-noise ratio (SNR) and excellent blood-myocardium contrast. In this study, various implementations of multiecho SSFP or EPI-SSFP for imaging in the heart are presented. EPI-SSFP has higher scan-time efficiency than single-echo SSFP, as two or more phase-encode lines are acquired per repetition time (TR) at the cost of a modest increase in TR. To minimize TR, a noninterleaved phase-encode order in conjunction with a phased-array ghost elimination (PAGE) technique was employed, removing the need for echo time shifting (ETS). The multishot implementation of EPI-SSFP was used to decrease the breath-hold duration for cine acquisitions or to increase the temporal or spatial resolution for a fixed breath-hold duration. The greatest gain in efficiency was obtained with the use of a three-echo acquisition. Image quality for cardiac cine applications using multishot EPI-SSFP was comparable to that of single-echo SSFP in terms of blood-myocardium contrast and contrast-to-noise ratio (CNR). The PAGE method considerably reduced flow artifacts due to both the inherent ghost suppression and the concomitant reduction in phase-encode blip size. The increased TR of multishot EPI-SSFP led to a reduced specific absorption rate (SAR) for a fixed RF flip angle, and allowed the use of a larger flip angle without increasing the SAR above the FDA-approved limits. Published 2002 Wiley-Liss, Inc. C1 NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA. RP Herzka, DA (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bldg 10,10 Ctr Dr,MSC-1061,B1D416, Bethesda, MD 20892 USA. OI Aletras, Anthony/0000-0002-3786-3817; Herzka, Daniel/0000-0002-9400-7814 FU Intramural NIH HHS [Z01 HL004608-08] NR 35 TC 28 Z9 28 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD APR PY 2002 VL 47 IS 4 BP 655 EP 664 DI 10.1002/mrm.10105 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 534NP UT WOS:000174592700006 PM 11948726 ER PT J AU Gach, HM Kam, AW Reid, ED Talagala, SL AF Gach, HM Kam, AW Reid, ED Talagala, SL TI Quantitative analysis of adiabatic fast passage for steady laminar and turbulent flows SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE arterial spin labeling; adiabatic fast passage; inversion efficiency; steady flow; labeling duty cycle ID CEREBRAL BLOOD-FLOW; PULSATILE VELOCITY-MEASUREMENTS; HUMAN ABDOMINAL-AORTA; ARTERIAL WATER; BRAIN PERFUSION; INVERSION; ANGIOGRAPHY; MODEL; MRI AB Adiabatic fast passage (AFP) is used in noninvasive quantitative perfusion experiments to invert (or label) arterial spins. Continuous arterial spin labeling (CASL) experiments conducted in vivo often assume the inversion efficiency based on the labeling field and steady flow conditions, without direct verification. In practice, the labeling field used in CASL is often amplitude- and duty cycle-limited due to hardware or specific absorption rate constraints. In this study, the effects of the labeling field amplitude and duty cycle, and flow dynamics on the inversion efficiency of AFP were examined under steady flow conditions in a saline flow phantom. The experimental results were in general agreement with models based on Zhernovoi's theory except at high labeling field amplitudes, when the spin inversion times are at least half of the duration of the labeling pulse. The nonlinear relation observed between the inversion efficiency and the labeling duty cycle implies that the practice of linear derating the inversion efficiency with the labeling duty cycle may be prone to significant error. A secondary finding was that the T-1 of the flowing fluid could be calculated based on the flow dynamics after varying the flow rate. (C) 2002 Wiley-Liss, Inc. C1 Univ Pittsburgh, Med Ctr, MR Res Ctr, Dept Radiol, Pittsburgh, PA 15213 USA. NIH, MRI Res Facil, Bethesda, MD 20892 USA. RP Gach, HM (reprint author), Univ Pittsburgh, Med Ctr, MR Res Ctr, Dept Radiol, PUH B804,200 Lothrop St, Pittsburgh, PA 15213 USA. NR 30 TC 8 Z9 8 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD APR PY 2002 VL 47 IS 4 BP 709 EP 719 DI 10.1002/mrm.10122 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 534NP UT WOS:000174592700012 PM 11948732 ER PT J AU Threadgill, DW Hunter, KW Williams, RW AF Threadgill, DW Hunter, KW Williams, RW TI Genetic dissection of complex and quantitative traits: from fantasy to reality via a community effort SO MAMMALIAN GENOME LA English DT Review ID EMBRYONIC STEM-CELLS; INBRED STRAINS; GENOME-WIDE; MOUSE; MUTAGENESIS; ETHYLNITROSOUREA; MICE C1 Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Genet, Chapel Hill, NC 27599 USA. NCI, DCEG, Lab Populat Genet, NIH, Bethesda, MD 20892 USA. Univ Tennessee, Ctr Hlth Sci, Ctr Genom & Bioinformat, Memphis, TN 38163 USA. RP Threadgill, DW (reprint author), Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Genet, CB7264,Rm 11-109, Chapel Hill, NC 27599 USA. RI Threadgill, David/N-4425-2013; OI Threadgill, David/0000-0003-3538-1635; Williams, Robert/0000-0001-8924-4447 NR 19 TC 112 Z9 116 U1 0 U2 3 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD APR PY 2002 VL 13 IS 4 BP 175 EP 178 DI 10.1007/s00335-001-4001-Y PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 542LX UT WOS:000175046300001 PM 11956758 ER PT J AU Brody, T Stivers, C Nagle, J Odenwald, WF AF Brody, T Stivers, C Nagle, J Odenwald, WF TI Identification of novel Drosophila neural precursor genes using a differential embryonic head cDNA screen SO MECHANISMS OF DEVELOPMENT LA English DT Article DE neural precursor genes; neuroblast; ganglion mother cell; central and peripheral nervous system development; expression patterns ID CENTRAL-NERVOUS-SYSTEM; TRANSCRIPTION FACTOR; BINDING-PROTEIN; DNA-REPLICATION; MOLECULAR CHARACTERIZATION; SEGMENTATION GENE; COLUMN IDENTITY; CELL FATE; MELANOGASTER; EXPRESSION AB During Drosophila neuroblast lineage development, temporally ordered transitions in neuroblast gene expression have been shown to accompany the changing repertoire of functionally diverse cells generated by neuroblasts. To broaden our understanding of the biological significance of these ordered transitions in neuroblast gene expression and the events that regulate them, additional genes have been sought that participate in the timing and execution of these temporally controlled events. To identify dynamically expressed neural precursor genes, we have performed a differential cDNA hybridization screen on a stage specific embryonic head cDNA library, followed by whole-mount embryo in situ hybridizations. Described here are the embryonic expression profiles of 57 developmentally regulated neural precursor genes. Information about 2389 additional genes identified in this screen, including 1614 uncharacterized genes, is available on-line at 'BrainGenes: a search for Drosophila neural precursor genes' (http://sdb.bio.purdue.edu/fly/brain/ahome,htm). Published by Elsevier Science Ireland Ltd. C1 NINCDS, Neurogenet Unit, Neurochem Lab, NIH, Bethesda, MD 20892 USA. NINCDS, DNA Sequencing Facil, NIH, Bethesda, MD 20892 USA. RP Odenwald, WF (reprint author), NINCDS, Neurogenet Unit, Neurochem Lab, NIH, Bldg 36,Rm 4D02,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 74 TC 37 Z9 39 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4773 J9 MECH DEVELOP JI Mech. Dev. PD APR PY 2002 VL 113 IS 1 BP 41 EP 59 AR PII S0925-4773(02)00010-2 DI 10.1016/S0925-4773(02)00010-2 PG 19 WC Developmental Biology SC Developmental Biology GA 543BY UT WOS:000175082300004 PM 11900973 ER PT J AU Ni, HY Simile, C Hardy, AM AF Ni, HY Simile, C Hardy, AM TI Utilization of complementary and alternative medicine by United States adults - Results from the 1999 National Health Interview Survey SO MEDICAL CARE LA English DT Article DE complementary and alternative medicines; utilization ID THERAPIES AB OBJECTIVE. To measure utilization of complementary and alternative medicine (CAM) by US adults. METHODS. We analyzed data from the 1999 National Health Interview Survey (NHIS), which covers the noninstitutionalized civilian US population. Information on 12 types of CAM use in the past 12 months was obtained from 30,801 respondents aged IS years and older. Statistical analyses were performed using the SUDAAN software package to account for the complex sample design of the NHIS. RESULTS. An estimated 28.9% of US adults used at least one CAM therapy in the past year. The three most commonly used therapies were spiritual healing or prayer (13.7%), herbal medicine (9.6%), and chiropractic therapies (7.6%). The use of CAM was most prevalent among women, persons aged 35 to 54 years, and persons with an educational attainment of greater than or equal to 16 years. The overall CAM use was higher for white non-Hispanic persons (30.8%) than for Hispanic (19.9%) and black non-Hispanic persons (24.1%). Although the use was higher for persons who had health insurance than for those who did not, the difference was not statistically significant after adjusting for age, gender and educational attainment. Compared with nonusers, CAM users were more likely to use conventional medical services. CONCLUSIONS. Estimates of CAM use in this nationally representative sample were considerably lower than have been reported in previous surveys. Most CAM therapies are used by US adults in conjunction with conventional medical services. C1 Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Div Hlth Interview Stat, Hyattsville, MD 20782 USA. NIH, Ctr Sci Review, Bethesda, MD 20892 USA. RP Ni, HY (reprint author), Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Div Hlth Interview Stat, 6525 Belcrest Rd, Hyattsville, MD 20782 USA. NR 17 TC 249 Z9 253 U1 5 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0025-7079 J9 MED CARE JI Med. Care PD APR PY 2002 VL 40 IS 4 BP 353 EP 358 DI 10.1097/00005650-200204000-00011 PG 6 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 536PX UT WOS:000174712000011 PM 12021691 ER PT J AU De Lucca, AJ Bland, JM Vigo, CB Cushion, M Selitrennikoff, CP Peter, J Walsh, TJ AF De Lucca, AJ Bland, JM Vigo, CB Cushion, M Selitrennikoff, CP Peter, J Walsh, TJ TI CAY-1, a fungicidal saponin from Capsicum sp fruit SO MEDICAL MYCOLOGY LA English DT Article DE saponin; fungicidal; Capsicum sp. ID TRITERPENOID SAPONINS; ANTIFUNGAL ACTIVITY; BINDING; CYTOTOXICITY; MEDICINE; PEPTIDES; AGENTS AB Saponins are steroidal or terpenoid-based glycosides with surface active properties. A steroidal saponin, CAY-1, with a molecular weight of 1243.35 Da, was isolated and purified to homogeneity from commercially available dry, ground fruit of Capsicum frutescens. CAY-1 was shown to be a potent fungicide for the germinating conidia of Aspergillus flavus, A. fumigatus, A. parasiticus and A. niger with species-dependent LD90 values between 3 and 20 mum. Activity against some Aspergillus species was affected by the test medium used. In vitro assays, CAY-1 was effective against Pneumocystis carinii (IC50: 9.5 mum) and Candida albicans (IC50: 6.2 muM). CAY-1 had no effect on the viability of the nongerminating conidia of the two filamentous fungi, P. carinii and C. albicans, nor on the conidial type of Fusarium oxysporum. It was ineffective against the bacteria Enterobacter agglomerans, Bacillus subtilis, Escherichia coli and Staphylococcus aureus. CAY-1 was not cytotoxic to A 549 lung carcinoma cells or HeLa cells at effective fungicidal concentrations. The results indicate that CAY-1 is an effective fungicide for Aspergillus species, C. albicans and P. carinii at concentrations below the threshold for mammalian cell toxicity. C1 ARS, So Reg Res Ctr, USDA, New Orleans, LA 70124 USA. Univ Cincinnati, Coll Med, Dept Internal Med, Div Infect Dis, Cincinnati, OH 45267 USA. Mycolog Inc, Denver, CO 80262 USA. NCI, Immunocompromised Host Sect, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. RP De Lucca, AJ (reprint author), ARS, So Reg Res Ctr, USDA, 1100 Robert E Lee Blvd, New Orleans, LA 70124 USA. NR 23 TC 27 Z9 30 U1 1 U2 11 PU B I O S SCIENTIFIC PUBLISHERS LTD PI OXFORD PA 9 NEWTEC PLACE, MAGDALEN RD, OXFORD OX4 1RE, ENGLAND SN 1369-3786 J9 MED MYCOL JI Med. Mycol. PD APR PY 2002 VL 40 IS 2 BP 131 EP 137 DI 10.1080/714031097 PG 7 WC Infectious Diseases; Mycology; Veterinary Sciences SC Infectious Diseases; Mycology; Veterinary Sciences GA 553FU UT WOS:000175665800004 PM 12058725 ER PT J AU Vuong, C Otto, M AF Vuong, C Otto, M TI Staphylococcus epidermidis infections SO MICROBES AND INFECTION LA English DT Review DE Staphylococcus epidermidis; cross-infection; biofilms ID POLYSACCHARIDE INTERCELLULAR ADHESIN; COAGULASE-NEGATIVE STAPHYLOCOCCI; BIOFILM FORMATION; GENE-EXPRESSION; BINDING-PROTEIN; AUREUS C55; AGR SYSTEM; LOCUS SAR; CELL-WALL; STRAINS AB The opportunistic human pathogen Staphylococcus epidermidis has become the most important cause of nosocomial infections in recent years. Its pathogenicity is mainly due to the ability to form biofilms on indwelling medical devices. In a biofilm, S. epidermidis is protected against attacks from the immune system and against antibiotic treatment, making S. epidermidis infections difficult to eradicate. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, NIH, Hamilton, MT 59840 USA. RP Otto, M (reprint author), NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, NIH, 903 S 4th St, Hamilton, MT 59840 USA. OI Otto, Michael/0000-0002-2222-4115 NR 75 TC 319 Z9 354 U1 4 U2 46 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 1286-4579 J9 MICROBES INFECT JI Microbes Infect. PD APR PY 2002 VL 4 IS 4 BP 481 EP 489 AR PII S1286-4579(02)01563-0 DI 10.1016/S1286-4579(02)01563-0 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 544KU UT WOS:000175157400011 PM 11932199 ER PT J AU Dorfman, JR Germain, RN AF Dorfman, JR Germain, RN TI MHC-dependent survival of naive T cells? A complicated answer to a simple question SO MICROBES AND INFECTION LA English DT Article DE cell survival; T lymphocytes; major histocompatibility complex ID CLASS-II MOLECULES; HOMEOSTATIC PROLIFERATION; THYMIC SELECTION; COMPLEX; MEMORY; CD4; MICE; LYMPHOCYTES; RECEPTOR; REPERTOIRE AB The differentiation and survival of developing alphabeta thymocytes depends on effective T-cell receptor (TCR) signaling upon recognition of self peptide/major histocompatibility complex (MHC) molecule ligands. Although this concept is uniformly accepted with regard to immature thymocytes, there are conflicting reports as to whether or not MHC recognition is required for survival of mature peripheral naive T cells. In this review, we assess these reports critically and conclude that in many cases, the differences observed in CD4(+) T-cell recovery between MHC-expressing and MHC-deficient animals can be attributed to proliferation occurring only in the MHC-expressing lymphopenic animals studied in these models systems, rather than to effects of MHC recognition on cell viability per se. Still other reports involve experimental manipulations that may have affected the intrathymic development of the T cells such that they receive a "poor" selecting signal, fail to fully mature, and thus behave more like thymocytes in their survival characteristics (i.e., show MHC dependence). With respect to CD8(+) T cells, we discuss data suggesting that some clones are more dependent upon the presence of MHC class I for survival than others. We propose that some CD8(+) T cells even in a wild-type host may behave like the manipulated CD4(+) T cells just described, and fail to mature completely with respect to their survival requirements. Although the proportion of CD8(+) cells in this MHC-dependent state is not known, the corresponding fraction among CD4(+) T cells seems to be rather small. Overall, our analysis of the available data suggests that most or all mature CD4(+) (and perhaps also many CD8(+)) T lymphocytes do not depend on self-recognition for their viability in the periphery. Published by Edtions scientifiques et medicales Elsevier SAS. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Germain, RN (reprint author), NIAID, Immunol Lab, NIH, Bldg 10 Rm 11N311,10 Ctr Dr MSC-1892, Bethesda, MD 20892 USA. RI Dorfman, Jeffrey/B-4854-2011 OI Dorfman, Jeffrey/0000-0001-9938-8911 NR 39 TC 26 Z9 26 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 1286-4579 J9 MICROBES INFECT JI Microbes Infect. PD APR PY 2002 VL 4 IS 5 BP 547 EP 554 AR PII S1286-4579(02)01571-X DI 10.1016/S1286-4579(02)01571-X PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 550GK UT WOS:000175495100004 PM 11959510 ER PT J AU Martinez, A AF Martinez, A TI Biology of adrenomedullin - Introduction SO MICROSCOPY RESEARCH AND TECHNIQUE LA English DT Editorial Material ID PEPTIDE; CALCITONIN C1 NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. RP Martinez, A (reprint author), NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. RI Martinez, Alfredo/A-3077-2013 OI Martinez, Alfredo/0000-0003-4882-4044 NR 11 TC 13 Z9 13 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-910X J9 MICROSC RES TECHNIQ JI Microsc. Res. Tech. PD APR 1 PY 2002 VL 57 IS 1 BP 1 EP 2 DI 10.1002/jemt.10045 PG 2 WC Anatomy & Morphology; Biology; Microscopy SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics; Microscopy GA 533ND UT WOS:000174535800001 PM 11921350 ER PT J AU Pio, R Elsassr, TH Martinez, A Cuttitta, F AF Pio, R Elsassr, TH Martinez, A Cuttitta, F TI Identification, characterization, and physiological actions of factor H as an adrenomedullin binding protein present in human plasma SO MICROSCOPY RESEARCH AND TECHNIQUE LA English DT Article DE adrenomedullin; factor H; binding protein; ligand blotting; complement ID COMPLEMENT FACTOR-H; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; ALTERNATIVE PATHWAY; NEISSERIA-GONORRHOEAE; VASODILATORY PEPTIDE; SERUM RESISTANCE; C3B; ENDOTOXIN; MONOCYTES; SITE AB A recently discovered adrenomedullin binding protein has been characterized as complement factor H, an important regulator of the complement cascade. This review will describe the evidence that led to the identification of factor H as an adrenomedullin binding protein and will address the implications that such binding has in the radioimmunoassay of AM in plasma. We will also describe the possible physiological implications of AM binding: namely, factor H suppresses the antimicrobial activity of AM, enhances AM-mediated induction of cyclic-AMP in rat fibroblasts, and augments the AM-mediated growth of a human cancer cell line. These initial studies suggest that factor H may be an important factor in the regulation of AM physiology. The elucidation of the mechanisms that modulate AM activity will be necessary for the understanding of the role of AM in normal and pathological conditions. (C) 2002 Wiley-Liss, Inc. C1 Univ Navarra, Sch Med, Dept Biochem, Pamplona 31080, Spain. Univ Navarra, Sch Med, Carcinogenesis Unit, Pamplona 31080, Spain. USDA, Agr Res Serv, Growth Biol Lab, Beltsville, MD 20705 USA. NCI, Dept Cell & Canc Biol, NIH, Bethesda, MD 20892 USA. RP Pio, R (reprint author), Univ Navarra, Sch Med, Dept Biochem, Pamplona 31080, Spain. RI Martinez, Alfredo/A-3077-2013; Pio, Ruben/F-5353-2017 OI Martinez, Alfredo/0000-0003-4882-4044; Pio, Ruben/0000-0002-6831-6111 NR 48 TC 13 Z9 16 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-910X J9 MICROSC RES TECHNIQ JI Microsc. Res. Tech. PD APR 1 PY 2002 VL 57 IS 1 BP 23 EP 27 DI 10.1002/jemt.10047 PG 5 WC Anatomy & Morphology; Biology; Microscopy SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics; Microscopy GA 533ND UT WOS:000174535800004 PM 11921353 ER PT J AU Garayoa, M Bodegas, E Cuttitta, F Montuenga, LM AF Garayoa, M Bodegas, E Cuttitta, F Montuenga, LM TI Adrenomedullin in mammalian embryogenesis SO MICROSCOPY RESEARCH AND TECHNIQUE LA English DT Review ID GENE-RELATED-PEPTIDE; EPIDERMAL GROWTH-FACTOR; SWISS 3T3 CELLS; HUMAN CYTOTROPHOBLAST DIFFERENTIATION; HUMAN CHORIONIC-GONADOTROPIN; PULMONARY BLOOD-FLOW; SMOOTH-MUSCLE CELLS; HUMAN-PREGNANCY; HYPOTENSIVE PEPTIDE; AMNIOTIC-FLUID AB Here are summarized data supporting that adrenomedullin (AM) is a multifunctional factor involved in the complex regulatory mechanisms of mammalian development. During rodent embryogenesis, AM is first expressed in the heart, followed by a broader but also defined spatio-temporal pattern of expression in vascular, neural, and skeletal-forming tissues as well as in the main embryonic internal organs. AM pattern of expression is suggestive of its involvement in the control of embryonic invasion, proliferation, and differentiation processes, probably through autocrine or paracrine modes of action. AM levels in fetoplacental tissues, uterus, maternal and umbilical plasma are highly increased during normal gestation. These findings in addition to other physiological and gene targeting studies support the importance of AM as a vasorelaxant factor implicated in the regulation of maternal vascular adaptation to pregnancy, as well as of fetal and fetoplacental circulations. AM is also present in amniotic fluid and milk, which is suggestive of additional functions in the maturation and immunological protection of the fetus. Altered expression of AM has been found in some gestational pathologies, although it is not yet clear whether this corresponds to causative or compensatory mechanisms, Future studies in regard to the distribution and expression levels of the molecules known to function as AM receptors, together with data on the action of complement factor H (an AM binding protein), may help to better define the roles of AM during embryonic development. (C) 2002 Wiley-Liss, Inc. C1 Univ Navarra, Dept Hist & Pathol, Carcinogenesis Unit, Pamplona 31080, Spain. NCI, Div Clin Sci, Med Branch, Dept Cell & Canc Biol, Bethesda, MD 20892 USA. RP Garayoa, M (reprint author), Univ Navarra, Dept Hist & Pathol, Carcinogenesis Unit, Pamplona 31080, Spain. NR 143 TC 25 Z9 27 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-910X J9 MICROSC RES TECHNIQ JI Microsc. Res. Tech. PD APR 1 PY 2002 VL 57 IS 1 BP 40 EP 54 DI 10.1002/jemt.10050 PG 15 WC Anatomy & Morphology; Biology; Microscopy SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics; Microscopy GA 533ND UT WOS:000174535800006 PM 11921355 ER PT J AU Hutter, D Chen, PL Barnes, J Liu, YS AF Hutter, D Chen, PL Barnes, J Liu, YS TI The carboxyl-terminal domains of MKP-1 and MKP-2 have inhibitory effects on their phosphatase activity SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article DE MAP kinase phosphatase; MAP kinase; inhibitory; regulation; dephosphorylation ID ACTIVATED PROTEIN-KINASE; DUAL-SPECIFICITY PHOSPHATASE; SIGNAL-TRANSDUCTION PATHWAY; IMMEDIATE-EARLY GENE; MAP KINASE; CATALYTIC ACTIVATION; TYROSINE-PHOSPHATASE; INFLAMMATORY CYTOKINES; HEAT-SHOCK; EXPRESSION AB Both the mitogen-activated protein kinase (MAPK) phosphatases MKP-1 and MKP-2 exert important feedback control of MAPK-mediated signaling events. The function of MKP-1 and MKP-2 is regulated via complex mechanisms, ranging from increased transcription of the MKP-1 and MKP-2 genes to post-translational catalytic activation of MKP-1 and MKP-2 proteins upon binding to their substrate MAPKs. In addition, MKP-1 stability increases upon ERK-dependent phosphorylation of two serine residues in its C-terminus. The C-terminal regions of MKP-1 and MKP-2, but not those of other MKPs, are homologous. To investigate the role of this domain, we have deleted the C-terminal tails from MKP-1 and MKP-2 and examined the effect of these deletions on their enzymatic activity. C-terminally truncated MKP-1 and MKP-2 exhibited, both in vivo and in vitro, substantially greater phosphatase activity towards their substrate MAPKs than did the full-length counterparts. However, C-terminal truncations did not significantly change either their substrate affinity, or their substrate-mediated catalytic activation. Basal phosphatase activity of the truncated proteins was also significantly higher than that of the wild-type counterparts. Collectively, these results suggest that the C-terminal domain may potentially play a role in the regulation of MKP-1 and MKP-2. C1 NIA, Stress Signal Unit, Cellular & Mol Biol Lab, Intramural Res Program, Baltimore, MD 21224 USA. RP Liu, YS (reprint author), NIA, Stress Signal Unit, Cellular & Mol Biol Lab, Intramural Res Program, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Liu, Yusen/E-3527-2011 NR 44 TC 10 Z9 10 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0300-8177 J9 MOL CELL BIOCHEM JI Mol. Cell. Biochem. PD APR PY 2002 VL 233 IS 1-2 BP 107 EP 117 DI 10.1023/A:1015502226940 PG 11 WC Cell Biology SC Cell Biology GA 552TC UT WOS:000175635300014 PM 12083364 ER PT J AU Roberts, C Sutherland, HF Farmer, H Kimber, W Halford, S Carey, A Brickman, JM Wynshaw-Boris, A Scambler, PJ AF Roberts, C Sutherland, HF Farmer, H Kimber, W Halford, S Carey, A Brickman, JM Wynshaw-Boris, A Scambler, PJ TI Targeted mutagenesis of the Hira gene results in gastrulation defects and patterning abnormalities of mesoendodermal derivatives prior to early embryonic lethality SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CONGENITAL HEART-DISEASE; LEFT-RIGHT SPECIFICATION; MOUSE EMBRYO; SACCHAROMYCES-CEREVISIAE; DIGEORGE-SYNDROME; PRIMITIVE STREAK; TRANSCRIPTIONAL REPRESSORS; EXPRESSION ANALYSIS; CANDIDATE GENE; MORPHOGENESIS AB The Hira gene encodes a nuclear WD40 domain protein homologous to the yeast transcriptional corepressors Hir1p and Hir2p. Using targeted mutagenesis we demonstrate that Hira is essential for murine embryogenesis. Analysis of inbred 129Sv embryos carrying the null mutation revealed an initial requirement during gastrulation, with many mutant embryos having a distorted primitive streak. Mutant embryos recovered at later stages have a range of malformations with axial and paraxial mesendoderm being particularly affected, a finding consistent with the disruption of gastrulation seen earlier in development. This phenotype could be partially rescued by a CD1 genetic background, although the homozygous mutation was always lethal by embryonic day 11, with death probably resulting from abnormal placentation and failure of cardiac morphogenesis. C1 Inst Child Hlth, Mol Med Unit, London WC1N 1EH, England. Univ Edinburgh, Ctr Genome Res, Edinburgh EH9 3JQ, Midlothian, Scotland. NIA, NIH, Baltimore, MD 21224 USA. Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA. RP Scambler, PJ (reprint author), Inst Child Hlth, Mol Med Unit, 30 Guilford St,Rm 211, London WC1N 1EH, England. RI Scambler, Peter/C-4998-2008; OI Scambler, Peter/0000-0002-1487-4628; Brickman, Joshua/0000-0003-1580-7491 NR 60 TC 83 Z9 92 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 7 BP 2318 EP 2328 DI 10.1128/MCB.22.7.2318-2328.2002 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 531GK UT WOS:000174407500032 PM 11884616 ER PT J AU Wu, ZQ Earle, J Saito, S Anderson, CW Appella, E Xu, Y AF Wu, ZQ Earle, J Saito, S Anderson, CW Appella, E Xu, Y TI Mutation of mouse p53 Ser23 and the response to DNA damage SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID INDUCED PHOSPHORYLATION; IONIZING-RADIATION; MDM2; APOPTOSIS; ACTIVATION; CHK2; CHECKPOINT; KINASE; SITES; MICE AB Recent studies have suggested that phosphorylation of human p53 at Ser20 is important for stabilizing p53 in response to DNA damage through disruption of the interaction between MDM2 and p53. To examine the requirement for this DNA damage-induced phosphorylation event in a more physiological setting, we introduced a missense mutation into the endogenous p53 gene of mouse embryonic stem (ES) cells that changes serine 23 (S23), the murine equivalent of human serine 20, to alanine (A). Murine embryonic fibroblasts harboring the p53(S23A) mutation accumulate p53 as well as p21 and Mdm2 proteins to normal levels after DNA damage. Furthermore, ES cells and thymocytes harboring the p53(S23A) mutation also accumulate p53 protein to wild-type levels and undergo p53-dependent apoptosis similarly to wild-type cells after DNA damage. Therefore, phosphorylation of murine p53 at Ser23 is not required for p53 responses to DNA damage induced by UV and ionizing radiation treatment. C1 Univ Calif San Diego, Div Biol, Mol Biol Sect, La Jolla, CA 92093 USA. NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA. RP Xu, Y (reprint author), Univ Calif San Diego, Div Biol, Mol Biol Sect, 9500 Gilman Dr, La Jolla, CA 92093 USA. NR 42 TC 76 Z9 77 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 8 BP 2441 EP 2449 DI 10.1128/MCB.22.8.2441-2449.2002 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 535FZ UT WOS:000174635700002 PM 11909939 ER PT J AU Fernandez-Medarde, A Esteban, LM Nunez, A Porteros, A Tessarollo, L Santos, E AF Fernandez-Medarde, A Esteban, LM Nunez, A Porteros, A Tessarollo, L Santos, E TI Targeted disruption of Ras-Grf2 shows its dispensability for mouse growth and development SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID NUCLEOTIDE EXCHANGE FACTOR; BETA-GAMMA-SUBUNITS; SIGNALING PATHWAYS; SEVENLESS GENE; ACTIVATES RAS; PROTEIN; EXPRESSION; CLONING; BINDING; DOMAINS AB The mammalian Grf1 and Grf2 proteins are Ras guanine nucleotide exchange factors (GEFs) sharing a high degree of structural homology, as well as an elevated expression level in central nervous system tissues. Such similarities raise questions concerning the specificity and/or redundancy at the functional level between the two Grf proteins. grf1-null mutant mice have been recently described which showed phenotypic growth reduction and long-term memory loss. To gain insight into the in vivo function of Grf2, we disrupted its catalytic CDC25-H domain by means of gene targeting. Breeding among grf2(+/-) animals gave rise to viable grf2(-/-) adult animals with a normal Mendelian pattern, suggesting that Grf2 is not essential for embryonic and adult mouse development. In contrast to Grf1-null mice, analysis of grf2(-/-) litters showed similar size and weight as their heterozygous or wild-type grf2 counterparts. Furthermore, adult grf2(-/-) animals reached sexual maturity at the same age as their wild-type littermates and showed similar fertility levels. No specific pathology was observed in adult Grf2-null animals, and histopathological studies showed no observable differences between null mutant and wild-type Grf2 mice. These results indicate that grf2 is dispensable for mouse growth, development, and fertility. Furthermore, analysis of double grf1/grf2 null animals did not show any observable phenotypic difference with single grf1(-/-) animals, further indicating a lack of functional overlapping between the two otherwise highly homologous Grf1 and Grf2 proteins. C1 Univ Salamanca, CSIC, IBMCC, Ctr Invest Canc, Salamanca 37007, Spain. Univ Salamanca, Dept Biol Celular & Patol, Salamanca 37007, Spain. NCI, Mammalian Genet Lab, Frederick, MD 21702 USA. RP Santos, E (reprint author), Univ Salamanca, CSIC, IBMCC, Ctr Invest Canc, Campus Unamuno, Salamanca 37007, Spain. RI Porteros, Angel/B-5749-2017 OI Porteros, Angel/0000-0002-0227-1141 NR 30 TC 26 Z9 28 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 8 BP 2498 EP 2504 DI 10.1128/MCB.22.8.2498-2504.2002 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 535FZ UT WOS:000174635700007 PM 11909944 ER PT J AU Miki, K Eddy, EM AF Miki, K Eddy, EM TI Tumor necrosis factor receptor 1 is an ATPase regulated by silencer of death domain SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HSP70 CHAPERONE ACTIVITY; FACTOR TNF RECEPTOR; SIGNALS CELL-DEATH; NEGATIVE REGULATOR; CRYSTAL-STRUCTURE; HSC70 CHAPERONE; PROTEIN; APOPTOSIS; BAG-1; ACTIVATION AB Self-aggregation of tumor necrosis factor receptor type 1 (TNFR1) induces spontaneous downstream signaling and results in cell death. It has been suggested that silencer of death domain (SODD) binds TNFR1 monomers to prevent self-aggregation. We found that SODD binds through its BAG domain to the ATPase domain of Hsp70. We also determined that SODD binds through its BAG domain to TNFR1. ATP, but not nonhydrolyzable ATP-gammaS, regulates the SODD binding by Hsp70 or TNFR1. ATP binding by TNFR1 was abolished when a point mutation was introduced into a phosphate-binding loop motif characteristic of ATP-binding proteins, suggesting that TNFR1 functions as an ATPase. Furthermore, TNFR1 was present in aggregates in ATP-depleted cells and SODD disassembled aggregates in vitro only in the presence of ATP. These data suggest that SODD functions as a cofactor analogous to the nucleotide exchange factor BAG-1, which modulates the ATPase cycle of Hsp70 proteins. We propose a new model in which a nucleotide-dependent conformational change in TNFR1 has a key role in regulating TNF signaling. C1 NIEHS, LRDT, Gamete Biol Sect, NIH, Res Triangle Pk, NC 27709 USA. RP Eddy, EM (reprint author), NIEHS, LRDT, Gamete Biol Sect, NIH, MD C4-01,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. NR 47 TC 32 Z9 38 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 8 BP 2536 EP 2543 DI 10.1128/MCB.22.8.2536-2543.2002 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 535FZ UT WOS:000174635700011 PM 11909948 ER PT J AU Bianco, C Adkins, HB Wechselberger, C Seno, M Normanno, N De Luca, A Sun, YP Khan, N Kenney, N Ebert, A Williams, KP Sanicola, M Salomon, DS AF Bianco, C Adkins, HB Wechselberger, C Seno, M Normanno, N De Luca, A Sun, YP Khan, N Kenney, N Ebert, A Williams, KP Sanicola, M Salomon, DS TI Cripto-1 activates nodal- and ALK4-dependent and -independent signaling pathways in mammary epithelial cells SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ONE-EYED PINHEAD; GROWTH-FACTOR-BETA; TYROSINE PHOSPHORYLATION; VERTEBRATE DEVELOPMENT; GENE FAMILY; I RECEPTOR; PROTEIN; EXPRESSION; GASTRULATION; GLAND AB Cripto-1 (CR-1), an epidermal growth factor-CFC (EGF-CFC) family member, has a demonstrated role in embryogenesis and mammary gland development and is overexpressed in several human tumors. Recently, EGF-CFC proteins were implicated as essential signaling cofactors for Nodal, a transforming growth factor beta family member whose expression has previously been defined as embryo specific. To identify a receptor for CR-1, a human brain cDNA phage display library was screened using CR-1 protein as bait. Phage inserts with identity to ALK4, a type I serine/threonine kinase receptor for Activin, were identified. CR-1 binds to cell surface ALK4 expressed on mammalian epithelial cells in fluorescence-activated cell sorter analysis, as well as by coimmunoprecipitation. Nodal is coexpressed with mouse Cr-1 in the mammary gland, and CR-1 can phosphorylate the transcription factor Smad-2 in EpH-4 mammary epithelial cells only in the presence of Nodal and ALK4. In contrast, CR-1 stimulation of mitogen-activated protein kinase and AKT in these cells is independent of Nodal and ALK4, suggesting that CR-1 may modulate different signaling pathways to mediate its different functional roles. C1 NCI, BRL, TGFS, NIH, Bethesda, MD 20892 USA. Okayama Univ, Fac Engn, Dept Biosci & Biotechnol, Okayama 7008530, Japan. ITN Fdn Pascale, Oncol Sperimentale D, I-80131 Naples, Italy. Hampton Univ, Dept Biol Sci, Hampton, VA 23665 USA. Free Univ Berlin, Dept Obstet & Gynecol, D-1000 Berlin, Germany. Biogen Inc, Cambridge, MA 02142 USA. RP Sanicola, M (reprint author), NCI, BRL, TGFS, NIH, Bldg 10,Rm 5B39,9000 Rockville Pike, Bethesda, MD 20892 USA. RI SENO, Masaharu /B-2092-2011; De Luca, Antonella/J-8737-2016; OI SENO, Masaharu /0000-0001-8547-6259; De Luca, Antonella/0000-0001-5762-447X; Normanno, Nicola/0000-0002-7158-2605 NR 50 TC 106 Z9 109 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 8 BP 2586 EP 2597 DI 10.1128/MCB.22.8.2586-2597.2002 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 535FZ UT WOS:000174635700016 PM 11909953 ER PT J AU Akiyama, TE Sakai, S Lambert, G Nicol, CJ Matsusue, K Pimprale, S Lee, YH Ricote, M Glass, CK Brewer, HB Gonzalez, FJ AF Akiyama, TE Sakai, S Lambert, G Nicol, CJ Matsusue, K Pimprale, S Lee, YH Ricote, M Glass, CK Brewer, HB Gonzalez, FJ TI Conditional disruption of the peroxisome proliferator-activated receptor gamma gene in mice results in lowered expression of ABCA1, ABCG1, and apoE in macrophages and reduced cholesterol efflux SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MONOCYTE-DERIVED MACROPHAGES; LOW-DENSITY-LIPOPROTEIN; FOAM CELL-FORMATION; E-DEFICIENT MICE; BINDING CASSETTE TRANSPORTER-1; MOUSE PERITONEAL-MACROPHAGES; BONE-MARROW TRANSPLANTATION; HUMAN APOLIPOPROTEIN-E; RETINOID-X-RECEPTOR; SMOOTH-MUSCLE CELLS AB Disruption of the peroxisome proliferator-activated receptor gamma (PPARgamma) gene causes embryonic lethality due to placental dysfunction. To circumvent this, a PPARgamma conditional gene knockout mouse was produced by using the Cre-loxP system. The targeted allele, containing loxP sites flanking exon 2 of the PPARgamma gene, was crossed into a transgenic mouse line expressing Cre recombinase under the control of the alpha/beta interferon-inducible (MX) promoter. Induction of the MX promoter by pIpC resulted in nearly complete deletion of the targeted exon, a corresponding loss of full-length PPARgamma mRNA transcript and protein, and marked reductions in basal and troglitazone-stimulated expression of the genes encoding lipoprotein lipase, CD36, LXRalpha, and ABCG1 in thioglycolate-elicited peritoneal macrophages. Reductions in the basal levels of apolipoprotein E (apoE) mRNA in macrophages and apoE protein in total plasma and high-density lipoprotein (HDL) were also observed in pIpC-treated PPARgamma-MXCre(+) mice. Basal cholesterol efflux from cholesterol-loaded macrophages to HDL was significantly reduced after disruption of the PPARgamma gene. Troglitazone selectively inhibited ABCA1 expression (while rosiglitazone, ciglitazone, and pioglitazone had little effect) and cholesterol efflux in both PPARgamma-deficient and control macrophages, indicating that this drug can exert paradoxical effects on cholesterol homeostasis that are independent of PPARgamma. Together, these data indicate that PPARgamma plays a critical role in the regulation of cholesterol homeostasis by controlling the expression of a network of genes that mediate cholesterol efflux from cells and its transport in plasma. C1 NCI, Div Basic Sci, Lab Metab, NIH, Bethesda, MD 20892 USA. NHLBI, Mol Dis Branch, NIH, Bethesda, MD 20892 USA. Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA. RP Gonzalez, FJ (reprint author), NCI, Div Basic Sci, Lab Metab, NIH, Bldg 37,Rm 3E-24, Bethesda, MD 20892 USA. RI Ricote, Mercedes/L-4615-2014 OI Ricote, Mercedes/0000-0002-8090-8902 NR 97 TC 278 Z9 295 U1 0 U2 14 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 2002 VL 22 IS 8 BP 2607 EP 2619 DI 10.1128/MCB.22.8.2607-2619.2002 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 535FZ UT WOS:000174635700018 PM 11909955 ER PT J AU Seigel, GM Lotery, A Kummer, A Bernard, DJ Greene, NDE Turmaine, M Derksen, T Nussbaum, RL Davidson, B Wagner, J Mitchison, HM AF Seigel, GM Lotery, A Kummer, A Bernard, DJ Greene, NDE Turmaine, M Derksen, T Nussbaum, RL Davidson, B Wagner, J Mitchison, HM TI Retinal pathology and function in a Cln3 knockout mouse model of juvenile neuronal ceroid lipofuscinosis (Batten disease) SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID NERVE-FIBER LAYER; MITOCHONDRIAL ATP SYNTHASE; SINGLE-STRANDED-DNA; MACULAR DEGENERATION; RETINITIS-PIGMENTOSA; MONOCLONAL-ANTIBODY; CELL-DEATH; SUBUNIT-C; APOPTOSIS; GLAUCOMA AB Batten disease or JNCL, is the juvenile form of Neuronal Ceroid Lipofuscinosis (NCL) an autosomal recessive neurodegenerative disorder. Since retinal degeneration is an early consequence of Batten disease, we examined the eyes of Cln3 knockout mice (1-20 months of age), along with heterozygotes and appropriate controls, to determine whether or not the Cln3 defect would lead to characteristic retinal degeneration and visual loss. Accumulation of autofluorescent material and intracellular inclusions were markedly increased in Cln3 knockout retinal ganglion cells, as well as most other nuclear layers. Nerve fiber density was also significantly decreased in Cln3 knockout retinae. Apoptosis was observed in the photoreceptor layer of Cln3 knockout. However, the degree of retinal degeneration up to age 20 months was not extensive. Fundus examinations of Cln3 knockout mice showed no significant abnormalities, while electroretinograms remained robust through 11 months of age. In summary, it appears that accumulation of autofluorescent material, carbohydrate storage material, as well as apoptotic cell death are retinal manifestations of the Cln3 defect that do not appear to extinguish retinal function in this mouse model of Batten disease. C1 Univ Rochester, Sch Med, Dept Ophthalmol, Rochester, NY USA. Univ Iowa, Dept Ophthalmol, Iowa City, IA 52242 USA. NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. Royal Free & UCL, Sch Med, Dept Paediat, London, England. UCL, Dept Anat & Dev Biol, London, England. RP Univ Buffalo, Dept Ophthalmol, Buffalo, NY 14222 USA. EM gseigel@frontiernet.net RI Mitchison, Hannah/C-1891-2008; OI Greene, Nicholas/0000-0002-4170-5248 FU NIDDK NIH HHS [P30DK54759] NR 52 TC 36 Z9 36 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 1044-7431 EI 1095-9327 J9 MOL CELL NEUROSCI JI Mol. Cell. Neurosci. PD APR PY 2002 VL 19 IS 4 BP 515 EP 527 DI 10.1006/mcne.2001.1099 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 550GE UT WOS:000175494600004 PM 11988019 ER PT J AU Lilliehook, C Chan, S Choi, EK Zaidi, NF Wasco, W Mattson, MP Buxbaum, JD AF Lilliehook, C Chan, S Choi, EK Zaidi, NF Wasco, W Mattson, MP Buxbaum, JD TI Calsenilin enhances apoptosis by altering endoplasmic reticulum calcium signaling SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID AMYLOID BETA-PEPTIDE; NF-KAPPA-B; ALZHEIMERS-DISEASE; MUTANT PRESENILIN-1; NEURONAL APOPTOSIS; CA2+ CONCENTRATION; BINDING PROTEIN; NERVOUS-SYSTEM; CALPAIN; CELLS AB Calsenilin (also called DREAM and KChIP3), a member of the neuronal calcium sensor family, was isolated in a yeast two-hybrid screen using an apoptotic domain of presenilin 2 as bait. Calsenilin is a cytoplasmic protein, but interacts with the COOH-termini of both presenilin I and presenilin 2 at the endoplasmic reticulum and the Golgi apparatus. In this study, we have investigated calsenilin's effect on apoptosis. In stable neuroglioma cell lines, we observed that calsenilin enhances apoptosis in response to serum withdrawal or thapsigargin. Consistent with these observations, caspase and apparently calpain activities were increased during apoptosis in calsenilin-overexpressing cells. Moreover, using calcium imaging we were able to show that cells treated with thapsigargin released more calcium from intracellular stores when calsenilin was overexpressed. Taken together, these data suggest that calsenilin causes cells to be more susceptible to apoptotic triggers, possibly by altering calcium dynamics. C1 Mt Sinai Med Ctr, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. Mt Sinai Med Ctr, Dept Neurobiol, New York, NY 10029 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Genet & Aging Unit, Charlestown, MA 02129 USA. NIA, Gerontol Res Ctr, Neurosci Lab, Baltimore, MD 21224 USA. RP Buxbaum, JD (reprint author), Mt Sinai Med Ctr, Dept Psychiat, Lab Mol Neuropsychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. EM buxbaj01@doc.mssm.edu RI Mattson, Mark/F-6038-2012; OI Buxbaum, Joseph/0000-0001-8898-8313 FU NIA NIH HHS [AG05138, AG15801] NR 46 TC 55 Z9 58 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell. Neurosci. PD APR PY 2002 VL 19 IS 4 BP 552 EP 559 DI 10.1006/mcne.2001.1096 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 550GE UT WOS:000175494600007 PM 11988022 ER PT J AU Zhang, JZ Rosenberg, HF AF Zhang, JZ Rosenberg, HF TI Diversifying selection of the tumor-growth promoter angiogenin in primate evolution SO MOLECULAR BIOLOGY AND EVOLUTION LA English DT Article DE angiogenin; diversifying selection; evolution; ribonuclease; cancer; primates ID POSITIVE DARWINIAN SELECTION; SINGLE-NUCLEOTIDE POLYMORPHISMS; RAPID EVOLUTION; ADAPTIVE EVOLUTION; CANCER PROGRESSION; CODING REGIONS; ATHYMIC MICE; GENES; PROTEIN; SERUM AB Diversifying selection drives the rapid differentiation of acne sequences and is one of the main forces behind adaptive evolution. Most genes known to be shaped by diversifying selection are those involved in host-pathogen or male-female interactions characterized as molecular "arms races." Here we report the unexpected detection of diversifying selection in the evolution of a tumor-growth promoter. angiogenin (ANG). A comparison among I I primate species demonstrates that ANG has a significantly higher rate of nucleotide substitution at nonsynonymous sites than at synonymous sites, a hallmark of positive selection acting at the molecular level. Furthermore, we observed significant charge diversity at the molecular surface, suggesting the presence of selective pressures in the microenvironment of ANG, including its binding molecules, A population survey of ANG in chimpanzees, however, reveals no polymorphism, which may have resulted from a recent selective sweep of a charge-altering Substitution in chimpanzee evolution. Functional assays of recombinant ANGs from the human and owl monkey indicate that primate ANGs retain angiogenic activity despite rapid evolution. Our study, together with findings of similar selection in the primate breast cancer suppressor gene, BRCA1, reveals an intriguing phenomenon of unusual selective pressures on. and adaptive evolution of. cancer-related genes in primate evolution. C1 Natl Inst Allergy & Infect Dis, Lab Host Def, NIH, Bethesda, MD 20892 USA. RP Rosenberg, HF (reprint author), Natl Inst Allergy & Infect Dis, Lab Host Def, NIH, Bldg 10 Rm 11N104 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 66 TC 33 Z9 45 U1 1 U2 3 PU SOC MOLECULAR BIOLOGY EVOLUTION PI LAWRENCE PA PO BOX 1897, LAWRENCE, KS 66044-8897 USA SN 0737-4038 J9 MOL BIOL EVOL JI Mol. Biol. Evol. PD APR PY 2002 VL 19 IS 4 BP 438 EP 445 PG 8 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA 541CE UT WOS:000174967000008 PM 11919285 ER PT J AU Griffis, ER Altan, N Lippincott-Schwartz, J Powers, MA AF Griffis, ER Altan, N Lippincott-Schwartz, J Powers, MA TI Nup98 is a mobile nucleoporin with transcription-dependent dynamics SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID NUCLEAR-PORE COMPLEX; CREB-BINDING-PROTEIN; MESSENGER-RNA EXPORT; IMPORTIN-BETA; INTRANUCLEAR FILAMENTS; CELL-PROLIFERATION; GLFG NUCLEOPORIN; CONSERVED MOTIF; DOCKING SITE; LIVING CELLS AB Nucleoporin 98 (Nup98), a glycine-leucine-phenylalanine-glycine (GLFG) amino acid repeat-containing nucleoporin, plays a critical part in nuclear trafficking. Injection of antibodies to Nup98 into the nucleus blocks the export of most RNAs. Nup98 contains binding sites for several transport factors; however, the mechanism by which this nucleoporin functions has remained unclear. Multiple subcellular localizations have been suggested for Nup98. Here we show that Nup98 is indeed found both at the nuclear pore complex and within the nucleus. Inside the nucleus, Nup98 associates with a novel nuclear structure that we term the GLFG body because the GLFG domain of Nup98 is required for targeting to this structure. Photobleaching of green fluorescent protein-Nup98 in living cells reveals that Nup98 is mobile and moves between these different localizations. The rate of recovery after photobleaching indicates that Nup98 interacts with other, less mobile, components in the nucleoplasm. Strikingly, given the previous link to nuclear export, the mobility of Nup98 within the nucleus and at the pore is dependent on ongoing transcription by RNA polymerases I and II. These data give rise to a model in which Nup98 aids in direction of RNAs to the nuclear pore and provide the first potential mechanism for the role of a mobile nucleoporin. C1 Emory Univ, Sch Med, Dept Cell Biol, Atlanta, GA 30322 USA. NICHHD, Biochem Cell & Dev Biol Grad Program, Bethesda, MD 20892 USA. NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. RP Powers, MA (reprint author), Emory Univ, Sch Med, Dept Cell Biol, Atlanta, GA 30322 USA. RI Griffis, Eric/A-4804-2015 OI Griffis, Eric/0000-0002-2832-6649 FU NIGMS NIH HHS [GM-59975, R01 GM059975] NR 74 TC 164 Z9 166 U1 0 U2 6 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD APR PY 2002 VL 13 IS 4 BP 1282 EP 1297 DI 10.1091/mbc.01-11-0538 PG 16 WC Cell Biology SC Cell Biology GA 547DU UT WOS:000175318400016 PM 11950939 ER PT J AU Solanas, M Escrich, E Rouzaut, A Costa, I Martinez, A Notario, V AF Solanas, M Escrich, E Rouzaut, A Costa, I Martinez, A Notario, V TI Deregulated expression of the PCPH proto-oncogene in rat mammary tumors induced with 7,12-dimethylbenz[a]anthracene SO MOLECULAR CARCINOGENESIS LA English DT Article DE carcinogenesis; oncogenes; breast cancer; gene expression ID EXPERIMENTAL DIETS; LIPID INFLUENCE; PROTOONCOGENE; CPH; LOCALIZATION; CARCINOMA; CELLS AB The PCPH proto-oncogene was identified by its frequent activation in Syrian hamster fetal cells exposed to 3-methylcholanthrene. We previously isolated human PCPH cDNA and studied its expression in normal human tissues. We report herein the pattern of PCPH expression in normal rat tissues. Each tissue expressed one major PCPH polypeptide that varied in molecular mass in different tissues. Normal mammary gland expressed a single PCPH polypeptide of 27 kDa, This PCPH form also was expressed in lactating mammary glands but at significantly greater levels. These results suggest the existence of tissue-specific regulatory mechanisms for PCPH expression that may be influenced by the differentiation stage. Our previous studies on the involvement of PCPH in human cancer showed that human breast tumor cell lines have frequent alterations in PCPH, including multiple PCPH polypeptide forms that are not expressed in normal cells. These cell lines also have frequent loss of a 27-kDa form identified as the only PCPH polypeptide expressed by normal human breast epithelial cells. In this study, we found that these same alterations occurred in vivo during mammary carcinogenesis in Sprague-Dawley rats treated with 7,12-dimethylbenz[a]anthracene, in both benign and malignant tumors, indicating that stable changes in PCPH expression took place early in the neoplastic process. Results showed that this experimental system is relevant to human breast carcinogenesis and provides an excellent model to study the molecular basis of the regulation of PCPH expression during normal differentiation and pathologic stages of neoplasia of the mammary gland and to analyze the role of PCPH in the carcinogenic process. Furthermore, the detection of atypical PCPH polypeptides in tumors suggests that PCPH immunodetection may be applied as a diagnostic tool for the early identification of neoplastic breast epithelial cells. (C) 2002 Wiley-Liss, Inc. C1 Georgetown Univ, Med Ctr, Dept Radiat Med, Expt Carcinogenesis Lab, Washington, DC 20007 USA. Univ Autonoma Barcelona, Dept Cell Biol Physiol & Immunol, E-08193 Barcelona, Spain. Hosp Gen Granollers, Dept Pathol, Barcelona, Spain. NCI, Dept Cell & Canc Biol, NIH, Bethesda, MD 20892 USA. RP Notario, V (reprint author), Georgetown Univ, Med Ctr, Dept Radiat Med, Expt Carcinogenesis Lab, Res Bldg,Room E215,3970 Reservoir Rd NW, Washington, DC 20007 USA. RI Martinez, Alfredo/A-3077-2013; Solanas Garcia, Montserrat /O-4684-2016 OI Martinez, Alfredo/0000-0003-4882-4044; Solanas Garcia, Montserrat /0000-0003-2949-1344 FU NCI NIH HHS [CA64472] NR 23 TC 17 Z9 17 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD APR PY 2002 VL 33 IS 4 BP 219 EP 227 DI 10.1002/mc.10039 PG 9 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA 539HY UT WOS:000174865500004 PM 11933075 ER PT J AU Singh, BB Liu, XB Tang, JS Zhu, MX Ambudkar, IS AF Singh, BB Liu, XB Tang, JS Zhu, MX Ambudkar, IS TI Calmodulin regulates Ca2+-dependent feedback inhibition of store-operated interaction with a site in the Ca2+ influx by C terminus of TrpC1 SO MOLECULAR CELL LA English DT Article ID ACTIVATED CALCIUM CURRENT; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTORS; PROTEIN-KINASE; DEPENDENT INACTIVATION; SIGNALING COMPLEX; GLAND CELLS; ENTRY; CHANNELS; RELEASE; DEPLETION AB The mechanism involved in [Ca2+](i)-dependent feedback inhibition of store-operated Ca2+ entry (SOCE) is not yet known. Expression of Call-insensitive calmodulin (Mut-CaM) but not wild-type CaM increased SOCE and decreased its Call-dependent inactivation. Expression of TrpC1 lacking C terminus aa 664-793 (TrpC1DeltaC) also attenuated Ca2+-dependent inactivation of SOCE. CaM interacted with endogenous and expressed TrpC1 and with GST-TrpC1 C terminus but not with TrpC1DeltaC. Two CaM binding domains, aa 715749 and aa 758-793, were identified. Expression of TrpC1Delta758-793 but not TrpC1Delta715-749 mimicked the effects of TrpC1DeltaC and Mut-CaM on SOCE. These data demonstrate that CaM mediates Ca2+-dependent feedback inhibition of SOCE via binding to a domain in the C terminus of TrpC1. These findings reveal an integral role for TrpC1 in the regulation of SOCE. C1 Natl Inst Dent & Craniofacial Res, Secretory Physiol Sect, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD 20892 USA. Ohio State Univ, Neurobiotechnol Ctr, Columbus, OH 43210 USA. RP Ambudkar, IS (reprint author), Natl Inst Dent & Craniofacial Res, Secretory Physiol Sect, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD 20892 USA. OI Singh, Brij/0000-0003-0535-5997 NR 43 TC 99 Z9 103 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD APR PY 2002 VL 9 IS 4 BP 739 EP 750 DI 10.1016/S1097-2765(02)00506-3 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 545YD UT WOS:000175244400008 PM 11983166 ER PT J AU Okamoto, K Li, HY Jensen, MR Zhang, TT Taya, Y Thorgeirsson, SS Prives, C AF Okamoto, K Li, HY Jensen, MR Zhang, TT Taya, Y Thorgeirsson, SS Prives, C TI Cyclin G recruits PP2A to dephosphorylate Mdm2 SO MOLECULAR CELL LA English DT Article ID PROTEIN PHOSPHATASE 2A; ATM-DEPENDENT PHOSPHORYLATION; DNA-DAMAGE; ONCOPROTEIN MDM2; CELL-GROWTH; IN-VIVO; NUCLEOLAR-LOCALIZATION; NUCLEAR EXPORT; G2/M ARREST; P53 AB The function of cyclin G, a commonly induced p53 target, has remained elusive. We show that cyclin G forms a quaternary complex in vivo and in vitro with enzymatically active phosphatase 2A (PP2A) holoenzymes containing B' subunits. Interestingly, cyclin G also binds in vivo and in vitro to Mdm2 and markedly stimulates the ability of PP2A to dephosphorylate Mdm2 at T216. Consistent with these data, cyclin G null cells have both Mdm2 that is hyperphosphorylated at T216 and markedly higher levels of p53 protein when compared to wild-type cells. Cyclin G expression also results in reduced phosphorylation of human Hdm2 at S166. Thus, our data suggest that cyclin G recruits PP2A in order to modulate the phosphorylation of Mdm2 and thereby to regulate both Mdm2 and p53. C1 Columbia Univ, Dept Biol Sci, New York, NY 10027 USA. NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. Natl Canc Ctr, Res Inst, Chuo Ku, Tokyo 104, Japan. RP Prives, C (reprint author), Columbia Univ, Dept Biol Sci, New York, NY 10027 USA. RI Jensen, Michael/E-9677-2011 FU NCI NIH HHS [CA 58316] NR 74 TC 147 Z9 159 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD APR PY 2002 VL 9 IS 4 BP 761 EP 771 DI 10.1016/S1097-2765(02)00504-X PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 545YD UT WOS:000175244400010 PM 11983168 ER PT J AU An, WJ Palhan, VB Karymov, MA Leuba, SH Roeder, RG AF An, WJ Palhan, VB Karymov, MA Leuba, SH Roeder, RG TI Selective requirements for histone H3 and H4N termini in p300-dependent transcriptional activation from chromatin SO MOLECULAR CELL LA English DT Article ID NUCLEOSOME CORE PARTICLES; RNA POLYMERASE-II; N-TERMINI; IN-VITRO; ACETYLTRANSFERASE ACTIVITY; RECOMBINANT CHROMATIN; TAIL DOMAINS; ACETYLATION; YEAST; DNA AB The N-terminal tails of the core histones play important roles in transcriptional regulation, but their mechanism(s) of action are poorly understood. Here, pure chromatin templates assembled with varied combinations of recombinant wild-type and mutant core histones have been employed to ascertain the role of individual histone tails, both in overall acetylation patterns and in transcription. In vitro assays show an indispensable role for H3 and H4 tails, especially major lysine substrates, in p300-dependent transcriptional activation, as well as activator-targeted acetylation of promoter-proximal histone tails by p300. These results indicate, first, that constraints to transcription are imposed by nucleosomal histone components other than histone N-terminal tails and, second, that the histone N-terminal tails have selective roles, which can be modulated by targeted acetylation, in transcriptional activation by p300. C1 Rockefeller Univ, Biochem & Mol Biol Lab, New York, NY 10021 USA. NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. RP Roeder, RG (reprint author), Rockefeller Univ, Biochem & Mol Biol Lab, New York, NY 10021 USA. NR 62 TC 68 Z9 69 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD APR PY 2002 VL 9 IS 4 BP 811 EP 821 DI 10.1016/S1097-2765(02)00497-5 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 545YD UT WOS:000175244400014 PM 11983172 ER PT J AU Akiyama, TE Baumann, CT Sakai, S Hager, GL Gonzalez, FJ AF Akiyama, TE Baumann, CT Sakai, S Hager, GL Gonzalez, FJ TI Selective intranuclear redistribution of PPAR isoforms by RXR alpha SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID PROLIFERATOR-ACTIVATED RECEPTOR; RETINOID-X-RECEPTOR; LIPID-METABOLISM; GENE-EXPRESSION; PEROXISOME PROLIFERATORS; GLUCOCORTICOID-RECEPTOR; FATTY-ACIDS; 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2); ADIPOCYTE DIFFERENTIATION; PROGESTERONE-RECEPTOR AB The intracellular localization of transcriptionally active green fluorescent protein (GFP) chimeras linked to PPARs for human PPARalpha (GFP-PPARhalpha) and mouse PPARalpha, beta, and gamma1 (GFP-PPARmalpha, GFPPPARmbeta, and GFP-PPARmgamma, respectively) was examined in the mouse hepatoma cell line, Hepa-1, using fluorescence microscopy. A predominantly nuclear and diffuse distribution of each isoform was found in both the presence and absence of specific ligands for each receptor. GFP-PPARmalpha-G (containing a Glu282Gly substitution of PPARmalpha) and a phosphorylation mutant, GFP-PPARmgamma-A (containing a Ser82Ala substitution of PPARmgamma), exhibited altered transcriptional activities, but displayed similar intracellular localization patterns compared with their respective wild-type receptors. Coexpression of nuclear receptor corepressor suppressed, whereas steroid receptor coactivator-1 enhanced the transcriptional activity of each of the GFP-PPAR isoforms, but did not discernibly alter their intracellular distributions, both in the presence and absence of PPAR ligands. Interestingly, coexpression of the obligate heterodimeric partner of PPARs, RXRalpha, resulted in an intranuclear redistribution of the GFP-PPARmgamma isoform characterized by a reticulated pattern of the green fluorescent label for PPARgamma within the nucleus, but not in nucleoli, and a heightened concentration of the fluorescent label surrounding nucleolar structures and at the nuclear membrane. Conversely, coexpression of yellow fluorescent protein-RXRalpha and native PPARmgamma resulted in a similar distribution of the yellow fluorescent tag. This localization pattern was not discernibly altered by PPARgamma or RXRalpha-specific ligands. These results implicate RXRalpha in the nuclear reorganization of PPARgamma and suggest that PPARgamma colocalizes with RXRalpha at specific locations within the nucleus independent of added ligand. C1 NCI, Lab Metab, Bethesda, MD 20892 USA. NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. RP NIH, Met Lab, Bldg 37,Room 3E-24,9000 Rockville Pike, Bethesda, MD 20892 USA. EM fjgonz@helix.nih.gov NR 79 TC 46 Z9 48 U1 0 U2 3 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 2002 VL 16 IS 4 BP 707 EP 721 DI 10.1210/me.16.4.707 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 535AN UT WOS:000174622100005 PM 11923467 ER PT J AU Wassif, CA Vied, D Tsokos, M Connor, WE Steiner, RD Porter, FD AF Wassif, CA Vied, D Tsokos, M Connor, WE Steiner, RD Porter, FD TI Cholesterol storage defect in RSH/Smith-Lemli-Opitz syndrome fibroblasts SO MOLECULAR GENETICS AND METABOLISM LA English DT Article DE Smith-Lemli-Opitz syndrome; RSH syndrome; SLOS cholesterol synthesis; LDL metabolism; lysosomal inclusions ID NIEMANN-PICK DISEASE; SONIC-HEDGEHOG; SKIN FIBROBLASTS; CHILD SYNDROME; 3-BETA-HYDROXYSTEROID DEHYDROGENASE; CHONDRODYSPLASIA PUNCTATA; DELTA-7-STEROL REDUCTASE; MOUSE MODEL; MUTATIONS; GENE AB The RSH/Smith-Lemli-Opitz syndrome (SLOS) is a multiple malformation/mental retardation syndrome caused by an inborn error of cholesterol synthesis. Mutations in the 3beta-hydroxysteroid Delta(7)-reductase gene result in impaired enzymatic reduction of 7-dehydrocholesterol (7-DHC) to cholesterol. Cells obtain cholesterol by either de novo synthesis or from exogenous sources by the binding and uptake of low density lipoprotein (LDL) particles. Because de novo synthesis of cholesterol is impaired in SLOS, current investigational therapy for SLOS consists of dietary cholesterol supplementation. However, the potential effects of elevated intracellular levels of 7-DHC on intracellular LDL metabolism have not been described. We now report that in addition to the primary defect in de novo cholesterol synthesis, SLOS fibroblasts have a secondary defect of LDL cholesterol metabolism. Staining of fibroblasts with filipin, a fluorescent polyene antibiotic which binds unesterified sterols, shows that SLOS fibroblasts accumulate unesterified sterols. Further studies show that this increased filipin staining was due to an abnormal accumulation of LDL derived cholesterol rather than due to storage of endogenously synthesized 7-dehydrocholesterol (7-DHC). We have also found that SLOS fibroblasts failed to degrade LDL at a normal rate, and examination of SLOS fibroblasts by electron microscopy demonstrated the formation of lysosomal inclusions similar to that seen in Niemann-Pick type C (NPC) cells. We propose that 7-DHC may directly or indirectly inhibit the function of the NPC protein through its sterol-sensing domain (SSD), and that 7-DHC may perturb the function of other SSD containing proteins in SLOS. (C) 2002 Elsevier Science (USA). All rights reserved. C1 NICHHD, Unit Mol Dysmorphol, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. Oregon Hlth & Sci Univ, Dept Med, Div Endocrinol Diabet & Clin Nutr, Portland, OR 97207 USA. Oregon Hlth Sci Univ, Doernbecher Mem Hosp Children, Dept Pediat, Child Dev & Rehabil Ctr, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Doernbecher Mem Hosp Children, Dept Mol & Med Genet, Child Dev & Rehabil Ctr, Portland, OR 97201 USA. RP Porter, FD (reprint author), NICHHD, Unit Mol Dysmorphol, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. OI Steiner, Robert/0000-0003-4177-4590; Wassif, Christopher/0000-0002-2524-1420 NR 65 TC 28 Z9 29 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 1096-7192 J9 MOL GENET METAB JI Mol. Genet. Metab. PD APR PY 2002 VL 75 IS 4 BP 325 EP 334 AR PII S1096-7192(02)00010-0 DI 10.1016/S1096-7192(02)00010-0 PG 10 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA 552QP UT WOS:000175631300005 PM 12051964 ER PT J AU Yang, XL Pratley, RE Tokraks, S Tataranni, PA Permana, PA AF Yang, XL Pratley, RE Tokraks, S Tataranni, PA Permana, PA TI UCP5/BMCP1 transcript isoforms in human skeletal muscle: relationship of the short-insert isoform with lipid oxidation and resting metabolic rates SO MOLECULAR GENETICS AND METABOLISM LA English DT Article DE uncoupling protein; UCP5; BMCP1; Isoforms; skeletal muscle; energy metabolism; Pima Indians ID BROWN-ADIPOSE-TISSUE; MITOCHONDRIAL UNCOUPLING PROTEIN; INSULIN SECRETORY DYSFUNCTION; MESSENGER-RNA EXPRESSION; ENERGY-EXPENDITURE; DIABETES-MELLITUS; PIMA-INDIANS; GENE-EXPRESSION; LEAN HUMANS; RESISTANCE AB Uncoupling protein 5 (UCP5) or brain mitochondrial carrier protein-1 (BMCP1) enhances mitochondrial proton leak in vitro and its hepatic and brain expression profiles are modulated by diet and cold exposure in mice. Alternative splicing generates three isoforms: a long form (UCP5L), a short form (UCPSS), and a short form with a 31 amino acid insert (UCP5SI). We investigated the relationship between skeletal muscle UCP5 expression and in vivo energy metabolism in 36 non-diabetic Pima Indians. We determined the expression levels of total UCP5 (UCP5T), and the isoforms UCP5L, UCP5S, and UCP5SI (66.8, 32.5, and 0.8% of UCP5T, respectively). None correlated with body weight or percent body fat. The transcript level of UCP5SI, but not the others, was positively correlated with resting metabolic rate (r = 0.38, P = 0.02, adjusted for age, sex, fat mass, and fat-free mass) and lipid oxidation rate (adjusted for age, sex, and percent body fat) during a euglycemic clamp with infusion of insulin at a physiologic concentration (r = 0.42, P = 0.01). (C) 2002 Elsevier Science (USA). All rights reserved. C1 NIDDKD, Clin Diabet & Nutr Sect, Phoenix Epidemiol & Clin Res Branch, NIH, Phoenix, AZ 85016 USA. RP Permana, PA (reprint author), NIDDKD, Clin Diabet & Nutr Sect, Phoenix Epidemiol & Clin Res Branch, NIH, 4212 N 16Th St, Phoenix, AZ 85016 USA. NR 29 TC 11 Z9 11 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 1096-7192 J9 MOL GENET METAB JI Mol. Genet. Metab. PD APR PY 2002 VL 75 IS 4 BP 369 EP 373 AR PII S1096-7192(02)00008-2 DI 10.1016/S1096-7192(02)00008-2 PG 5 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA 552QP UT WOS:000175631300010 PM 12051969 ER PT J AU Khil, PP Camerini-Otero, RD AF Khil, PP Camerini-Otero, RD TI Over 1000 genes are involved in the DNA damage response of Escherichia coli SO MOLECULAR MICROBIOLOGY LA English DT Article ID SACCHAROMYCES-CEREVISIAE; EXPRESSION ANALYSIS; AGENTS; REPAIR; IDENTIFICATION; REPLICATION; INDUCTION; SEQUENCE; PATTERNS; ARRAY AB Changes in gene expression after treatment of Escherichia coli cultures with mitomycin C were assessed using gene array technology. Unexpectedly, a large number of genes (nearly 30% of all genes) displayed significant changes in their expression level. Analysis and classification of expression profiles of the corresponding genes allowed us to assign this large number of genes into one or two dozen small clusters of genes with similar expression profiles. This assignment allowed us to describe systematically the changes in the level of gene expression in response to DNA damage. Among the damage-induced genes, more than 100 are novel. From those genes involved in DNA metabolism that have not previously been shown to be induced by DNA damage, the mutS gene involved in mismatch repair is especially noteworthy. In addition to the SOS response, we observed the induction of other stress response pathways, such as those of oxidative stress and osmotic protection. Among the genes that are downregulated in response to DNA damage are numerous protein biosynthesis genes. Analysis of the gene expression data highlighted the essential involvement of sigma (s) -regulated genes and the general stress response network in the response to DNA damage. C1 NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA. RP Camerini-Otero, RD (reprint author), NIDDK, Genet & Biochem Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA. OI Khil, Pavel/0000-0002-4903-8777 NR 46 TC 130 Z9 136 U1 1 U2 5 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD APR PY 2002 VL 44 IS 1 BP 89 EP 105 DI 10.1046/j.1365-2958.2002.02878.x PG 17 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA 542PB UT WOS:000175052300008 PM 11967071 ER PT J AU Lazo, JS Nemoto, K Pestell, KE Cooley, K Southwick, EC Mitchell, DA Furey, W Gussio, R Zaharevitz, DW Joo, B Wipf, P AF Lazo, JS Nemoto, K Pestell, KE Cooley, K Southwick, EC Mitchell, DA Furey, W Gussio, R Zaharevitz, DW Joo, B Wipf, P TI Identification of a potent and selective pharmacophore for Cdc25 dual specificity phosphatase inhibitors. SO MOLECULAR PHARMACOLOGY LA English DT Article ID CELL-CYCLE; CRYSTAL-STRUCTURE; TYROSINE-PHOSPHATASE; CATALYTIC DOMAIN; SMALL-MOLECULE; CANCER-CELLS; MITOSIS; HOMOLOG; LIBRARY; DESIGN AB Small molecules provide powerful tools to interrogate biological pathways but many important pathway participants remain refractory to inhibitors. For example, Cdc25 dual-specificity phosphatases regulate mammalian cell cycle progression and are implicated in oncogenesis, but potent and selective inhibitors are lacking for this enzyme class. Thus, we evaluated 10,070 compounds in a publicly available chemical repository of the National Cancer Institute for in vitro inhibitory activity against oncogenic, full-length, recombinant human Cdc25B. Twenty-one compounds had mean inhibitory concentrations of <1 μM; >75% were quinones and >40% were of the para-naphthoquinone structural type. Most notable was NSC 95397 (2,3-bis-[2-hydroxyethylsulfanyl]-[1,4]naphthoquinone), which displayed mixed inhibition kinetics with in vitro K-i values for Cdc25A, -B, and -C of 32, 96, and 40 nM, respectively. NSC 95397 was more potent than any inhibitor of dual specificity phosphatases described previously and 125- to 180-fold more selective for Cdc25A than VH1-related dual-specificity phosphatase or protein tyrosine phosphatase 1b, respectively. Modification of the bis-thioethanol moiety markedly decreased enzyme inhibitory activity, indicating its importance for bioactivity. NSC 95397 showed significant growth inhibition against human and murine carcinoma cells and blocked G(2)/M phase transition. A potential Cdc25 site of interaction was postulated based on molecular modeling with these quinones. We propose that inhibitors based on this chemical structure could serve as useful tools to probe the biological function of Cdc25. C1 Univ Pittsburgh, Dept Pharmacol, Pittsburgh, PA 15261 USA. Univ Pittsburgh, Dept Chem, Pittsburgh, PA 15260 USA. Vet Affairs Med Ctr, Biocrystallog Lab, Pittsburgh, PA USA. NCI, Dev Therapeut Program, NIH, Rockville, MD USA. RP Lazo, JS (reprint author), Univ Pittsburgh, Dept Pharmacol, Biomed Sci Tower E1340, Pittsburgh, PA 15261 USA. RI Mitchell, Douglas/C-4400-2011; Mitchell, Doug/B-6349-2012; OI Mitchell, Doug/0000-0002-9564-0953; Barnes, Katharine/0000-0003-4968-3028 FU NCI NIH HHS [CA52995, CA78039, CA82723] NR 35 TC 127 Z9 129 U1 1 U2 4 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 2002 VL 61 IS 4 BP 720 EP 728 AR UNSP 1385/972845 DI 10.1124/mol.61.4.720 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 536ZB UT WOS:000174730800003 PM 11901209 ER PT J AU King, LM Ma, JX Srettabunjong, S Graves, J Bradbury, JA Li, LP Spiecker, M Liao, JK Mohrenweiser, H Zeldin, DC AF King, LM Ma, JX Srettabunjong, S Graves, J Bradbury, JA Li, LP Spiecker, M Liao, JK Mohrenweiser, H Zeldin, DC TI Cloning of CYP2J2 gene and identification of functional polymorphisms SO MOLECULAR PHARMACOLOGY LA English DT Article ID CYTOSOLIC EPOXIDE HYDROLASE; ARACHIDONIC-ACID EPOXIDES; MOLECULAR-CLONING; EPOXYEICOSATRIENOIC ACIDS; PARKINSONS-DISEASE; LUNG-CANCER; HYPERPOLARIZING FACTORS; CDNA CLONING; CYTOCHROME-P450; EXPRESSION AB CYP2J2 is abundant in cardiovascular tissue and active in the metabolism of arachidonic acid to eicosanoids that possess potent anti-inflammatory, vasodilatory, and fibrinolytic properties. We cloned and sequenced the entire CYP2J2 gene (similar to40.3 kb), which contains nine exons and eight introns. We then sequenced the CYP2J2 exons and intron-exon boundaries in 72 healthy persons representing African, Asian, and European/ white populations as part of the National Institutes of Health/ National Institute of Environmental Health Sciences Environmental Genome Single Nucleotide Polymorphism Program. A variety of polymorphisms were found, four of which resulted in coding changes (Arg158Cys, Ile192Asn, Asp342Asn, and Asn404Tyr). A fifth variant (Thr143Ala) was identified by screening a human heart cDNA library. All five variant cDNAs of CYP2J2 were generated by site-directed mutagenesis and expressed in Sf9 insect cells by using a baculovirus system. The recombinant wild-type and variant CYP2J2 proteins immunoreacted with peptide-based antibodies to CYP2J2 and displayed typical cytochrome P450 (P450) CO-difference spectra; however, the Asn404Tyr and Ile192Asn variants also had prominent spectral peaks at 420 nm. The ability of these variants to metabolize arachidonic acid and linoleic acid was compared with that of wild-type CYP2J2. Three variants (Asn404Tyr, Arg158Cys, and Thr143Ala) showed significantly reduced metabolism of both arachidonic acid and linoleic acid. The Ile192Asn variant showed significantly reduced activity toward arachidonic acid only. The Asp342Asn variant showed similar metabolism to wild-type CYP2J2 for both endogenous substrates. Based on these data, we conclude that allelic variants of the human CYP2J2 gene exist and that some of these variants result in a P450 protein that has reduced catalytic function. Insofar as CYP2J2 products have effects in the cardiovascular system, we speculate that these variants may be functionally relevant. C1 NIEHS, Div Intramural Res, Res Triangle Pk, NC 27709 USA. Univ Mainz, Dept Med 2, D-6500 Mainz, Germany. Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Lawrence Livermore Natl Lab, Livermore, CA USA. RP Zeldin, DC (reprint author), NIEHS, Div Intramural Res, 111 TW Alexander Dr,Bldg 101,Room D236, Res Triangle Pk, NC 27709 USA. FU NIEHS NIH HHS [Y1-ES8054-05] NR 61 TC 84 Z9 91 U1 0 U2 5 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 2002 VL 61 IS 4 BP 840 EP 852 AR UNSP 1423/971867 DI 10.1124/mol.61.4.840 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 536ZB UT WOS:000174730800017 PM 11901223 ER PT J AU Lin, ZC Uhl, GR AF Lin, ZC Uhl, GR TI Dopamine transporter mutants with cocaine resistance and normal dopamine uptake provide targets for cocaine antagonism SO MOLECULAR PHARMACOLOGY LA English DT Article ID SEROTONIN TRANSPORTER; NOREPINEPHRINE TRANSPORTERS; TRANSMEMBRANE DOMAIN; SUBSTRATE TRANSPORT; STRUCTURAL DOMAINS; ANALOG RECOGNITION; BINDING; MUTATIONS; RESIDUES; 1-METHYL-4-PHENYLPYRIDINIUM AB Cocaine's blockade of dopamine reuptake by brain dopamine transporters (DAT) is a central feature of current understanding of cocaine reward and addiction. Empirical screening of small-molecule chemical libraries has thus far failed to provide successful cocaine blockers that allow dopamine reuptake in the presence of cocaine and provide cocaine "antagonism". We have approached this problem by assessing expression, dopamine uptake, and cocaine analog affinities of 56 DAT mutants in residues located in or near transmembrane domains likely to play significant roles in cocaine recognition and dopamine uptake. A phenylalanine-to-alanine mutant in putative DAT transmembrane domain 3, F154A, retains normal dopamine uptake, lowers cocaine affinity 10-fold, and reduces cocaine stereospecificity. Such mutants provide windows into DAT structures that could serve as targets for selective cocaine blockers and document how combined strategies of mutagenesis and small molecule screening may improve our abilities to identify and design compounds with such selective properties. C1 NIDA, Mol Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Uhl, GR (reprint author), NIDA, Mol Neurobiol Branch, Intramural Res Program, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 30 TC 32 Z9 32 U1 0 U2 1 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 2002 VL 61 IS 4 BP 885 EP 891 AR UNSP 1468/974120 DI 10.1124/mol.61.4.885 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 536ZB UT WOS:000174730800022 PM 11901228 ER PT J AU Mastakov, MY Baer, K Kotin, RM During, MJ AF Mastakov, MY Baer, K Kotin, RM During, MJ TI Recombinant adeno-associated virus serotypes 2-and 5-mediated gene transfer in the mammalian brain: Quantitative analysis of heparin co-infusion SO MOLECULAR THERAPY LA English DT Article DE rAAV; heparin; injection parameters; CNS; gene therapy ID HERPES-SIMPLEX VIRUS; CENTRAL-NERVOUS-SYSTEM; ADENOASSOCIATED VIRUS; SULFATE PROTEOGLYCAN; TYROSINE-HYDROXYLASE; BEHAVIORAL RECOVERY; NEUROTROPHIC FACTOR; TYPE-2 INFECTION; AAV VECTOR; EXPRESSION AB Recombinant adeno-associated viruses (rAAVs) are among the most promising vectors for gene delivery into the CNS. However, a major hurdle for gene transfer to the mammalian brain is to achieve high transduction levels in target cells beyond the immediate injection site. Therefore, building upon the optimization of injection parameters on which we have recently reported, it is important to define additional methods to increase the volume of distribution. Here, we establish an optimal heparin concentration, and show that co-injection of heparin together with rAAV2 leads to a significantly higher and more homogeneous distribution of transduced cells. In contrast, the diffusion pattern of rAAV serotype 5 differs from that of rAAV2, in that its distribution is less homogeneous, more variable, and patchy. Furthermore, this study illustrates the influence of receptor binding on the expression pattern following injection of rAAV in the CNS. In addition to improvements in expression cassettes and viral titers and the use of very slow infusion rates, gene transfer studies in the CNS where the goal is to obtain widespread transduction should consider co-injecting the viral vector rAAV2 with heparin to maximize transduction efficiency and viral spread. C1 Univ Auckland, Fac Med & Hlth Sci, Div Mol Med, Funct Genom & Transiat Neuorsci Lab, Auckland 1, New Zealand. NHLBI, Lab Biochem Genet, NIH, Bethesda, MD 20892 USA. Jefferson Med Coll, CNS Gene Therapy Ctr, Philadelphia, PA 19107 USA. RP During, MJ (reprint author), Univ Auckland, Fac Med & Hlth Sci, Div Mol Med, Funct Genom & Transiat Neuorsci Lab, Auckland 1, New Zealand. RI kotin, robert/B-8954-2008 FU NINDS NIH HHS [R01 NS39144] NR 60 TC 49 Z9 52 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 1525-0016 J9 MOL THER JI Mol. Ther. PD APR PY 2002 VL 5 IS 4 BP 371 EP 380 DI 10.1006/mthe.2002.0564 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 539LL UT WOS:000174871500007 PM 11945063 ER PT J AU Wu, XFS Rao, K Zhang, H Wang, F Sellers, JR Matesic, LE Copeland, NG Jenkins, NA Hammer, JA AF Wu, XFS Rao, K Zhang, H Wang, F Sellers, JR Matesic, LE Copeland, NG Jenkins, NA Hammer, JA TI Identification of an organelle receptor for myosin-Va SO NATURE CELL BIOLOGY LA English DT Article ID MELANOSOME DISTRIBUTION; DILUTE MELANOCYTES; MUTATIONS; TRANSPORT; PROTEIN; MOTOR; LOCUS; GENE; MICE AB Little is known about how molecular motors bind to their vesicular cargo. Here we show that myosin-Va, an actin-based vesicle motor, binds to one of its cargoes, the melanosome, by interacting with a receptor-protein complex containing Rab27a and melanophilin, a postulated Rab27a effector. Rab27a binds to the melanosome first and then recruits melanophilin, which in turn recruits myosin-Va. Melanophilin creates this link by binding to Rab27a in a GTP-dependent fashion through its amino terminus, and to myosin-Va through its carboxy terminus. Moreover, this latter interaction, similar to the ability of myosin-Va to colocalize with melanosomes and influence their distribution in vivo, is absolutely dependent on the presence of exon-F, an alternatively spliced exon in the myosin-Va tall. These results provide the first molecular description of an organelle receptor for an actin-based motor, illustrate how alternate exon usage can be used to specify cargo, and further expand the functional repertoire of Rab GTPases and their effectors. C1 NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA. NCI, Mouse Canc Genet Program, NIH, Bethesda, MD 20892 USA. RP Wu, XFS (reprint author), NHLBI, Cell Biol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 37 TC 314 Z9 318 U1 1 U2 14 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1465-7392 J9 NAT CELL BIOL JI Nat. Cell Biol. PD APR PY 2002 VL 4 IS 4 BP 271 EP 278 DI 10.1038/ncb670 PG 8 WC Cell Biology SC Cell Biology GA 541PY UT WOS:000174994000014 PM 11887186 ER PT J AU Pece, S Gutkind, JS AF Pece, S Gutkind, JS TI E-cadherin and Hakai: signalling, remodeling or destruction? SO NATURE CELL BIOLOGY LA English DT Editorial Material ID CELLS AB Activation of tyrosine kinase receptors in epithelial cells results in the rapid disassembly of E-cadherin-mediated cell-cell adhesions. New research has identified Hakai, an E3-uiquitin-ligase related to Cbl that binds E-cadherin in a tyrosine phosphorylation-dependent manner. By promoting the endocytosis and dynamic recycling or destruction of E-cadherin complexes, Hakai may control epithelial-mesenchymal transitions under physiological and pathological conditions. C1 Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. European Inst Oncol, Dept Expt Oncol, I-20141 Milan, Italy. RP Pece, S (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, Bethesda, MD 20892 USA. RI Gutkind, J. Silvio/A-1053-2009; Pece, Salvatore/B-9609-2013 OI Pece, Salvatore/0000-0003-1764-3929 NR 15 TC 44 Z9 48 U1 0 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1465-7392 J9 NAT CELL BIOL JI Nat. Cell Biol. PD APR PY 2002 VL 4 IS 4 BP E72 EP E74 DI 10.1038/ncb0402-e72 PG 3 WC Cell Biology SC Cell Biology GA 541PY UT WOS:000174994000005 PM 11944035 ER PT J AU Yamada, KM Even-Ram, S AF Yamada, KM Even-Ram, S TI Integrin regulation of growth factor receptors SO NATURE CELL BIOLOGY LA English DT Editorial Material ID PROTEIN-COUPLED RECEPTORS; TYROSINE KINASES; EGF RECEPTOR; PHOSPHORYLATION; ACTIVATION AB Integrins are receptors for extracellular matrix proteins that engage in reciprocal crosstalk with growth factor receptors. Recent work identifies a unique mechanism for the regulation of growth factor receptor phosphorylation by integrins, indicating multiple ways of achieving cooperation between these major signalling systems. C1 Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. RP Yamada, KM (reprint author), Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 15 TC 189 Z9 193 U1 2 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1465-7392 J9 NAT CELL BIOL JI Nat. Cell Biol. PD APR PY 2002 VL 4 IS 4 BP E75 EP E76 DI 10.1038/ncb0402-e75 PG 2 WC Cell Biology SC Cell Biology GA 541PY UT WOS:000174994000007 PM 11944037 ER PT J AU Zhang, JZ Zhang, YP Rosenberg, HF AF Zhang, JZ Zhang, YP Rosenberg, HF TI Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey SO NATURE GENETICS LA English DT Article ID POSITIVE DARWINIAN SELECTION; RAPID EVOLUTION; SUBSTITUTIONS; FEATURES; PROTEIN; RATES AB Although the complete genome sequences of over 50 representative species have revealed the many duplicated genes in all three domains of life(1-4), the roles of gene duplication in organismal adaptation and biodiversity are poorly understood. In addition, the evolutionary forces behind the functional divergence of duplicated genes are often unknown, leading to disagreement on the relative importance of positive Darwinian selection versus relaxation of functional constraints in this process(5-10). The methodology of earlier studies relied largely on DNA sequence analysis but lacked functional assays of duplicated genes, frequently generating contentious results(11,12). Here we use both computational and experimental approaches to address these questions in a study of the pancreatic ribonuclease gene (RNASE1) and its duplicate gene (RNASE1B) in a leaf-eating colobine monkey, douc langur. We show that RNASE1B has evolved rapidly under positive selection for enhanced ribonucleolytic activity in an altered microenvironment, a response to increased demands for the enzyme for digesting bacterial RNA. At the same time, the ability to degrade double-stranded RNA, a non-digestive activity characteristic of primate RNASE1, has been lost in RNASE1B, indicating functional specialization and relaxation of purifying selection. Our findings demonstrate the contribution of gene duplication to organismal adaptation and show the power of combining sequence analysis and functional assays in delineating the molecular basis of adaptive evolution. C1 NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. Univ Michigan, Dept Ecol & Evolutionary Biol, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA. Chinese Acad Sci, Kunming Inst Zool, Kunming, Yunnan, Peoples R China. RP Zhang, JZ (reprint author), NIAID, Host Def Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 33 TC 215 Z9 243 U1 3 U2 37 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 2002 VL 30 IS 4 BP 411 EP 415 DI 10.1038/ng852 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 536BZ UT WOS:000174682000019 PM 11925567 ER PT J AU Lincoln, AJ Wickramasinghe, D Stein, P Schultz, RM Palko, ME De Miguel, MP Tessarollo, L Donovan, PJ AF Lincoln, AJ Wickramasinghe, D Stein, P Schultz, RM Palko, ME De Miguel, MP Tessarollo, L Donovan, PJ TI Cdc25b phosphatase is required for resumption of meiosis during oocyte maturation SO NATURE GENETICS LA English DT Article ID MEIOTIC COMPETENCE; MOUSE OOCYTES; CELL-CYCLE; PROTEIN; YEAST; HOMOLOG; DEPHOSPHORYLATION; ACTIVATION; MITOSIS; ACQUISITION AB In a wide variety of animal species, oocyte maturation is arrested temporarily at prophase of meiosis I (ref. 1). Resumption of meiosis requires activation of cyclin-dependent kinase-1 (CDK1, p34cdc2), one component of maturation-promoting factor (MPF)(2,3). The dual specificity phosphatases Cdc25a, Cdc25b and Cdc25c are activators of cyclin-dependent kinases(4-8); consequently, they are postulated to regulate cell-cycle progression in meiosis and mitosis as well as the DNA-damage response(9-12). We generated Cdc25b-deficient (Cdc25b(-/-)) mice and found that they are viable. As compared with wildtype cells, fibroblasts from Cdc25b(-/-) mice grew vigorously in culture and arrested normally in response to DNA damage. Female Cdc25b(-/-) mice were sterile, and Cdc25b(-/-) oocytes remained arrested at prophase with low MPF activity. Microinjection of wildtype Cdc25b mRNA into Cdc25b(-/-) oocytes caused activation of MPF and resumption of meiosis. Thus, Cdc25b(-/-) female mice are sterile because of permanent meiotic arrest resulting from the inability to activate MPF. Cdc25b is therefore essential for meiotic resumption in female mice. Mice lacking Cdc25b provide the first genetic model for studying the mechanisms regulating prophase arrest in vertebrates. C1 NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Univ Penn, Dept Biol, Philadelphia, PA 19104 USA. RP Donovan, PJ (reprint author), Thomas Jefferson Univ, Kimmel Canc Ctr, Dept Microbiol & Immunol, Philadelphia, PA 19107 USA. NR 26 TC 161 Z9 177 U1 3 U2 13 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 2002 VL 30 IS 4 BP 446 EP 449 DI 10.1038/ng856 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 536BZ UT WOS:000174682000026 PM 11912493 ER PT J AU Shih, TAY Roederer, M Nussenzweig, MC AF Shih, TAY Roederer, M Nussenzweig, MC TI Role of antigen receptor affinity in T cell-independent antibody responses in vivo SO NATURE IMMUNOLOGY LA English DT Article ID SIGNAL-TRANSDUCTION MOLECULE; GERMINAL CENTER FORMATION; LYN-DEFICIENT MICE; HEAVY-CHAIN GENE; B-CELL; IMMUNE-RESPONSE; PNEUMOCOCCAL POLYSACCHARIDE; C57BL-6 MICE; MOUSE; CD19 AB To examine how B cell receptor affinity affects clonal selection in thymus-independent type 2 (T1-2) immune responses, we produced mice with antibodies that showed a 40-fold difference in affinity for the hapten (4-hydroxy-3-nitrophenyl) acetyl (NP). The difference in the responses of high- and low-affinity B cells to NP-Ficoll was only twofold. However, in competition experiments only the high-affinity B cells responded to antigen. CD19 deficiency increased the affinity threshold of T1-2 responses, whereas Lyn deficiency enhanced clonal expansion but abrogated B cell terminal differentiation. Thus, in T1-2 immune responses, large differences in affinity produce only small differences in the intrinsic ability of B cells to respond to antigen, and selection for high- affinity clones is due to clonal competition during the earliest stages of the response. C1 Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA. NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. Howard Hughes Med Inst, New York, NY 10021 USA. RP Nussenzweig, MC (reprint author), Rockefeller Univ, Lab Mol Immunol, 1230 York Ave, New York, NY 10021 USA. RI Roederer, Mario/G-1887-2011 FU NIGMS NIH HHS [GM07739] NR 56 TC 109 Z9 113 U1 0 U2 2 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD APR PY 2002 VL 3 IS 4 BP 399 EP 406 DI 10.1038/ni776 PG 8 WC Immunology SC Immunology GA 535BD UT WOS:000174623600022 PM 11896394 ER PT J AU Grossman, Z Meier-Schellersheim, M Sousa, AE Victorino, RMM Paul, WE AF Grossman, Z Meier-Schellersheim, M Sousa, AE Victorino, RMM Paul, WE TI CD4(+) T-cell depletion in HIV infection: Are we closer to understanding the cause? SO NATURE MEDICINE LA English DT Editorial Material ID ACTIVE ANTIRETROVIRAL THERAPY; RHESUS MACAQUES; RAPID TURNOVER; ACTIVATION; HOMEOSTASIS; AIDS; DYSFUNCTION; LYMPHOCYTES; POPULATION; DIVISION AB Is CD4(+) cell depletion due to rapid elimination by HIV and failure of the immune system to replace these cells at the required rate? Increasing evidence suggests that this is not the case, and that infection-induced immune activation drives both viral replication and CD4(+) cell depletion. C1 Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. Fac Med Lisbon, Inst Mol Med, Lisbon, Portugal. RP Grossman, Z (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel. RI Grossman, Zvi/A-9643-2008; Sousa, Ana E./L-2642-2014; Victorino, Rui/N-7948-2013 OI Sousa, Ana E./0000-0002-4618-9799; Victorino, Rui/0000-0001-7567-1704 NR 36 TC 324 Z9 333 U1 0 U2 8 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 2002 VL 8 IS 4 BP 319 EP 323 DI 10.1038/nm0402-319 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 536ML UT WOS:000174704800016 PM 11927927 ER PT J AU Diamond, JS AF Diamond, JS TI A broad view of glutamate spillover SO NATURE NEUROSCIENCE LA English DT Editorial Material ID SILENT SYNAPSES; HIPPOCAMPUS; RECEPTOR; ACTIVATION C1 NINCDS, Synapt Physiol Unit, NIH, Bethesda, MD 20892 USA. RP Diamond, JS (reprint author), NINCDS, Synapt Physiol Unit, NIH, 36 Convent Dr, Bethesda, MD 20892 USA. RI Diamond, Jeffrey/C-1835-2015 OI Diamond, Jeffrey/0000-0002-1770-2629 NR 14 TC 37 Z9 39 U1 0 U2 1 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1097-6256 J9 NAT NEUROSCI JI Nat. Neurosci. PD APR PY 2002 VL 5 IS 4 BP 291 EP 292 DI 10.1038/nn0402-291 PG 2 WC Neurosciences SC Neurosciences & Neurology GA 534UQ UT WOS:000174606900004 PM 11914716 ER PT J AU Koslow, SH AF Koslow, SH TI Sharing primary data: a threat or asset to discovery? SO NATURE REVIEWS NEUROSCIENCE LA English DT Review ID BRAIN AB The degree of complexity of neuroscience data is a sufficient reason both for sharing and for not sharing primary data. Sharing data should make research more efficient and greatly facilitate our understanding of brain function. The intellectual challenges are identical with or without data sharing. Sharing increases the value of the data and provides new knowledge and understanding. C1 NIMH, Off Neuroinformat, NIH, Bethesda, MD 20892 USA. RP Koslow, SH (reprint author), NIMH, Off Neuroinformat, NIH, 6001 Execut Blvd, Bethesda, MD 20892 USA. NR 8 TC 41 Z9 42 U1 1 U2 4 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1471-0048 J9 NAT REV NEUROSCI JI Nat. Rev. Neurosci. PD APR PY 2002 VL 3 IS 4 BP 311 EP 313 DI 10.1038/nrn787 PG 3 WC Neurosciences SC Neurosciences & Neurology GA 537CE UT WOS:000174739200017 PM 11967561 ER PT J AU Aldosari, N Wiltshire, RN Dutra, A Schrock, E McLendon, RE Friedman, HS Bigner, DD Bigner, SH AF Aldosari, N Wiltshire, RN Dutra, A Schrock, E McLendon, RE Friedman, HS Bigner, DD Bigner, SH TI Comprehensive molecular cytogenetic investigation of chromosomal abnormalities in human medulloblastoma cell lines and xenograft SO NEURO-ONCOLOGY LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; IN-SITU HYBRIDIZATION; BRAIN-TUMORS; AMPLIFICATION; LIMITATIONS; GENE AB Cell lines and xenografts derived from medulloblastomas are useful tools to investigate the chromosomal changes in these tumors. Here we used G-banding, fluorescence in situ hybridization (FISH), spectral karyotyping (SKY), and comparative genomic hybridization to study 4 medulloblastoma cell lines and 1 xenograft. Cell line D-425 Med had a relatively simple karyotype, with a terminal deletion of 10q and amplification of MYC in double-minutes (dmins). FISH demonstrated that an apparent isochromosome (17q) by routine karyotyping was actually an unbalanced translocation between 2 copies of chromosome 17. Cell line D-556 Med also had a simple near-diploid stemline with an unbalanced 1;13 translocation resulting in a gain of 1q, an isochromosome (17q), and dmins. These findings were initially described using routine G-banded preparations, and FISH showed that the dmins were an amplification of MYC and the i(17q) was an isodicentric 17q chromosome. The other finding was confirmed by FISH, SKY, and comparative genomic hybridization. Cell lines D-721 Med and D-581 Med had complex karyotypic patterns that could be completely characterized only when FISH and SKY were used. Xenograft D-690 Med also had a complex pattern that FISH and SKY were helpful in completely elucidating. Interestingly, balanced reciprocal translocations were seen as well as complicated unbalanced translocations and marker chromosomes. Comparative genomic hybridization demonstrated only a deletion of 10q22-10q24, supporting the idea that despite the complexity of the chromosomal rearrangements, minimal alterations in the overall chromosomal content had occurred. This study demonstrates that routine cytogenetic preparations are adequate to describe chromosomal abnormalities in occasional medulloblastoma samples, but a broader spectrum of molecular cytogenetic methods is required to completely analyze most of these tumor samples. C1 Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA. Inst Mol Biotechnol, D-07745 Jena, Germany. NHGRI, NIH, Bethesda, MD 20892 USA. RP Bigner, SH (reprint author), Duke Univ, Med Ctr, Dept Pathol, POB 3712, Durham, NC 27710 USA. FU NCI NIH HHS [CA-68119] NR 29 TC 26 Z9 26 U1 0 U2 3 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA SN 1522-8517 J9 NEURO-ONCOLOGY JI Neuro-Oncology PD APR PY 2002 VL 4 IS 2 BP 75 EP 85 DI 10.1215/15228517-4-2-75 PG 11 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 534RJ UT WOS:000174600300001 PM 11916498 ER PT J AU Kamitani, H Taniura, S Watanabe, K Sakamoto, M Watanabe, T Eling, T AF Kamitani, H Taniura, S Watanabe, K Sakamoto, M Watanabe, T Eling, T TI Histone acetylation may suppress human glioma cell proliferation when p21WAF/Cip1 and gelsolin are induced SO NEURO-ONCOLOGY LA English DT Article ID HUMAN CANCER-CELLS; DEACETYLASE INHIBITORS; ERYTHROLEUKEMIA-CELLS; GROWTH-INHIBITION; MALIGNANT GLIOMA; DOWN-REGULATION; IN-VIVO; DIFFERENTIATION; EXPRESSION; BUTYRATE AB Histone deacetylase inhibitors that increase histone acetylation on transformed cells are being investigated as unique anticancer drugs. The aim of this investigation was to evaluate an anti proliferative activity of the histone deacetylase inhibitors sodium butyrate (NaBT) and trichostatin A on 5 glioma cell lines, T98G, A172, U-87 MG, U-118 MG, and U-373 MG, with the examination of the altered expressions in p21 and gelsolin genes. Treatment with 5-mM NaBT and 40 ng/ml trichostatin A for 48 h caused more than a 50% growth inhibition in 5 cell lines as measured by cell proliferation assays. An increase in histone acetylation was confirmed in each cell line. After treatment with 5 mM NaBT, T98G, A172, and U118 cells undergo apoptosis as indicated by DNA ladder formation. Treatment with NaBT and trichostatin A also decreased DNA synthesis as examined by the fluorescence-activated cell sorting analysis in T98G and U87 cells. In addition to the suppression of cell growth, the up regulation of p21 and gelsolin expression was observed after treatment with NaBT, especially in T98G cells. Maximum expression of p21 and gelsolin was observed within 24 h after treatment. Results from our in vitro studies indicate that the treatment of human glioma cells with one of the histone deacetylase inhibitors suppresses cell growth with decreasing DNA synthesis and stimulates apoptosis, and that associated molecular mechanisms responsible for these effects include increased histone acetylation as well as enhanced expression of p21 and gelsolin. C1 Tottori Univ, Fac Med, Inst Neurol Sci, Dept Neurosurg, Tottori 6838504, Japan. NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. RP Kamitani, H (reprint author), 36-1 Nishi Cho, Tottori 6838504, Japan. NR 36 TC 37 Z9 46 U1 0 U2 1 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA SN 1522-8517 J9 NEURO-ONCOLOGY JI Neuro-Oncology PD APR PY 2002 VL 4 IS 2 BP 95 EP 101 DI 10.1215/15228517-4-2-95 PG 7 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 534RJ UT WOS:000174600300003 PM 11916500 ER PT J AU Tendi, EA Bosetti, F DasGupta, SF Stella, AMG Drieu, K Rapoport, SI AF Tendi, EA Bosetti, F DasGupta, SF Stella, AMG Drieu, K Rapoport, SI TI Ginkgo biloba extracts EGb 761 and bilobalide increase NADH dehydrogenase mRNA level and mitochondrial respiratory control ratio in PC12 cells SO NEUROCHEMICAL RESEARCH LA English DT Article DE Ginkgo biloba EGb 761; bilobalide; PC12 cells; NADH dehydrogenase; mitochondria; respiration ID CYTOCHROME-C-OXIDASE; PARKINSONS-DISEASE; HUNTINGTONS-DISEASE; HEART-MITOCHONDRIA; CEREBRAL-CORTEX; EGB-761; BRAIN; PEROXIDATION; INVOLVEMENT; EXPRESSION AB In the present study, we investigated the effect of Ginkgo biloba extract, EGb 761, and one of its components, bilobalide, on gene expression of subunit I of mitochondrial NADH dehydrogenase (ND1) in PC12 cells. By Northern blot analysis we found a similar to2-fold significant increase in ND1 mRNA level, after 48 and 72 h exposure to 100 mug/ml EGb 761 and to 10 mug/ml bilobalide. We also evaluated, by oxygraphy measurements, mitochondrial respiration during state 3 and state 4. In cells treated with EGb 761 and bilobalide for 48 and 72 h, state 4 respiration was significantly decreased, and the respiratory control ratio was increased. These results provide evidence that EGb 761 and bilobalide exert their protective effects by up-regulating mitochondrial ND1 gene expression and by decreasing state 4 respiration, whose increase is thought to be responsible for oxidative damage. C1 NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA. Univ Catania, Fac Med, Dept Chem, Sect Biochem & Mol Bio, I-95125 Catania, Italy. IHB IPSEN, F-75781 Paris, France. RP Tendi, EA (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bldg 49,Rm 5A78,49 Convent Drive, Bethesda, MD 20892 USA. NR 32 TC 38 Z9 41 U1 1 U2 3 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0364-3190 J9 NEUROCHEM RES JI Neurochem. Res. PD APR PY 2002 VL 27 IS 4 BP 319 EP 323 AR UNSP 0364-3190/02/0400-0319/0 DI 10.1023/A:1014963313559 PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 539DJ UT WOS:000174854300009 PM 11958534 ER PT J AU Schueler, U Kaneski, C Murray, G Sandhoff, K Brady, RO AF Schueler, U Kaneski, C Murray, G Sandhoff, K Brady, RO TI Uptake of mannose-terminal glucocerebrosidase in cultured human cholinergic and dopaminergic neuron cell lines SO NEUROCHEMICAL RESEARCH LA English DT Article DE Gaucher disease; glucocerebrosidase delivery to neurons ID MACROPHAGE-TARGETED GLUCOCEREBROSIDASE; GAUCHERS-DISEASE; HORSERADISH-PEROXIDASE; REPLACEMENT THERAPY; PARKINSONS-SYNDROME; MODEL; GLYCOPROTEINS; DEFICIENCY; CEREBELLUM; INFANTILE AB Enzyme replacement therapy has been shown to be particularly effective for patients with type I (non-neuronopathic) Gaucher disease. However, intravenously administered glucocerebrosidase does not reverse or halt the progression of brain damage in patients with type 2 (acute neuronopathic) Gaucher disease. A previous investigation revealed that intracerebral infusion of mannose-terminal glucocerebrosidase was safe in experimental animals. The enzyme had a comparatively long half-life in the brain. It was transported by convection from the site of infusion along white matter fiber tracts to the cerebral cortex where it was endocytosed by neurons. In anticipation of intracerebral administration of mannose-terminal glucocerebrosidase to patients with type 2 Gaucher disease, it was important to learn the mechanism involved in its cellular uptake. We therefore compared the endocytosis of this enzyme by J774 macrophage cells with that in two human neuronal cell lines and a human astrocyte cell line. Mannose-terminal glucocerebrosidase was taken up by cholinergic LA-N-2 cells, but to a much lower extent than by macrophages. Considerably less of the enzyme was endocytosed by dopaminergic SH-SY5Y cells. It was not taken up by NHA astrocytes. The findings provide encouragement for an exploration of intracerebral administration of glucocerebrosidase in patients with type 2 Gaucher disease. C1 NINCDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA. Univ Bonn, Inst Chem & Biochem, D-5300 Bonn, Germany. RP Schueler, U (reprint author), NIMH, Lab Cellular & Mol Regulat, Funct Neuroanat Sect, NIH, Bldg 36,Room 2D15, Bethesda, MD 20892 USA. OI Kaneski, Christine/0000-0003-1453-2502 NR 28 TC 9 Z9 9 U1 0 U2 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0364-3190 J9 NEUROCHEM RES JI Neurochem. Res. PD APR PY 2002 VL 27 IS 4 BP 325 EP 330 AR UNSP 0364-3190/02/0400-0325/0 DI 10.1023/A:1014915430398 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 539DJ UT WOS:000174854300010 PM 11958535 ER PT J AU Leong, DS Terron, JA Falcon-Neri, A Armando, I Ito, T Johren, O Tonelli, LH Hoe, KL Saavedra, JM AF Leong, DS Terron, JA Falcon-Neri, A Armando, I Ito, T Johren, O Tonelli, LH Hoe, KL Saavedra, JM TI Restraint stress modulates brain, pituitary and adrenal expression of angiotensin II AT(1A), AT(1B) and AT(2) receptors SO NEUROENDOCRINOLOGY LA English DT Article DE angiotensin; angiotensin receptors; in situ hybridization; stress; paraventricular nucleus; subfornical organ; adrenal gland ID HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; MESSENGER-RNA EXPRESSION; RAT-BRAIN; GENE-EXPRESSION; PHOSPHOINOSITIDE HYDROLYSIS; ANTERIOR-PITUITARY; SUBFORNICAL ORGAN; TYPE-1 RECEPTOR; BINDING-SITES; SUBTYPES AB Angiotensin II (Ang II) AT(1) receptors are involved in the regulation of the stress response. In adult male rats, acute restraint increased AT(1A) mRNA in paraventricular nucleus. Repeated restraint increased AT(1A) mRNA and AT(1) binding in paraventricular nucleus and AT(1) binding in subfornical organ and median eminence. AT(1B) and AT(2) receptors were not expressed in brain areas involved in the stress response. Acute restraint increased anterior pituitary AT(1A) mRNA and AT(1) binding and decreased AT(1B) mRNA. During repeated restraint, the increase in AT(1A) mRNA in the anterior pituitary was maintained, but AT(1B) mRNA and AT, binding returned to normal levels. In adrenal zona glomerulosa, AT(1B) mRNA, AT(1) binding, AT(2) mRNA and AT(2) binding decreased during acute restraint. Receptor mRNA and binding returned to normal after repeated stress, with the exception of rebound increase in adrenal zona glomerulosa AT(2) mRNA. In adrenal medulla, AT(1A) mRNA increased and AT(2) mRNA decreased during acute restraint. AT(1A) mRNA remained increased during repeated restraint, while alterations in AT(2) mRNA were no longer present. Expression of AT(1A), AT(1B) and AT(2) receptors in the hypothalamic-pituitary-adrenal axis is tissue specific and is different in acute and repeated stress. Increased brain, pituitary and adrenomedullary AT(1A) receptor expression correlates with hypothalamic-pituitary-adrenal axis stimulation, supporting the hypothesis of Ang II, through selective AT(1A) receptor stimulation, as an important determinant of the acute and repeated stress response. Decreased adrenal zona glomerulosa and anterior pituitary AT(1B) receptors during acute stress can be interpreted as compensatory to increased stimulation by Ang II. There may be additional roles for adrenal AT(2) receptors during acute stress, possibly related to interaction or cross-talk with AT(1) receptors. C1 NIMH, Pharmacol Sect, Bethesda, MD 20892 USA. RP Saavedra, JM (reprint author), NIMH, Pharmacol Sect, 10 Ctr Dr,MSC 1514,Bld 10,Rm 2D-57, Bethesda, MD 20892 USA. RI Johren, Olaf/G-6967-2011 NR 57 TC 56 Z9 57 U1 0 U2 5 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD APR PY 2002 VL 75 IS 4 BP 227 EP 240 DI 10.1159/000054714 PG 14 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 546WL UT WOS:000175299000003 PM 11979053 ER PT J AU Crawley, JN Mufson, EJ Hohmann, JG Teklemichael, D Steiner, RA Holmberg, K Xu, ZQD Blakeman, KH Xu, XJ Wiesenfeld-Hallin, Z Bartfai, T Hokfelt, T AF Crawley, JN Mufson, EJ Hohmann, JG Teklemichael, D Steiner, RA Holmberg, K Xu, ZQD Blakeman, KH Xu, XJ Wiesenfeld-Hallin, Z Bartfai, T Hokfelt, T TI Galanin overexpressing transgenic mice SO NEUROPEPTIDES LA English DT Article ID CENTRALLY ADMINISTERED GALANIN; NEURONS FOLLOWING AXOTOMY; NERVE GROWTH-FACTOR; ALZHEIMERS-DISEASE; BASAL FOREBRAIN; SENSORY NEURONS; ACETYLCHOLINE-RELEASE; MESSENGER PLASTICITY; HIPPOCAMPAL GALANIN; VENTRAL HIPPOCAMPUS AB Galanin overexpressing transgenic mice (GAL-tg) were generated on two different promoters. Both lines of GAL-tg displayed high levels of galanin in the hippocampus and reduced sensitivity to seizures, as compared to their respective wildtype littermate controls (WT). Performance deficits on learning and memory tasks, impaired long-term potentiation, reduced hippocampal excitability, lower evoked glutamate release, and reduced numbers of choline acetyltransferase immunoreactive neurons in the horizontal limb of the diagonal band were detected in GAL-tg as compared to WT. Changes in sensitivity to nociceptive stimuli were demonstrated in one line. GAL-tg represent a new model for investigating the biological actions of endogenous galanin, and for testing novel therapeutics based on galanin receptor ligands. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 NIMH, Sect Behav Genom, NIH, Bethesda, MD 20892 USA. Rush Presbyterian St Lukes Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA. Rush Presbyterian St Lukes Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA. Univ Washington, Sch Med, Dept Obstet & Gynecol, Seattle, WA 98195 USA. Univ Washington, Sch Med, Dept Physiol & Biophys, Seattle, WA 98195 USA. Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden. Huddinge Univ Hosp, Karolinska Inst, Clin Neurophysiol Sect, S-14186 Huddinge, Sweden. Karolinska Inst, Dept Biochem & Biophys, S-17177 Stockholm, Sweden. Scripps Res Inst, Res Inst, Dept Neuropharmacol, Harold L Dorris Neurol Res Ctr, La Jolla, CA 92037 USA. RP Crawley, JN (reprint author), NIMH, Sect Behav Genom, NIH, Bldg 10 Room 4D11, Bethesda, MD 20892 USA. EM crawleyj@intra.nimh.nih.gov FU NIA NIH HHS [AG10668]; NICHD NIH HHS [R01 HD27142, U54 HD 12629] NR 78 TC 44 Z9 44 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0143-4179 EI 1532-2785 J9 NEUROPEPTIDES JI Neuropeptides PD APR-JUN PY 2002 VL 36 IS 2-3 BP 145 EP 156 DI 10.1054/npep.2002.0891 PG 12 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 597AV UT WOS:000178200500010 PM 12359505 ER PT J AU Jiang, Y Luo, YJ Parasuraman, R AF Jiang, Y Luo, YJ Parasuraman, R TI Priming of two-dimensional visual motion is reduced in older adults SO NEUROPSYCHOLOGY LA English DT Article; Proceedings Paper CT Cognitive Aging Conference CY APR, 2000 CL ATLANTA, GEORGIA ID AGE-RELATED DIFFERENCES; APPARENT MOTION; PERCEPTION; DIRECTION; SENSITIVITY; MECHANISMS; INERTIA; BRAIN; AREA; MT AB Previously, Y. Jiang, P. Greenwood, and R. Parasuraman (1999) reported that priming of rotating three-dimensional visual objects is age sensitive. The current study investigated whether there is also an age-related difference in priming with simple two-dimensional (2-D) moving stimuli (i.e., whether a prime stimulus moving in a particular direction causes a subsequent ambiguous target stimulus to be seen moving in the same direction as the prime). In 2 experiments, younger and older adults judged the directions of moving sine-wave gratings. Groups differed neither in determining the direction of a single 2-D movement nor in detecting motion reversals in successively moving gratings. However, the older group showed a significant reduction in the extent of 2-D motion priming. The decrement in older adults for visual motion priming may reflect age-related changes in temporal processing in human visual cortex. C1 NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA. Catholic Univ Amer, Cognit Sci Lab, Washington, DC 20064 USA. Chinese Acad Sci, Inst Psychol, Beijing 10101, Peoples R China. Catholic Univ Amer, Cognit Sci Lab, Washington, DC 20064 USA. RP Jiang, Y (reprint author), NIMH, Lab Brain & Cognit, NIH, Bldg 10,4C-104,MSC 1366, Bethesda, MD 20892 USA. FU NIA NIH HHS [K01 AG000986, AG07569, AG00986] NR 38 TC 8 Z9 10 U1 0 U2 4 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD APR PY 2002 VL 16 IS 2 BP 140 EP 145 DI 10.1037//0894-4105.16.2.140 PG 6 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 539CR UT WOS:000174852600003 PM 11949705 ER PT J AU Lamar, M Zonderman, AB Resnick, S AF Lamar, M Zonderman, AB Resnick, S TI Contribution of specific cognitive processes to executive functioning in an aging population SO NEUROPSYCHOLOGY LA English DT Article ID ISCHEMIC VASCULAR DEMENTIA; FRONTAL-LOBE FUNCTIONS; ALZHEIMERS-DISEASE; AGE-DIFFERENCES; CATEGORY TEST; DEFICITS; PERFORMANCE; FLUENCY; DAMAGE; TRAIL AB The Current study investigated executive function measures emphasizing Alpha Span (ASp) to understand relationships among executive and nonexecutive tasks. Nondemented older participants (N = 417) received a comprehensive cognitive battery. Age and vocabulary adjusted correlations revealed associations among ASp, Wechsler Adult Intelligence Scale-Revised (D. Wechsler, 1981) Digit Span subtests, and fluency tasks. Principal-components analysis with varimax rotation revealed a 4 component solution (86.4% of the variance) with executive variables contributing to all loadings. Calculated component indices were submitted to a regression analysis predicting Asp performance. After accounting for age (6.3% of the variance), Component 3 reflecting brief attention-mental manipulation accounted for 13.4% of ASp variance, Component 1, verbal language ability, 11.5%; Component 2, sustained attention-mental tracking, 1.9% and Component 4, visuoperceptual spatial organization-planning, 0.9%. Results stress the importance of considering executive and nonexecutive aspects of cognition when conceptualizing executive functioning. C1 NIA, GRC, LPC, Baltimore, MD 21224 USA. RP Lamar, M (reprint author), NIA, GRC, LPC, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM lamarm@lpc.grc.nia.nih.gov OI Zonderman, Alan B/0000-0002-6523-4778 FU NIA NIH HHS [AG05146, AG08325] NR 49 TC 30 Z9 31 U1 4 U2 8 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 EI 1931-1559 J9 NEUROPSYCHOLOGY JI Neuropsychology PD APR PY 2002 VL 16 IS 2 BP 156 EP 162 DI 10.1037//0894-4105.16.2.156 PG 7 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 539CR UT WOS:000174852600005 PM 11949707 ER PT J AU Parasuraman, R Greenwood, PM Sunderland, T AF Parasuraman, R Greenwood, PM Sunderland, T TI The apolipoprotein E gene, attention, and brain function SO NEUROPSYCHOLOGY LA English DT Review ID POSITRON-EMISSION-TOMOGRAPHY; FAMILIAL ALZHEIMERS-DISEASE; E-DEFICIENT MICE; TRANSCRANIAL MAGNETIC STIMULATION; LOWER COGNITIVE PERFORMANCE; SELECTIVE VISUAL-ATTENTION; FEATURE-INTEGRATION-THEORY; POSTERIOR PARIETAL CORTEX; E ALLELE EPSILON-4; E TYPE-4 ALLELE AB The epsilon4 allele of the apolipoprotein E (ApoE) gene is associated with alterations in brain function and is a risk factor for Alzheimer's disease (AD). Changes in components of visuospatial attention with ApoE-epsilon4, aging, and AD are described. Healthy middle-aged adults without dementia who have the ApoE-epsilon4 gene show deficits in spatial attention and working memory that are qualitatively similar to those seen in clinically diagnosed AD patients. The findings support an association between ApoE polymorphism and specific components of visuospatial attention. Molecular mechanisms that may mediate the ApoE-attention link by modulating cholinergic neurotransmission to the posterior parietal cortex are discussed. Studies of attention and brain function in ApoE-epsilon4 carriers without dementia can advance knowledge of the genetics of visual attention, may enhance understanding of the preclinical phase of AD, and may lead to better methods for early AD detection. C1 Catholic Univ Amer, Cognit Sci Lab, Washington, DC 20064 USA. NIMH, Geriatr Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Parasuraman, R (reprint author), Catholic Univ Amer, Cognit Sci Lab, Washington, DC 20064 USA. EM parasuraman@cua.edu FU NIA NIH HHS [R01 AG019653, U01 AG019653, AG19653] NR 228 TC 83 Z9 89 U1 10 U2 13 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD APR PY 2002 VL 16 IS 2 BP 254 EP 274 DI 10.1037//0894-4105.16.2.254 PG 21 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 539CR UT WOS:000174852600016 PM 11949718 ER PT J AU Monk, CS Nelson, CA AF Monk, CS Nelson, CA TI The effects of hydrocortisone on cognitive and neural function: A behavioral and event-related potential investigation SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE cortisol; hydrocortisone; memory; cognition; evoked potentials ID RECEPTOR MESSENGER-RNA; PROLONGED GLUCOCORTICOID EXPOSURE; LONG-TERM POTENTIATION; DECLARATIVE MEMORY; CORTISOL-LEVELS; HIPPOCAMPAL-FORMATION; RECOGNITION MEMORY; STRESS IMPAIRS; INSITU HYBRIDIZATION; NOVELTY DETECTION AB Research indicates that glucocorticoids affect hippocampal function and the form of cognition that the hippocampus is thought to subserve, explicit memory. However, some studies suggest that glucocorticoids affect the frontal lobe, attention and working memory. Thus, it is not clear whether glucocorticoids specifically target the hippocampus and explicit memory or if the effects are more ubiquitous. By simultaneously measuring event-related potentials and behavioral performance in tasks designed to tap particular cognitive and neural processes, the present study examined the effects of hydrocortisone on 24 healthy humans. In an intentional face recognition memory task where the stimuli were presented again after a brief delay (6-18 s) and a long delay (30 min), hydrocortisone altered the P600 component (an electrophysiological index of recognition memory and hippocampal activity) following, the brief delay and impaired behavioral performance after the long delay. ERPs and behavioral performance were not affected in the attention and working memory tasks. These findings are consistent with reports indicating that glucocorticoids affect explicit memory and hippocampal function. (C) 2002 American College of Neuropsychopharmacology. Published by Elsevier Science Inc. C1 Univ Minnesota, Inst Child Dev, Minneapolis, MN 55455 USA. Ctr Cognit Sci, Minneapolis, MN USA. Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA. RP Monk, CS (reprint author), NIMH, Sect Dev & Affect Neurosci, Mood & Anxiety Disorders Program, 15K North Dr, Bethesda, MD 20892 USA. RI Monk, Christopher/J-1805-2014 FU NCRR NIH HHS [RR 00400]; NICHD NIH HHS [5T32 HD 07151]; NINDS NIH HHS [NS 32976] NR 64 TC 49 Z9 50 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD APR PY 2002 VL 26 IS 4 BP 505 EP 519 AR PII S0893-133X(01)00384-0 DI 10.1016/S0893-133X(01)00384-0 PG 15 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 533WV UT WOS:000174554000010 PM 11927175 ER PT J AU Stevens, B Fields, RD AF Stevens, B Fields, RD TI Regulation of the cell cycle in normal and pathological glia SO NEUROSCIENTIST LA English DT Article DE Ras; glioma; neurofibromatosis-type 1 (NF1); Schwann cell; cyclindependent kinase inhibitor; tumor suppressor protein ID DEPENDENT KINASE INHIBITORS; MALIGNANT GLIOMA GROWTH; NEUROFIBROMATOSIS TYPE-1; THERAPEUTIC STRATEGY; SIGNAL-TRANSDUCTION; SCHWANN-CELLS; LIFE-SPAN; RAS; GENE; ARREST AB Precise regulation of the glial cell cycle is essential during nervous system development and in response to injury, whereas disruption of cell cycle control is associated with malignant glial tumors and other nervous system diseases. The Ras signaling pathway plays a central role in regulating the mammalian cell cycle, and uncontrolled Ras signaling has been implicated in a wide range of human cancers, including malignant gliomas. Recent studies in glia have demonstrated that activation of Ras can either induce or inhibit proliferation through complex interactions among downstream signaling pathways impinging on cell cycle regulatory proteins. Studies in Schwann cells have begun to delineate the pathways by which Ras regulates the cell cycle in normal and pathological glia, and have identified promising targets for therapeutic intervention in the treatment of PNS and CNS malignant glial tumors. C1 NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20895 USA. NR 42 TC 7 Z9 7 U1 0 U2 2 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-8584 J9 NEUROSCIENTIST JI Neuroscientist PD APR PY 2002 VL 8 IS 2 BP 93 EP 97 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 536AY UT WOS:000174679600010 PM 11954563 ER PT J AU Butler, AA Yakar, S LeRoith, D AF Butler, AA Yakar, S LeRoith, D TI Insulin-like growth factor-I: Compartmentalization within the somatotropic axis? SO NEWS IN PHYSIOLOGICAL SCIENCES LA English DT Article ID POSTNATAL-GROWTH; GENE; MICE; MANIPULATION; DELETION AB Insulin-like growth factor-I (IGF-I) is essential for normal growth; igf-1 gene mutations are associated with extreme growth retardation in mice and, very rarely, in humans. The relative contributions of tissue vs. endocrine (hepatic) IGF-I to the regulation of growth has been a fundamental question. New gene targeting technologies are providing answers for these questions. C1 Oregon Hlth Sci Univ, Vollum Inst, Portland, OR 97201 USA. NIDDKD, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Butler, AA (reprint author), Oregon Hlth Sci Univ, Vollum Inst, Portland, OR 97201 USA. NR 13 TC 21 Z9 24 U1 0 U2 0 PU NEWS IN PHYSIOLOGICAL SCIENCES PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0886-1714 J9 NEWS PHYSIOL SCI JI News Physiol. Sci. PD APR PY 2002 VL 17 BP 82 EP 85 DI 10.1152/nips.01351.2001 PG 4 WC Physiology SC Physiology GA 542UZ UT WOS:000175063800008 PM 11909998 ER PT J AU Anantharaman, V Koonin, EV Aravind, L AF Anantharaman, V Koonin, EV Aravind, L TI Comparative genomics and evolution of proteins involved in RNA metabolism SO NUCLEIC ACIDS RESEARCH LA English DT Review ID 60S RIBOSOMAL-SUBUNITS; DNA-BINDING-PROTEIN; DOUBLE-STRANDED-RNA; HEAT-SHOCK-PROTEIN; MESSENGER-RNA; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; CRYSTAL-STRUCTURE; ADENOSINE-DEAMINASE; C-ELEGANS AB RNA metabolism, broadly defined as the compendium of all processes that involve RNA, including transcription, processing and modification of transcripts, translation, RNA degradation and its regulation, is the central and most evolutionarily conserved part of cell physiology. A comprehensive, genome-wide census of all enzymatic and non-enzymatic protein domains involved in RNA metabolism was conducted by using sequence profile analysis and structural comparisons. Proteins related to RNA metabolism comprise from 3 to 11% of the complete protein repertoire in bacteria, archaea and eukaryotes, with the greatest fraction seen in parasitic bacteria with small genomes. Approximately one-half of protein domains involved in RNA metabolism are present in most, if not all, species from all three primary kingdoms and are traceable to the last universal common ancestor (LUCA). The principal features of LUCA's RNA metabolism system were reconstructed by parsimony-based evolutionary analysis of all relevant groups of orthologous proteins. This reconstruction shows that LUCA possessed not only the basal translation system, but also the principal forms of RNA modification, such as methylation, pseudouridylation and thiouridylation, as well as simple mechanisms for polyadenylation and RNA degradation. Some of these ancient domains form paralogous groups whose evolution can be traced back in time beyond LUCA, towards low-specificity proteins, which probably functioned as cofactors for ribozymes within the RNA world framework. The main lineage-specific innovations of RNA metabolism systems were identified. The most notable phase of innovation in RNA metabolism coincides with the advent of eukaryotes and was brought about by the merge of the archaeal and bacterial systems via mitochondrial endosymbiosis, but also involved emergence of several new, eukaryote-specific RNA-binding domains. Subsequent, vast expansions of these domains mark the origin of alternative splicing in animals and probably in plants. In addition to the reconstruction of the evolutionary history of RNA metabolism, this analysis produced numerous functional predictions, e.g. of previously undetected enzymes of RNA modification. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, 8600 Rockville Pike,Bldg 389, Bethesda, MD 20894 USA. EM koonin@ncbi.nlm.nih.gov OI Anantharaman, Vivek/0000-0001-8395-0009 NR 284 TC 297 Z9 302 U1 4 U2 29 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 1 PY 2002 VL 30 IS 7 BP 1427 EP 1464 DI 10.1093/nar/30.7.1427 PG 38 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 535QB UT WOS:000174654200001 PM 11917006 ER PT J AU Parvathy, VR Bhaumik, SR Chary, KVR Govil, G Liu, KL Howard, FB Miles, HT AF Parvathy, VR Bhaumik, SR Chary, KVR Govil, G Liu, KL Howard, FB Miles, HT TI NMR structure of a parallel-stranded DNA duplex at atomic resolution SO NUCLEIC ACIDS RESEARCH LA English DT Article ID IRREGULAR NUCLEIC-ACIDS; BASE-PAIRS; MOLECULAR-STRUCTURE; MAGNETIC-RESONANCE; WATSON-CRICK; DOUBLE HELIX; SPECTROSCOPY; SEQUENCE; OLIGONUCLEOTIDES; MACROMOLECULES AB DNA dodecamers have been designed with two cytosines on each end and intervening A and T stretches, such that the oligomers have fully complementary A:T base pairs when aligned in the parallel orientation. Spectroscopic (UV, CD and IR), NMR and molecular dynamics studies have shown that oligomers having the sequences d(CCATAATTTACC) and d(CCTATTAAATCC) form a parallel-stranded duplex when dissolved at 1:1 stoichiometry in aqueous solution. This is due to the C:C+ clamps on either end and extensive mismatches in the antiparallel orientation. The structure is stable at neutral and acidic pH. At higher temperatures, the duplex melts into single strands in a highly cooperative fashion. All adenine, cytosine and thymine nucleotides adopt the anti conformation with respect to the glycosidic bond. The A:T base pairs form reverse Watson-Crick base pairs. The duplex shows base stacking and NOEs between the base protons T(H6)/A(H8) and the sugar protons (H1'/H2'/H2") of the preceding nucleotide, as has been observed in antiparallel duplexes. However, no NOEs are observed between base protons H2/H6/H8 of sequential nucleotides, though such NOEs are observed between T(CH3) and A(H8). A three-dimensional structure of the parallel-stranded duplex at atomic resolution has been obtained using molecular dynamics simulations under NMR constraints. The simulated structures have torsional angles very similar to those found in B-DNA duplexes, but the base stacking and helicoid parameters are significantly different. C1 Tata Inst Fundamental Res, Dept Chem Sci, Colaba 400005, Mumbai, India. NIDDKD, NIH, Bethesda, MD 20892 USA. RP Chary, KVR (reprint author), Tata Inst Fundamental Res, Dept Chem Sci, Homi Bhabha Rd, Colaba 400005, Mumbai, India. EM chary@tifr.res.in NR 50 TC 45 Z9 48 U1 1 U2 10 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 1 PY 2002 VL 30 IS 7 BP 1500 EP 1511 DI 10.1093/nar/30.7.1500 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 535QB UT WOS:000174654200005 PM 11917010 ER PT J AU Ahmad, A Murthy, M Greiner, RS Moriguchi, T Salem, N AF Ahmad, A Murthy, M Greiner, RS Moriguchi, T Salem, N TI A decrease in cell size accompanies a loss of docosahexaenoate in the rat hippocampus SO NUTRITIONAL NEUROSCIENCE LA English DT Article DE n-3 deficiency; phospholipids; hippocampal morphology; CA1 neuron size; stereology; infant nutrition ID FATTY-ACID COMPOSITION; NERVE GROWTH-FACTOR; AGE-RELATED-CHANGES; PROTEIN-KINASE-C; CEREBRAL-CORTEX; BRAIN PHOSPHATIDYLSERINES; WHITE-MATTER; DEFICIENCY; MEMORY; NEURONS AB Rats raised on n-3 essential fatty acid deficient diets demonstrate spatial memory deficits. To investigate neuroanatomical correlates of these deficits, morphological analysis of the hippocampus were carried out. Adult, female rats were raised for three generations on n-3 deficient or n-3 supplemented diets. Two n-3 deficient diets contained adequate linoleic acid (LA), or high linoleic acid (high LA), and two supplemented diets contained LA supplemented with alpha-linolenic acid (+LNA), or linoleic supplementation with alpha-linolenic and docosahexaenoic acids (+LNA/DHA). The total fatty acid composition of the hippocampus revealed a profound loss (90%) in docosahexaenoic acid (DHA) in the hippocampi of LA and high LA animals compared to those on + LNA and + LNA/DHA diets with a reciprocal increase in docosapentaenoic acid (DPAn-6) in all phospholipid species. The volume, density, total number, and cell body size of neurons in CA1-3, granular and hilar layers of the hippocampus were measured at septal and temporal locations using unbiased stereology. No differences were detected in any of these measures except for in cell body size; CA1 pyramidal neurons in the LA group were significantly (p < 0.04) smaller than neurons in the +LNA/DHA group at the septal location. C1 NIAAA, Sect Nutr Neurosci, Lab Membrane Biochem & Biophys, Div Intramural Clin & Biol Res,NIH, Rockville, MD USA. RP Salem, N (reprint author), 12420 Parklawn Dr,Room 158, Rockville, MD 20852 USA. NR 64 TC 55 Z9 58 U1 0 U2 3 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1028-415X J9 NUTR NEUROSCI JI Nutr. Neurosci. PD APR PY 2002 VL 5 IS 2 BP 103 EP 113 DI 10.1080/10284150290018973 PG 11 WC Neurosciences; Nutrition & Dietetics SC Neurosciences & Neurology; Nutrition & Dietetics GA 564HM UT WOS:000176309000003 PM 12004794 ER PT J AU Solomon, D Schiffman, M Tarone, R AF Solomon, D Schiffman, M Tarone, R CA ALTS Grp TI ASCUS LSIL Triage study (ALTS) conclusions reaffirmed: Response to a November 2001 commentary SO OBSTETRICS AND GYNECOLOGY LA English DT Editorial Material C1 NCI, Div Canc Prevent, EPN, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Solomon, D (reprint author), NCI, Div Canc Prevent, EPN, Room 2130,MSC 7333,6130 Execut Blvd, Bethesda, MD 20892 USA. FU NCI NIH HHS [CN55157, CN-55153, CN-55159, CN-55154, CN-55156, CN-55105, CN-55155, CN-55158] NR 6 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 2002 VL 99 IS 4 BP 671 EP 674 AR PII S002907844(02)01922-1 DI 10.1016/S0029-7844(02)01922-1 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 535FU UT WOS:000174635200030 PM 12039132 ER PT J AU Freedman, DM Dosemeci, M McGlynn, K AF Freedman, DM Dosemeci, M McGlynn, K TI Sunlight and mortality from breast, ovarian, colon, prostate, and non-melanoma skin cancer: a composite death certificate based case-control study SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID VITAMIN-D METABOLITES; UNITED-STATES; COLORECTAL-CANCER; SOCIOECONOMIC-STATUS; PHYSICAL-ACTIVITY; SOLAR-RADIATION; RISK; CALCIUM; HEALTH; EXPOSURE AB Objectives: To explore whether mortality from female breast, ovarian, colon, and prostate cancer were negatively associated with exposure to sunlight. Methods: A death certificate based case-control study of mortality was conducted into five cancers: female breast, ovarian, colon, prostate, and non-melanoma skin cancer (as a positive control) to examine associations with residential and occupational exposure to sunlight. Cases were all deaths from these cancers between 1984 and 1995 in 24 states of the United States. Controls, which were age frequency matched to a series of cases, excluded deaths from cancer and certain neurological diseases. Multiple logistic regression was used in a model that included age, sex, race, residential exposure to sunlight (based on region), and socioeconomic status, occupational exposure to sunlight, and physical activity (the lost three based on usual occupation). Results: Residential exposure to sunlight was negatively and significantly associated with mortality from Female breast, ovarian, prostate, and colon cancer. Only female breast and colon cancer, however, also showed significant negative associations with jobs with the highest occupational exposure to sunlight (odds ratio (OR) 0.82 (95% confidence interval (95% CI) 0.70 to 0.97) for Female breast cancer; OR 0.90 (95% CI 0.86 to 0.94) For colon cancer). For both cancers, the negative association with, occupational sunlight was greatest in the geographical region of highest exposure to sunlight and was independent of physical activity on the job. Non-melanoma skin cancer, as expected, was positively associated with both residential and occupational sunlight. Conclusions: In this exploratory study, unlike mortality from non-melanoma skin cancer, mortality from female breast cancer and colon cancer were negatively associated with both residential and occupational sunlight. C1 NCI, Radiat Epidemiol Branch, Bethesda, MD 20892 USA. NCI, Occupat Epidemiol Branch, Bethesda, MD 20892 USA. NCI, Environm Epidemiol Branch, Bethesda, MD 20892 USA. RP Freedman, DM (reprint author), NCI, Radiat Epidemiol Branch, Room 7087,6120 Execut Blvd, Bethesda, MD 20892 USA. NR 48 TC 212 Z9 215 U1 2 U2 8 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1351-0711 J9 OCCUP ENVIRON MED JI Occup. Environ. Med. PD APR PY 2002 VL 59 IS 4 BP 257 EP 262 DI 10.1136/oem.59.4.257 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 543VN UT WOS:000175122000007 PM 11934953 ER PT J AU Thylefors, B Chylack, LT Konyama, K Sasaki, K Sperduto, R Taylor, HR West, S AF Thylefors, B Chylack, LT Konyama, K Sasaki, K Sperduto, R Taylor, HR West, S CA WHO Cataract Grading Syst TI A simplified cataract grading system SO OPHTHALMIC EPIDEMIOLOGY LA English DT Article DE cataract grading; World Health Organization; nuclear cataract; cortical cataract; posterior subcapsular cataract ID LENS OPACITIES; CLASSIFICATION; PROGRESSION AB A simplified method for grading the presence and severity of different cataract types is needed for field use in assessment of the magnitude of the cataract problem. A cataract grading system was developed by a panel of experts with the objective of making available a simple system for use with a slit lamp to allow for the reliable grading of the most common forms of cataract by relatively inexperienced observers. Three levels, reflecting progressive severity, for grading of nuclear, cortical and posterior subcapsular (PSC) cataract were included in the classification; three standard photos were used for grading nuclear cataract. Field evaluation from four different sites indicated very good to fair interobserver agreement with the use of this system following minimal training of residents in ophthalmology at each site. Further testing of this system is warranted. The WHO simplified cataract grading system should allow for the obtaining of comparable data across countries based on field assessment of the most common forms of cataract. C1 Univ Melbourne, Dept Ophthalmol, Melbourne, Vic, Australia. Kanazawa Med Univ, Dept Ophthalmol, Kanazawa, Ishikawa, Japan. Juntendo Univ, Sch Med, Dept Ophthalmol, Tokyo 113, Japan. Johns Hopkins Univ, Dana Ctr Prevent Ophthalmol, Baltimore, MD USA. NEI, Bethesda, MD 20892 USA. Brigham & Womens Hosp, Ctr Ophthalm Res, Boston, MA 02115 USA. WHO, Programme Prevent Blindness & Deafness, CH-1211 Geneva, Switzerland. RP Chylack, LT (reprint author), 221 Longwood Ave, Boston, MA 02115 USA. OI Taylor, Hugh/0000-0002-9437-784X NR 16 TC 62 Z9 65 U1 2 U2 3 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 0928-6586 J9 OPHTHALMIC EPIDEMIOL JI Ophthalmic Epidemiol. PD APR PY 2002 VL 9 IS 2 BP 83 EP 95 DI 10.1076/opep.9.2.83.1523 PG 13 WC Ophthalmology SC Ophthalmology GA 606EY UT WOS:000178722200001 PM 11821974 ER PT J AU Max, MB AF Max, MB TI Clarifying the definition of nenropathic pain SO PAIN LA English DT Letter ID NEUROPATHIC PAIN C1 Natl Inst Dent & Craniofacial Res, Pain & Neurosensory Mech Branch, NIH, Bethesda, MD 20892 USA. RP Max, MB (reprint author), Natl Inst Dent & Craniofacial Res, Pain & Neurosensory Mech Branch, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 7 TC 30 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD APR PY 2002 VL 96 IS 3 BP 406 EP 407 AR PII S0304-3959(02)00422-5 DI 10.1016/S0304-3959(01)00422-5 PG 2 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA 554VT UT WOS:000175758400025 PM 11973017 ER PT J AU Savarino, SJ Hall, ER Bassily, S Wierzba, TF Youssef, FG Peruski, LF Abu-Elyazeed, R Rao, M Francis, WM El Mohamady, H Safwat, M Naficy, AB Svennerholm, AM Jertborn, M Lee, YJ Clemens, JD AF Savarino, SJ Hall, ER Bassily, S Wierzba, TF Youssef, FG Peruski, LF Abu-Elyazeed, R Rao, M Francis, WM El Mohamady, H Safwat, M Naficy, AB Svennerholm, AM Jertborn, M Lee, YJ Clemens, JD CA Pride Study Grp TI Introductory evaluation of an oral, killed whole cell enterotoxigenic Escherichia coli plus cholera toxin B subunit vaccine in Egyptian infants SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE Escherichia coli infections/diarrhea/prevention and control; bacterial vaccines/safety and immunogenicity; cholera toxin/immunology; human/infant; developing countries; clinical trials; double blind method; random allocation ID MONOCLONAL-ANTIBODIES; COLONIZATION FACTORS; IMMUNOSORBENT-ASSAY; RURAL BANGLADESH; DIARRHEA; IMMUNOGENICITY; CHILDREN; RESPONSES; SAFETY; ADULTS AB Background. We conducted the first trial to assess the safety and immunogenicity of an oral, killed enterotoxigenic Escherichia coli plus cholera toxin B-subunit vaccine in children <2 years old. Methods. Three doses of vaccine or killed E. coli K-12 control were given at 2-week intervals to 64 Egyptian infants, 6 to 18 months old, in a randomized, double blind manner. Adverse events were monitored for 3 days after each dose. Blood was collected before immunization and 7 to 10 days after each dose to assess vaccine-specific serologic responses. Results. There was no statistically significant intergroup difference in the percentage of subjects reporting the primary safety endpoint (diarrhea or vomiting) after the first (31%, vaccine; 30%, control) or third (14%, vaccine; 18%, control) dose, whereas there was a trend toward greater reporting in the vaccine group after Dose 2 (36%, vaccine; 18%, control; P = 0.052). The percentage of children showing IgA seroconversion after any dose was higher in the vaccine than the control group for recombinant cholera toxin B-subunit (97% vs. 46%), colonization factor antigen 1 (61% vs. 18%) and coli surface antigen 4 (39% vs. 4%) (P < 0.001 for each comparison). IgG seroconversion rates in the vaccine and control groups were 97 and 21% to recombinant cholera toxin B-subunit (P < 0.001), 64 and 29% for colonization factor antigen I (P < 0.01), 53 and 21% for coli surface antigen 2 (P < 0.05) and 58 and 4% for coli surface antigen 4 (P < 0.001), respectively. The third vaccine dose was followed by augmented IgG antitoxin titers. Conclusion. The oral enterotoxigenic E. coli vaccine was safe and immunogenic in this setting in Egyptian infants. C1 USN, Med Res Unit 3, Cairo, Egypt. Egyptian Minist Hlth & Populat, Al Qalyubiyah Governorate, Banha, Egypt. NICHHD, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. Univ Gothenburg, Dept Med Microbiol & Immunol, Gothenburg, Sweden. Int Vaccine Inst, Seoul, South Korea. RP Savarino, SJ (reprint author), USN, Med Res Ctr, 503 Robert Grant Ave, Silver Spring, MD 20910 USA. FU NICHD NIH HHS [Y1-HD-0026-01] NR 35 TC 42 Z9 46 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0891-3668 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD APR PY 2002 VL 21 IS 4 BP 322 EP 330 DI 10.1097/00006454-200204000-00012 PG 9 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA 544GU UT WOS:000175150500011 PM 12075764 ER PT J AU Ron, E AF Ron, E TI Ionizing radiation and cancer risk: evidence from epidemiology SO PEDIATRIC RADIOLOGY LA English DT Article ID DIAGNOSTIC-X-RAY; CHILDHOOD-CANCER; THYROID-CANCER; EXPOSURE C1 NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA. RP Ron, E (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd, Rockville, MD 20852 USA. NR 8 TC 62 Z9 65 U1 0 U2 3 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD APR PY 2002 VL 32 IS 4 BP 232 EP 237 AR PII 10.1007/s00247-002-0672-0 DI 10.1007/s00247-002-0672-0 PG 6 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA 547UN UT WOS:000175350800007 PM 11956701 ER PT J AU Bleyer, A Ron, E Rosen, N Brenner, D Slovis, T Staab, E Berdon, W Strife, J AF Bleyer, A Ron, E Rosen, N Brenner, D Slovis, T Staab, E Berdon, W Strife, J TI Panel discussion SO PEDIATRIC RADIOLOGY LA English DT Editorial Material C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 83 Z9 84 U1 1 U2 1 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD APR PY 2002 VL 32 IS 4 BP 242 EP 244 DI 10.1007/s00247-002-0674-y PG 3 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA 547UN UT WOS:000175350800009 ER PT J AU Gadomski, AM Bennett, SM Wissow, LS AF Gadomski, AM Bennett, SM Wissow, LS TI Clinical utility of the GAPS in a rural setting SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Bassett Healthcare, Res Inst, Cooperstown, NY USA. NIAAA, Clin Studies Lab, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 20 BP 4A EP 4A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600021 ER PT J AU Perrin, EM Murphy, ML Pichichero, ME Casey, J Garrett, JM Swedo, SE AF Perrin, EM Murphy, ML Pichichero, ME Casey, J Garrett, JM Swedo, SE TI Behaviors and thoughts in the wake of error parental vs child assessment SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Univ N Carolina, Robert Wood Johnson Clin Scholars Program, Chapel Hill, NC USA. Elmwood Pediat Grp, Rochester, NY USA. NIMH, Pediat & Dev Neuropsychiat Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 113 BP 20A EP 20A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600114 ER PT J AU Tanofsky-Kraff, M Yanovski, SZ Wilfley, DE Yanovski, JA AF Tanofsky-Kraff, M Yanovski, SZ Wilfley, DE Yanovski, JA TI Eating disordered behaviors, body fat and psychopathology in overweight and normal weight children SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, Unit Growth & Obes, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 152 BP 27A EP 27A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600153 ER PT J AU Berra, L Panigada, M Lorenzo, DM Gianluca, G Lewandowski, R Kolobow, T AF Berra, L Panigada, M Lorenzo, DM Gianluca, G Lewandowski, R Kolobow, T TI Bacterial colonization of the respiratory tract following tracheal intubation and mechanical ventilation effect of gravity SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 289 BP 50A EP 50A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600290 ER PT J AU McCune, SK Brenneman, DE Hill, JM AF McCune, SK Brenneman, DE Hill, JM TI Signal transduction and cytokine gene expression profile in control and VIP-stimulated E9.5 mouse neural tubes SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 George Washington Univ, Childrens Natl Med Ctr, Washington, DC USA. NICHHD, Dev Neurobiol Lab, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 343 BP 59A EP 59A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600344 ER PT J AU Cabral, WA Mertts, M Tekin, M Pandya, A Leikin, S Marini, JC AF Cabral, WA Mertts, M Tekin, M Pandya, A Leikin, S Marini, JC TI Type I collagen mutation that shifts the register of alpha chains by one Gly-X-Y triplet disrupts incorporation of mutant trimers into fibrils and ECM and causes lethal osteogenesis imperfecta SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, Heritable Disorders Branch, Bethesda, MD 20892 USA. NIH, Lab Phys & Struct Biol, Bethesda, MD 20892 USA. Virginia Commonwealth Univ, Med Coll Virginia, Dept Human Genet, Richmond, VA 23298 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 395 BP 68A EP 68A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600396 ER PT J AU Marini, JC Kozloff, KM Bergwitz, C Forlino, A Goldstein, SA Gronowicz, G AF Marini, JC Kozloff, KM Bergwitz, C Forlino, A Goldstein, SA Gronowicz, G TI Making brittle bones better, lessons from the Brittle (Brtl) mouse model for osteogenesis imperfecta in post-pubertal adaptation of the OI skeleton SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, Heritable Disorders Branch, Bethesda, MD 20892 USA. Univ Michigan, Orthopaed Res Labs, Ann Arbor, MI 48109 USA. Univ Connecticut, Dept Orthopaed Surg, Farmington, CT USA. RI Forlino, Antonella/H-5385-2015 OI Forlino, Antonella/0000-0002-6385-1182 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 397 BP 68A EP 68A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600398 ER PT J AU Scayo, LM Karas, M Murray, M LeRoith, D AF Scayo, LM Karas, M Murray, M LeRoith, D TI IGF-I regulates the differentiation of human mesenchymal stem cells into adipocytes SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIDDK, CEB, NIH, Bethesda, MD USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. BioWhittaker Co, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 656 BP 112A EP 113A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600657 ER PT J AU Charmandari, E Weise, M Eisenhofer, G Keil, MF Bornstein, SR Chrousos, GP Merke, DP AF Charmandari, E Weise, M Eisenhofer, G Keil, MF Bornstein, SR Chrousos, GP Merke, DP TI Children with classic congenital adrenal hyperplasia have elevated serum leptin concentrations and insulin resistance SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NIH, Pediat & Reprod Endocrinol Branch, Bethesda, MD USA. NINCDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA. Univ Dusseldorf, Dept Endocrinol, D-4000 Dusseldorf, Germany. RI Charmandari, Evangelia/B-6701-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 679 BP 116A EP 117A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600680 ER PT J AU Weise, M Pacak, K Merke, D Walther, M Eisnhofer, G AF Weise, M Pacak, K Merke, D Walther, M Eisnhofer, G TI Plasma metanephrines for detecting childhood pheochromocytoma SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, DEB, Bethesda, MD 20892 USA. NIH, PREB, Bethesda, MD 20892 USA. NINCDS, CNS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 675 BP 116A EP 116A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600676 ER PT J AU Elberg, J Goldbar, LR Fallon, EM Parikh, SJ Yanoyski, JA AF Elberg, J Goldbar, LR Fallon, EM Parikh, SJ Yanoyski, JA TI Air displacement plethysmography accurately estimates changes of body fatness in African-American and Caucasian children SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, Unit Growth & Obes, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 701 BP 120A EP 120A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600702 ER PT J AU Yanovski, JA Rose, SR Municchi, G Pescovitz, OH Hill, SC Cassorla, FG Cutler, GB AF Yanovski, JA Rose, SR Municchi, G Pescovitz, OH Hill, SC Cassorla, FG Cutler, GB TI Luteinizing hormone-releasing hormone agonist-induced delay of epiphyseal fusion prolongs the growth period and increases adult height of adolescents with short stature: Results of a randomized, placebo-controlled, trial SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, Dev Endocrinol Branch, Bethesda, MD 20892 USA. Childrens Hosp, Med Ctr, Dept Pediat Endocrinol, Cincinnati, OH 45229 USA. Univ Siena, Dept Pediat, I-53100 Siena, Italy. Indiana Univ, Dept Pediat, Indianapolis, IN USA. Univ Chile, Inst Invest Materno Infantil, Santiago, Chile. Eli Lilly & Co, Indianapolis, IN 46285 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 742 BP 127A EP 127A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600743 ER PT J AU Sandrini, F Matyakhina, LD Bourdeau, I Farmakidis, C Keil, M Kirschner, LS Stratakis, CA AF Sandrini, F Matyakhina, LD Bourdeau, I Farmakidis, C Keil, M Kirschner, LS Stratakis, CA TI PRKAR1A a regulator of protein kinase A, is mutated in children with carney comples and isolated micronodular adrenal hyperplasia SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA. RI Levesque, Isabelle/A-1899-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 755 BP 130A EP 130A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714600756 ER PT J AU Fallon, EM McDuffie, JR Hubbard, VS Uwaifo, GL Salaita, CG Yanovski, JA AF Fallon, EM McDuffie, JR Hubbard, VS Uwaifo, GL Salaita, CG Yanovski, JA TI A 6 month pilot study of the efficacy of orlistat in overweight adolescents SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Unit Growth & Obes, NIH, Bethesda, MD USA. NIDDK, DNRC, NIH, Bethesda, MD USA. RI Uwaifo, Gabriel/M-2361-2016 OI Uwaifo, Gabriel/0000-0002-6962-9304 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1094 BP 188A EP 188A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601093 ER PT J AU Brenner, R Simons-Morton, B Bhaskar, B Revenis, M Das, A Clemens, J AF Brenner, R Simons-Morton, B Bhaskar, B Revenis, M Das, A Clemens, J TI Infant-parent bedsharing in an inner-city population SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Bethesda, MD USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. IVI, Seoul, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1126 BP 193A EP 193A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601125 ER PT J AU England, L Ruth, B Brinda, B Abhik, D Bruce, SM Mary, R Nintin, M Millicent, C John, C AF England, L Ruth, B Brinda, B Abhik, D Bruce, SM Mary, R Nintin, M Millicent, C John, C TI Breastfeeding practices in a cohort of inner city women: The role of contraindications SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Bethesda, MD USA. RTI, Rockville, MD USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. Georgetown Univ, Med Ctr, Washington, DC 20007 USA. DC Gen Hosp, Washington, DC USA. IVI, Seoul, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1190 BP 205A EP 205A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601189 ER PT J AU Hirschhorn, JN Loomer, M Platko, J O'Donnell, C Daly, MJ Lander, ES AF Hirschhorn, JN Loomer, M Platko, J O'Donnell, C Daly, MJ Lander, ES TI Surveying linkage disequilibrium in genes: Implications for disease studies SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Harvard Med Childrens Hosp, Boston, MA USA. Whitehead Inst, Cambridge, MA 02142 USA. MIT, Cambridge, MA 02139 USA. NHLBI, Cardiogenom PGA, Boston, MA USA. NHLBI, Framingham Heart Study, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1310 BP 225A EP 225A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601309 ER PT J AU Kaler, SG Holmes, CS Goldstein, DS AF Kaler, SG Holmes, CS Goldstein, DS TI Perfect sensitivity and specificity of plasma catechol analyses for neonatal diagnosis of Menkes disease SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Unit Pediat Genet, Lab Clin Genom, NIH, Bethesda, MD USA. NINCDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1309 BP 225A EP 225A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601308 ER PT J AU Anikster, Y Kleta, R Skovby, F Rosenberg, T Shaag, A Anderson, PD Elpeleg, O Gahl, WA AF Anikster, Y Kleta, R Skovby, F Rosenberg, T Shaag, A Anderson, PD Elpeleg, O Gahl, WA TI Type III 3-methylglutaconic aciduria (MGA): Discovery of the OPA3 gene, its founder mutation in Iraqi Jews, and a milder mutation in a type IV MGA patient SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD USA. UH Rigshosp, Copenhagen, Denmark. SZMC, Jerusalem, Israel. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1314 BP 226A EP 226A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601313 ER PT J AU Rao, DA Veszelovszky, E Plotz, PH Hoffman, EP AF Rao, DA Veszelovszky, E Plotz, PH Hoffman, EP TI Expression profiling in dysferlin deficiency: Insights into molecular pathogenesis and protein function SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Natl Med Ctr, Res Ctr Genet Med, Washington, DC 20010 USA. George Washington Univ, Childrens Natl Med Ctr, Washington, DC 20052 USA. NIAMS, Arthritis & Rheumatism Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1313 BP 226A EP 226A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601312 ER PT J AU Liu, PC Chen, YW Hoffman, EP Kaler, SG AF Liu, PC Chen, YW Hoffman, EP Kaler, SG TI Brain gene expression profile in classical Menkes disease SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NIH, Unit Pediat Genet, Lab Clin Genom, Bethesda, MD USA. Childrens Natl Med Ctr, Res Ctr Genet Med, Washington, DC 20010 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1319 BP 227A EP 227A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601318 ER PT J AU Phornphutkul, C Introne, W D'Souza, M Anderson, P Huizing, M Anikster, Y Bernadini, I Gahl, W AF Phornphutkul, C Introne, W D'Souza, M Anderson, P Huizing, M Anikster, Y Bernadini, I Gahl, W TI Mutation analysis of the human homogentisate 1,2 dioxygenase gene in American-based alkaptonuria patients SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Heritable Disorder Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1322 BP 227A EP 227A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601321 ER PT J AU Correa-Cerro, LS Krakowiak, PA Wassif, CA Porter, FD AF Correa-Cerro, LS Krakowiak, PA Wassif, CA Porter, FD TI Suppression of Nonsense Mediated Decay in Smith-Lemli-Opitz syndrome SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1326 BP 228A EP 228A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601325 ER PT J AU Porter, FD Wassif, CA Kratz, L Kelley, RL Krakowiak, PA AF Porter, FD Wassif, CA Kratz, L Kelley, RL Krakowiak, PA TI Disruption of the mouse lathosterol 5-desaturase gene: A new inborn error of cholesterol biosynthesis SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD USA. Kennedy Krieger Inst, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1327 BP 228A EP 228A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601326 ER PT J AU Goker-Alpan, O Park, JK Schiffmann, R Orvisky, E Stubblefield, BK Tayebi, N Sidransky, E AF Goker-Alpan, O Park, JK Schiffmann, R Orvisky, E Stubblefield, BK Tayebi, N Sidransky, E TI Neuronopathic Gaucher disease has a phenotypic continuum: An intermediary phenotype between type 2 and type 3 Gaucher disease SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIMH, NSB, NIH, Bethesda, MD 20892 USA. NINCDS, DMNB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1331 BP 229A EP 229A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601330 ER PT J AU Porter, FD Wright, BS Wassif, CA Nwokoro, NA AF Porter, FD Wright, BS Wassif, CA Nwokoro, NA TI Smith-Lemli-Opitz syndrome in African Americans: Rare or undiagnosed? SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, HDB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1334 BP 229A EP 229A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601333 ER PT J AU Tayebi, N Park, JK Schiffmann, R Orvisky, E Kaneski, C LaMarca, ME Sidransky, E AF Tayebi, N Park, JK Schiffmann, R Orvisky, E Kaneski, C LaMarca, ME Sidransky, E TI Myoclonic epilepsy and Gaucher disease: A genotype and phenotype assessment SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIMH, NSB, Bethesda, MD 20892 USA. NINCDS, DMNB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1335 BP 229A EP 229A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601334 ER PT J AU Wright, BS Wassif, CA Porter, FD AF Wright, BS Wassif, CA Porter, FD TI Investigation of Simvastatin therapy in Smith-Lemli-Opitz syndrome SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1336 BP 229A EP 229A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601335 ER PT J AU Pitney, A Fox, E Cole, D Widemann, B Balis, F AF Pitney, A Fox, E Cole, D Widemann, B Balis, F TI Comparison of farnesyltransferase (FTase) activity in normal peripheral blood mononuclear cells (PBMCs) and leukemia blasts (LBs) from children with acute leukemia SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Walter Reed Army Med Ctr, Washington, DC 20307 USA. NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1365 BP 234A EP 235A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601364 ER PT J AU Byrne, J Fears, TR Mills, J Zeltzer, L Sklar, C Meadows, AT Reaman, G Robison, LL AF Byrne, J Fears, TR Mills, J Zeltzer, L Sklar, C Meadows, AT Reaman, G Robison, LL TI Fertility impairments among men and women treated for leukemia during childhood or adolescence SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Natl Med Ctr, Washington, DC 20010 USA. NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. Univ Minnesota, Sch Med, Minneapolis, MN 55455 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1420 BP 244A EP 244A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601419 ER PT J AU Dickens, DS Kozielski, R Leavey, P Timmons, C Khan, J Cripe, TP AF Dickens, DS Kozielski, R Leavey, P Timmons, C Khan, J Cripe, TP TI Efficacy and mechanism of combined doxycycline and celecoxib therapy for the treatment of pediatric sarcomas SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA. Hop St Justine, Montreal, PQ H3T 1C5, Canada. Univ Texas, SW Med Ctr, Dallas, TX USA. Childrens Med Ctr, Dallas, TX 75235 USA. NCI, Pediat Oncol Grp, Gaithersburg, MD USA. RI Khan, Javed/P-9157-2014 OI Khan, Javed/0000-0002-5858-0488 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1431 BP 246A EP 246A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601430 ER PT J AU Lin, EYC Weisman, LE Adams, KM Moyer, P Lodinger, BS Troendle, J AF Lin, EYC Weisman, LE Adams, KM Moyer, P Lodinger, BS Troendle, J TI Clinical spectrum and determinants of risk for late-onset group B streptoccal disease SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Epidemiol Branch, Bethesda, MD 20892 USA. Baylor Coll Med, Sect Neonatol, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1538 BP 264A EP 264A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601537 ER PT J AU Stoll, BJ Hansen, N Wright, LL Fanaroff, AA Carlo, WA Ehrenkranz, RA Poole, K AF Stoll, BJ Hansen, N Wright, LL Fanaroff, AA Carlo, WA Ehrenkranz, RA Poole, K TI High likelihood of meningitis without sepsis among VLBW infants SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1540 BP 265A EP 265A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601539 ER PT J AU Truong, HHM Shin, M Dillon, M Uittenbogaart, CH Dickover, R Plaeger, S Bryson, Y AF Truong, HHM Shin, M Dillon, M Uittenbogaart, CH Dickover, R Plaeger, S Bryson, Y TI Effect of short course antepartum zidovudine (ZDV) on HIV-RNA, CD4 T-cells and serum activation markers during pregnancy and postpartum SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA 90024 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1555 BP 267A EP 267A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601554 ER PT J AU Domachowske, JB Bonville, CA Rosenberg, HF AF Domachowske, JB Bonville, CA Rosenberg, HF TI Combination immunomodulatory and antiviral therapy results in improved survival in response to acute pneumovirus infection SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 SUNY Upstate Med Univ, Syracuse, NY USA. NIH, Host Def Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1559 BP 268A EP 268A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601558 ER PT J AU Anderson, EL Belshe, RB Newman, FK Karron, R Wright, P Roberton, D Reisinger, K Henderson, F King, J Loh, R Sly, P McIntyre, P Ziegler, J Keyserling, H Schwartz, R Weinberg, G Murphy, B Tatem, J Gohs, F Tsai, T Hackell, J Gruber, W AF Anderson, EL Belshe, RB Newman, FK Karron, R Wright, P Roberton, D Reisinger, K Henderson, F King, J Loh, R Sly, P McIntyre, P Ziegler, J Keyserling, H Schwartz, R Weinberg, G Murphy, B Tatem, J Gohs, F Tsai, T Hackell, J Gruber, W TI Phase II evaluation of PIV3 cp45 live, attenuated parainfluenza type 3 vaccine in healthy children 6-18 months of age SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 St Louis Univ, St Louis, MO 63103 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Vanderbilt Univ, Nashville, TN USA. Womens & Childrens Hosp, Adelaide, SA, Australia. Univ N Carolina, Chapel Hill, NC USA. Univ Maryland, Baltimore, MD 21201 USA. Princess Margaret Hosp Children, Subiaco, WA, Australia. Sydney Childrens Hosp, Randwick, NSW, Australia. Emory Univ, Atlanta, GA 30322 USA. Vienna Pediat, Vienna, Austria. Univ Rochester, Rochester, NY 14627 USA. NIAID, LID, NIH, Bethesda, MD 20892 USA. Wyeth Lederle Vaccines, Pearl River, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1637 BP 281A EP 281A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601636 ER PT J AU Karron, RA Wright, PF Belshe, RB Randolph, V Collins, PL Murphy, BR AF Karron, RA Wright, PF Belshe, RB Randolph, V Collins, PL Murphy, BR TI Evaluation of live rRSVA2 vaccines in infants and children SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Johns Hopkins Univ, BSPH, Baltimore, MD 21218 USA. Vanderbilt Univ, Nashville, TN USA. St Louis Univ, St Louis, MO 63103 USA. Wyeth Lederle Vaccines, Pearl River, NY USA. NIAID, LID, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1638 BP 281A EP 281A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601637 ER PT J AU Passwell, JH Ashkenazi, S Robbins, JB Schneerson, R AF Passwell, JH Ashkenazi, S Robbins, JB Schneerson, R CA Israeli Shigella Study Grp TI Safety and immunogenicity of experimental Shigella conjugate vaccine in toddlers SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Schneider Childrens Hosp, Tel Aviv, Israel. Chaim Sheba Med Ctr, Tel Aviv, Israel. NICHHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1642 BP 282A EP 282A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601641 ER PT J AU Ehrenkranz, RA Ohls, RK Das, A Vohr, BR AF Ehrenkranz, RA Ohls, RK Das, A Vohr, BR TI Neurodevelopmental outcome and growth at 18-22 months in extremely low birth weight infants treated with early erythropoietin and iron SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1697 BP 291A EP 291A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601696 ER PT J AU Johnson, YR Shankaran, S Yao, Q Wright, LL Vohr, B Fanaroff, AA AF Johnson, YR Shankaran, S Yao, Q Wright, LL Vohr, B Fanaroff, AA TI Risk factors associated with postneonatal mortality among extremely low birth weight infants SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1693 BP 291A EP 291A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601692 ER PT J AU Wadhawan, R Vohr, BR Fanaroff, AA Perritt, R Duara, S Stoll, BJ Goldberg, R Laptook, A Poole, K Wright, LL Oh, W AF Wadhawan, R Vohr, BR Fanaroff, AA Perritt, R Duara, S Stoll, BJ Goldberg, R Laptook, A Poole, K Wright, LL Oh, W TI Does labor influence neonatal outcomes of extremely low birth weight infants delivered by C-section? SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Brown Univ, Women & Infants Hosp, Providence, RI USA. NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1714 BP 294A EP 294A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601713 ER PT J AU Duara, S Stoll, BJ Wright, LL Gard, C Oh, W Fanaroff, AA Poole, K Goldberg, RN Laptook, ARAR AF Duara, S Stoll, BJ Wright, LL Gard, C Oh, W Fanaroff, AA Poole, K Goldberg, RN Laptook, ARAR TI Early death in extremely low birthweight infants: A changing profile over the past decade SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1722 BP 296A EP 296A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601721 ER PT J AU Lefkowitz, W Lim, SY Lin, YH Loewke, J Majchrzak, S Salem, N AF Lefkowitz, W Lim, SY Lin, YH Loewke, J Majchrzak, S Salem, N TI Where does the developing brain get its docosahexaenoic acid? SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 USUHS, Bethesda, MD USA. NIAAA, Metab & Mol Biol Lab, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1792 BP 308A EP 308A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601791 ER PT J AU Messinger, DS Bauer, CR Das, A Seifer, R Lester, B LaGasse, L Wright, LL Shankaran, S Bada, H Smeriglio, V Poole, K AF Messinger, DS Bauer, CR Das, A Seifer, R Lester, B LaGasse, L Wright, LL Shankaran, S Bada, H Smeriglio, V Poole, K TI Maternal lifestyle study (MLS): Prenatal cocaine (C) & opiate (O) exposure and Bayley II performance at 1, 2, & 3 years (NICHD neonatal research network, NIDA, ACYF, CSAT) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Univ Miami, Coral Gables, FL 33124 USA. Brown Univ, Providence, RI 02912 USA. NICHHD, Bethesda, MD USA. Wayne State Univ, Detroit, MI USA. Univ Tennessee, Memphis, TN USA. NIDA, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1880 BP 323A EP 323A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601879 ER PT J AU Shankaran, S Johnson, Y Langer, J Vohr, B Wright, L Fanaroff, A Poole, K AF Shankaran, S Johnson, Y Langer, J Vohr, B Wright, L Fanaroff, A Poole, K TI ELBW infants at highest risk (birth weight <= 750 grams, gestational age <= 24 weeks, and 1 minute Apgar score <= 3): Predicting outcome SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1888 BP 324A EP 325A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601887 ER PT J AU Hintz, SR Kendrick, DE Wright, LL Poole, WK Fanaroff, AA Laptook, AR Goldberg, R Duara, S Stoll, BJ Oh, W AF Hintz, SR Kendrick, DE Wright, LL Poole, WK Fanaroff, AA Laptook, AR Goldberg, R Duara, S Stoll, BJ Oh, W TI Mortality and major morbidity among very low birth weight (VLBW) infants born at < 25 weeks: How are we doing in the post-surfactant era? SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1893 BP 325A EP 325A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601892 ER PT J AU Shankaran, S Das, A Bauer, CR Bada, H Lester, B Wright, L Poole, K Smeriglio, V AF Shankaran, S Das, A Bauer, CR Bada, H Lester, B Wright, L Poole, K Smeriglio, V TI Cocaine exposure (EXP) and small for gestational age status (SGA) at birth: Effects on growth at 6-years. The maternal lifestyle study SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 1895 BP 326A EP 326A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714601894 ER PT J AU Haberman, B Shankaran, S Stevenson, DK Papile, LA Stark, A Korones, S McDonald, S Poole, K Wright, LL Donovan, EF AF Haberman, B Shankaran, S Stevenson, DK Papile, LA Stark, A Korones, S McDonald, S Poole, K Wright, LL Donovan, EF TI Does surfactant (S) and immediate extubation to nasal continuous positive airway pressure (CPAP) reduce use of mechanical ventilation? SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2030 BP 349A EP 349A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602028 ER PT J AU Oh, W Carlo, WA Fanaroff, AA McDonald, S Donovan, EE Poole, K Wright, LJ AF Oh, W Carlo, WA Fanaroff, AA McDonald, S Donovan, EE Poole, K Wright, LJ TI Delayed cord clamping in extremely low birth weight infants - A pilot randomized controlled trial SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 5 Z9 5 U1 1 U2 3 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2126 BP 365A EP 366A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602124 ER PT J AU Wadhawan, R Fanaroff, AA Perritt, R Duara, S Stoll, BJ Goldberg, R Laptook, A Polle, K Wright, LL Oh, W AF Wadhawan, R Fanaroff, AA Perritt, R Duara, S Stoll, BJ Goldberg, R Laptook, A Polle, K Wright, LL Oh, W TI Lack of early postnatal weight loss in very low birth weight infants is associated with a higher incidence of bronchopulmonary dysplasia SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Brown Univ, Women & Infants Hosp, Providence, RI USA. NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2150 BP 370A EP 370A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602148 ER PT J AU Vernacchio, L Corwin, MJ Lesko, SM Vezina, RM Hunt, CE Hoffman, HI Willinger, M Mitchell, AA AF Vernacchio, L Corwin, MJ Lesko, SM Vezina, RM Hunt, CE Hoffman, HI Willinger, M Mitchell, AA TI Sleep position of low-birthweight infants SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Boston Univ, Sch Publ Hlth, Slone Epidemiol Unit, Boston, MA 02215 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NIDCD, NIH, Bethesda, MD USA. NICHHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2176 BP 374A EP 374A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602174 ER PT J AU Cotten, M Oh, W McDonald, S Fanaroff, AA Duara, S Laptook, A Carlo, WA Stoll, BJ Poole, K Wright, LL Goldberg, RN AF Cotten, M Oh, W McDonald, S Fanaroff, AA Duara, S Laptook, A Carlo, WA Stoll, BJ Poole, K Wright, LL Goldberg, RN TI Predictors of prolonged hospital stay (PHS) for extremely low birth weight (ELBW) infants SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, Neonatal Res Network, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2184 BP 375A EP 375A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602182 ER PT J AU Kolobow, T Aly, H Berra, L DeMarchi, L Panigada, M AF Kolobow, T Aly, H Berra, L DeMarchi, L Panigada, M TI Ultra-thin wall, two-stages-twin tracheal tube (UTTS-T-ETT), of low resistance (R) and low dead space (DS) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NHLBI, NIH, Crit Care Med Branch, Bethesda, MD 20892 USA. George Washington Univ Hosp, Newborn Serv, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2281 BP 392A EP 392A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602279 ER PT J AU Kleta, R AF Kleta, R TI Clues for the diagnosis and treatment of Bartter and Gitelman syndromes SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Unikinderklin, Munster, Germany. NICHHD, HDB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2484 BP 426A EP 427A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602482 ER PT J AU Lester, BM Tronick, EZ Seifer, R LaGasse, L Bauer, CR Shankaran, S Bada, H Wright, LL Smeriglio, V Liu, J Poole, K AF Lester, BM Tronick, EZ Seifer, R LaGasse, L Bauer, CR Shankaran, S Bada, H Wright, LL Smeriglio, V Liu, J Poole, K TI The maternal lifestyles study: Effects of polydrug use on 1 month neurobehavior SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHD Neonatal Res Network, NIDA, ACYF, CSAT, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2562 BP 440A EP 440A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602560 ER PT J AU Salisbury, A Lester, B Tronick, E Seifer, R LaGasse, L Bauer, C Shankaran, S Bada, H Wright, L Smeriglio, V Liu, J Poole, K AF Salisbury, A Lester, B Tronick, E Seifer, R LaGasse, L Bauer, C Shankaran, S Bada, H Wright, L Smeriglio, V Liu, J Poole, K TI The maternal lifestyles study: Maternal depression and cocaine effects on infant neurobehavior SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHD Neonatal Res Network, NIDA, ACYF, CSAT, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2563 BP 440A EP 441A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602561 ER PT J AU Warner, JP Balsamo, LM Xu, B Ross, N Theodore, WH Gaillard, WD AF Warner, JP Balsamo, LM Xu, B Ross, N Theodore, WH Gaillard, WD TI fMRI comparison of neural substrates for prose and musical sight-reading SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Natl Med Ctr, Washington, DC 20010 USA. NINCDS, Epilepsy Res Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 3 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2672 BP 459A EP 459A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602670 ER PT J AU Jungbluth, GL Welshman, IR Hopkins, NK Bruss, JB James, LP Kearns, GL AF Jungbluth, GL Welshman, IR Hopkins, NK Bruss, JB James, LP Kearns, GL TI Linezolid pharmacokinetics in adolescents SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Arkansas Childrens Hosp, Little Rock, AR 72202 USA. Pharmacia, Kalamazoo, MI USA. Childrens Mercy Hosp, Kansas City, MO 64108 USA. NICHHD, PPRU Network, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2695 BP 462A EP 463A PN 2 PG 2 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602693 ER PT J AU Jungbluth, GL Welshman, IR Hopkins, NK Bruss, JB Wu, E Kearns, GL AF Jungbluth, GL Welshman, IR Hopkins, NK Bruss, JB Wu, E Kearns, GL TI Impact of gestational and postnatal age on linezolid disposition in neonates and young infants SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Pharmacia & Upjohn Inc, Kalamazoo, MI 49001 USA. Hosp San Juan Dios, Santiago, Chile. Childrens Mercy Hosp, Kansas City, MO 64108 USA. NICHHD, PPRU Network, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2002 VL 51 IS 4 SU S MA 2712 BP 465A EP 465A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 536RA UT WOS:000174714602710 ER PT J AU Tassaneeyakul, W Tawalee, A Tassaneeyakul, W Kukongviriyapan, V Blaisdell, J Goldstein, JA Gaysornsiri, D AF Tassaneeyakul, W Tawalee, A Tassaneeyakul, W Kukongviriyapan, V Blaisdell, J Goldstein, JA Gaysornsiri, D TI Analysis of the CYP2C19 polymorphism in a North-eastern Thai population SO PHARMACOGENETICS LA English DT Article DE CYP2C19; polymorphism; Thai; omeprazole; phenotye and genotype ID POOR METABOLIZER PHENOTYPE; MEPHENYTOIN OXIDATION POLYMORPHISM; S-MEPHENYTOIN; GENETIC-DEFECT; HYDROXYLATION PHENOTYPE; HIGH-FREQUENCIES; HUMAN-LIVER; OMEPRAZOLE; PROGUANIL; GENOTYPE AB CYP2C19 is a polymorphically expressed cytochrome P450 responsible for the metabolism of several clinically used drugs, including some barbiturates, diazepam, proguanil, propranolol and several proton pump inhibitors. Genetic polymorphism of this enzyme shows marked interracial differences, with the poor metabolizer (PM) phenotype representing 2-5% of Caucasian and 11-23% of Oriental populations. In the present study, CYP2C19 phenotype and genotype were investigated in 107 North-eastern Thai subjects using the omeprazole hydroxylation index (HI) and polymerase chain reaction-restriction fragment length polymorphism technique, respectively. It was found that the distribution of HI in these subjects was bimodal. Seven subjects [6.54%, 95% confidence (CI) 1.86-11.22%] were identified as PM, with an HI > 7. Analysis of CYP2C19 genotypes in these 107 Thai subjects revealed that the allele frequencies for CYP2C19*1, CYP2C19*2 and CYP2C19*3 were 0.71 (95% CI 0.65-0.77), 0.27 (95% CI 0.21-0.33) and 0.02 (95% CI 0.01-0.05), respectively. The PM phenotype and the frequencies of CYP2C19 defective alleles in Thais, particularly CYP2C19*3, were lower than those observed in other Oriental populations. It is noteworthy that there was a case of nonaccordance between phenotype and genotype in one of the PMs. Whether this PM represents a novel defective allele requires further investigation. Pharmacogenetics 12: 221-225 (C) 2002 Lippincott Williams Wilkins. C1 Khon Kaen Univ, Fac Med, Dept Pharmacol, Khon Kaen 40002, Thailand. Khon Kaen Univ, Fac Pharmaceut Sci, Dept Toxicol, Khon Kaen 40002, Thailand. NIEHS, Res Triangle Pk, NC 27709 USA. RP Tassaneeyakul, W (reprint author), Khon Kaen Univ, Fac Med, Dept Pharmacol, Khon Kaen 40002, Thailand. EM wichit-t@md.kku.ac.th RI Khon Kaen University, Faculty of Medicine/A-3133-2009; Goldstein, Joyce/A-6681-2012 NR 41 TC 27 Z9 30 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD APR PY 2002 VL 12 IS 3 BP 221 EP 225 DI 10.1097/00008571-200204000-00006 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA 542RF UT WOS:000175057600006 PM 11927837 ER PT J AU Lee, CR Goldstein, JA Pieper, JA AF Lee, CR Goldstein, JA Pieper, JA TI Cytochrome P4502C9 polymorphisms: a comprehensive review of the in-vitro and human data SO PHARMACOGENETICS LA English DT Review DE CYP2C9; polymorphisms; warfarin; phenytoin ID HUMAN LIVER-MICROSOMES; HUMAN CYP2C SUBFAMILY; ALLELIC VARIANT; GENETIC-POLYMORPHISM; JAPANESE PATIENTS; CYP2C9-ASTERISK-3 ALLELE; BLEEDING COMPLICATIONS; TORSEMIDE METABOLISM; HEALTHY-VOLUNTEERS; DOSE REQUIREMENT AB The discovery of six distinct polymorphisms in the genetic sequence encoding for the cytochrome P450 2C9 (CYP2C9) protein has stimulated numerous investigations in an attempt to characterize their population distribution and metabolic activity. Since the CYP2C9*1, *2 and *3 alleles were discovered first, they have undergone more thorough investigation than the recently identified *4, *5 and *6 alleles. Population distribution data suggest that the variant *2 and *3 alleles are present in approximately 35% of Caucasian individuals; however, these alleles are significantly less prevalent in African-American and Asian populations. In-vitro data have consistently demonstrated that the CYP2C9*2 and *3 alleles are associated with significant reductions in intrinsic clearance of a variety of 2C9 substrates compared with CYP2C9* 1; however, the degree of these reductions appear to be highly substrate-dependent. In addition, multiple in-vivo investigations and clinical case reports have associated genotypes expressing the CYP2C9*2 and *3 alleles with significant reductions in both the metabolism and daily dose requirements of selected CYP2C9 substrates. Individuals expressing these variant genotypes also appear to be significantly more susceptible to adverse events with the narrow therapeutic index agents warfarin and phenytoin, particularly during the initiation of therapy. These findings have subsequently raised numerous questions regarding the potential clinical utility of genotyping for CYP2C9 prior to initiation of therapy with these agents. However, further clinical investigations evaluating the metabolic consequences in individuals expressing the CYP2C9*2, *3, *4, *5, or *6 alleles are required before large-scale clinical genotyping can be recommended. Pharmacogenetics 12:251-263 (C) 2002 Lippincott Williams Wilkins. C1 Univ N Carolina, Div Pharmacotherapy, Chapel Hill, NC 27599 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Pieper, JA (reprint author), Univ N Carolina, Div Pharmacotherapy, CB7360,Beard Hall, Chapel Hill, NC 27599 USA. OI Lee, Craig/0000-0003-3595-5301 NR 81 TC 396 Z9 417 U1 0 U2 16 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD APR PY 2002 VL 12 IS 3 BP 251 EP 263 DI 10.1097/00008571-200204000-00010 PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA 542RF UT WOS:000175057600010 PM 11927841 ER PT J AU Rothman, RB Baumann, MH AF Rothman, RB Baumann, MH TI Serotonin releasing agents - Neurochemical therapeutic and adverse effects SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Review DE serotonin; serotonin releaser; SERT; serotonin transporter; serotonin receptor; obesity; drug addiction; depression ID PRIMARY PULMONARY-HYPERTENSION; APPETITE-SUPPRESSANT DRUGS; D-FENFLURAMINE; NEUROTRANSMITTER TRANSPORTERS; RAT-BRAIN; PHARMACOLOGICAL PROPERTIES; DEXFENFLURAMINE TREATMENT; SUBSTITUTED AMPHETAMINES; PARA-CHLOROAMPHETAMINE; RECEPTOR ANTAGONISTS AB This review summarizes the neurochemical, therapeutic and adverse effects of serotonin (5-HT) releasing agents. The 5-HT releaser (+/-)-fenfluramine is composed of two stereoisomers, (+)-fenfluramine and (-)-fenfluramine, which are N-de-ethylated to yield the metabolites, (+)-norfenfluramine and (-)-norfenfluramine. Fenfluramines and norfenfluramines are 5-HT transporter substrates and potent 5-HT releasers. Other 5-HT releasing agents include m-chlorophenylpiperazine (mCPP), a major metabolite of the antidepressant drug trazodone. Findings from in vitro and in vivo studies support the hypothesis that fenfluramines and mCPP release neuronal 5-HT via a nonexocytotic carrier-mediated exchange mechanism involving 5-HT transporters. (+)-Norfenfluramine is a potent 5-HT2B and 5-HT2C receptor agonist. The former activity may increase the risk of developing valvular heart disease (VHD), whereas the latter activity is implicated in the anorectic effect of systemic fenfluramine. Anorectic agents that increase the risk of developing primary pulmonary hypertension (PPH) share the common property of being 5-HT transporter substrates. However, these drugs vary considerably in their propensity to increase the risk of PPH. In this regard, neither trazodone nor mCPP is associated with PPH. Similarly, although some 5-HT substrates can deplete brain 5-HT (fenfluramine), others do not (mCPP). In addition to the established indication of obesity, 5-HT releasers may be helpful in treating psychiatric problems such as drug and alcohol dependence, depression and premenstrual syndrome. Viewed collectively, it seems possible to develop new medications that selectively release 5-HT without the adverse effects of PPH, VHD or neurotoxicity. Such agents may have utility in treating a variety of psychiatric disorders. (C) 2002 Elsevier Science Inc. All rights reserved. C1 NIDA, Clin Psychopharmacol Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Rothman, RB (reprint author), NIDA, Clin Psychopharmacol Sect, Intramural Res Program, NIH, POB 5180,5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 125 TC 86 Z9 86 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 2002 VL 71 IS 4 BP 825 EP 836 AR PII S0091-3057(01)00669-4 DI 10.1016/S0091-3057(01)00669-4 PG 12 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA 540VN UT WOS:000174951100029 PM 11888573 ER PT J AU Le, AD Shaham, Y AF Le, AD Shaham, Y TI Neurobiology of relapse to alcohol in rats SO PHARMACOLOGY & THERAPEUTICS LA English DT Review DE alcohol-deprivation effect; conditioned drug cues; extinction; reinstatement; review; stress ID CORTICOTROPIN-RELEASING FACTOR; COCAINE-SEEKING BEHAVIOR; STRESS-INDUCED RELAPSE; VOLUNTARY ETHANOL-CONSUMPTION; EXTRACELLULAR DOPAMINE LEVELS; 5-HT3 ANTAGONIST ONDANSETRON; FREE-FEEDING RATS; NUCLEUS-ACCUMBENS; DRUG-SEEKING; PREFERRING RATS AB Relapse to alcohol use after prolonged withdrawal periods is the major problem in the treatment of alcohol dependence in humans. However, until recently, relatively few preclinical studies concentrated on the elucidation of the neurochemical events underlying relapse to alcohol. In this article we will review recent data from studies in which alcohol-deprivation and reinstatement models were used to determine the mechanisms underlying relapse to alcohol in rats. In the alcohol-deprivation model, the intake of alcohol is determined after prolonged periods of forced abstinence in drug-experienced rats. In the reinstatement model, the ability of acute non-contingent exposure to drug or non-drug stimuli to reinstate drug seeking is determined following training for drug self-administration and subsequent extinction of the drug-reinforced behavior. We will review studies, which used these preclinical models, on the effect of specific pharmacological agents on relapse to alcohol seeking induced by re-exposure to alcohol and to alcohol-associated cues and by exposure to stress. Subsequently, we will describe potential neuronal circuits that may underlie relapse to alcohol. Finally, future directions and clinical implications of the study of relapse to alcohol in laboratory animals will be discussed briefly. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Ctr Addict & Mental Hlth, Dept Neurosci, Biobehav Pharmacol Sect, Toronto, ON M5S 2S1, Canada. NIDA, Behav Neurosci Branch, IRP, Baltimore, MD 21224 USA. RP Le, AD (reprint author), Ctr Addict & Mental Hlth, Dept Neurosci, Biobehav Pharmacol Sect, 33 Russell St, Toronto, ON M5S 2S1, Canada. RI shaham, yavin/G-1306-2014 NR 204 TC 150 Z9 157 U1 2 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0163-7258 J9 PHARMACOL THERAPEUT JI Pharmacol. Ther. PD APR-MAY PY 2002 VL 94 IS 1-2 BP 137 EP 156 AR PII S0163-7258(02)00200-0 DI 10.1016/S0163-7258(02)00200-0 PG 20 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 571VZ UT WOS:000176741000009 PM 12191599 ER PT J AU Sato, H Nagashima, Y Chrousos, GP Ichihashi, M Funasaka, Y AF Sato, H Nagashima, Y Chrousos, GP Ichihashi, M Funasaka, Y TI The expression of corticotropin-releasing hormone in melanoma SO PIGMENT CELL RESEARCH LA English DT Article DE POMC; immunohistochemistry; agonist; antagonist ID PROOPIOMELANOCORTIN-DERIVED PEPTIDES; CUTANEOUS MALIGNANT-MELANOMA; BENIGN MELANOCYTIC NEVI; STIMULATING-HORMONE; HUMAN SKIN; RECEPTOR EXPRESSION; MURINE MELANOMA; BETA-ENDORPHIN; RAT; ALPHA AB We previously demonstrated that advanced melanoma cells express high amounts of proopiomelanocortin (POMC) that correlate with tumor progression. We now investigated whether the high expression of POMC derives from increased expression of corticotropin-releasing hormone (CRH) and the possible role of CRH as a melanoma growth factor. Forty-five cases of melanoma [25 primary malignant melanoma; 20 metastatic melanoma (MetM)] were immunohistochemically analysed for coexpression of POMC and CRH peptides. The ability of CRH to induce POMC expression in cultured melanoma cells was examined using CRH and a CRH antagonist. In CRH positive melanomas, seven out of nine cases (78%) of primary melanoma, and 7 out of 12 cases (58%) of MetM showed colocalization of CRH and POMC peptides. CRH induced POMC mRNA expression, an effect that was inhibited by a CRH antagonist. These results provide evidence for the existence of the CRH/POMC axis in pigmented lesions. C1 Kobe Univ, Sch Med, Dept Dermatol, Chuo Ku, Kobe, Hyogo 6500017, Japan. Yokohama City Univ, Sch Med, Dept Pathol, Yokohama, Kanagawa 232, Japan. NIH, Pediat & Reprod Endocrinol Branch, Bethesda, MD 20892 USA. RP Funasaka, Y (reprint author), Kobe Univ, Sch Med, Dept Dermatol, Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan. NR 52 TC 18 Z9 19 U1 0 U2 1 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0893-5785 J9 PIGM CELL RES JI Pigm. Cell. Res. PD APR PY 2002 VL 15 IS 2 BP 98 EP 103 DI 10.1034/j.1600-0749.2002.1o063.x PG 6 WC Cell Biology; Dermatology SC Cell Biology; Dermatology GA 534XG UT WOS:000174614600004 PM 11936276 ER PT J AU Mehta, DV Kim, YS Dixon, D Jetten, AM AF Mehta, DV Kim, YS Dixon, D Jetten, AM TI Characterization of the expression of the retinoid-related, testis-associated receptor (RTR) in trophoblasts SO PLACENTA LA English DT Article ID CELL NUCLEAR FACTOR; ORPHAN RECEPTOR; MOLECULAR-CLONING; RESPONSE ELEMENT; XENOPUS-LAEVIS; PPAR-GAMMA; GENE; DIFFERENTIATION; BINDING; GCNF AB Previous studies have provided evidence indicating that the nuclear orphan receptor RTR plays an important role during embryonic development and in spermatogenesis. In this study, we examine the expression of RTR in murine placenta and several human placental choriocarcinoma cell lines. Northern blot analysis showed high expression of RTR mRNA in placental tissue. In contrast to murine testis, which contains 7.4 and 2.3 kb transcripts, placental tissue expressed only the larger transcript. Examination of RTR expression in murine placental tissue by immunohistochemistry demonstrated the presence of RTR protein in the nuclei of giant trophoblasts and spongiotrophoblasts. RTR mRNA was also expressed in rat choriocarcinoma Rcho-1 cells and in the human placental choriocarcinoma cell lines BcWo, JAR, and JEG-3. In trophoblasts, RTR was co-expressed with the estrogen-related receptors ERRalpha and ERRbeta. Giant trophoblast differentiation in Rcho-1 cells, characterized by induction of placental lactogen I (PL-I), was accompanied by a steady decrease in the expression of RTR mRNA and down-regulation of ERRP expression while levels of ERRalpha mRNA did not change significantly. RTR was able to inhibit ERRalpha-mediated transactivation through the consensus RTR-response element (RTRE) likely by competing with ERRalpha, for binding to the RTRE. These results suggest the possibility of cross-talk between RTR and ERRalpha receptor signalling pathways in trophoblasts. (C) 2002 Elsevier Science Ltd. C1 NIEHS, Cell Biol Sect, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Pathol Lab, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA. RP Jetten, AM (reprint author), NIEHS, Cell Biol Sect, Div Intramural Res, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. OI Jetten, Anton/0000-0003-0954-4445 NR 42 TC 11 Z9 11 U1 0 U2 1 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0143-4004 J9 PLACENTA JI Placenta PD APR PY 2002 VL 23 IS 4 BP 281 EP 287 DI 10.1053/plac.2001.0779 PG 7 WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology GA 548NU UT WOS:000175395200004 PM 11969338 ER PT J AU Kloczkowski, A Erman, B Mark, JE AF Kloczkowski, A Erman, B Mark, JE TI Effect of non-Gaussian chains on fluctuations of junctions in bimodal networks SO POLYMER LA English DT Article DE non-Gaussian; bimodal networks; tetrahedron ID RUBBERLIKE ELASTICITY; ELASTOMERIC NETWORKS; POLY(DIMETHYLSILOXANE); LENGTH; STATE AB A simple tetrahedron model is used to study the effect of non-Gaussian chains on fluctuations of junctions in bimodal networks. The four chains are assumed to meet at a junction with their other ends being fixed at the vertices of the tetrahedron. It is assumed that the angles between mean end-to-end vectors of all four chains connected at the junction are tetrahedral, but the lengths of edges of the tetrahedron may differ due to the difference in the lengths of the chains. The central junction is free to fluctuate, subject to the constraints imposed by the pendant chains. The long chains are chosen to be Gaussian. The short chains are assumed to be non-Gaussian. Calculations show that the non-Gaussian nature of the short chains imposes severe restrictions on the fluctuations of the central junction. The strength of these restrictions directs attention to the importance of anharmonic modes in networks. (C) 2002 Published by Elsevier Science Ltd. C1 NCI, Lab Expt & Computat Biol, NIH, Bethesda, MD 20892 USA. Sabanci Univ, Fac Engn & Nat Sci, Lab Computat Biol, TR-81474 Istanbul, Turkey. Univ Cincinnati, Dept Chem, Cincinnati, OH 45221 USA. Univ Cincinnati, Ctr Polymer Res, Cincinnati, OH 45221 USA. RP Kloczkowski, A (reprint author), NCI, Lab Expt & Computat Biol, NIH, 12 South Dr,Bldg 12B,Rm B116, Bethesda, MD 20892 USA. RI Kloczkowski, Andrzej/B-9868-2012; OI ERMAN, BURAK/0000-0002-2496-6059 NR 21 TC 3 Z9 3 U1 3 U2 5 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0032-3861 J9 POLYMER JI Polymer PD APR PY 2002 VL 43 IS 8 BP 2569 EP 2574 AR PII S0032-3861(01)00797-2 DI 10.1016/S0032-3861(01)00797-2 PG 6 WC Polymer Science SC Polymer Science GA 524UA UT WOS:000174030200051 ER PT J AU Gerald, MS AF Gerald, MS TI The finding of an inverse relationship between social dominance and feeding priority among pairs of unfamiliar adult male vervet monkeys (Cercopithecus aethiops sabaeus) SO PRIMATES LA English DT Article DE social dominance; feeding priority; scrotal colour; vervet monkeys ID PRIMATE COLOR; BEHAVIOR AB Dominance is often presumed to confer priority of access to resources. This study evaluated the relationship between two assessments of dominance: (1) social dominance, based on agonistic interactions and (2) feeding priority among pairs of unfamiliar adult vervet monkeys (Cercopithecus aethiops sabaeus) differing in scrotal colour, but matched for height, weight and testicular volume, during paired introduction experiments. Results of this investigation showed that neither size differences nor scrotal colour were predictive of feeding priority, and social dominance was inversely related to feeding priority. This finding demonstrates that different assessments of dominance can yield different outcomes even within the same primate taxon. I propose that male dominance rank may best predict access to resources when there is direct contest competition over a resource, which is not immediately exhaustible, whereas highly impulsive low ranking males may gain a competitive edge in scramble competitions for ephemeral and small resources. C1 Natl Inst Hlth, Bethesda, MD 20892 USA. RP Gerald, MS (reprint author), Caribbean Primate Res Ctr, POB 906, Punta Santiago, PR 00741 USA. NR 21 TC 8 Z9 8 U1 1 U2 6 PU SPRINGER-VERLAG TOKYO PI TOKYO PA 3-3-13, HONGO, BUNKYO-KU, TOKYO, 113-0033, JAPAN SN 0032-8332 J9 PRIMATES JI Primates PD APR PY 2002 VL 43 IS 2 BP 127 EP 132 DI 10.1007/BF02629672 PG 6 WC Zoology SC Zoology GA 549HE UT WOS:000175437800004 PM 12082301 ER PT J AU Onaivi, ES Leonard, CM Ishiguro, H Zhang, PW Lin, ZC Akinshola, BE Uhl, GR AF Onaivi, ES Leonard, CM Ishiguro, H Zhang, PW Lin, ZC Akinshola, BE Uhl, GR TI Endocannabinoids and cannabinoid receptor genetics SO PROGRESS IN NEUROBIOLOGY LA English DT Review ID CEREBELLAR GRANULE NEURONS; ACID AMIDE HYDROLASE; RECTIFYING POTASSIUM CHANNELS; LONG-TERM POTENTIATION; RAT HIPPOCAMPAL SLICES; NITRIC-OXIDE RELEASE; CB1 RECEPTOR; ENDOGENOUS CANNABINOIDS; MESSENGER-RNA; KNOCKOUT MICE AB This review presents the remarkable advances that have been achieved in marijuana (cannabinoid) research, with the discovery of specific receptors and the existence of naturally occurring cannabis-like substances in the human body and brain. The last decade has seen more rapid progress in marijuana research than any time in the thousands of years that marijuana has been used by humans, particularly in cannabinoid genomics. The cDNA and genomic sequences encoding G protein-coupled cannabinoid receptors (Cnrs) from several species have now, been cloned. Endogenous cannabinoids (endocannabinoids), synthetic and hydrolyzing enzymes and transporters that define neurochemically-specific cannabinoid brain pathways have been identified. Endocannabinoid lipid signaling molecules alter activity at G protein-coupled receptors (GPCR) and possibly at anandamide-gated ion channels, such as vanilloid receptors. Availability of increasingly-specific CB1 and CB2 Cnr antagonists and of CBI and CB2 Cnr knockout mice have increased our understanding of these cannabinoid systems and provides tantalizing evidence for even more G protein-coupled Cnrs. Initial studies of the Cnr gene structure, regulation and polymorphisms whet our appetite for more information about these interesting genes, their variants and roles in vulnerabilities to addictions and other neuropsychiatric disorders. Behavioral studies of cannabinoids document the complex interactions between rewarding and aversive effects of these drugs. Pursuing cannabinoid-related molecular, pharmacological and behavioral leads will add greatly to our understanding of endogenous brain neuromodulator systems, abused substances and potential therapeutics. This review of CBI and CB2 Cnr genes in human and animal brain and their neurobiological effects provide a basis for many of these studies. Therefore, understanding the physiological cannabinoid control system in the human body and brain will contribute to elucidating this natural regulatory mechanism in health and disease. Published by Elsevier Science Ltd. C1 William Paterson Univ, Dept Biol, Wayne, NJ 07470 USA. NIDA, Intramural Program, Mol Neurobiol Branch, NIH, Baltimore, MD 21224 USA. Howard Univ, Sch Med, Dept Pharmacol, Washington, DC 20059 USA. RP Onaivi, ES (reprint author), William Paterson Univ, Dept Biol, Wayne, NJ 07470 USA. FU PHS HHS [263-MI-107518] NR 229 TC 60 Z9 66 U1 0 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0301-0082 J9 PROG NEUROBIOL JI Prog. Neurobiol. PD APR PY 2002 VL 66 IS 5 BP 307 EP 344 AR PII S0301-0082(02)00007-2 DI 10.1016/S0301-0082(02)00007-2 PG 38 WC Neurosciences SC Neurosciences & Neurology GA 564XL UT WOS:000176338800002 PM 12015198 ER PT J AU Wubah, JA Fischer, CM Rolfzen, LN Khalili, M Kang, J Green, JE Bieberich, CJ AF Wubah, JA Fischer, CM Rolfzen, LN Khalili, M Kang, J Green, JE Bieberich, CJ TI Ventral prostate predominant I, a novel mouse gene expressed exclusively in the prostate SO PROSTATE LA English DT Article DE prostate-unique; development; androgen regulation; prostate lobes; TRAMP ID TRAMP MODEL; TRANSGENIC ADENOCARCINOMA; CANCER; PROGRESSION; SECRETION; RECEPTOR; BIOLOGY; SIGNALS; MICE; RIG AB BACKGROUND. Despite the region-specific nature of human prostate disease, there is a paucity of information regarding the molecular basis of prostate regionalization and patterning. To elucidate genetic mechanisms that underlie prostate growth and development, we investigated differential gene expression in mouse prostate lobes. METHODS. mRNA differential display analysis was used to identify differentially expressed genes during development of ventral, anterior, and dorsolateral prostate lobes. Differential gene expression was confirmed by Northern blot analysis and RT-PCR. RESULTS. A novel gene, Ventral prostate predominant1 (Vpp1) was identified. Vpp1 mRNA was evident in all lobes but accumulated predominantly in the ventral prostate, and was detected on postnatal day 7 through adulthood exclusively in the prostate gland. The steady-state level of Vpp1. mRNA decreased markedly in response to castration, suggesting androgen regulation of Vpp1 expression. Analysis of TRAMP tumors demonstrated a dramatic decrease in the level of Vppl mRNA. CONCLUSIONS. The spatial distribution and early postnatal onset of Vppl expression is consistent with a role for this gene in prostate regionalization. The absolute prostate specificity of Vppl expression may allow this gene to serve as a paradigm to study the molecular basis of gene expression that is restricted exclusively to the prostate gland. Prostate 51: 21-29, 2001 (C) 2002 Wiley-Liss, Inc. C1 Univ Maryland, Dept Biol Sci, Baltimore, MD 21250 USA. Natl Canc Inst, Lab Cell Regulat & Carinogenesis, Bethesda, MD USA. RP Bieberich, CJ (reprint author), Univ Maryland, Dept Biol Sci, Baltimore, MD 21250 USA. FU NIDDK NIH HHS [R01DK54067, F22DK10094-01] NR 28 TC 4 Z9 4 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0270-4137 J9 PROSTATE JI Prostate PD APR 1 PY 2002 VL 51 IS 1 BP 21 EP 29 DI 10.1002/pros.10060 PG 9 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA 538RW UT WOS:000174829700003 PM 11920954 ER PT J AU Gulnik, SV Afonina, EI Gustchina, E Yu, B Silva, AM Kim, Y Erickson, JW AF Gulnik, SV Afonina, EI Gustchina, E Yu, B Silva, AM Kim, Y Erickson, JW TI Utility of (His)(6) tag for purification and refolding of proplasmepsin-2 and mutants with altered activation properties SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID PARASITE PLASMODIUM-FALCIPARUM; PLASMEPSIN-II; ASPARTIC PROTEINASES; CATHEPSIN-D; MALARIA; EXPRESSION; INHIBITION; CHROMATOGRAPHY; PEPSINOGEN; PROTEASES AB Plasmepsin-2 is a malarial aspartic proteinase that has been implicated in the initial steps of hemoglobin degradation in parasites and thus represents an attractive antimalarial. target. Escherichia coli expressed proplasmepsin-2 is capable of activation at acidic pH by autocatalytic cleavage of the pro part region, which results in products of different length. We designed a 10-amino-acid deletion in the pro part region that allows faster generation of homogeneous enzyme upon activation. Incorporation of a (HiS)(6) tag onto the N-terminus of the pro part enables on-column refolding of proplasmepsin-2 and simplifies proenzyme purification and pro part separation after activation. The proposed purification procedure results in highly pure and easily crystallizable enzyme. (C) 2002 Elsevier Science (USA). C1 NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD 21702 USA. RP Gulnik, SV (reprint author), NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, POB B, Frederick, MD 21702 USA. FU NCI NIH HHS [N01-CO-56000] NR 21 TC 13 Z9 13 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 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 2002 VL 24 IS 3 BP 412 EP 419 DI 10.1006/prep.2001.1590 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA 541AQ UT WOS:000174963400011 PM 11922757 ER PT J AU Chen, PL Hutter, D Liu, PH Liu, YS AF Chen, PL Hutter, D Liu, PH Liu, YS TI A mammalian expression system for rapid production and purification of active MAP kinase phosphatases SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID PROTEIN-TYROSINE-PHOSPHATASE; CATALYTIC ACTIVATION; RECOMBINANT PROTEINS; ESCHERICHIA-COLI; HUMAN HEMOGLOBIN; GENE; MUTATION; CLONING; VECTOR; STRESS AB Expression of enzymatically active mammalian proteins in Escherichia coli can proven to be a challenging task due to poor solubility, improper folding, and lack of adequate posttranslational modification. Expression of mammalian proteins using baculovirus or yeast systems is time-consuming and may also be subject to inadequate modification. In order to overcome these technical difficulties, we have developed a mammalian expression system for the convenient subcloning of cDNA fragments, high-level expression, and one-step purification of enzymatically active proteins. The mammalian expression vector pEBG that expresses glutathione S-transferase fusion proteins was modified to create an SrfI restriction site in the multiple cloning site. The protein coding sequences of ALAP kinase phosphatase-1 (MKP-1), MAP kinase phosphatase-2 (MKP2), and the tumor suppressor PTEN were PCR-amplified using Pfu DNA polymerase and cloned into the SrfI site through SrfI digestion-coupled ligation. The resulting plasmids were transiently transfected into 293T cells using FuGENE 6 transfection reagent. Forty eight hours after transfection, cells were harvested and bioactive recombinant proteins were purified by glutathione-Sepharose beads. Protein yield, which ranged from 200 to 700 jug, was more than adequate for biochemical studies. The usefulness of this versatile system for studying protein function and its potential application for proteomics research are discussed. (C) 2002 Elsevier Science (USA). C1 NIA, Stress Signaling Unit, Cellular & Mol Biol Lab, NIH,Intramural Res Program, Baltimore, MD 21224 USA. RP Liu, YS (reprint author), NIA, Stress Signaling Unit, Cellular & Mol Biol Lab, NIH,Intramural Res Program, Box 12,5600 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Liu, Yusen/E-3527-2011 NR 29 TC 23 Z9 24 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 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 2002 VL 24 IS 3 BP 481 EP 488 DI 10.1006/prep.2001.1599 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA 541AQ UT WOS:000174963400019 PM 11922765 ER PT J AU Grisshammer, R Grunwald, T Sohal, AK AF Grisshammer, R Grunwald, T Sohal, AK TI Characterization of an antibody Fv fragment that binds to the human, but not to the rat neurotensin receptor NTS-1 SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article DE Fv antibody fragment; G-protein-coupled receptor; neurotensin; Escherichia coli; antibody receptor complex ID CYTOCHROME-C-OXIDASE; ESCHERICHIA-COLI; PURIFICATION; EXPRESSION; PROTEIN; AFFINITY; SITE; CRYSTALLIZATION; IDENTIFICATION; RESOLUTION AB The cDNAs coding for the heavy and light chain variable domains of an antibody, recognizing the human G-protein-coupled receptor for neurotensin, NTS-1, were obtained from a hybridoma cell line, B-N6. The Fv BN6 fragment was expressed in Escherichia coli and purified. To characterize the properties of the antibody fragment, human and rat high-affinity neurotensin receptors were expressed in E. coli in functional form, linked at their N-termini to the maltose-binding protein. Fv B-N6 was found to compete for [H-3]neurotensin binding to the human neurotensin receptor, but not to the rat neurotensin receptor, with IC50 values of 1.6 muM (membrane-bound receptor) and 1.9 muM (detergent-solubilized, purified receptor). The formation of a relatively stable complex of Fv B-N6 with purified human neurotensin receptor fusion protein was also demonstrated by gel filtration experiments. The Fv B-N6 fragment will be used to isolate a high-affinity binder to the human neurotensin receptor as a valuable tool for cocrystallization and receptor structure determination. (C) 2002 Elsevier Science (USA). C1 MRC, Mol Biol Lab, Cambridge CB2 2QH, England. MRC Ctr, Ctr Prot Engn, Cambridge CB2 2QH, England. RP Grisshammer, R (reprint author), NIDDK, Mol Biol Lab, NIH, Bldg 50,Room 4503,50 South Dr, Bethesda, MD 20892 USA. RI Grisshammer, Reinhard/C-3089-2015 NR 28 TC 3 Z9 3 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 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 2002 VL 24 IS 3 BP 505 EP 512 DI 10.1006/prep.2001.1591 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA 541AQ UT WOS:000174963400022 PM 11922768 ER PT J AU Anderson, GM Bennett, AJ Weld, KP Pushkas, JG Ocame, DM Higley, JD AF Anderson, GM Bennett, AJ Weld, KP Pushkas, JG Ocame, DM Higley, JD TI Serotonin in cisternal cerebrospinal fluid of rhesus monkeys: basal levels and effects of sertraline administration SO PSYCHOPHARMACOLOGY LA English DT Article DE serotonin; cerebrospinal fluid (CSF); rhesus monkey; cisternal CSF; sertraline; selective serotonin reuptake inhibitor (SSRI) ID RAT FRONTAL-CORTEX; IN-VIVO; EXTRACELLULAR SEROTONIN; 5-HYDROXYINDOLEACETIC ACID; MACACA-MULATTA; RAPHE NUCLEI; 5-HT RELEASE; FLUOXETINE; 5-HYDROXYTRYPTAMINE; NOREPINEPHRINE AB Rationale: Studies of rodents suggest that extracellular fluid and cerebrospinal fluid (CSF) serotonin (5-HT) concentrations provide a better index of released 5-HT than the frequently obtained measure of CSF 5-hydroxyindoleacetic acid (5-HIAA). The measurement of cisternal CSF 5-HT levels in the monkey might offer a method of assessing the effects of agents and actions on central 5-HT functioning in primate brain. Objective: To address methodological issues related to the determination of monkey cisternal CSF 5-HT and to examine the effects of a selective serotonin reuptake inhibitor (SSRI) on the measure. Methods: Monkey CSF was obtained by cisternal puncture and 5-HT levels determined by high performance liquid chromatography, after screening for blood contamination. Results: When blood contamination was minimized, a mean (+/-SD) basal concentration of cisternal CSF 5-HT 87+/-36 pg/ml (n=13) was observed. Good longitudinal stability (variances of 16 and 20%) of CSF 5-HT was demonstrated in two monkeys sampled over a 3-month period. A two-fold increase in CSF 5-HT was seen in seven animals treated with the SSRI sertraline (20 mg/kg PO, mean treatment period of 12 days): pre- and post-drug 5-HT concentrations were 85+/-39 and 162+/-53 pg/ml (P=0.0007); in contrast, levels of 5-HIAA decreased from 40.0+/-5.7 to 20.4+/-2.2 ng/ml (P=0.0001). Conclusions: The measurement of monkey cisternal CSF 5-HT appears to provide a useful index of central 5-HT release. Initial results tend to support a role for increased extracellular 5-HT in the mechanism of action of chronically administered SSRIs. C1 Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06510 USA. NIAAA, Clin Studies Lab, Primate Unit, Poolesville, MD USA. RP Anderson, GM (reprint author), Yale Univ, Sch Med, Dept Child Psychiat, 230 S Frontage Rd, New Haven, CT 06510 USA. NR 32 TC 29 Z9 29 U1 0 U2 4 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD APR PY 2002 VL 161 IS 1 BP 95 EP 99 DI 10.1007/s00213-002-1034-1 PG 5 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 552GA UT WOS:000175610100012 PM 11967636 ER PT J AU Nyberg, U Nilsson, B Travis, LB Holm, LE Hall, P AF Nyberg, U Nilsson, B Travis, LB Holm, LE Hall, P TI Cancer incidence among Swedish patients exposed to radioactive Thorotrast: A forty-year follow-up survey SO RADIATION RESEARCH LA English DT Article ID GERMAN THOROTRAST; LIVER; MORTALITY; SERIES; SITES AB Thorotrast is an alpha-particle-emitting radiological contrast medium that caused chronic exposure to internal alpha-particle radiation when it was administered systemically. Cancer incidence in 432 Swedish patients exposed to Thorotrast was evaluated by computerized linkage of the cohort with the Swedish Cancer Register. Standardized incidence ratios (SIRs) were calculated as the ratio of observed cases in the cohort to expected cases in the general population. A total of 170 cancers occurring in 152 individuals were reported, whereas only 57 cases were expected. The SIR was significantly increased for cancer at all sites (3.0), with the largest excesses noted for primary liver and gallbladder cancer (SIR = 39.2). Other significantly elevated risks were observed for liver cancer not specified as primary, small intestine cancer, stomach cancer, leukemia, kidney cancer, CNS tumors, and pancreatic cancer. Among women, there was a significantly increased risk for lung cancer, based on a small number. Our results show that cumulative radiation exposure is directly related to carcinogenesis in the liver and gallbladder, which is consistent with earlier findings. In addition, there may be a relationship between radiation exposure and the development of other solid tumors. (C) 2002 by Radiation Research Society. C1 Karolinska Inst, Dept Med Epidemiol, S-17177 Stockholm, Sweden. Karolinska Univ Hosp, Dept Canc Epidemiol, Radiumhemmet, Stockholm, Sweden. NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Swedish Radiat Protect Inst, Stockholm, Sweden. RP Karolinska Inst, Dept Med Epidemiol, POB 281, S-17177 Stockholm, Sweden. EM ullakarin.nyberg@telia.com FU NCI NIH HHS [N01-CP-33059-01] NR 33 TC 15 Z9 15 U1 0 U2 1 PU RADIATION RESEARCH SOC PI LAWRENCE PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA SN 0033-7587 EI 1938-5404 J9 RADIAT RES JI Radiat. Res. PD APR PY 2002 VL 157 IS 4 BP 419 EP 425 DI 10.1667/0033-7587(2002)157[0419:CIASPE]2.0.CO;2 PG 7 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA 536VQ UT WOS:000174722900009 PM 11893244 ER PT J AU Sigurdson, AJ Stovall, M Kleinerman, RA Maor, MH Taylor, ME Boice, JD Ron, E AF Sigurdson, AJ Stovall, M Kleinerman, RA Maor, MH Taylor, ME Boice, JD Ron, E TI Feasibility of assessing the carcinogenicity of neutrons among neutron therapy patients SO RADIATION RESEARCH LA English DT Editorial Material ID MYELOID-LEUKEMIA; CANCER INCIDENCE; GAMMA-RAYS; RISK; IRRADIATION; INDUCTION; PILOTS; MICE; ATTENDANTS; MORTALITY AB Nuclear workers, oil well loggers, astronauts, air flight crews, and frequent fliers can be exposed to low doses of neutrons, but the long-term human health consequences of neutron exposure are unknown. While few of these exposed populations are suitable for studying the effects of neutron exposure, patients treated with neutron-beam therapy might be a source of information. To assess the feasibility of conducting a multi-center international study of the late effects of neutron therapy, we surveyed 23 cancer centers that had used neutron beam therapy. For the 17 responding institutions, only 25% of the patients treated with neutrons (2,855 of 11,191) were alive more than 2 years after treatment. In a two-center U.S. pilot study of 484 neutron-treated cancer patients, we assessed the feasibility of obtaining radiotherapy records, cancer incidence and other follow-up data, and of estimating patient organ doses. Patients were treated with 42 MeV neutrons between 1972 and 1989. Applying a clinical equivalence factor of 3.2 for neutrons, total average organ doses outside the treatment beam ranged from 0.14 to 0.29 Gy for thyroid, 0.40 to 2.50 Gy for breast, 0.63 to 2.35 Gy for kidney, and 1.12 to 1.76 Gy for active bone marrow depending upon the primary cancer treatment site. We successfully traced 97% of the patients, but we found that patient survival was poor and that chemotherapy was not confirmable in a quarter of the patients. Based on our findings from the international survey and the feasibility study, we conclude that a large investigation could detect a fivefold or higher leukemia risk, but would be inadequate to evaluate the risk of solid cancers with long latent periods and therefore would likely not be informative with respect to neutron-related cancer risk in humans. (C) 2002 by Radiation Research Society. C1 NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Univ Texas, MD Anderson Canc Ctr, Dept Radiat Therapy, Houston, TX 77030 USA. Washington Univ, Sch Med, Radiat Oncol Ctr, St Louis, MO 63110 USA. Int Epidemiol Inst, Rockville, MD 20850 USA. RP Sigurdson, AJ (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 7092,MSC 7238, Bethesda, MD 20892 USA. OI Kleinerman, Ruth/0000-0001-7415-2478 FU NCI NIH HHS [N01-CP-81121, N01-CP-40535] NR 32 TC 2 Z9 2 U1 0 U2 1 PU RADIATION RESEARCH SOC PI OAK BROOK PA 820 JORIE BOULEVARD, OAK BROOK, IL 60523 USA SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD APR PY 2002 VL 157 IS 4 BP 483 EP 489 DI 10.1667/0033-7587(2002)157[0483:FOATCO]2.0.CO;2 PG 7 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA 536VQ UT WOS:000174722900018 PM 11893253 ER PT J AU Knopp, MV Himmelhan, N Radeleff, J Junkermann, H Hess, T Sinn, HP Brix, G AF Knopp, MV Himmelhan, N Radeleff, J Junkermann, H Hess, T Sinn, HP Brix, G TI Comparison of quantification techniques for dynamic contrast enhancement MRI analyzed using MR mammography SO RADIOLOGE LA German DT Article DE MR-mammography; gadolinium-chelate; quantification; ROC analysis; comparative study ID BREAST-TUMORS; GD-DTPA; CERVICAL-CARCINOMA; MICROCIRCULATION; PARAMETERS; DIAGNOSIS; CURVES; CANCER AB Aim. Aim of this study was to demonstrate and compare different quantification techniques to assess contrast enhancement in dynamic MRI studies. The diagnostic potential of dynamic MRI studies is increasingly appreciated and already used in different organ systems. Method. A patient population of 314 histologically verified breast lesions (138 malignant,176 benign) were evaluated using a high temporal resolved dynamic sequence. Different quantification techniques such as the use of a cutoff line,time dependent and pharmacokinetic assessment were comparatively evaluated. Results. Time dependent quantification methods revealed higher diagnostic potential which was further improved by in vivo normalization of the contrast availability in the vascular system. Significant differences in the enhancement characteristics were determined between malignant and benign as well within the different histological entities. Conclusion. Time dependent quantification methods enable an angiogenic characterization of lesions to improve diagnostic interpretation as well as monitoring during therapy. They are also the basis for automated, color-coded visualization of dynamic studies. C1 NIH, Ctr Clin, Abt Diagnost Radiol, Bethesda, MD 20892 USA. Univ Klinikum Heidelberg, Abt Gynakol Radiol, Heidelberg, Germany. Univ Klinikum Heidelberg, Abt Pathol, Heidelberg, Germany. RP Knopp, MV (reprint author), Ohio State Univ, Univ Hosp, Dept Radiol, 163 Means Hall,1654 Upham Dr, Columbus, OH 43210 USA. RI Sinn, Hans-Peter/C-5661-2008 NR 36 TC 6 Z9 6 U1 0 U2 1 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0033-832X J9 RADIOLOGE JI Radiologe PD APR PY 2002 VL 42 IS 4 BP 280 EP 290 DI 10.1007/s00117-002-0728-z PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 552JX UT WOS:000175618200007 PM 12063736 ER PT J AU Avila, NA Kelly, JA Dwyer, AJ Johnson, DL Jones, EC Moss, J AF Avila, NA Kelly, JA Dwyer, AJ Johnson, DL Jones, EC Moss, J TI Lymphangioleiomyomatosis: Correlation of qualitative and quantitative thin-section CT with pulmonary function tests and assessment of dependence on pleurodesis SO RADIOLOGY LA English DT Article DE computed tomography (CT), thin-section; lung, CT; lymphangiomyomatosis ID DIFFUSING-CAPACITY; COMPUTED-TOMOGRAPHY; LYMPHANGIOMYOMATOSIS AB PURPOSE: To explore the relationship between findings at thin-section computed tomography (CT) and pulmonary function tests in lymphangioleiomyomatosis (LAM) and to evaluate the influence of pleurodesis on this relation and the effectiveness of quantitative versus qualitative CT in the assessment of disease severity. MATERIALS AND METHODS: Thirty-seven patients with LAM (17 with pleurodesis) underwent CT and pulmonary function tests. The severity of pulmonary cystic involvement was graded qualitatively by two independent readers and measured quantitatively at CT with a thresholding technique. Relationships between findings at CT and pulmonary function tests and the influence of pleurodesis on these findings were assessed with regression analysis and analysis of covariance. RESULTS: Qualitative ratings had good agreement between observers (kappa = 0.75). Quantitative CT had good repeatability and showed significant correlation with the percent predicted forced expiratory volume in 1 second (FEV1%) (r = 0.67, P < .001), percent predicted diffusing capacity of lung for carbon monoxide (DLCO%) (r = 0.48, P < .005), percent predicted ratio of residual volume to total lung capacity (RV/TLC%) (r = -0.65, P < .001), and percent predicted TLC (r = 0.34, P < .04). Quantitative CT results were somewhat better than qualitative CT results. The standard error of the FEV1% for the quantitative CT was about 85% of that for the qualitative CT. Pleurodesis had no statistically significant effect on the slope of the regression line between quantitative CT findings, FEV1%, and DLCO% (corrected for alveolar volume). The slope between quantitative CT and RV/TLC% was significantly (P = .044) more negative in patients with pleurodesis. CONCLUSION: Qualitative and quantitative CT findings correlate with pulmonary dysfunction over a wide range of disease severity in patients with LAM. Pleurodesis influences the relationship between CT measurements and pulmonary function test results. (C) RSNA, 2002. C1 NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bethesda, MD 20892 USA. NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. RP Avila, NA (reprint author), NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bldg 10,Rm 1C-660,10 Ctr Dr,MSC 1182, Bethesda, MD 20892 USA. NR 33 TC 25 Z9 26 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 2002 VL 223 IS 1 BP 189 EP 197 DI 10.1148/radiol.2231010315 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 534WC UT WOS:000174611900025 PM 11930066 ER PT J AU Thayer, JF Friedman, BH AF Thayer, JF Friedman, BH TI Stop that! Inhibition, sensitization, and their neurovisceral concomitants SO SCANDINAVIAN JOURNAL OF PSYCHOLOGY LA English DT Article DE sensitization; inhibition; heart rate variability; anxiety; emotion ID HEART-RATE-VARIABILITY; GENERALIZED ANXIETY DISORDER; AUTONOMIC CHARACTERISTICS; PERIOD VARIABILITY; PREFRONTAL CORTEX; MECHANISMS; SYSTEM; WORRY; PERSPECTIVE; PSYCHIATRY AB There is increasing evidence that the behavior of living systems can be conceptualized as a self-organizing dynamical system. Moreover, evidence suggests that inhibitory processes give these systems the flexibility that is necessary for efficient functioning in the face of changing environmental demands, The process of sensitization can be conceived as a breakdown of inhibitory neural processes that can lead to maladaptive, perseverative behavior. In this paper we describe a model of inhibition and sensitization from a dynamical systems perspective. We show that inhibition is important for adaptive behavior across a number of levels of system functioning. Using our work on attention, emotion, and anxiety disorders we show the importance of both central - for example gamma-aminobutyric acid (GABA)-ergic - and peripheral - for example heart rate variability (HRV) - inhibitory processes and how they may be linked by a network of neural structures that guide the organism from one state of relative stability to another. C1 NIA, GRC, LPC, Baltimore, MD 21224 USA. Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA. RP Thayer, JF (reprint author), NIA, GRC, LPC, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 63 TC 65 Z9 66 U1 4 U2 14 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0036-5564 J9 SCAND J PSYCHOL JI Scand. J. Psychol. PD APR PY 2002 VL 43 IS 2 BP 123 EP 130 DI 10.1111/1467-9450.00277 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 543RJ UT WOS:000175114700005 PM 12004949 ER PT J AU Sorg, BA Newlin, DB AF Sorg, BA Newlin, DB TI Sensitization as a mechanism for multiple chemical sensitivity: Relationship to evolutionary theory SO SCANDINAVIAN JOURNAL OF PSYCHOLOGY LA English DT Article DE avoidance; mesocorticolimbic system; multiple chemical sensitivity; sensitization; conditioned fear ID CORTICOTROPIN-RELEASING HORMONE; POSTTRAUMATIC-STRESS-DISORDER; MEDIATED LOCOMOTOR-ACTIVITY; PARAVENTRICULAR NUCLEUS; MESSENGER-RNA; ADRENOCORTICOTROPIN SECRETION; SOMATIC COMPLAINTS; MAJOR DEPRESSION; LIMBIC SYSTEM; YOUNG-ADULTS AB Multiple chemical sensitivity (MCS) is a disorder in humans attributed to prior chemical exposure. Sensitization is an amplification of neuronal responsiveness that elicits increased behavioral responding to stimuli, and occurs in a recently developed rat model of MCS. Rats were exposed to repeated formaldehyde (Form) and their response in three behavioral tests, including locomotor activity after a cocaine challenge, conditioned fear, and behavioral avoidance of Form, was assessed. In all three tests, rats demonstrated sensitized behaviors, implicating amplified responding within specific limbic brain regions. Evolutionary theory in the context of MCS specifies how the behavioral strategies of those with MCS are consistent with the notion that their self-perceived sense of survival and reproductive Fitness may be threatened by chemical exposures, This behavior may be mediated by the same limbic brain regions that become sensitized after repeated chemical exposure in animals. C1 Washington State Univ, Dept VCAPP, Alcohol & Drug Abuse Program, Pullman, WA 99164 USA. Washington State Univ, Dept VCAPP, Program Neurosci, Pullman, WA 99164 USA. NIDA, Intramural Res Program, Baltimore, MD USA. RP Sorg, BA (reprint author), Washington State Univ, Dept VCAPP, Alcohol & Drug Abuse Program, Pullman, WA 99164 USA. NR 62 TC 7 Z9 7 U1 2 U2 3 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0036-5564 J9 SCAND J PSYCHOL JI Scand. J. Psychol. PD APR PY 2002 VL 43 IS 2 BP 161 EP 167 DI 10.1111/1467-9450.00282 PG 7 WC Psychology, Multidisciplinary SC Psychology GA 543RJ UT WOS:000175114700010 PM 12004954 ER PT J AU Johnsen, BH Eid, J Laberg, JC Thayer, JF AF Johnsen, BH Eid, J Laberg, JC Thayer, JF TI The effect of sensitization and coping style on post-traumatic stress symptoms and quality of life: Two longitudinal studies SO SCANDINAVIAN JOURNAL OF PSYCHOLOGY LA English DT Article DE sensitization; coping style; PTSD symptoms; quality of life ID MULTIPLE CHEMICAL-SENSITIVITY; TRAFFIC ACCIDENT VICTIMS; MOTOR-VEHICLE ACCIDENTS; POSTTRAUMATIC-STRESS; IMMUNOLOGICAL REACTIVITY; CRISIS SUPPORT; DISORDER; DISASTER; PREDICTORS; RESPONSES AB The present study investigated the effects of multiple trauma exposure and coping style on post-traumatic stress symptoms and quality of life, It was hypothesized that sensitization would occur in subjects repeatedly exposed to life-threatening situations (study 1), and different coping styles would act as a resilience or facilitating factor in symptom development (study 2). The results showed that the single-exposure group revealed a decrease in trauma specific stress reactions from three weeks to four months, with a persistent reduction at 12-month follow-up, while the repeated-exposure group showed an increase in symptom reporting over the 12-month period. The same pattern emerged for perceived quality of life-measured by the General Health Questionnaire (GHQ-30). The second study revealed a correlation between scores on avoidant-focused coping style and the Impact of Event Scale-avoidance dimension, Post-traumatic Symptom Scale and GHQ-30. Furthermore, only subjects with a dominant coping style of emotion-focused or task-focused coping showed a reduction in trauma-specific symptom scores over time. C1 Univ Bergen, Dept Psychol Sci, N-5015 Bergen, Norway. Royal Norwegian Naval Acad, Bergen, Norway. Univ Bergen, Dept Psychosocial Sci, Bergen, Norway. NIA, Baltimore, MD 21224 USA. RP Johnsen, BH (reprint author), Univ Bergen, Dept Psychol Sci, Christiesgt 12, N-5015 Bergen, Norway. RI Eid, Jarle/G-1346-2014 NR 46 TC 40 Z9 41 U1 0 U2 10 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0036-5564 J9 SCAND J PSYCHOL JI Scand. J. Psychol. PD APR PY 2002 VL 43 IS 2 BP 181 EP 188 DI 10.1111/1467-9450.00285 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 543RJ UT WOS:000175114700013 PM 12004957 ER PT J AU Freedman, MH Alter, BP AF Freedman, MH Alter, BP TI Risk of myelodysplastic syndrome and acute myeloid leukemia in congenital neutropenias SO SEMINARS IN HEMATOLOGY LA English DT Article ID COLONY-STIMULATING-FACTOR; SHWACHMAN-DIAMOND-SYNDROME; FACTOR-RECEPTOR GENE; ACUTE MYELOGENOUS LEUKEMIA; G-CSF RECEPTOR; GRANULOCYTE; MUTATIONS; AGRANULOCYTOSIS; TRANSFORMATION; MONOSOMY-7 C1 Univ Toronto, Hosp Sick Children, Div Hematol Oncol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Inst Res, Toronto, ON M5G 1X8, Canada. NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA. RP Freedman, MH (reprint author), Univ Toronto, Hosp Sick Children, Div Hematol Oncol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. NR 41 TC 54 Z9 55 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD APR PY 2002 VL 39 IS 2 BP 128 EP 133 DI 10.1053/shem.2002.31912 PG 6 WC Hematology SC Hematology GA 540WV UT WOS:000174954600010 PM 11957196 ER PT J AU Weinreich, DM Alexander, HR AF Weinreich, DM Alexander, HR TI Transarterial perfusion of liver metastases SO SEMINARS IN ONCOLOGY LA English DT Review ID TUMOR-NECROSIS-FACTOR; ISOLATED HEPATIC PERFUSION; ISOLATED LIMB PERFUSION; OCULAR MELANOMA; UVEAL MELANOMA; COLORECTAL-CANCER; PHASE-I; SYSTEMIC FLUOROURACIL; ARTERIAL INFUSION; VENOUS ISOLATION C1 NCI, Metab Sect, Surg Branch, Bethesda, MD 20892 USA. RP Alexander, HR (reprint author), NCI, Metab Sect, Surg Branch, Room 2B07,10 Ctr Dr, Bethesda, MD 20892 USA. NR 45 TC 14 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 2002 VL 29 IS 2 BP 136 EP 144 DI 10.1053/sonc.2002.31681 PG 9 WC Oncology SC Oncology GA 539ER UT WOS:000174858000005 PM 11951211 ER PT J AU Kadiiska, MB Mason, RP AF Kadiiska, MB Mason, RP TI In vivo copper-mediated free radical production: an ESR spin-trapping study SO SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY LA English DT Article; Proceedings Paper CT 7th International Workshop on Electron Magnetic Resonance of Disorded Systems CY JUN 09-18, 2001 CL SOFIA BOYANA, BULGARIA DE rats; spin trap; ESR; free radicals ID PERFUSED RAT-LIVER; DIETARY VITAMIN-E; LIPID-PEROXIDATION; CARBON-TETRACHLORIDE; ASCORBIC-ACID; GLUTATHIONE-PEROXIDASE; BIOLOGICAL DAMAGE; HYDROGEN-PEROXIDE; OXIDATIVE DAMAGE; INVIVO AB Copper has been suggested to facilitate oxidative tissue injury through a free radical-mediated pathway analogous to the Fenton reaction. By applying the electron spin resonance (ESR) spin-trapping technique, evidence for hydroxyl radical formation in vivo was obtained in rats treated simultaneously with copper and ascorbic acid or paraquat. A secondary radical spin-trapping technique was used in which the hydroxyl radical formed the methyl radical upon reaction with dimethylsulfoxide. The methyl radical was then detected by ESR spectroscopy as its adduct with the spin trap phenyl-N-t-butyl- nitrone (PBN). In contrast, lipid derived radical was detected in vivo in copper-challenged, vitamin E and selenium-deficient rats. These findings support the proposal that dietary selenium and vitamin E can protect against lipid peroxidation and copper toxicity. Since copper excreted into the bile from treated animals is expected to be maintained in the Cu(I) state (by ascorbic acid or glutathione), a chelating agent that would redox-stablilize it in the Cu(I) state was used to prevent ex vivo redox chemistry. Bile samples were collected directly into solutions of bathocuproinedisulfonic acid, a Cu(l)-stabilizing agent, and 2,2'-dipyridyl, a Fe(II)-stabilizing agent. If these precautions were not taken, radical adducts generated ex vivo could be mistaken for radical adducts produced in vivo and excreted into the bile. (C) 2002 Elsevier Science B.V. All rights reserved. C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. RP Kadiiska, MB (reprint author), NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 74 TC 42 Z9 47 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1386-1425 J9 SPECTROCHIM ACTA A JI Spectroc. Acta Pt. A-Molec. Biomolec. Spectr. PD APR PY 2002 VL 58 IS 6 SI SI BP 1227 EP 1239 AR PII S1386-1425(01)00713-2 DI 10.1016/S1386-1425(01)00713-2 PG 13 WC Spectroscopy SC Spectroscopy GA 536KL UT WOS:000174699200014 PM 11993471 ER PT J AU Borkowf, CB AF Borkowf, CB TI Computing the non-null asymptotic variance of n-way contingency tables with fixed one-way marginal totals, with applications to gene-environment interaction studies SO STATISTICA SINICA LA English DT Article DE contingency table; epidemiology; gene-environment interaction; multinomial; multivariate extended hypergeometric (MXH) distribution; permutation test ID EMPIRICAL QUANTILES AB Consider first the set of all possible n-way multinomial tables defined by certain mean cell proportions with a given number of total counts. Consider next the subset of these n-way tables that, in addition, satisfies certain one-way marginal totals obtained by summing the cell counts over all but one subscript. The subset of tables that satisfies these marginal constraints is said to have the multivariate extended hypergeometric (MXH) distribution. In this paper we develop a general algorithm for calculating the asymptotic variance of n-way MXH tables and present some explicit covariance formulas under independence and in other special cases. We also note that permutation tests defined by certain mean cell proportions and one-way marginal constraints essentially enumerate the entire set of MXH tables with those proportions and constraints. Thus, one can use the asymptotic MXH distribution to approximate the finite sample variances of statistics calculated under permutation tests for various null and alternative hypotheses. One can then use these results to construct confidence intervals for parameters of interest and to approximate the percentiles of test statistics under permutation tests, which is a significant advantage when these tests are computationally prohibitive. We illustrate the use of methods based on the asymptotic MXH distribution as complements and alternatives to permutation tests in the analysis of epidemiological studies of gene-environment interactions. C1 NCI, CCR, CPSB, Bethesda, MD 20893 USA. RP Borkowf, CB (reprint author), NCI, CCR, CPSB, 6116 Execut Blvd,Suite 705,MSC 8314, Bethesda, MD 20893 USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU STATISTICA SINICA PI TAIPEI PA C/O DR H C HO, INST STATISTICAL SCIENCE, ACADEMIA SINICA, TAIPEI 115, TAIWAN SN 1017-0405 J9 STAT SINICA JI Stat. Sin. PD APR PY 2002 VL 12 IS 2 BP 491 EP 504 PG 14 WC Statistics & Probability SC Mathematics GA 555TQ UT WOS:000175809700007 ER PT J AU Ezzeddine, MA Lev, MH McDonald, CT Rordorf, G Oliveira-Filho, J Aksoy, FG Farkas, J Segal, AZ Schwamm, LH Gonzalez, RG Koroshetz, WJ AF Ezzeddine, MA Lev, MH McDonald, CT Rordorf, G Oliveira-Filho, J Aksoy, FG Farkas, J Segal, AZ Schwamm, LH Gonzalez, RG Koroshetz, WJ TI CT angiography with whole brain perfused blood volume imaging - Added clinical value in the assessment of acute stroke SO STROKE LA English DT Article DE angiography; diagnostic imaging; stroke assessment; stroke classification; tomography, x-ray computed ID ACUTE ISCHEMIC STROKE; ACUTE CEREBRAL-ISCHEMIA; INTEROBSERVER AGREEMENT; INTERRATER RELIABILITY; TRANSCRANIAL DOPPLER; SUBTYPE DIAGNOSIS; CLASSIFICATION; ARTERY; TRIAL; INFARCTION AB Background and Purpose-In CT angiographic and perfusion imaging (CTA/CTP), rapid CT scanning is performed during the brief steady state administration of a contrast bolus, creating both vascular phase images of the major intracranial vessels and perfused blood volume-weighted parenchymal phase images of the entire brain. We assessed the added clinical value of the data provided by CTA/CTP over that of clinical examination and noncontrast CT (NCCT) alone. Methods-NCCT and CTA/CTP imaging was performed in 40 patients presenting with an acute stroke. Short clinical vignettes were retrospectively prepared. After concurrent review of the vignettes and NCCT, a stroke neurologist rated infarct location, vascular territory, vessel(s) occluded, and Trial of Org 10172 in Acute Stroke Treatment (TOAST) and Oxfordshire Community Stroke Project classifications. The ratings were repeated after serial review of each of the CTA/CTP components: (1) axial CTA source images; (2) CTP whole brain blood volume-weighted source images; and (3) maximum-intensity projection 3-dimensional reformatted images. The sequential ratings for each case were compared with the final discharge assessment. Results-Compared with the initial review after NCCT, CTA/CTP improved the overall accuracy of infarct localization (P<0.001), vascular territory determination (P=0.003), vessel occlusion identification (P<0.001), TOAST classification (P=0.039), and Oxfordshire Community Stroke Project classification (P<0.001) by 40%, 28%, 38%, 18%, and 32%, respectively. Conclusions-Admission CTA/CTP imaging significantly improves accuracy, over that of initial clinical assessment and NCCT imaging alone, in the determination of infarct localization, site of vascular occlusion, and Oxfordshire classification in acute stroke patients. C1 Massachusetts Gen Hosp, Dept Radiol, Div Neuroradiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. NINCDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. Cornell Univ, Med Ctr, Dept Neurol, New York, NY 10021 USA. RP Lev, MH (reprint author), Massachusetts Gen Hosp, Dept Radiol, Div Neuroradiol, 55 Fruit St, Boston, MA 02114 USA. OI Schwamm, Lee/0000-0003-0592-9145 FU NCRR NIH HHS [RR-13213]; NINDS NIH HHS [NS-34626] NR 29 TC 83 Z9 89 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD APR PY 2002 VL 33 IS 4 BP 959 EP 966 DI 10.1161/hs0402.105388 PG 8 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 539EL UT WOS:000174857400014 PM 11935044 ER PT J AU Leker, RR Teichner, A Grigoriadis, N Ovadia, H Brenneman, DE Fridkin, M Giladi, E Romano, J Gozes, I AF Leker, RR Teichner, A Grigoriadis, N Ovadia, H Brenneman, DE Fridkin, M Giladi, E Romano, J Gozes, I TI NAP, a femtomolar-acting peptide, protects the brain against ischemic injury by reducing apoptotic death SO STROKE LA English DT Article DE animal models; cerebral ischemia; neuropeptides; neuroprotection; vasoactive intestinal peptide; rats ID CEREBRAL-ARTERY OCCLUSION; NITRIC-OXIDE; RAT; NEUROPROTECTION; SENSORIMOTOR; NECROSIS; CULTURES; STROKE AB Background and Purpose-We sought to determine the cerebroprotective potential of NAP, a synthetic octapeptide related to vasoactive intestinal peptide. Activity-dependent neuroprotective protein mediates some of the protective effects of vasoactive intestinal peptide. The neuroprotective NAP sequence is derived from activity-dependent neuroprotective protein. Methods-Spontaneously hypertensive rats underwent permanent middle cerebral artery occlusion by craniotomy and electrocoagulation. After dose-response and time-course experiments, the animals were injected with NAP (3 mug/kg) or vehicle intravenously 1 hour after stroke onset. Another group of rats was injected with the D-amino acid isomer of NAP (D-NAP) and served as a negative control. Rats were examined for motor and behavioral deficits 24 hours to 30 days later, and infarct volumes were determined. The effect of NAP administration on apoptotic death was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase-3 stainings. Results-NAP significantly reduced motor disability and infarct volumes compared with vehicle or D-NAP when tested at 24 hours after stroke onset (9.67+/-1.4% versus 17.04+/-1.18% and 19.19+/-1.9% of hemispheric volume, respectively; P<0.05). NAP given 4 but not 6 hours after permanent middle cerebral artery occlusion still conferred significant neuroprotection (infarct volume 10.9+/-3.9% of hemispheric volume; P<0.05 versus vehicle). Long-term studies demonstrated that infarct volumes and disability scores remained significantly lower after 30 days in NAP-treated animals. NAP significantly reduced the number of apoptotic cells. Conclusions-Our results indicate that the durable cerebroprotection by NAP involves antiapoptotic mechanisms. C1 Hadassah Univ Hosp, Dept Neurol, Agnes Ginges Ctr Human Neurogenet, Hadassah Med Sch, IL-91120 Jerusalem, Israel. Univ Roma La Sapienza, Dept Neurol Sci, I-00185 Rome, Italy. NIH, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, Bethesda, MD 20892 USA. Weizmann Inst Sci, Dept Organ Chem, IL-76100 Rehovot, Israel. Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. RP Leker, RR (reprint author), Hadassah Univ Hosp, Dept Neurol, Agnes Ginges Ctr Human Neurogenet, Hadassah Med Sch, POB 12000, IL-91120 Jerusalem, Israel. NR 22 TC 86 Z9 89 U1 2 U2 9 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD APR PY 2002 VL 33 IS 4 BP 1085 EP 1092 DI 10.1161/01.STR.0000014207.05597.D7 PG 8 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 539EL UT WOS:000174857400035 PM 11935065 ER PT J AU Cone, EJ Preston, KL AF Cone, EJ Preston, KL TI Toxicologic aspects of heroin substitution treatment SO THERAPEUTIC DRUG MONITORING LA English DT Article DE heroin; methadone; levomethadyl acetate; urinalysis ID METHADONE-MAINTENANCE TREATMENT; SUBLINGUAL BUPRENORPHINE; OPIOID DEPENDENCE; PLASMA-LEVELS; FOLLOW-UP; DRUG-USE; ADDICTS; TRIAL; BENZODIAZEPINES; PHARMACOLOGY AB Heroin abuse is an international problem with which all countries must continually cope. Many countries have implemented heroin substitution therapy as an effective means of decreasing illicit heroin use, crime, HIV risk, and death, and in improving employment and social adjustment. Although methadone is the most commonly used medication for heroin substitution, other agonists in current use include levomethadyl acetate (LAAM), buprenorphine, and pharmaceutical-grade heroin. This report reviews toxicologic issues that arise in these programs. A broad array of testing methodologies are available that allow selection of on-site testing or laboratory-based methodology. Urine specimens may be monitored for nonprescribed drugs on a qualitative or semiquantitative basis. Methods for differentiating opiate sources by urinalysis have been proposed to distinguish poppy seed consumption from heroin abuse and for distinguishing pharmaceutical-grade heroin from illicit heroin. Therapeutic drug monitoring for methadone in plasma continues to be evaluated for use in establishing adequate dosing and detecting diversion, and new methods have been devised for measurement of the optical isomers of methadone in plasma. Biologic specimens, in addition to plasma and urine, have been evaluated for use in drug monitoring, including sweat, hair, and oral fluid, with promising results. Overall, the many recent developments in testing methodology provide more effective means to assess patients in heroin substitution programs and should contribute to improvements in public health. C1 NIDA, Intramural Res Program, Baltimore, MD 21224 USA. ConeChem Res, Baltimore, MD USA. RP Preston, KL (reprint author), NIDA, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 NR 45 TC 17 Z9 17 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0163-4356 J9 THER DRUG MONIT JI Ther. Drug Monit. PD APR PY 2002 VL 24 IS 2 BP 193 EP 198 DI 10.1097/00007691-200204000-00001 PG 6 WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology GA 533BX UT WOS:000174510500001 PM 11897965 ER PT J AU Williams, ML Wainer, IW AF Williams, ML Wainer, IW TI Role of chiral chromatography in therapeutic drug monitoring and in clinical and forensic toxicology SO THERAPEUTIC DRUG MONITORING LA English DT Article DE chiral chromatography; drug transport; drug metabolism ID KETAMINE ISOMERS; P-GLYCOPROTEIN; PHARMACOLOGY; RAT; METABOLISM AB Advances in chiral chromatographic separations have given pharmacologists and toxicologists the tools to examine unexpected clinical results involving chiral drugs. The ability to unravel complex phenomena associated with drug transport and drug metabolism is presented in this manuscript. The relation between the chirality of the drug mefloquine and the intracellular concentrations of the drug cyclosporine is illustrated by examining the effect of the enantiomers of mefloquine on the transport activity of P-glycoprotein (Pgp). These studies were conducted using a liquid chromatographic column containing immobilized Pgp. The results demonstrated that mefloquine competitively displaced the Pgp substrate cyclosporine whereas mefloquine had no effect on cyclosporine-P-p binding. The data suggest that cyclosporine cellular and CNS concentrations can be increased through the concomitant administration of (+)-mefloquine. The use of chirality in clinical and forensic situations is also illustrated by the metabolism of the enantiomers of ketamine (KET). The plasma concentrations of (+)-KET and (-)-KET and the norketamine metabolites (+)-NK and (-)-NK were measured in rat plasma using enantioselective gas chromatography. The separations were accomplished using a gas chromatography chiral stationary phase based on P-cyclodextrin. The pharmacokinetic profiles of (+)-, (-)-KET and (,+)-, (-)-NK were determined in control and protein-calorie malnourished (PCM) rats to determine the effect of PCM on ketamine metabolism and clearance. The results indicate that PCM produced a significant and stereoselective decrease in KET and NK metabolism. The data suggest that the effects of environmental factors (smoking, alcohol use, diet) and drug interactions (coadministered agents) can be measured using the changes in stereochemical metabolic and pharmacokinetic patterns of KET and similar drugs. C1 Univ Leicester, Dept Oncol, Leicester, Leics, England. Georgetown Univ, Med Ctr, Dept Pharmacol, Washington, DC 20007 USA. RP Wainer, IW (reprint author), NIA, Natl Inst Hlth, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 32 TC 26 Z9 26 U1 0 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0163-4356 J9 THER DRUG MONIT JI Ther. Drug Monit. PD APR PY 2002 VL 24 IS 2 BP 290 EP 296 DI 10.1097/00007691-200204000-00010 PG 7 WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology GA 533BX UT WOS:000174510500010 PM 11897974 ER PT J AU Schneider, AB Becker, DV Robbins, J AF Schneider, AB Becker, DV Robbins, J TI Protecting the thyroid from accidental or terrorist- instigated I-131 releases SO THYROID LA English DT Editorial Material ID REACTOR ACCIDENT; PROPHYLAXIS; IODINE C1 Univ Illinois, Chicago, IL 60612 USA. New York Weill Cornell Med Ctr, New York, NY USA. NIH, Bethesda, MD 20892 USA. RP Schneider, AB (reprint author), Univ Illinois, Endo & Metab M-C 640,1819 Polk St, Chicago, IL 60612 USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1050-7256 J9 THYROID JI Thyroid PD APR PY 2002 VL 12 IS 4 BP 271 EP 272 DI 10.1089/10507250252949379 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 547CV UT WOS:000175316200001 PM 12034049 ER PT J AU Wolff, J AF Wolff, J TI A miss for NIS? SO THYROID LA English DT Editorial Material ID RE-188-PERRHENATE; SYMPORTER; BALLOON; CELLS C1 NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Wolff, J (reprint author), NIDDKD, Lab Biochem & Genet, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 28 TC 5 Z9 5 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1050-7256 J9 THYROID JI Thyroid PD APR PY 2002 VL 12 IS 4 BP 295 EP 297 DI 10.1089/10507250252949414 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 547CV UT WOS:000175316200005 PM 12034053 ER PT J AU Robbins, J AF Robbins, J TI Lectio doctoralis: The geometric progress of knowledge and the erratic course of a life: A memoir SO THYROID LA English DT Article C1 NIH, Bethesda, MD 20892 USA. RP Robbins, J (reprint author), NIH, Bldg 10,Rm 7C432B,10 Ctr Dr, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1050-7256 J9 THYROID JI Thyroid PD APR PY 2002 VL 12 IS 4 BP 338 EP 341 DI 10.1089/10507250252949496 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 547CV UT WOS:000175316200013 PM 12034061 ER PT J AU Wu, GG Cheng, LH Deng, ZH Wang, LX Wei, TL Yang, CS Zhao, TM AF Wu, GG Cheng, LH Deng, ZH Wang, LX Wei, TL Yang, CS Zhao, TM TI Cloning and complete sequence of a novel HLA-A null allele, A*0253N, with a termination codon generated by a C to G mutation in exon 2 SO TISSUE ANTIGENS LA English DT Article DE cloning of HLA-A*0253N; HLA-A null allele; PCR-SSP; point mutation AB A novel HLA-A null allele, A*0253 N, has been identified in two generations of a Chinese family using combined serological and molecular cloning approaches. Full-length genomic DNA sequencing indicated that this new allele differs from HLA-A*02011 by a single C to G substitution at nucleotide position 324 in exon 2. This mutation results in an amino acid change from a tyrosine codon to a stop codon at position 108. A PCR-SSP based method was developed to distinguish A*0253 N from A*02 alleles. No further individuals of A*0253 N were found in 718 Chinese blood donors who carry the HLA-A*02 allele1. C1 NIAID, Mol & Cellular Immunogenet Sect, NIH, Bethesda, MD 20892 USA. Shenzhen Inst Transfus Med, Shenzhen, Peoples R China. RP Zhao, TM (reprint author), NIAID, Mol & Cellular Immunogenet Sect, NIH, Bldg 50,Room 5516,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 4 TC 7 Z9 16 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD APR PY 2002 VL 59 IS 4 BP 328 EP 330 DI 10.1034/j.1399-0039.2002.590414.x PG 3 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA 575AW UT WOS:000176924200014 PM 12135435 ER PT J AU Boley, SE Wong, VA French, JE Recio, L AF Boley, SE Wong, VA French, JE Recio, L TI p53 heterozygosity alters the mRNA expression of p53 target genes in the bone marrow in response to inhaled benzene SO TOXICOLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT 6th International Symposium on Biological Reactive Intermediates CY JUL 16-20, 2000 CL UNIV RENE DESCARTES, PARIS, FRANCE SP CNRS, European Commiss, US EPA, Natl Inst Environm Hlth Sci HO UNIV RENE DESCARTES DE p53; haploinsufficiency; DNA damage; altered expression; benzene; tumor; mouse ID CELL-CYCLE CHECKPOINT; WILD-TYPE P53; IN-VITRO; MICE; APOPTOSIS; GADD45; MDM2; RADIATION; PATHWAY; TUMORS AB C57BL/6 Trp53 heterozygous (N5) mice (p53(+/-) mice)Show an increased sensitivity to tumorigenesis following exposure to genotoxic compounds and are being used as an alternate animal model for carcinogenicity testing. However, there is relatively little data regarding the effect of p53 heterozygosity on the genomic and cellular responses of target tissues in these mice to toxic insult, especially under chronic exposure conditions used in carcinogenicity bioassays. We hypothesized that heterozygosity at the p53 locus in p53(+/-) mice alters the expression of bone marrow p53-regulated genes involved in cell cycle control and apoptosis during chronic genotoxic stress. We used real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) to examine gene expression alterations in bone marrow cells from C57BL/6 p53(+/+) and isogenic p53(+/-) mice chronically exposed for 15 weeks to genotoxic and carcinogenic levels (100 ppm) of inhaled benzene. Examination of mRNA levels of p53-regulated genes involved in cell cycle control (p21, gadd45, and cyclin G) or apoptosis (bax and bcl-2) showed that during chronic genotoxic stress, bone marrow cells from p53(+/+) mice expressed significantly higher levels of a majority of these genes compared to p53(+/-) bone marrow cells. Our results indicate that p53 heterozygosity results in a haploinsufficient phenotype in p53(+/-) bone marrow cells as evident by significantly altered mRNA levels of key genes involved in the p53-regulated DNA damage response pathway. C1 Chem Ind Inst Toxicol, Ctr Hlth Res, Res Triangle Pk, NC 27709 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Recio, L (reprint author), Chem Ind Inst Toxicol, Ctr Hlth Res, 6 Davis Dr, Res Triangle Pk, NC 27709 USA. NR 40 TC 41 Z9 42 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1096-6080 J9 TOXICOL SCI JI Toxicol. Sci. PD APR PY 2002 VL 66 IS 2 BP 209 EP 215 DI 10.1093/toxsci/66.2.209 PG 7 WC Toxicology SC Toxicology GA 534CA UT WOS:000174566000005 PM 11896287 ER PT J AU Morgan, DL Chanda, SM Price, HC Fernando, R Liu, J Brambila, E O'Connor, RW Beliles, RP Barone, S AF Morgan, DL Chanda, SM Price, HC Fernando, R Liu, J Brambila, E O'Connor, RW Beliles, RP Barone, S TI Disposition of inhaled mercury vapor in pregnant rats: Maternal toxicity and effects on developmental outcome SO TOXICOLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT 6th International Symposium on Biological Reactive Intermediates CY JUL 16-20, 2000 CL UNIV RENE DESCARTES, PARIS, FRANCE SP CNRS, European Commiss, US EPA, Natl Inst Environm Hlth Sci HO UNIV RENE DESCARTES DE mercury vapor; elemental mercury; metallic mercury; inhalation; developmental toxicity; maternal toxicity; fetal toxicity; metallothionein; developmental neurotoxicity ID ELEMENTAL MERCURY; SQUIRREL-MONKEYS; NERVOUS-SYSTEM; EXPOSURE; BRAIN; METALLOTHIONEIN; CONSEQUENCES; TISSUES AB The disposition and toxicity of inhaled elemental mercury (Hg-0) vapor for pregnant Long-Evans rats, and potential adverse effects on reproductive outcome were investigated. Rats were exposed to 0, 1, 2, 4, or 8 mg Hg-0/m(3) for 2 h/day from gestation day (GD) 6 through GD 15. Maternal toxicity occurred primarily in rats exposed to 4 and 8 mg/m(3) and was manifested as a concentration-related decrease in body weight gain and mild nephrotoxicity. Control rats gained about 13% of their initial body weight during the 10-day exposure. Rats exposed to 4 mg/m(3) Hg-0 gained about 7% less than controls, and rats exposed to 8 mg/m(3) Hg-0 lost about 17% of their initial body weight during the 10-day exposure period. Maternal kidney weights were significantly increased in the 4 and 8 mg/m(3) concentration groups, and urinalysis revealed increased levels of protein and alkaline phosphatase activity in urine of all Hg-0-exposed rats. Dams exposed to 8 mg/m(3) were euthanized in moribund condition on postnatal day (PND) 1. There was no histopathological evidence of toxicity in maternal lung, liver, or kidney of exposed rats at GD 6, GD 15, or PND 1. The incidence of resorptions was significantly increased, litter size and PND 1 neonatal body weights were significantly decreased only in the 8-mg/m(3) group. Total Hg concentrations in maternal tissues increased with increasing number of exposure days and concentration. In general, approximately 70% of Hg was eliminated from maternal tissues during the week following the last exposure (GD 15 to PND 1). Elimination of Hg from maternal brain and kidney was slower than in other tissues, possibly due to higher levels of metallothionein. Total Hg concentrations in fetal tissues increased with increasing number of exposure days and concentration, demonstrating that a significant amount of Hg crossed the placenta. One week after the last exposure, significant amounts of Hg were still present in brain, liver, and kidney of PND 1 neonates. Metallothionein levels in neonatal tissues were not significantly increased by exposure to 4 mg/m3 Hg-0. The total amount of Hg in neonatal brain (ng/brain) continued to increase after termination of inhalation exposure, suggesting a redistribution of Hg from the dam to neonatal brain. These data demonstrate that inhaled Hg-0 vapor is distributed to all maternal and fetal tissues in a dose-dependent manner. Adverse effects of Hg on developmental outcome occurred only at a concentration that caused maternal toxicity. C1 NIEHS, NCI, Res Triangle Pk, NC 27709 USA. ManTech Environm Technol Inc, Res Triangle Pk, NC 27709 USA. Res Triangle Inst, Res Triangle Pk, NC 27709 USA. US EPA, Off Res & Dev, NCEA, Washington, DC 20460 USA. US EPA, Div Neurotoxicol, NHEERL, ORD, Res Triangle Pk, NC 27709 USA. RP Morgan, DL (reprint author), NIEHS, NCI, Mail Stop IF-00,POB 12233, Res Triangle Pk, NC 27709 USA. NR 41 TC 26 Z9 27 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1096-6080 J9 TOXICOL SCI JI Toxicol. Sci. PD APR PY 2002 VL 66 IS 2 BP 261 EP 273 DI 10.1093/toxsci/66.2.261 PG 13 WC Toxicology SC Toxicology GA 534CA UT WOS:000174566000011 PM 11896293 ER PT J AU Weaver, JL Broud, DD McKinnon, K Germolec, DR AF Weaver, JL Broud, DD McKinnon, K Germolec, DR TI Serial phenotypic analysis of mouse peripheral blood leukocytes SO TOXICOLOGY MECHANISMS AND METHODS LA English DT Article DE leukocyte; mouse; peripheral blood; phenotypic analysis; repeat sampling ID FLOW-CYTOMETRY; INTERLABORATORY EVALUATION; LYMPHOCYTE; QUANTIFICATION; INJURY; CELLS; MICE AB Repeated phenotypic analysis of mouse peripheral blood leukocytes over short periods of time (2 weeks) has been difficult because of the very limited volumes of blood available under guidelines of the Institutional Animal Care and Use Committee. The loss of leukocytes and variations among laboratories during conventional flow cytometry sample preparation based on lysing and repeated washing have been limiting factors when measuring multiple parameters in small samples. We describe a method of phenotypic analysis using a no-lyse, no-wash staining technique combined with fluorescent triggering for data collection that can be performed on volumes of 20 muL or less of whole blood per set of markers in one tube. This method allows repeated phenotypic analysis of peripheral whole blood from mice. Fluorescent triggering with anti-CD45-PE/Cy5 antibody allows high-quality phenotypic data to be collected for CD4, CD8, TcR-beta, CD45R (B220), CD11b, and Gr-1 epitopes on leukocytes from mouse peripheral blood without lysis. The markers selected cover the major populations in peripheral mouse blood. Reproducibility and time-course data are presented for sampling periods as long as 4 weeks. Data produced by flow cytometers manufactured by two different companies show well-correlated results. An instrument equipped with a gated amplifier or a photomultiplier tube suitable for Cy7 conjugates could measure additional parameters. Because of interference from unlysed erythrocytes, scatter parameters are not useful for identifying cell populations with this method. C1 US FDA, Div Appl Pharmacol Res, Off Testing & Res, Ctr Drug Evaluat & Res, Laurel, MD 20708 USA. Celera Genom Inc, Rockville, MD USA. NIEHS, Toxicol Lab, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA. RP Weaver, JL (reprint author), US FDA, Div Appl Pharmacol Res, Off Testing & Res, Ctr Drug Evaluat & Res, MOD-1,8301 Muirkirk Rd, Laurel, MD 20708 USA. NR 13 TC 6 Z9 8 U1 0 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1537-6524 J9 TOXICOL MECH METHOD JI Toxicol. Mech. Methods PD APR-JUN PY 2002 VL 12 IS 2 BP 95 EP 118 DI 10.1080/10517230290075341 PG 24 WC Toxicology SC Toxicology GA 555MX UT WOS:000175798800001 PM 20021196 ER PT J AU Kozlov, MM Chernomordik, LV AF Kozlov, MM Chernomordik, LV TI The protein coat in membrane fusion: Lessons from fission SO TRAFFIC LA English DT Article DE hemagglutinin; membrane curvature; membrane fission; membrane fusion; protein coat ID INFLUENZA-VIRUS HEMAGGLUTININ; SYNAPTIC VESICLE ENDOCYTOSIS; PLANAR BILAYER-MEMBRANES; INDUCED CELL-FUSION; LOW-PH; HEMIFUSION INTERMEDIATE; MEDIATED FUSION; TRANSMEMBRANE DOMAIN; AIR/WATER INTERFACE; RECEPTOR-BINDING AB Multiple cell biological processes involve two opposite rearrangements of membrane configuration, referred to as fusion and fission. While membrane intermediates in protein-mediated fusion have been studied in some detail, the global force which drives sequential stages of the fusion reaction from early local intermediates to an expanding fusion pore remains unknown. Fusion proceeds via stages, which are analogous but in the opposite direction to that of membrane budding-off and fission driven by protein coats. On the basis of this analogy, we propose that an interconnected coat formed by membrane-bound activated fusion proteins surrounding the membrane contact zone generates the driving force for fusion. This fusion protein coat has a strongly curved intrinsic shape opposite to that of the protein coat driving fission. To relieve internal stresses, the fusion protein coat spontaneously bends out of the initial shape of the membrane surface. This bending produces elastic stresses in the underlying lipid bilayer and drives its fusion with the apposing membrane. The hypothesis that 'bystander' proteins (i.e. fusion proteins outside the contact zone) generate the driving force for fusion offers a new interpretation for a number of known features of the fusion reaction mediated by the prototype fusion protein, influenza hemagglutinin, and might bring new insights into mechanisms of other fusion reactions. C1 Tel Aviv Univ, Sackler Sch Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel. NICHHD, Sect Membrane Biol, LCMB, NIH, Bethesda, MD 20892 USA. RP Kozlov, MM (reprint author), Tel Aviv Univ, Sackler Sch Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel. NR 89 TC 55 Z9 56 U1 0 U2 5 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1398-9219 J9 TRAFFIC JI Traffic PD APR PY 2002 VL 3 IS 4 BP 256 EP 267 DI 10.1034/j.1600-0854.2002.030403.x PG 12 WC Cell Biology SC Cell Biology GA 540NB UT WOS:000174934100003 PM 11929607 ER PT J AU Stroncek, D Bux, J AF Stroncek, D Bux, J TI Is it time to standardize granulocyte alloantigen nomenclature? SO TRANSFUSION LA English DT Editorial Material ID NEONATAL NEUTROPENIA; SH; GENES; NA1; FORMS; NB1; PATHOGENESIS; NEUTROPHILS; POPULATION; EXPRESSION C1 NIH, Warren Grant Magnuson Clin Ctr, Dept Transfus Med, Bethesda, MD 20892 USA. Univ Giessen, Inst Clin Immunol & Transfus Med, D-6300 Giessen, Germany. RP Stroncek, D (reprint author), NIH, Warren Grant Magnuson Clin Ctr, Dept Transfus Med, Bethesda, MD 20892 USA. NR 26 TC 3 Z9 4 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 USA SN 0041-1132 J9 TRANSFUSION JI Transfusion PD APR PY 2002 VL 42 IS 4 BP 393 EP 395 DI 10.1046/j.1525-1438.2002.00107.x PG 3 WC Hematology SC Hematology GA 550MM UT WOS:000175506900003 PM 12076283 ER PT J AU Wolkow, CA AF Wolkow, CA TI Life span: getting the signal from the nervous system SO TRENDS IN NEUROSCIENCES LA English DT Review ID CU/ZN-SUPEROXIDE-DISMUTASE; CAENORHABDITIS-ELEGANS; OXIDATIVE STRESS; DROSOPHILA-MELANOGASTER; CATALASE; EXPRESSION; RESISTANCE; OVEREXPRESSION; LONGEVITY; EXTENSION AB Life span is determined by both environmental and genetic influences. The importance of genes is illustrated by the fact that single gene mutations extend life span in nematodes, fruit flies and mice. Recent reports reveal that the life span of Caenorhabditis elegans is controlled by insulin-like signals from the nervous system. Hormones that control life span have recently been identified in fruit flies and mice. These findings suggest that neuroendocrine pathways could constitute an important determinant of life span across phylogeny. This review examines the evidence for nervous system control of longevity and discusses the implications for popular models for aging. C1 NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. RP Wolkow, CA (reprint author), NIA, Neurosci Lab, Intramural Res Program, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 37 TC 38 Z9 38 U1 1 U2 7 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD APR PY 2002 VL 25 IS 4 BP 212 EP 216 DI 10.1016/S0166-2236(02)02133-1 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 533CQ UT WOS:000174512200012 PM 11998690 ER PT J AU Shahabuddin, M AF Shahabuddin, M TI Do Plasmodium ookinetes invade a specific cell type in the mosquito midgut? SO TRENDS IN PARASITOLOGY LA English DT Article ID AEDES-AEGYPTI MIDGUT; ANOPHELES-GAMBIAE; GALLINACEUM; ATPASE; MECHANISM; INVASION; SITES AB Recent debate in Plasmodium ookinete invasion has been centered on whether the parasite chooses a specific cell type to cross the midgut epithelium in the mosquito. A few publications have described the mosquito midgut being composed of complex surface-structures, histochemically and biochemically diverse cell types, and have proposed that Plasmodium gallinaceum ookinetes prefers a specific cell type (Ross cell) in Aedes aegypti for crossing the midgut epithelium. Two recent publications reported, however, that with differential interference contrast microscopy, all midgut epithelia[ cells in uninfected mosquitoes appear structurally similar and argued that ookinetes do not invade a specific cell type. These observations are discussed here in the context of the 'Ross cell' hypothesis. C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Shahabuddin, M (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NR 22 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1471-4922 J9 TRENDS PARASITOL JI Trends Parasitol. PD APR PY 2002 VL 18 IS 4 BP 157 EP 161 AR PII S1471-4922(01)02219-X DI 10.1016/S1471-4922(01)02219-X PG 5 WC Parasitology SC Parasitology GA 533CM UT WOS:000174511900007 PM 11998702 ER PT J AU Pautler, SE Harrington, FS McWilliams, GW Walther, MM AF Pautler, SE Harrington, FS McWilliams, GW Walther, MM TI A novel laparoscopic specimen entrapment device to facilitate morcellation of large renal tumors SO UROLOGY LA English DT Article ID RADICAL NEPHRECTOMY; EXPERIENCE AB A reusable laparoscopic instrument consisting of a flexible deployment ring and a barrel was fabricated, and an impermeable sac was sutured to the flexible ring before entrapment of the specimen and morcellation. The laparoscopic specimen entrapment device facilitated placement of large renal tumors within a sac for morcellation. C1 NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA. NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA. RP Walther, MM (reprint author), NCI, Urol Oncol Branch, NIH, Bldg 10,Room 2B47,10 Ctr Dr, Bethesda, MD 20892 USA. NR 7 TC 9 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0090-4295 J9 UROLOGY JI UROLOGY PD APR PY 2002 VL 59 IS 4 BP 591 EP 593 AR PII S0090-4295(01)01622-3 DI 10.1016/S0090-4295(01)01622-3 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA 536DX UT WOS:000174686400032 PM 11927323 ER PT J AU Messam, CA Hou, J Berman, JW Major, EO AF Messam, CA Hou, J Berman, JW Major, EO TI Analysis of the temporal expression of nestin in human fetal brain derived neuronal and glial progenitor cells SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article; Proceedings Paper CT 4th Brain Research Interactive Symposium CY NOV 08-10, 2001 CL SAN DIEGO, CA DE stem cell; glia; astrocyte; astrocyte progenitor; neuronal progenitor; GFAP ID CENTRAL-NERVOUS-SYSTEM; INTERMEDIATE FILAMENT PROTEIN; NEURAL STEM-CELLS; REACTIVE ASTROCYTES; SPINAL-CORD; IDENTIFICATION; CULTURE; PROLIFERATION; COEXPRESSION; INDUCTION AB Nestin expression in the developing human brain was examined with the use of unique human specific anti-nestin antibodies. Double immunostaining of cell cultures and tissue sections derived from first and second trimester human fetal brain (HFB) examined the co-expression of nestin with other cell type specific phenotypic markers. The immunocytochemical analysis shows that from first to second trimester, the majority of developing glial cells exhibited a transitional state marked by cc-expression of nestin and GFAP. However, the corresponding transitional state for developing neuronal cells, co-expressing nestin and MAP-2, was rarely detected. These results imply different temporal patterns of nestin expression in cells of glial and neuronal lineages. Confocal microscopy of HFB tissue section staining also revealed a similar pattern of nestin co-expression with glial and neuronal markers. Our results suggest that nestin expression alone may not identify an undifferentiated stein cell, and that progenitor cells in glial and neuronal lineages express nestin in different temporal patterns. Published by Elsevier Science B.V. C1 NINCDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA. RP NINCDS, Lab Mol Med & Neurosci, NIH, 36 Convent Dr,Bldg 36,Room 5W21, Bethesda, MD 20892 USA. EM messam@codon.nih.gov; eomajor@codon.nih.gov NR 31 TC 46 Z9 47 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD MAR 31 PY 2002 VL 134 IS 1-2 SI SI BP 87 EP 92 AR PII S0165-3806(01)00325-X DI 10.1016/S0165-3806(01)00325-X PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 547VX UT WOS:000175354200009 PM 11947939 ER PT J AU Carp, RI Meeker, HC Chung, R Kozak, CA Hosokawa, M Fujisawa, H AF Carp, RI Meeker, HC Chung, R Kozak, CA Hosokawa, M Fujisawa, H TI Murine leukemia virus in organs of senescence-prone and -resistant mouse strains SO MECHANISMS OF AGEING AND DEVELOPMENT LA English DT Article DE murine leukemia virus; accelerated senescence; mouse strain ID AGE-RELATED-CHANGES; ACCELERATED MOUSE; PROVIRAL SEQUENCES; MICE; SAMP8; MODEL; MEMORY; BRAIN AB A series of inbred strains of mice have been developed that are either prone (SAMP) or resistant (SAMR) to accelerated senescence. All of these strains originated from an inadvertent cross or crosses between the AKR/J mouse strain and an unknown strain(s). The characteristics of the nine senescence-prone lines differ, with all strains showing generalized aspects of accelerated aging but with each line having a specific aging-related change that is emphasized, e.g. learning and memory deficits, osteoporosis and senile amyloidosis. The senescence-resistant strains have normal patterns of aging and do not show the specific aging-related changes seen in SAMP strains. The fact that AKR mice have high levels of endogenous, ecotropic murine leukemia virus (MuLV) prompted an examination of the expression levels of MuLV in SAM strains. Analysis of brain, spleen and thymus samples revealed that seven of nine SAMP strains had high levels of MuLV and contained the Emv11 provirus, (previously termed Akv1) that encodes the predominant MuLV found in AKR mice. In contrast, none of the SAMR strains had Emv11 or significant amounts of virus. The current findings represent an initial step in determining the role of MuLV in the accelerated senescence seen in SAMP strains. Published by Elsevier Science Ireland Ltd. C1 New York State Inst Basic Res Dev Disabil, Staten Isl, NY 10314 USA. NIH, Bethesda, MD 20892 USA. Kyoto Univ, Inst Frontier Med Sci, Field Regenerat Control, Kyoto 6068507, Japan. RP Carp, RI (reprint author), New York State Inst Basic Res Dev Disabil, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. EM richard.carp@omr.state.ny.us NR 26 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0047-6374 J9 MECH AGEING DEV JI Mech. Ageing Dev. PD MAR 31 PY 2002 VL 123 IS 6 BP 575 EP 584 AR PII S0047-6374(01)00377-3 DI 10.1016/S0047-6374(01)00377-3 PG 10 WC Cell Biology; Geriatrics & Gerontology SC Cell Biology; Geriatrics & Gerontology GA 580MJ UT WOS:000177238100003 PM 11850021 ER PT J AU Kotzin, S AF Kotzin, S TI Medline and PubMed will be able to synthesise clinical data SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Natl Lib Med, Bibli Serv Div, Rockville, MD 20850 USA. RP Kotzin, S (reprint author), Natl Lib Med, Bibli Serv Div, Rockville, MD 20850 USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD MAR 30 PY 2002 VL 324 IS 7340 BP 791 EP 791 DI 10.1136/bmj.324.7340.791 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 538KY UT WOS:000174816200039 PM 11923173 ER PT J AU Wacholder, S Garcia-Closas, M Rothman, N AF Wacholder, S Garcia-Closas, M Rothman, N TI Study of genes and environmental factors in complex diseases SO LANCET LA English DT Letter ID MISCLASSIFICATION C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Wacholder, S (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,M-S 7244, Bethesda, MD 20892 USA. RI Garcia-Closas, Montserrat /F-3871-2015 OI Garcia-Closas, Montserrat /0000-0003-1033-2650 NR 5 TC 6 Z9 6 U1 0 U2 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 30 PY 2002 VL 359 IS 9312 BP 1155 EP 1155 DI 10.1016/S0140-6736(02)08137-0 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 536YJ UT WOS:000174729200042 PM 11943292 ER PT J AU Lore, K Sonnerborg, A Brostrom, C Goh, LE Perrin, L McDade, H Stellbrink, HJ Gazzard, B Weber, R Napolitano, LA van Kooyk, Y Andersson, J AF Lore, K Sonnerborg, A Brostrom, C Goh, LE Perrin, L McDade, H Stellbrink, HJ Gazzard, B Weber, R Napolitano, LA van Kooyk, Y Andersson, J TI Accumulation of DC-SIGN+CD40+ dendritic cells with reduced CD80 and CD86 expression in lymphoid tissue during acute HIV-1 infection SO AIDS LA English DT Article DE HIV-1; dendritic cell; cytokines; co-stimulatory molecule; DC-SIGN; lymphoid tissue; primary HIV-1 infection ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOKINE PRODUCTION; T-LYMPHOCYTES; HUMAN TONSILS; MOLECULES; INDIVIDUALS; CD40; SUPPRESSION; STIMULATION; ACTIVATION AB Background: Dendritic cells (DC) are target cells for HIV-1 and play a key role in antigen presentation and activation of T cells. Objective: To characterize interdigitating DC in lymphoid tissue (LT) with regard to maturation, expression of cytokines and co-stimulatory molecules in HIV-1-positive patients. Methods: DC were characterized by immunohistochemistry and in situ imaging in LT from patients with acute HIV-1 infection (aHI), antiretroviral treated patients, long-term non-progressors/slow progressors with HIV-1 infection (LTNP/SLP), patients with AIDS, HIV-1-negative controls and patients with acute Epstein-Barr virus (EBV) infection. Results: A significant increase of interdigitating DC expressing CD1a, S-100b, CD83 and DC-SIGN was found in LT from patients with aHI (P < 0.02). The co-stimulatory molecules CD80 and CD86 were, however, only partially upregulated and the complete parafollicular network found in acute EBV infection was not generated, despite increased expression of interleukins 1alpha, 1beta, 12; interleukin 1alpha receptor antagonist; interferon alpha; and CD40 expression. LTNP/SLP and treated aviremic subjects had increased frequency of interdigitating DC, albeit lower than in aHI, and low expression of CD80 and CD86. In contrast, patients with AIDS had fewer DC and reduced cytokine expression in LT. Conclusions: In the early phase of HIV-1 infection, there was a migration of DC to LT comparable to that found in acute EBV infection. The infiltration of DC in LT in acute EBV infection was accompanied by upregulation of CD80 and CD86 expression, which did not occur in aHI. This co-stimulatory defect in aHI may have an impact on the development of HIV-1-specific T cell immunity. (C) 2002 Lippincott Williams Wilkins. C1 Huddinge Univ Hosp, Karolinska Inst, Dept Microbiol Pathol & Immunol, Div Clin Virol, Stockholm, Sweden. Huddinge Univ Hosp, Karolinska Inst, Ctr Infect Med, Dept Med, Stockholm, Sweden. GlaxoWellcome R&D, HIV Dept, Greenford, Middx, England. Univ Hosp Geneva, Dept Infect Dis, Geneva, Switzerland. Univ Hamburg, Hosp Eppendorf, Med Poliklin, D-20246 Hamburg, Germany. Chelsea & Westminster Hosp, St Stephens Clin, London, England. Royal Free Hosp, Dept Clin Immunol, London NW3 2QG, England. Univ San Francisco, Gladstone Inst Virol & Immunol, San Francisco, CA 94117 USA. Free Univ Amsterdam, Med Ctr, Dept Mol Cell Biol, Amsterdam, Netherlands. RP Lore, K (reprint author), NIH, Vaccine Res Ctr, Bldg 4 Room 3612B,40 Convent Dr, Bethesda, MD 20892 USA. RI Weber, Rainer/D-5175-2012; Infektiologie, USZ/A-6921-2011 FU NCI NIH HHS [CA66529]; NIMH NIH HHS [P30 MH59037]; PHS HHS [A141536] NR 37 TC 116 Z9 120 U1 1 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD MAR 29 PY 2002 VL 16 IS 5 BP 683 EP 692 DI 10.1097/00002030-200203290-00003 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 538JD UT WOS:000174811200003 PM 11964524 ER PT J AU Sugatani, J Yamakawa, K Yoshinari, K Machida, T Takagi, H Mori, M Kakizaki, S Sueyoshi, T Negishi, M Miwa, M AF Sugatani, J Yamakawa, K Yoshinari, K Machida, T Takagi, H Mori, M Kakizaki, S Sueyoshi, T Negishi, M Miwa, M TI Identification of a defect in the UGT1A1 gene promoter and its association with hyperbilirubinemia SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE UDP-glucuronosyltransferase; UGT1A1; Gilbert's syndrome; hyperbilirubinemia; bilirubin; single nucleotide polymorphism (SNP); phenobarbital-responsive enhancer module (PBREM); constitutive active receptor (CAR) ID BILIRUBIN UDP-GLUCURONOSYLTRANSFERASE; NAJJAR TYPE-I; GILBERTS-SYNDROME; CRIGLER-NAJJAR; EXPRESSION; UDP-GLUCURONOSYLTRANSFERASE-1; POLYMORPHISM AB The UDP-glucuronosyltransferase UGT1A1 plays a critical role in the detoxification of potentially neurotoxic bilirubin by conjugating it with glucuronic acid. We identified a polymorphism that results in a T to G substitution at nucleotide number -3263 of the phenobarbital-responsive enhancer module of the UGT1A1 gene, thereby significantly decreasing transcriptional activity as indicated by the luciferase-reporter assay. At least one T-3263G allele was found in 21 of 25 subjects with mild hyperbilirubinemia (Gilbert's syndrome); this frequency (0.58) was significantly higher than that in normobilirubinemic controls (0.17; n = 8 of 27). Homozygous mutations in the TATA element (A[TA](7)TAA) or at nucleotide 211 of exon 1 (G to A substitution) were found in 5 and 2 of the hyperbilirubinemic group, respectively, while 12 of these subjects were double heterozygotes for the T-3263G and G211A mutations. Plasma total bilirubin levels in these double heterozygotes were significantly higher than those in control subjects carrying one or other of these mutations singly, indicating that compound heterozygous mutations may result in more strongly reduced UGT1A1 activity. Our results indicate that homozygosity and compound heterozygosity for mutations in the UGT1A1 gene promoter (T-3263G and A[TA](7)TAA) and/or exon 1 of the gene (G211A) could explain the hyperbilirubinemia seen in the majority of individuals with Gilbert's syndrome. (C) 2002 Elsevier Science (USA). C1 Univ Shizuoka, Sch Pharmaceut Sci, Dept Pharmacobiochem, Shizuoka 4228526, Japan. Gunma Univ, Sch Med, Dept Internal Med 1, Maebashi, Gumma 3718511, Japan. NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. RP Miwa, M (reprint author), Univ Shizuoka, Sch Pharmaceut Sci, Dept Pharmacobiochem, 52-1 Yada, Shizuoka 4228526, Japan. EM miwa@ys7.u-shizuoka-ken.ac.jp NR 24 TC 149 Z9 157 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 29 PY 2002 VL 292 IS 2 BP 492 EP 497 DI 10.1006/bbrc.2002.6683 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 538BB UT WOS:000174793200030 PM 11906189 ER PT J AU Stefanski, R Lee, SH Yasar, S Cadet, JL Goldberg, SR AF Stefanski, R Lee, SH Yasar, S Cadet, JL Goldberg, SR TI Lack of persistent changes in the dopaminergic system of rats withdrawn from methamphetamine self-administration SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE methamphetamine; drug self-administration; neuroadaptation; dopamine; (Rat) ID VENTRAL TEGMENTAL AREA; FREELY MOVING RATS; BEHAVIORAL SENSITIZATION; NUCLEUS-ACCUMBENS; AUTORECEPTOR SUBSENSITIVITY; EXTRACELLULAR DOPAMINE; AMPHETAMINE TREATMENT; TIME-COURSE; COCAINE; SENSITIVITY AB A continuing challenge for studies in the neurobiology of drug abuse is to identify and characterize long-lived neuroadaptations that can trigger craving and relapse, We previously reported that rats that had actively self administered methamphetamine for 5 weeks and were then withdrawn from methamphetamine for 24 h showed marked decreases in somatodendritic dopamine D-2 autoreceptor levels in the ventral tegmental area and median and dorsal part of the substantia nigra zona compacta with a corresponding down-regulation of dopamine D-1 receptors in the shell of the nucleus accumbens. The purpose of the present study was to determine whether neuroadaptive changes in dopamine receptors or transporters in the brains of rats withdrawn for 24 h from chronic methamphetamine self-administration are persistent changes that can be demonstrated long after withdrawal. A "yoked" procedure was used in which rats were tested simultaneously in groups of three, with only one rat actively self-administering methamphetamine while the other two received yoked injections of either methamphetamine or saline. In vitro quantitative autoradiography was used to determine densities of dopamine uptake sites and dopamine D-1 and D-2 receptors in different brain regions following 7- and 30-day periods of withdrawal from chronic methamphetamine self-administration. No changes in dopamine transporter and dopamine receptor numbers were detected in any brain region examined in rats self-administering methamphetamine compared with littermates receiving yoked infusions of either methamphetamine or saline. Thus, neuroadaptive changes in densities of dopamine receptors or transporters in certain brain areas may contribute to the reinforcing effects of methamphetamine during the acquisition and maintenance phases of self-administration, but do not appear to contribute to the long-lasting neuroadaptive effects of chronic methamphetamine self-administration, which may trigger craving and relapse. (C) 2002 Elsevier Science B.V. All rights reserved. C1 NIDA, Preclin Pharmacol Sect, NIH, Intramural Res Program, Baltimore, MD 21224 USA. Inst Psychiat & Neurol, Dept Pharmacol, PL-02957 Warsaw, Poland. Korea Food & Drug Adm, Dept Toxicol, Natl Inst Toxicol Res, Eunpyung Gu, Seoul 122704, South Korea. Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Johns Hopkins Bayview Med Ctr, Baltimore, MD 21224 USA. NIDA, Mol Neuropsychiat Sect, NIH, Intramural Res Program, Baltimore, MD 21224 USA. RP Goldberg, SR (reprint author), NIDA, Preclin Pharmacol Sect, NIH, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 29 TC 32 Z9 32 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 29 PY 2002 VL 439 IS 1-3 BP 59 EP 68 AR PII S0014-2999(02)01301-8 DI 10.1016/S0014-2999(02)01301-8 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 545QZ UT WOS:000175230100008 PM 11937093 ER PT J AU Hayashi, H Szaszi, K Coady-Osberg, N Orlowski, J Kinsella, JL Grinstein, S AF Hayashi, H Szaszi, K Coady-Osberg, N Orlowski, J Kinsella, JL Grinstein, S TI A slow pH-dependent conformational transition underlies a novel mode of activation of the epithelial Na+/H+ exchanger-3 isoform SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RENAL PROXIMAL TUBULE; HAMSTER OVARY CELLS; DIFFICILE TOXIN-B; PROTEIN-KINASE-C; NA/H EXCHANGER; THYMIC LYMPHOCYTES; MEMBRANE-VESICLES; APICAL MEMBRANE; MODIFIER SITE; NHE3 ACTIVITY AB Allosteric control of Na+/H- exchange by intracellular protons ensures rapid and accurate regulation of the intracellular pH. Although this allosteric effect was heretofore thought to occur almost instantaneously, we report here the occurrence of a slower secondary activation of the epithelial Na+/H- exchanger (NHE)-3 isoform. This slow activation mode developed over the course of minutes and was unique to NHE3 and the closely related isoform NHE5, but was not observed in NHE1 or NHE2. Activation of NHE3 was not due to increased density of exchangers at the cell surface, nor was it accompanied by detectable changes in phosphorylation. The association of NHE3 with the cytoskeleton, assessed by its retention in the detergent-insoluble fraction, was similarly unaffected by acidification. In contrast to the slow progressive activation elicited by acidification, deactivation occurred very rapidly upon restoration of the physiological pH. We propose that NHE3 undergoes a slow pH-dependent transition from a less active to a more active state, likely by changing its conformation or state of association. C1 Hosp Sick Children, Res Inst, Cell Biol Program, Toronto, ON M5G 1X8, Canada. McGill Univ, Dept Physiol, Montreal, PQ H3G 1Y6, Canada. NIA, Cardiovasc Sci Lab, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. RP Grinstein, S (reprint author), Hosp Sick Children, Res Inst, Cell Biol Program, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. RI Szaszi, Katalin/J-7522-2012; Hayashi, Hisayoshi/K-5883-2013 NR 38 TC 28 Z9 28 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 29 PY 2002 VL 277 IS 13 BP 11090 EP 11096 DI 10.1074/jbc.M111868200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 534WQ UT WOS:000174613100045 PM 11792708 ER PT J AU Yang, FJ Li, XY Sharma, M Sasaki, CY Longo, DL Lim, B Sun, ZJ AF Yang, FJ Li, XY Sharma, M Sasaki, CY Longo, DL Lim, B Sun, ZJ TI Linking beta-catenin to androgen-signaling pathway SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEAR-RECEPTOR FUNCTION; E-CADHERIN; PROSTATE-CANCER; TRANSCRIPTIONAL COACTIVATOR; COLORECTAL-CANCER; ESTROGEN-RECEPTOR; GASTRIC-CANCER; REPEAT REGION; ALPHA-CATENIN; EXPRESSION AB The androgen-signaling pathway is important for the growth and progression of prostate cancer cells. The growth-promoting effects of androgen on prostate cells are mediated mostly through the androgen receptor (AR). There is increasing evidence that transcription activation by AR is mediated through interaction with other cofactors. beta-Catenin plays a critical role in embryonic development and tumorigenesis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction. Here, we demonstrate that a specific protein-protein interaction occurs between beta-catenin and AR. Unlike the steroid hormone receptor coactivator 1 (SRC1), beta-catenin showed a strong interaction with AR but not with other steroid hormone receptors such as estrogen receptor alpha, progesterone receptor beta, and glucocorticoid receptor. The ligand binding domain of AR and the NH2 terminus combined with the first six armadillo repeats of beta-catenin were shown to be necessary for the interaction. Through this specific interaction, beta-catenin augments the ligand-dependent activity of AR in prostate cancer cells. Moreover, expression of E-cadherin in E-cadherin-negative prostate cancer cells results in redistribution of the cytoplasmic beta-catenin to the cell membrane and reduction of AR-mediated transcription. These data suggest that loss of E-cadherin can elevate the cellular levels of beta-catenin in prostate cancer cells, which may directly contribute to invasiveness and a more malignant tumor phenotype by augmenting AR activity during prostate cancer progression. C1 Stanford Univ, Sch Med, Dept Surg, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Beth Israel Deaconess Med Ctr, Dept Med, Div Hematol Oncol, Boston, MA 02215 USA. NIA, NIH, Immunol Lab, Baltimore, MD 21224 USA. RP Sun, ZJ (reprint author), Stanford Univ, Sch Med, Dept Surg, R135,Edwards Bldg, Stanford, CA 94305 USA. FU NCI NIH HHS [R01 CA087767-01A2, CA70297, R01 CA070297, R01 CA070297-06A1, R01 CA070297-07, R01 CA070297-08, R01 CA070297-09, R01 CA070297-10, R01 CA070297-11A2, R01 CA070297-12, R01 CA087767, R01 CA087767-02, R01 CA087767-03, R01 CA087767-04, R01 CA087767-05, R01 CA151623, R29 CA070297, R29 CA070297-03, R29 CA070297-04, R29 CA070297-04S1, R29 CA070297-05, R29 CA070297-05S1]; NIDDK NIH HHS [DK47636, DK54417, R01 DK061002, R01 DK061002-01A1, R01 DK061002-02, R01 DK061002-03, R01 DK061002-04, R01 DK061002-05, R56 DK061002, R56 DK061002-06A1] NR 54 TC 232 Z9 237 U1 2 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 29 PY 2002 VL 277 IS 13 BP 11336 EP 11344 DI 10.1074/jbc.M111962200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 534WQ UT WOS:000174613100075 PM 11792709 ER PT J AU Arthos, J Cicala, C Steenbeke, TD Chun, TW Cruz, CD Hanback, DB Khazanie, P Nam, D Schuck, P Selig, SM Van Ryk, D Chaikin, MA Fauci, AS AF Arthos, J Cicala, C Steenbeke, TD Chun, TW Cruz, CD Hanback, DB Khazanie, P Nam, D Schuck, P Selig, SM Van Ryk, D Chaikin, MA Fauci, AS TI Biochemical and biological characterization of a dodecameric CD4-Ig fusion protein - Implications for therapeutic and vaccine strategies SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; RECOMBINANT SOLUBLE CD4; T-CELL LINE; CONFORMATIONAL-CHANGES; PEPTIDE INHIBITOR; HIV; BINDING; GP120; INFECTION; NEUTRALIZATION AB Drug toxicities associated with HAART lend urgency to the development of new anti-HIV therapies. Inhibition of viral replication at the entry stage of the viral life cycle is an attractive strategy because it prevents de novo infection. Soluble CD4 (sCD4), the first drug in this class, failed to suppress viral replication in vivo. At least three factors contributed to this failure: sCD4 demonstrated poor neutralizing activity against most primary isolates of HIV in vitro; it demonstrated an intrinsic capacity to enhance viral replication at low concentrations; and it exhibited a relatively short half-life in vivo. Many anti-gp120 monoclonal antibodies, including neutralizing monoclonal antibodies also enhance viral replication at suboptimal concentrations. Advances in our understanding of the events leading up to viral entry suggest strategies by which this activity can be diminished. We hypothesized that by constructing a sCD4-based molecule that is large, binds multiple gp120s simultaneously, and is highly avid toward gp120, we could remove its capacity to enhance viral entry. Here we describe the construction of a polymeric CD4-IgG1 fusion protein. The hydrodynamic radius of this molecule is similar to12 nM. It can bind at least 10 gp120 subunits with binding kinetics that suggest a highly avid interaction toward virion-associated envelope. This protein does not enhance viral replication at suboptimal concentrations. These observations may aid in the design of new therapeutics and vaccines. C1 NIAID, Lab Immunoregulat, Bethesda, MD 20892 USA. Mol Interact Resource Div Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA. RP Arthos, J (reprint author), 10 Ctr Dr MSC 1876 Bldg 10 Rm 6A08, Bethesda, MD 20892 USA. OI Schuck, Peter/0000-0002-8859-6966 NR 51 TC 58 Z9 60 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 29 PY 2002 VL 277 IS 13 BP 11456 EP 11464 DI 10.1074/jbc.M111191200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 534WQ UT WOS:000174613100090 PM 11805109 ER PT J AU Phillips, RS Ramso, SBV Blackshear, PJ AF Phillips, RS Ramso, SBV Blackshear, PJ TI Members of the tristetraprolin family of tandem CCCH zinc finger proteins exhibit CRM1-dependent nucleocytoplasmic shuttling SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEAR EXPORT SIGNAL; AU-RICH ELEMENTS; MESSENGER-RNA DEGRADATION; EARLY-RESPONSE GENES; CYTOPLASMIC LOCALIZATION; TRANSCRIPTION FACTOR; NUCLEOTIDE-SEQUENCE; BINDING PROTEIN; HUMAN HOMOLOG; PORE COMPLEX AB Members of the tristetraprolin (TTP) family of CCCH tandem zinc finger proteins can bind directly to certain types of AU-rich elements (AREs) in mRNA. Experiments in TTP-deficient mice have shown that TTP is involved in the physiological destabilization of at least two cytokine mRNAs, those encoding tumor necrosis factor a and granulocyte-macrophage colony-stimulating factor. The two other known mammalian members of the TTP family, CMG1 and TIS11D, also contain ARE-binding CCCH tandem zinc finger domains and can also destabilize ARE-containing mRNAs. To investigate the effects of primary sequence on the subcellular localization of these proteins, we constructed green fluorescent protein fusions with TTP, CMG1, and TIS11D; these were predominantly cytoplasmic when expressed in 293 or HeLa cells. Deletion and mutation analyses revealed functional nuclear export signals in the amino terminus of TTP and in the carboxyl termini of CMG1 and TIS11D. This type of leucine-rich nuclear export signal interacts with the nuclear export receptor CRM1; abrogation of CRM1 activity resulted in nuclear accumulation of TTP, CMG1, and TIS11D. These proteins are thus nucleocytoplasmic shuttling proteins and rely on CRM1 for their export from the nucleus. Although TTP, CMG1, and TIS11D lack known nuclear import sequences, mapping experiments revealed that their nuclear accumulation required an intact tandem zinc finger domain but did not require RNA binding ability. These findings suggest possible roles for nuclear import and export in the regulation of cellular TTP, CMG1, and TIS11D activity. C1 NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Off Clin Res & Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA. RP Blackshear, PJ (reprint author), NIEHS, Lab Signal Transduct, NIH, A2-05,111 Alexander Dr, Res Triangle Pk, NC 27709 USA. NR 73 TC 65 Z9 69 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 29 PY 2002 VL 277 IS 13 BP 11606 EP 11613 DI 10.1074/jbc.M111457200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 534WQ UT WOS:000174613100109 PM 11796723 ER PT J AU Lavedan, C Buchholtz, S Nussbaum, RL Albin, RL Polymeropoulos, MH AF Lavedan, C Buchholtz, S Nussbaum, RL Albin, RL Polymeropoulos, MH TI A mutation in the human neurofilament M gene in Parkinson's disease that suggests a role for the cytoskeleton in neuronal degeneration SO NEUROSCIENCE LETTERS LA English DT Article DE Parkinson's disease; Gly336Ser; cytoskeleton; mutation; neurofilament M; Lewy bodies ID ALPHA-SYNUCLEIN; INTERMEDIATE FILAMENTS; MONOCLONAL-ANTIBODIES; LEWY BODIES; SUBUNIT AB Parkinson's disease (PD) is a common neurodegenerative movement disorder characterized by the destruction of dopaminergic neurons of the substantia nigra. We have identified a new mutation (Gly336Ser) in the medium neurofilament subunit in a patient of French-Canadian origin with early onset severe PD. This finding suggests, for the first time, that aberrations in neuronal molecules involved in the cytoskeleton could lead to the development of the pathology seen in PD. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Novartis Pharmaceut Corp, Gaithersburg, MD 20878 USA. Natl Human Genome Res Inst, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. Univ Michigan, Dept Neurol, Ann Arbor, MI USA. Educ & Clin Ctr, Ann Arbor, MI USA. RP Polymeropoulos, MH (reprint author), Novartis Pharmaceut Corp, 9 W Watkins Mill Rd, Gaithersburg, MD 20878 USA. NR 21 TC 35 Z9 36 U1 1 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAR 29 PY 2002 VL 322 IS 1 BP 57 EP 61 AR PII S0304-3940(01)02513-7 DI 10.1016/S0304-3940(01)02513-7 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 539CT UT WOS:000174852700015 PM 11958843 ER PT J AU Nemoto, S Finkel, T AF Nemoto, S Finkel, T TI Redox regulation of forkhead proteins through a p66shc-dependent signaling pathway SO SCIENCE LA English DT Article ID TRANSCRIPTION FACTOR; OXIDATIVE STRESS; LIFE-SPAN; SURVIVAL; ELEGANS; FKHR; AKT; AFX AB Genetic determinants of longevity include the forkhead-related transcription factor DAF-16 in the worm Caenorhabditis elegans and the p66shc locus in mice. We demonstrate that p66shc regulates intracellular oxidant levels in mammalian cells and that hydrogen peroxide can negatively regulate forkhead activity. In p66shc(-/-) cells, the activity of the mammalian forkhead homolog FKHRL1 is increased and redox-dependent forkhead inactivation is reduced. In addition, expression of FKHRL1 results in an increase in both hydrogen peroxide scavenging and oxidative stress resistance. These results demonstrate an important functional relation between three distinct elements linked to aging: forkhead proteins, p66shc, and intracellular oxidants. C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. RP Finkel, T (reprint author), NHLBI, Cardiovasc Branch, NIH, Bldg 10-6N-240,10 Ctr Dr, Bethesda, MD 20892 USA. NR 24 TC 553 Z9 576 U1 1 U2 26 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD MAR 29 PY 2002 VL 295 IS 5564 BP 2450 EP 2452 DI 10.1126/science.1069004 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 536QD UT WOS:000174712600055 PM 11884717 ER PT J AU Lee, SJ Cho, SH Park, SK Kim, SW Park, MS Choi, HY Choi, JY Lee, SY Im, HJ Kim, JY Yoon, YJ Choi, H Shin, SG Park, TW Rothman, N Hirvonen, A Kang, DH AF Lee, SJ Cho, SH Park, SK Kim, SW Park, MS Choi, HY Choi, JY Lee, SY Im, HJ Kim, JY Yoon, YJ Choi, H Shin, SG Park, TW Rothman, N Hirvonen, A Kang, DH TI Combined effect of glutathione S-transferase M1 and T1 genotypes on bladder cancer risk SO CANCER LETTERS LA English DT Article DE GSTM1; GSTT1; combined effect; genetic polymorphisms; bladder cancer ID GENETIC-POLYMORPHISM; UROTHELIAL CANCER; HOMOZYGOUS DELETION; NULL GENOTYPES; GSTM1; GSTT1; SUSCEPTIBILITY; LUNG; MU AB To evaluate the association between genetic polymorphism of GSTM1, GSTT1 and development of bladder cancer, a hospital-based case-control study was conducted in South Korea. The study population consisted of 232 histologically confirmed male bladder cancer cases and 165 male controls enrolled from urology departments with no previous history of cancer or systemic diseases in Seoul during 1997-1999. The GSTM1 null genotype was significantly associated with bladder cancer (OR: 1.6, 95% CI: 1.0-2.4), whereas the association observed for GSTT1 null genotype did not reach statistical significance (OR: 1.3, 95% CI: 0.9-2.0). There was a statistically significant multiple interaction between GSTM1 and GSTT1 genotype for risk of bladder cancer (P = 0.04); the risk associated with the concurrent lack of both of the genes (OR: 2.2, 95% CI: 1.2-4.3) was greater than the product of risk in men with GSTM1 null/GSTT1 present (OR: 1.3,95% CI: 0.7-2.5) or GSTM1 present/GSTT1 null (OR: 1.1, 95% CI 0.6-2.2) genotype combinations. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Seoul Natl Univ, Coll Med, Dept Prevent Med, Chongno Gu, Seoul 110799, South Korea. Hallym Univ, Coll Med, Dept Internal Med, ChooChun, South Korea. Dongguk Univ, Coll Med, Dept Prevent Med, Kyongju, South Korea. Seoul Natl Univ, Coll Med, Dept Urol, Chongno Gu, Seoul 110799, South Korea. Sungkyunkwan Univ, Dept Urol, Coll Med, Suwon, South Korea. Seoul Natl Univ, Coll Med, Inst Environm Med, Dept Pharmacol,SNUMRC,Chongno Gu, Seoul 110799, South Korea. Chonbuk Natl Univ Hosp, Dept Psychiat, Chonju, South Korea. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Inst Occupat Hlth, Dept Ind Hyg & Toxicol, SF-00250 Helsinki, Finland. Seoul Natl Univ, Coll Med, Canc Res Inst, Chongno Gu, Seoul 110799, South Korea. RP Kang, DH (reprint author), Seoul Natl Univ, Coll Med, Dept Prevent Med, Chongno Gu, 28 Yongon Dong, Seoul 110799, South Korea. EM dhkang@snu.ac.kr RI Kang, Dae Hee/E-8631-2012; Choi, Ji-Yeob/J-2796-2012; Shin, Sang-Goo/J-5522-2012; Park, Sue Kyung/J-2757-2012 NR 28 TC 39 Z9 47 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD MAR 28 PY 2002 VL 177 IS 2 BP 173 EP 179 AR PII S0304-3835(01)00820-5 DI 10.1016/S0304-3835(01)00820-5 PG 7 WC Oncology SC Oncology GA 540PB UT WOS:000174936400008 PM 11825664 ER PT J AU Hayallah, AM Sandoval-Ramirez, J Reith, U Schobert, U Preiss, B Schumacher, B Daly, JW Muller, CE AF Hayallah, AM Sandoval-Ramirez, J Reith, U Schobert, U Preiss, B Schumacher, B Daly, JW Muller, CE TI 1,8-disubstituted xanthine derivatives: Synthesis of potent A(2B)-selective adenosine receptor antagonists SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID RAT STRIATAL MEMBRANES; A(2B) RECEPTORS; MOLECULAR-CLONING; A(3) RECEPTOR; HIGH-AFFINITY; ANALOGS; CELLS; 3-POSITION; AGONISTS; SUBTYPES AB 3-Unsubstituted xanthine derivatives bearing a cyclopentyl or a phenyl residue in the 8-position were synthesized and developed as A(2)B adenosine receptor antagonists. Compounds bearing polar substituents were prepared to obtain water-soluble derivatives. 1-Alkyl-8-phenylxanthine derivatives were found to exhibit high affinity for A(2B) adenosine receptors (ARs). 1,8-Disubstituted xanthine derivatives were equipotent to or more potent than 1,3,8-trisubstituted xanthines at A(2B) ARs, but generally less potent at A(1) and A(2A), and much less potent at A(3) ARs. Thus, the new compounds exhibited increased A2B selectivity versus all other AR subtypes. 9-Deazaxanthines (pyrrolo[2,3-d]pyrimidindiones) appeared to be less potent at A(2B) ARs than the corresponding xanthine derivatives. 1-Propyl-8-p-sulfophenylxanthiiie (17) was the most selective compound of the present series, exhibiting a K-i value of 53 nM at human A(2B) ARs and showing greater than 180-fold selectivity versus human A, ARs. Compound 17 was also highly selective versus rat A, ARs (41-fold) and versus the other human AR subtypes (A(2A) > 400-fold and A3 > 180-fold). The compound is highly water-soluble due to its sulfonate function. 1-Butyl-8-p-carboxyphenylxanthine (10), another polar analogue bearing a carboxylate function, exhibited a K-i value of 24 nM for A(2B) ARs, 49-fold selectivity versus human and 20-fold selectivity versus rat A, ARs, and greater than 150-fold selectivity versus human A2A and A3 ARs. 8-[4-(2-Hydroxyethylamino)-2-oxoethoxy)phenyl]-1-propylxanthine (29) and 1-butyl-8-[4(4-benzyl)piperazino-2-oxoethoxy)phenyl]xanthine (35) were among the most potent A(2B) antagonists showing K-i values at A(2B) ARs of 1 nM, 57-fold (29) and 94-fold (35) selectivity versus human A(1), ca. 30-fold selectivity versus rat A(1), and greater than 400-fold selectivity versus human A(2A) and A(3) ARs. The new potent, selective, water-soluble A(2B) antagonists may be useful research tools for investigating A(2B) receptor function. C1 Univ Bonn, Pharmazeut Inst Poppelsdorf, D-53115 Bonn, Germany. NIH, Bioorgan Chem Lab, Bethesda, MD 20892 USA. Univ Wurzburg, Inst Pharm & Food Chem, Wurzburg, Germany. RP Muller, CE (reprint author), Univ Bonn, Pharmazeut Inst Poppelsdorf, Kreuzbergweg 26, D-53115 Bonn, Germany. RI Muller, Christa/C-7748-2014 OI Muller, Christa/0000-0002-0013-6624 NR 56 TC 97 Z9 100 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAR 28 PY 2002 VL 45 IS 7 BP 1500 EP 1510 DI 10.1021/jm011049y PG 11 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 534LP UT WOS:000174588100013 PM 11906291 ER PT J AU Liu, YL Yakar, S Otero-Corchon, V Low, MJ Liu, JL AF Liu, YL Yakar, S Otero-Corchon, V Low, MJ Liu, JL TI Ghrelin gene expression is age-dependent and influenced by gender and the level of circulating IGF-1 SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE ghrelin mRNA; age-dependence; gender; IGF-I ID GROWTH-FACTOR-I; HORMONE SECRETION; SEXUAL DIMORPHISM; POSTNATAL-GROWTH; RECEPTOR; RELEASE; MICE; IDENTIFICATION; PITUITARY; PEPTIDE AB Ghrelin activates GH release and is implicated in growth and metabolic regulation. The regulation of its biosynthesis has not been well studied. The current investigation was designed to examine some of the factors that may influence ghrelin gene expression in the stomach. Thus. in C57BL/6 mice. ghrelin mRNA was detectable by Northern blots throughout the age groups studied, but the levels changed markedly over time. Levels were low at E18.5 and increased rapidly after birth to 6-fold at P14 before peaking to 8-fold at P21. The levels then exhibited a gradual decline at P60 (75% of the peak level) and at 6 months (67%) and a drastic decrease as the animals aged to 19 months (only 5%). Furthermore, sexual dimorphic gene expression. the effect of liver-derived IGF-I deficiency, as well as ghrelin secretion were studied. Our results support a role of ghrelin in growth, metabolism in juvenile and young adult mice of both sexes and in sexually dimorphic regulation of GH secretion in aged mice. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 McGill Univ, Royal Victoria Hosp, Dept Med, Fraser Labs, Montreal, PQ H3A 1A1, Canada. NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Oregon Hlth Sci Univ, Vollum Inst, Portland, OR 97201 USA. RP Liu, JL (reprint author), McGill Univ, Royal Victoria Hosp, Dept Med, Fraser Labs, M3-15,687 Pine Ave W, Montreal, PQ H3A 1A1, Canada. NR 27 TC 52 Z9 56 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD MAR 28 PY 2002 VL 189 IS 1-2 BP 97 EP 103 AR PII S0303-7207(01)00742-0 DI 10.1016/S0303-7207(01)00742-0 PG 7 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 543CA UT WOS:000175082500009 PM 12039068 ER PT J AU Beauchamp, MS Lee, KE Haxby, JV Martin, A AF Beauchamp, MS Lee, KE Haxby, JV Martin, A TI Parallel visual motion processing streams for manipulable objects and human movements SO NEURON LA English DT Article ID EVENT-RELATED FMRI; BIOLOGICAL MOTION; TEMPORAL CORTEX; FACE PERCEPTION; AREAS; STIMULI; SYSTEMS; PSYCHOPHYSICS; ACTIVATION; KNOWLEDGE AB We tested the hypothesis that different regions of lateral temporal cortex are specialized for processing different types of visual motion by studying the cortical responses to moving gratings and to humans and manipulable objects (tools and utensils) that were either stationary or moving with natural or artificially generated motions. Segregated responses to human and tool stimuli were observed in both ventral and lateral regions of posterior temporal cortex. Relative to ventral cortex, lateral temporal cortex showed a larger response for moving compared with static humans and tools. Superior temporal cortex preferred human motion, and middle temporal gyrus preferred tool motion. A greater response was observed in STS to articulated compared with unarticulated human motion. Specificity for different types of complex motion (in combination with visual form) may be an organizing principle in lateral temporal cortex. C1 NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA. RP Beauchamp, MS (reprint author), NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA. RI martin, alex/B-6176-2009 NR 45 TC 307 Z9 310 U1 2 U2 12 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD MAR 28 PY 2002 VL 34 IS 1 BP 149 EP 159 DI 10.1016/S0896-6273(02)00642-6 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 536HR UT WOS:000174695100017 PM 11931749 ER PT J AU Suzukawa, K Colburn, NH AF Suzukawa, K Colburn, NH TI AP-1 transrepressing retinoic acid does not deplete coactivators or AP-1 monomers but may target specific Jun or Fos containing dimers SO ONCOGENE LA English DT Article DE AP-1; JB6 cells; retinoic acid; transrepression; GAL4 transactivation assay ID ACTIVATOR PROTEIN-1 ACTIVATION; ANCHORAGE-INDEPENDENT GROWTH; MOUSE EPIDERMAL-CELLS; TUMOR PROMOTION; JB6 CELLS; TRANSCRIPTIONAL ACTIVATION; NEOPLASTIC TRANSFORMATION; HORMONE RECEPTORS; NUCLEAR RECEPTORS; KAPPA-B AB Retinoic acid (RA) inhibits tumor promotion in many models in vivo and in vitro, among them mouse epidermal JB6 cells. RA treatment suppresses 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced AP-1 activity, an activity that is required for transformation of JB6 P+ cells. The molecular mechanism of AP-1 transrepression by retinoids is unclear, especially as related to inhibition of transformation. Overexpression of AP-1 components did not rescue TPA induced AP-1 activation nor did a GST pull down experiment implicate direct binding, thus rendering unlikely both a Jun/Fos-RA-RAR direct interaction and a Jun/Fos sequestration mechanism. Overexpression of p300, SRC-1 or pCAF did not abrogate AP-1 suppression by RA, thus arguing against coactivator competition. Overexpression of the corepressor silencing mediator for retinoic acid and thyroid hormone receptors (SMRT) suppressed AP-1 activity. However, SMRT but not RA inhibited cJun transactivation, suggesting SMRT does not mediate RA transrepression. RA treatment also did not block TPA induced ERK phosphorylation, Jun/Fos family protein expression except for cFos, or DNA binding of the AP-1 complex. The transcriptional activities of full-length JunB and full-length Fra-1, but not the transactivation domain fusions, were increased by TPA treatment and suppressed by RA. Since these full-length fusions have bzip domains, the results suggest that JunB and/or Fra-1-containing dimers may constitute one target of RA for transrepression of AP-1. C1 Natl Canc Inst Frederick, Basic Res Lab, Gene Regulat Sect, Ft Detrick, MD 21702 USA. RP Colburn, NH (reprint author), Natl Canc Inst Frederick, Basic Res Lab, Gene Regulat Sect, Bldg 560 Rm 21-89 POB B, Ft Detrick, MD 21702 USA. NR 58 TC 26 Z9 26 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 28 PY 2002 VL 21 IS 14 BP 2181 EP 2190 DI 10.1038/sj/onc/1205281 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 533XJ UT WOS:000174555300007 PM 11948401 ER PT J AU Day, RM Soon, L Breckenridge, D Bridges, B Patel, BKR Wang, LM Corey, SJ Bottaro, DP AF Day, RM Soon, L Breckenridge, D Bridges, B Patel, BKR Wang, LM Corey, SJ Bottaro, DP TI Mitogenic synergy through multilevel convergence of hepatocyte growth factor and interleukin-4 signaling pathways SO ONCOGENE LA English DT Article DE growth factor; cytokine; signal transduction; cell proliferation ID FACTOR SCATTER FACTOR; MAP KINASE KINASE; C-MET; TYROSINE KINASE; FACTOR RECEPTOR; FACTOR ISOFORMS; PHOSPHATIDYLINOSITOL 3-KINASE; HEMATOPOIETIC-CELLS; EPITHELIAL-CELLS; MYELOID CELLS AB Hepatocyte growth factor (HGF) regulates various physiological and developmental processes in concerti with other growth factors, cytokines and hormones. We examined interactions between cell signaling events elicited by HGF and the cytokine interleukin (IL)-4, in the IL-3-dependent murine myeloid cell line 32D transfected with the human HGF receptor, c-Met. HGF was a potent mitogen in these cells, and prevented apoptosis in response to IL-3 withdrawal. IL-4 showed modest anti-apoptotic activity, but no significant mitogenic activity. IL-4 synergistically enhanced HGF-stimulated DNA synthesis, whereas only additive prevention of apoptosis was observed. IL-4 did not enhance HGF-dependent tyrosine phosphorylation of c-Met or She. In contrast, HGF-stimulated activation of MAP kinases was enhanced by IL-4, suggesting that the IL-4 and HGF signaling pathways converge upstream of these events. Although phosphatidylinositol 3-kinase (PI3K) inhibitors diminished HGF-induced mitogenesis, antiapoptosis, and MAP kinase activation, IL-4 enhanced HGF signaling persisted even in the presence of these inhibitors. IL-4 enhancement of HGF signaling was partially blocked in 32D/c-Met cells treated with inhibitors of MEK1 or c-Src kinases, completely blocked by expression of a catalytically inactive mutant of Janus kinase 3 (Jak3), and increased in 32D/c,Met cells overexpressing STAT6. Our results suggest that the IL-4 and HGF pathways converge at multiple levels, and that IL-4-dependent Jak3 and STAT6 activities modulate signaling events independent of PI3K to enhance, HGF-dependent mitogenesis in myeloid cells, and possibly other common cellular targets. C1 NCI, Cellular & Mol Biol Lab, Div Basic Sci, Natl Inst Hlth, Bethesda, MD USA. Univ Pittsburgh, Dept Pediat, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Dept Pharmacol, Pittsburgh, PA 15261 USA. RP Bottaro, DP (reprint author), EntreMed Inc, Dept Cell & Mol Biol, Rockville, MD 20850 USA. EM donb@entremed.com RI Bottaro, Donald/F-8550-2010 OI Bottaro, Donald/0000-0002-5057-5334 NR 61 TC 8 Z9 8 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 28 PY 2002 VL 21 IS 14 BP 2201 EP 2211 DI 10.1038/sj/onc/1205289 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 533XJ UT WOS:000174555300009 PM 11948403 ER PT J AU Lee, HY Bae, GU Jung, ID Lee, JS Kim, YK Noh, SH Stracke, ML Park, CG Lee, HW Han, JW AF Lee, HY Bae, GU Jung, ID Lee, JS Kim, YK Noh, SH Stracke, ML Park, CG Lee, HW Han, JW TI Autotaxin promotes motility via G protein-coupled phosphoinositide 3-kinase gamma in human melanoma cells SO FEBS LETTERS LA English DT Article DE autotaxin; phosphoinositide 3-kinase; p110 gamma; tumor cell motility ID G-BETA-GAMMA; ACTIVATION; KINASE; STIMULATION; PI3K-GAMMA; EXPRESSION; MIGRATION AB Autotaxin (ATX), an exo-nucleotide pyrophosphatase and phosphodiesterase, stimulates tumor cell motility at subnanomolar levels and augments invasiveness and angiogenesis. We investigated the role of G protein-coupled phosphoinositide 3-kinase gamma (PI3Kgamma) in ATX-mediated tumor cell motility stimulation. Pretreatment of human melanoma cell line A2058 with wortmannin or LY294002 inhibited ATX-induced motility. ATX increased the PI3K activity in p110gamma, but not p85, immunoprecipitates. This effect was abrogated by PI3K inhibitors or inhibited by pertussis toxin. Furthermore, stimulation of tumor cell motility by ATX was inhibited by catalytically inactive form of PI3Kgamma, strongly indicating the crucial role of PI3Kgamma for ATX-mediated motility in human melanoma cells. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved. C1 Sungkyunkwan Univ, Coll Pharm, Suwon 440746, South Korea. Konyang Univ, Coll Med, Nonsan 320711, South Korea. Yonsei Univ, Coll Med, Canc Metastasis Res Ctr, Seoul 120752, South Korea. Natl Canc Inst, NIH, Pathol Lab, Bethesda, MD 20892 USA. RP Han, JW (reprint author), Sungkyunkwan Univ, Coll Pharm, Suwon 440746, South Korea. EM jhhan@yurim.skku.ac.kr NR 27 TC 26 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 27 PY 2002 VL 515 IS 1-3 BP 137 EP 140 AR PII S0014-5793(02)02457-2 DI 10.1016/S0014-5793(02)02457-2 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 542AZ UT WOS:000175022500026 PM 11943209 ER PT J AU O'Brien, TR Engels, EA Rosenberg, PS Goedert, JJ AF O'Brien, TR Engels, EA Rosenberg, PS Goedert, JJ TI Relationship between Kaposi sarcoma-associated herpesvirus and HIV SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID HOMOSEXUAL MEN; RISK-FACTORS; COHORT C1 NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20857 USA. NCI, Biostat Branch, Rockville, MD USA. RP O'Brien, TR (reprint author), NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20857 USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 27 PY 2002 VL 287 IS 12 BP 1525 EP 1526 DI 10.1001/jama.287.12.1525 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 533VF UT WOS:000174550400017 PM 11911748 ER PT J AU Clore, GM Kuszewski, J AF Clore, GM Kuszewski, J TI chi(1) Rotamer populations and angles of mobile surface side chains are accurately predicted by a torsion angle database potential of mean force SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID PROTEINS; QUALITY; NMR C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NIH, Ctr Informat Technol, Computat Biosci & Engn Lab, Bethesda, MD 20892 USA. RP Clore, GM (reprint author), NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 13 TC 67 Z9 67 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 27 PY 2002 VL 124 IS 12 BP 2866 EP 2867 DI 10.1021/ja017712p PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA 533GF UT WOS:000174520500007 PM 11902865 ER PT J AU Caravan, P Cloutier, NJ Greenfield, MT McDermid, SA Dunham, SU Bulte, JWM Amedio, JC Looby, RJ Supkowski, RM Horrocks, WD McMurry, TJ Lauffer, RB AF Caravan, P Cloutier, NJ Greenfield, MT McDermid, SA Dunham, SU Bulte, JWM Amedio, JC Looby, RJ Supkowski, RM Horrocks, WD McMurry, TJ Lauffer, RB TI The interaction of MS-325 with human serum albumin and its effect on proton relaxation rates SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID MRI CONTRAST AGENTS; NMR RELAXOMETRIC INVESTIGATIONS; SPHERE WATER-MOLECULES; DRUG BINDING-SITES; O-17 NMR; GD-DTPA; GD3+-DIETHYLENETRIAMINEPENTAACETIC ACID; PARAMAGNETIC PROPERTIES; CRYSTAL-STRUCTURE; COMPLEXES AB MS-325 is a novel blood pool contrast agent for magnetic resonance imaging currently undergoing clinical trials to assess blockage in arteries. MS-325 functions by binding to human serum albumin (HSA) in plasma. Binding to HSA serves to prolong plasma half-life, retain the agent in the blood pool, and increase the relaxation rate of water protons in plasma. Ultrafiltration studies with a 5 kDa molecular weight cutoff filter show that MS-325 binds to HSA with stepwise stoichiometric affinity constants (mM(-1)) of K-a1 = 11.0 +/- 2.7, K-a2 = 0.84 +/- 0.16, K-a3 = 0.26 +/- 0.14, and K-a4 = 0.43 +/- 0.24. Under the conditions 0.1 mM MS-325, 4.5% HSA, pH 7.4 (phosphate-buffered saline), and 37 degreesC, 88 +/- 2% of MS-325 is bound to albumin. Fluorescent probe displacement studies show that MS-325 can displace dansyl sarcosine and dansyl-L-asparagine from HSA with inhibition constants (K-i) of 85 +/- 3 muM and 1500 +/- 850 muM, respectively; however, MS-325 is unable to displace warfarin. These results suggest that MS-325 binds primarily to site 11 on HSA. The relaxivity of MS-325 when bound to HSA is shown to be site dependent. The Eu(III) analogue of MS-325 is shown to contain one inner-sphere water molecule in the presence and in the absence of HSA. The synthesis of an MS-325 analogue, 5, containing no inner-sphere water molecules is described. Compound 5 is used to estimate the contribution to relaxivity from the outer-sphere water molecules surrounding MS-325. The high relaxivity of MS-325 bound to HSA is primarily because of a 60-100-fold increase in the rotational correlation time of the molecule upon binding (tau(R) = 10.1 +/- 2.6 ns bound vs 115 ps free). Analysis of the nuclear magnetic relaxation dispersion (T-1 and T-2) profiles also suggests a decrease in the electronic relaxation rate (1/T-1e at 20 MHz = 2.0 x 10(8) s(-1) bound vs 1.1 x 10(9) s(-1) free) and an increase in the inner-sphere water residency time (tau(m) = 170 +/- 40 ns bound vs 69 +/- 20 ns free). C1 EPIX Med Inc, Cambridge, MA 02142 USA. NIH, Lab Diagnost Radiol Res, Bethesda, MD 20892 USA. Penn State Univ, Dept Chem, University Pk, PA 16802 USA. RP Caravan, P (reprint author), EPIX Med Inc, 71 Rogers St, Cambridge, MA 02142 USA. RI Bulte, Jeff/A-3240-2008 OI Bulte, Jeff/0000-0003-1202-1610 NR 56 TC 303 Z9 308 U1 4 U2 44 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 27 PY 2002 VL 124 IS 12 BP 3152 EP 3162 DI 10.1021/ja017168k PG 11 WC Chemistry, Multidisciplinary SC Chemistry GA 533GF UT WOS:000174520500046 PM 11902904 ER PT J AU Stubbe, BG Braeckmans, K Horkay, F Hennink, WE De Smedt, SC Demeester, J AF Stubbe, BG Braeckmans, K Horkay, F Hennink, WE De Smedt, SC Demeester, J TI Swelling pressure observations on degrading dex-HEMA hydrogels SO MACROMOLECULES LA English DT Article ID RELEASE; BEHAVIOR; DEXTRAN; GELS; DEGRADATION; NETWORKS; DESIGN AB The variation of the swelling pressure of dextran hydroxyethyl methacrylate (dex-HEMA) hydrogels is determined as a function of the degradation time. In the first stage of the degradation process a moderate increase in the swelling pressure is observed due to the decrease of the elastic pressure. In this period the cross-link density of the polymer network gradually decreases, but only a small amount of free polymer (dextran) is released. Toward the end of the degradation process, however, a sudden increase in the swelling pressure occurs which is accompanied by the release of a major amount of dextran chains. It is demonstrated that the chemical composition of the network (dex-HEMA content and the number of HEMA groups on the dextran chains) strongly affects the degradation rate of dex-HEMA hydrogels. These observations are important to design degrading hydrogel systems with tailored swelling pressure profile for pulsed drug delivery. C1 State Univ Ghent, Dept Pharmaceut, Lab Gen Biochem & Phys Pharm, B-9000 Ghent, Belgium. NICHHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA. Univ Utrecht, Utrecht Inst Pharmaceut Sci, Dept Pharmaceut, NL-3508 TB Utrecht, Netherlands. RP De Smedt, SC (reprint author), State Univ Ghent, Dept Pharmaceut, Lab Gen Biochem & Phys Pharm, Harelbekestr 72, B-9000 Ghent, Belgium. NR 27 TC 17 Z9 20 U1 1 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0024-9297 J9 MACROMOLECULES JI Macromolecules PD MAR 26 PY 2002 VL 35 IS 7 BP 2501 EP 2505 DI 10.1021/ma011408z PG 5 WC Polymer Science SC Polymer Science GA 533ZF UT WOS:000174559600018 ER PT J AU Lipton, RB Scher, AI Kolodner, K Liberman, J Steiner, TJ Stewart, WF AF Lipton, RB Scher, AI Kolodner, K Liberman, J Steiner, TJ Stewart, WF TI Migraine in the United States - Epidemiology and patterns of health care use SO NEUROLOGY LA English DT Article ID OLMSTED-COUNTY; YOUNG-ADULTS; HEADACHE; PREVALENCE; POPULATION; DIAGNOSIS; MINNESOTA; IMPACT; RACE AB Objective: To determine the prevalence and distribution of migraine in the United States as well as current patterns of health care use. Methods: A random-digit-dial, computer-assisted telephone interview (CATI) survey was conducted in Philadelphia County, PA, in 1998. The CATI identifies individuals with migraine (categories 1.1 and 1.2) as defined by the diagnostic criteria of the International Headache Society with high sensitivity (85%) and specificity (96%). Interviews were completed in 4,376 subjects to identify 568 with migraine. Those with 6 or more attacks per year (n = 410) were invited to participate in a follow-up interview about health care utilization and family impact of migraine; 246 (60.0%) participated. Results: The 1-year prevalence of migraine was 17.2% in females and 6.0% in males. Prevalence was highest between the ages of 30 and 49. Whereas 48% of migraine sufferers had seen a doctor for headache within the last year (current consulters), 31% had never done so in their lifetimes and 21% had not seen a doctor for headache for at least 1 year (lapsed consulters). Of current or lapsed consulters, 73% reported a physician-made diagnosis of migraine; treatments varied. Of all migraine sufferers, 49% were treated with over-the-counter medications only, 23% with prescription medication only, 23% with both, and 5% with no medications at all. Conclusion: Relative to prior cross-sectional surveys, epidemiologic profiles for migraine have remained stable in the United States over the last decade. Self-reported rates of current medical consultation have more than doubled. Moderate increases were seen in the percentage of migraine sufferers who use prescription medications and in the likelihood of receiving a physician diagnosis of migraine. C1 Univ London Imperial Coll Sci Technol & Med, Sch Med, Div Neurosci, London, England. Johns Hopkins Sch Publ Hlth, Baltimore, MD USA. NINCDS, Neuroepidemiol Branch, NIH, Baltimore, MD USA. Innovat Med Res, Towson, MD USA. Montefiore Med Coll, Headache Unit, Bronx, NY USA. Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. Albert Einstein Coll Med, Dept Epidemiol, Bronx, NY 10467 USA. Albert Einstein Coll Med, Dept Social Med, Bronx, NY 10467 USA. RP Lipton, RB (reprint author), Innovat Med Res, 1200 High Ridge Rd, Stamford, CT 06905 USA. NR 30 TC 339 Z9 345 U1 0 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 26 PY 2002 VL 58 IS 6 BP 885 EP 894 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 533BB UT WOS:000174508600010 PM 11914403 ER PT J AU Shelby, MD AF Shelby, MD TI A simplified and rapid method for scoring micronucleated erythrocytes in human blood SO MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS LA English DT Editorial Material C1 NIEHS MD EC32, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA. RP Shelby, MD (reprint author), NIEHS MD EC32, Environm Toxicol Program, Box 12233, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1383-5718 J9 MUTAT RES-GEN TOX EN JI Mutat. Res. Genet. Toxicol. Environ. Mutagen. PD MAR 25 PY 2002 VL 515 IS 1-2 BP 1 EP 1 AR PII S1383-5718(02)00020-7 DI 10.1016/S1383-5718(02)00020-7 PG 1 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 536FZ UT WOS:000174691200001 PM 11909750 ER PT J AU Allen, DD Cardenas, AM Arriagada, C Bennett, LB Garcia, CJ Caviedes, R Rapoport, SI Caviedes, P AF Allen, DD Cardenas, AM Arriagada, C Bennett, LB Garcia, CJ Caviedes, R Rapoport, SI Caviedes, P TI A dorsal root ganglia cell line derived from trisomy 16 fetal mice, a model for Down syndrome SO NEUROREPORT LA English DT Article DE calcium signaling; choline uptake; Down syndrome; murine trisomy 16 ID CHOLINERGIC FUNCTION; CEREBRAL-CORTEX; SYNDROME BRAINS; ANIMAL-MODEL; MOUSE MODEL; NEURONS; IMMUNOREACTIVITY; ABNORMALITIES; RECEPTORS; CURRENTS AB We have established two immortalized cell lines from dorsal root ganglia of normal (G4b) and trisomy 16 mice (GTI), a model for Down syndrome. By immunohistochemistry, both cell lines exhibit neuronal traits and lack glial markers. GTI cells exhibited greater [H-3]choline uptake than G4b cells. K+ and nicotine-mediated acetylcholine release was greater in GTI cells. Basal intracellular Ca2+ concentration ([Ca2+](i)) was significantly lower in GTI cells. More GTI cells responded to neurotransmitters with a transient [Ca2+](i) increase compared to G4b cells, but both cell types showed similar amplitudes of [Ca2+](i) responses. The results show that both cell lines retain neuronal characteristics and respond to specific neurotransmitter stimuli. Altered GTI cell responses could be related to neuronal pathophysiology in Down's syndrome. C1 Univ Chile, Fac Med, ICBM, Program Mol & Clin Pharmacol, Santiago 7, Chile. Texas Tech Univ, Hlth Sci Ctr, Dept Pharmaceut Sci, Amarillo, TX USA. Univ Valparaiso, Sch Med, Pharmacol Lab, Valparaiso, Chile. Univ Valparaiso, Valparaiso Ctr Cellular & Mol Neurosci, Valparaiso, Chile. Univ Chile, Fac Med, ICBM, Morphol Program, Santiago 7, Chile. NIA, Sect Brain Physiol & Metab, NIH, Bethesda, MD 20892 USA. Sansum Med Res Inst, Santa Barbara, CA USA. RP Caviedes, P (reprint author), Univ Chile, Fac Med, ICBM, Program Mol & Clin Pharmacol, Casilla 70000,Correo 7, Santiago 7, Chile. NR 25 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR 25 PY 2002 VL 13 IS 4 BP 491 EP 496 DI 10.1097/00001756-200203250-00027 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 541EB UT WOS:000174971300027 PM 11930168 ER PT J AU Xing, GQ Russell, S Hough, C O'Grady, J Zhang, L Yang, ST Zhang, LX Post, R AF Xing, GQ Russell, S Hough, C O'Grady, J Zhang, L Yang, ST Zhang, LX Post, R TI Decreased prefrontal CaMKII alpha mRNA in bipolar illness SO NEUROREPORT LA English DT Article DE bipolar disorder; CaM kinase II; mRNA; prefrontal cortex; postmortem ID DEPENDENT PROTEIN-KINASE; HIPPOCAMPAL DENTATE GYRUS; LONG-TERM POTENTIATION; II MUTANT MICE; RAT-BRAIN; EXPRESSION; CORTEX; NEURONS; NEUROPATHOLOGY; DEFICIENT AB Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays critical roles in neurotransmission, synaptic plasticity, learning and memory. The aim of this study was to examine, by in situ hybridization, prefrontal cortical expression of CaMKII alpha mRNA in postmortem brains of unipolar, bipolar, schizophrenic, and control subjects. Compared to controls, bipolar patients had significantly lower levels of CaMKII cc m RNA in laminae I-VI of Brodmanns area 9 and laminae I-Ill and A of area 46. Unipolar patients also exhibited significantly lower levels of CaMKII alpha mRNA in laminae I-IV of area 9 than did controls. The significant decrease in CaMKII a mRNA in bipolar patients could be associated With some of the affective and cognitive alterations that have been linked to prefrontal cortical dysfunction in bipolar disorder, although this requires further direct examination. C1 Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA. NIMH, Biol Psychiat Branch, NIH, Bethesda, MD 20892 USA. NIMH, Behav Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Mol Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Xing, GQ (reprint author), Uniformed Serv Univ Hlth Sci, Dept Psychiat, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA. NR 27 TC 40 Z9 47 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR 25 PY 2002 VL 13 IS 4 BP 501 EP 505 DI 10.1097/00001756-200203250-00029 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 541EB UT WOS:000174971300029 PM 11930170 ER PT J AU Greenwald, P AF Greenwald, P TI Science, medicine, and the future - Cancer chemoprevention SO BRITISH MEDICAL JOURNAL LA English DT Review ID CARDIOVASCULAR-DISEASE; BREAST-CANCER; BETA-CAROTENE; PREVENTION; TAMOXIFEN; PROGRESS; PROMISE; MICE C1 NCI, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. RP Greenwald, P (reprint author), NCI, Div Canc Prevent, NIH, 6130 Execut Blvd,Suite 2040, Bethesda, MD 20892 USA. NR 27 TC 74 Z9 77 U1 0 U2 2 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD MAR 23 PY 2002 VL 324 IS 7339 BP 714 EP 718 DI 10.1136/bmj.324.7339.714 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 535ML UT WOS:000174648200021 PM 11909790 ER PT J AU Zhang, MD Schmid, S Carrington, M O'Brien, TR AF Zhang, MD Schmid, S Carrington, M O'Brien, TR TI Antibodies to varicella-zoster virus in blood donors with genetic variance in CC chemokine receptor 5 SO LANCET LA English DT Article ID HIV-1 INFECTION; ALLELE; AIDS AB Carriers of a 32 bp deletion (Delta32) allele of the CC chemokine receptor 5 (CCR5) gene are reported to be more likely to lack antibodies to varicella-zoster virus than CCR5 wild-type individuals. To find out whether CCR5-Delta32 Is associated with the seroprevalence of varicella-zoster virus Infection, we tested blood donors with different CCR5-Delta32 genotypes for varicella-zoster virus IgG. Antibody to varicella-zoster virus was present In 209 (99.5%) of 210 CCR5-Delta32 carriers and exactly the same proportion of CCR5 wild-type Individuals (209 of 210). We have therefore found no evidence that the CCR5-Delta32 allele is associated with decreased seroprevalence of varicella-zoster virus Infection. C1 NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA. Ctr Dis Control & Prevent, Atlanta, GA USA. NCI, Intramural Res Support Program, Sci Applicat Int Corp, Frederick, MD 21701 USA. RP O'Brien, TR (reprint author), NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC 7248, Rockville, MD 20852 USA. FU NCI NIH HHS [N01-CO-56000] NR 5 TC 2 Z9 3 U1 0 U2 1 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 23 PY 2002 VL 359 IS 9311 BP 1034 EP 1036 DI 10.1016/S0140-6736(02)08066-2 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 534KP UT WOS:000174585800013 PM 11937186 ER PT J AU Kapikian, AZ AF Kapikian, AZ TI Ecological studies, rotavirus vaccination, and intussusception SO LANCET LA English DT Letter C1 NIAID, Epidemiol Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA. RP Kapikian, AZ (reprint author), NIAID, Epidemiol Sect, Infect Dis Lab, NIH, 6700 Brockledge Dr, Bethesda, MD 20892 USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 23 PY 2002 VL 359 IS 9311 BP 1065 EP 1066 DI 10.1016/S0140-6736(02)08072-8 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 534KP UT WOS:000174585800035 PM 11937208 ER PT J AU Simonsen, L Morens, DM Blackwelder, WC AF Simonsen, L Morens, DM Blackwelder, WC TI Ecological studies, rotavirus vaccination, and intussusception SO LANCET LA English DT Letter C1 NIAID, NIH, Bethesda, MD 20892 USA. RP Simonsen, L (reprint author), NIAID, NIH, 6700-B Rockledge Dr, Bethesda, MD 20892 USA. OI Simonsen, Lone/0000-0003-1535-8526 NR 5 TC 7 Z9 8 U1 0 U2 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 23 PY 2002 VL 359 IS 9311 BP 1066 EP 1067 DI 10.1016/S0140-6736(02)08074-1 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 534KP UT WOS:000174585800037 PM 11937210 ER PT J AU Hodge, DR Li, DP Qi, SM Farrar, WL AF Hodge, DR Li, DP Qi, SM Farrar, WL TI IL-6 induces expression of the Fli-1 proto-oncogene via STAT3 SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ENDOTHELIAL GROWTH-FACTOR; ETS TRANSCRIPTION FACTORS; MULTIPLE-MYELOMA; GENE; PROTEINS; DIFFERENTIATION; INTERLEUKIN-6; PROMOTER; BINDING; FAMILY AB Induction of gene expression by IL-6 has become an area of intense interest due to the role this cytokine plays in mediating aspects of inflammation, cellular differentiation, and proliferation. The ETS family of transcription factors represents a group of positive and negative regulators of transcription, that are differentially expressed in a cell and tissue specific manner. The ETS protein Fli-I is known to induce differentiation in the erythroblastic leukemia cell line K562 along megakaryocytic developmental pathways. Here we show that IL-6 treatment of K562 induces the expression of Fli-1 via the STAT3 transcription factor. Upregulation of Fli-1 expression can be abrogated by the addition of AG490, a chemical inhibitor of JAK kinases, and by transfecting the cells with a dominant negative STAT3 expression construct. C1 NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Cytokine Mol Mech Sect, Frederick, MD 21702 USA. Aphton Corp, Mol Med Lab, Miami, FL 33130 USA. RP Farrar, WL (reprint author), NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, POB B,Bldg 560,Rm 31-76, Frederick, MD 21702 USA. FU NCI NIH HHS [N01 CO 56000] NR 27 TC 26 Z9 27 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 22 PY 2002 VL 292 IS 1 BP 287 EP 291 DI 10.1006/bbrc.2002.6652 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 534NF UT WOS:000174591900044 PM 11890706 ER PT J AU Agarwal, RK Silver, PB Su, SB Chan, CC Caspi, R AF Agarwal, RK Silver, PB Su, SB Chan, CC Caspi, R TI Vaccination with a plasmid encoding retinal interphotoreceptor retinoid-binding protein (IRBP) protects mice against experimental autoimmune uveitis (EAU). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1066 EP A1066 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901878 ER PT J AU Ali, AA Mohamed, AI Hansen, CT Wang, TTY Velasquez, MT Bhathena, SJ AF Ali, AA Mohamed, AI Hansen, CT Wang, TTY Velasquez, MT Bhathena, SJ TI Effect of probiotics and isoflavones on metabolic parameters in a genetic model of obesity and diabetes. SO FASEB JOURNAL LA English DT Meeting Abstract C1 USDA, Phytonutr Lab, Beltsville, MD 20705 USA. Virginia State Univ, Petersburg, VA USA. NIH, Bethesda, MD 20892 USA. George Washington Univ, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1014 EP A1014 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901593 ER PT J AU Babu, S Nutman, TB AF Babu, S Nutman, TB TI The cellular immune response to the human lymphatic filarial parasite Brugia malayi: NK- and T-cell activation in parasite-infected and uninfected hosts SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, LPD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1070 EP A1070 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901901 ER PT J AU Barton, LF Runnels, HA Ginsburg, DB Cho, YJ Schell, TD Tevethia, SS Monaco, JJ AF Barton, LF Runnels, HA Ginsburg, DB Cho, YJ Schell, TD Tevethia, SS Monaco, JJ TI Characterizing the role of the mouse PA28 proteasome activator family in antigen processing SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Cincinnati, Howard Hughes Med Inst, Cincinnati, OH 45267 USA. NIAID, Viral Immunol Sect, Bethesda, MD USA. Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Hershey, PA 17033 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1237 EP A1237 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902831 ER PT J AU Belkaid, Y Piccirillo, CA Shevach, EM Sacks, DL AF Belkaid, Y Piccirillo, CA Shevach, EM Sacks, DL TI Role for CD4+CD25+regulatory T cells in Leishmaniasis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID LPD, NIH, Bethesda, MD 20852 USA. NIAID LI, NIH, Bethesda, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1070 EP A1071 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901903 ER PT J AU Bhathena, SJ Ali, AA Mohamed, AA Hansen, CT Velasquez, MT AF Bhathena, SJ Ali, AA Mohamed, AA Hansen, CT Velasquez, MT TI Effects of dietary soybean and flaxseed meal on metabolic parameters in a genetic model of obesity and diabetes. SO FASEB JOURNAL LA English DT Meeting Abstract C1 USDA, Phytonutr Lab, Beltsville, MD 20705 USA. Ain Shams Univ, Dept Food Sci, Cairo, Egypt. Virginia State Univ, Petersburg, VA USA. NIH, Vet Resources Branch, Bethesda, MD USA. George Washington Univ, Dept Med, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1013 EP A1013 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901592 ER PT J AU Bocek, P Paul, WE AF Bocek, P Paul, WE TI IFN gamma can enhance in vitro priming of naive CD4 T cells for IL-4 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1226 EP A1226 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902770 ER PT J AU Candon, S McHugh, R Natarajan, K Shevach, EM Margulies, DH AF Candon, S McHugh, R Natarajan, K Shevach, EM Margulies, DH TI Autoimmune gastritis in mice expressing a transgenic TCR specific for the gastric parietal cell H/K ATPase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1221 EP A1221 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902739 ER PT J AU Caspi, RR Avichezer, D Chan, CC Lewis, GM Wiggert, B Liou, GI AF Caspi, RR Avichezer, D Chan, CC Lewis, GM Wiggert, B Liou, GI TI Immunologically privileged expression of a sequestered ocular antigen results in tolerance. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NEI, LRCMB, NIH, Bethesda, MD 20892 USA. Med Coll Georgia, Dept Ophthalmol, Augusta, GA 30912 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1066 EP A1066 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901877 ER PT J AU Caven, TH Ma, C Beavil, R Beavil, A Ghirlando, R Gould, H Conrad, D AF Caven, TH Ma, C Beavil, R Beavil, A Ghirlando, R Gould, H Conrad, D TI Antibodies against the stalk region of huCD23 block binding of IgE and inhibit in vitro IgE synthesis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Virginia Commonwealth Univ, Richmond, VA 23298 USA. Kings Coll London, London WC2R 2LS, England. NIH, Bethesda, MD 20892 USA. RI Ghirlando, Rodolfo/A-8880-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1239 EP A1239 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902845 ER PT J AU Chen, LY Lin, BC Pan, CJ Chou, JY AF Chen, LY Lin, BC Pan, CJ Chou, JY TI A mouse model of glycogen storage disease type 1b SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, Hertiable Disorders Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1102 EP A1103 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902085 ER PT J AU Chen, WJ Sim, D Jin, WW Kim, E Hardegen, N Bluestone, JA Wahl, SN AF Chen, WJ Sim, D Jin, WW Kim, E Hardegen, N Bluestone, JA Wahl, SN TI A functional link between CTLA-4 and cell surface associated TGF-beta in CD4(+)CD25(+) suppressor T cell-mediated immunosuppression SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDCR, OIIB, Bethesda, MD 20892 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1056 EP A1056 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901822 ER PT J AU Chen, ZM O'Shaughnessy, M Murphy, W Taub, D Ber, L Blazar, B AF Chen, ZM O'Shaughnessy, M Murphy, W Taub, D Ber, L Blazar, B TI Ex vivo targeting of the janus kinase 3 (Jak3) pathway in an MLR culture induces alloantigen-specific T cell hyporesponsiveness and prevention of graft-versus-host disease (GVHD) in vivo SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 USA. NCI, SAIC, Frederick, MD 21701 USA. NCI, Lab Leukocyte Biol, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1035 EP A1035 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901709 ER PT J AU Cohen-Fix, O Agarwal, R AF Cohen-Fix, O Agarwal, R TI Mitotic regulation: the dual nature of the securin-separase interaction SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, LMCB, NIH, Bethesda, MD 20892 USA. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A740 EP A740 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900081 ER PT J AU Coppinger, RJ Carlson, BA Esser, K Hatfield, DL Diamond, AM AF Coppinger, RJ Carlson, BA Esser, K Hatfield, DL Diamond, AM TI Selenium influences turnover of selenocysteine tRNA([Ser]Sec) in Chinese hamster ovary cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Illinois, Dept Human Nutr, Chicago, IL 60612 USA. NCI, BRL, CCR, NIH, Bethesda, MD USA. Univ Illinois, Dept Kinesiol, Chicago, IL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A992 EP A992 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901478 ER PT J AU Cui, XL Alsaaty, S Lawrance, M Combs, CA Rouhani, F Levine, SJ AF Cui, XL Alsaaty, S Lawrance, M Combs, CA Rouhani, F Levine, SJ TI Identification and characterization of a novel zinc metalloproteinase that up-regulates type I tumor necrosis factor receptor shedding SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA. NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1193 EP A1194 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902589 ER PT J AU De Carli, M Frossi, B Daniel, KC Rivera, J Pucillo, C AF De Carli, M Frossi, B Daniel, KC Rivera, J Pucillo, C TI IgE independent IL-4 production by RBL-2H3 cells: role of oxidative stress SO FASEB JOURNAL LA English DT Meeting Abstract C1 Azienda Osped Santa Maria Misericordia, Dept Internal Med, I-33100 Udine, Italy. Univ Udine, Immunol Sect, I-33100 Udine, Italy. GKT Sch Med, Dept Immunol, London, England. NIAMS, Mol Inflammat Sect, Bethesda, MD USA. RI Pucillo, Carlo/A-5515-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1241 EP A1242 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902858 ER PT J AU Diaw, L Siwarsky, D Wellington, T Taylor, BJ duBois, W Huppi, K AF Diaw, L Siwarsky, D Wellington, T Taylor, BJ duBois, W Huppi, K TI Expression of kappa : lambda cells in mouse B cell development SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1075 EP A1075 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901930 ER PT J AU Dobbins, DE Hashiramoto, A Wilder, RL Remmers, EF AF Dobbins, DE Hashiramoto, A Wilder, RL Remmers, EF TI The mutation causing osteopetrosis in tl rats maps to a 2.5 cM interval on rat chromosome 2. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NIAMS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A881 EP A881 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900862 ER PT J AU Dohke, Y Turner, RJ AF Dohke, Y Turner, RJ TI The transmembrane biogenesis of the water channel aquaporin 1 (AQP1) in intact mammalian cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 Natl Inst Dent & Craniofacial REs, GTTB, Membrane Biol Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A807 EP A807 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900457 ER PT J AU Dye, JM Gao, JL Kuziel, W Zajac, AJ Murphy, PM Quinn, DG AF Dye, JM Gao, JL Kuziel, W Zajac, AJ Murphy, PM Quinn, DG TI The role of MIP-1 alpha in protective immunity against lymphocytic choriomeningitis virus (LCMV) infection SO FASEB JOURNAL LA English DT Meeting Abstract C1 Loyola Univ, Maywood, IL 60153 USA. NIAID, Host Def Lab, Bethesda, MD 20892 USA. Univ Texas, Austin, TX 78712 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1080 EP A1080 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901958 ER PT J AU Ecelbarger, CA Goodenow, B Doud, MS Knepper, MA Verbalis, JG AF Ecelbarger, CA Goodenow, B Doud, MS Knepper, MA Verbalis, JG TI Insulin infusion or dietary PPAR-gamma agonists may stimulate aldosterone and aldosterone-sensitive renal proteins SO FASEB JOURNAL LA English DT Meeting Abstract C1 Georgetown Univ, Dept Med, Washington, DC 20007 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A842 EP A842 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900647 ER PT J AU Fedorova, IM Hernandez-Sanchez, C Basile, AS AF Fedorova, IM Hernandez-Sanchez, C Basile, AS TI Mice transgenically overexpressing sulfonylurea receptor 1 in forebrain resist seizure induction and excitotoxic neuron death SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, LBCK, NIH, Bethesda, MD 20892 USA. NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A950 EP A951 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901253 ER PT J AU Fisher, JT Vincent, SG Gomeza, J Yamada, M Wess, J AF Fisher, JT Vincent, SG Gomeza, J Yamada, M Wess, J TI M2 and M3 muscarinic receptor gene deletion abolishes vagally-induced bradycardia and bronchoconstriction. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Queens Univ, Kingston, ON K7L 3N6, Canada. NIDDK, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A879 EP A879 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900850 ER PT J AU Gaussin, V Van de Putte, T Mishina, Y Hanks, MC Zwijsen, A Huylebroeck, D Behringer, RR Schneider, MD AF Gaussin, V Van de Putte, T Mishina, Y Hanks, MC Zwijsen, A Huylebroeck, D Behringer, RR Schneider, MD TI Endocardial cushion and myocardial defects following heart-specific conditional deletion fo the BMP receptor ALK3 SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Med & Dent New Jersey, Inst Cardiovasc Res, Hackensack, NJ 07601 USA. Catholic Univ Louvain, B-3000 Louvain, Belgium. NIH, Res Triangle Pk, NC USA. Procter & Gamble Pharmaceut, Cincinnati, OH 45202 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Baylor Coll Med, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1094 EP A1094 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902036 ER PT J AU Ghosh, A Shieh, JJ Sun, MS Pan, CJ Chou, JY AF Ghosh, A Shieh, JJ Sun, MS Pan, CJ Chou, JY TI The catalytic center of glucose-6-phosphatase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A896 EP A896 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900943 ER PT J AU Hakim, FT Memon, SA Gress, RE AF Hakim, FT Memon, SA Gress, RE TI Recovery of CD8+T cell populations post transplant SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA. RI Memon, Sarfraz/E-1198-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1029 EP A1029 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901675 ER PT J AU Hartman, TJ Davies, MJ Huth, PJ Baer, DJ Judd, JT Remaley, AT Martini, MC Dorgan, JF Mosbacher, TL Taylor, PR AF Hartman, TJ Davies, MJ Huth, PJ Baer, DJ Judd, JT Remaley, AT Martini, MC Dorgan, JF Mosbacher, TL Taylor, PR TI The effects of animal (non-fat milk) versus soy protein replete with isoflavones on prostate-specific antigen and insulin-like growth factor in men SO FASEB JOURNAL LA English DT Meeting Abstract C1 Penn State Univ, University Pk, PA 16802 USA. Res Diets, Somerset, NJ USA. Kraft Gen Foods Inc, Glenview, IL 60025 USA. USDA ARS, Beltsville Agr Res Ctr, Beltsville Human Nutr Res Ctr, Beltsville, MD 20705 USA. NIH, Bethesda, MD 20892 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 4 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1004 EP A1004 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901542 ER PT J AU Hesse, M Modolell, M La Flamme, AC Schito, M Fuentes, JM Cheever, AW Pearce, EJ Wynn, TA AF Hesse, M Modolell, M La Flamme, AC Schito, M Fuentes, JM Cheever, AW Pearce, EJ Wynn, TA TI Differential regulation of NO Synthase-2 and Arginase-1 by Type1/Type2 cytokines controls pathology in murine schistosomiasis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, LPD, NIH, Bethesda, MD 20892 USA. Max Planck Inst Immunbiol, D-7800 Freiburg, Germany. Cornell Univ, Ithaca, NY USA. Univ Extremadura, Caceres, Spain. Biomed Res Inst, Rockville, MD 20852 USA. RI Wynn, Thomas/C-2797-2011; Fuentes, Jose/H-9490-2014 OI Fuentes, Jose/0000-0001-6910-2089 NR 0 TC 0 Z9 0 U1 0 U2 5 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1225 EP A1225 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902766 ER PT J AU Hoagland, KM Flasch, AK Knepper, MA Roman, RJ AF Hoagland, KM Flasch, AK Knepper, MA Roman, RJ TI Targeted proteomics reveals that abnormalities in expression of ROMK and CYP4A proteins contribute to elevated Cl transport in TALH of Dahl S rats SO FASEB JOURNAL LA English DT Meeting Abstract C1 Med Coll Wisconsin, Milwaukee, WI 53226 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A842 EP A842 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900648 ER PT J AU Hong, L Ton, TV Dunnick, JK Devereux, TR Sills, RC Boorman, GA AF Hong, L Ton, TV Dunnick, JK Devereux, TR Sills, RC Boorman, GA TI Genetic alterations in ras, p53, and b-catenin genes in hemangiosarcomas of B6C3F, mice following exposure to o-nitrotoluene for 2 years SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, DIR LEP, Res Triangle Pk, NC 27709 USA. NIEHS, DIR EDMP, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1202 EP A1202 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902635 ER PT J AU Huang, LYC Aliberti, J Inoue, S Mikolajczyk, M Golding, B AF Huang, LYC Aliberti, J Inoue, S Mikolajczyk, M Golding, B TI Role of dendritic cell-derived IFN-gamma in response to a microbial stimulus SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA, CBER, DH, Rockville, MD 20852 USA. NIAID, LPD, NIH, Bethesda, MD 20892 USA. RI Aliberti, Julio/G-4565-2012; Aliberti, Julio/I-7354-2013 OI Aliberti, Julio/0000-0003-3420-8478 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1230 EP A1230 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902794 ER PT J AU Hudson, MJ Chitnis, A AF Hudson, MJ Chitnis, A TI Identification and analysis of zebrafish neurogenesis mutants SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Maryland Baltimore Cty, Baltimore, MD 21250 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A730 EP A731 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900025 ER PT J AU Ikeyama, S Kokkonen, G Wang, XT Holbrook, NJ AF Ikeyama, S Kokkonen, G Wang, XT Holbrook, NJ TI Effects of aging and calorie restriction on growth factor- and oxidant-induced mitogenesis in rat hepatocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, LMBC, Baltimore, MD 21224 USA. Yale Univ, Dept Med, New Haven, CT 06520 USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1163 EP A1163 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902416 ER PT J AU Iribarren, P Cui, YH Le, YY Abe, K Gong, WH Dunlop, NM Wang, JM AF Iribarren, P Cui, YH Le, YY Abe, K Gong, WH Dunlop, NM Wang, JM TI Interleukin 4 attenuates mouse microglial cell activation by LPS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Mol Immunoregulat Lab, Ft Detrick, MD 21702 USA. SAIC, IRSP, Mol Immunoregulat Lab, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1086 EP A1086 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901990 ER PT J AU Jankovic, D Kullberg, MC Hieny, S Caspar, P Collazo, CM Sher, A AF Jankovic, D Kullberg, MC Hieny, S Caspar, P Collazo, CM Sher, A TI IL-12-independent development of host-protective Th1 cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, NIH, Parasit Dis Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1069 EP A1069 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901892 ER PT J AU Jayachandran, M Owen, W Korach, K Miller, VM AF Jayachandran, M Owen, W Korach, K Miller, VM TI Turnover and ATP secretion in platelets of female ER alpha knockout and wild-type mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. NIEHS, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A821 EP A821 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900534 ER PT J AU Khin, EK Smith, J Freebern, W Gardner, K AF Khin, EK Smith, J Freebern, W Gardner, K TI The influence of protein acetylation on gene expression and cell cycle progression in lymphoid cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Ctr Adv Technol, Pathol Lab, Div Clin Sci,NIH, Gaithersburg, MD 20877 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1203 EP A1203 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902640 ER PT J AU Kilmon, MA Holmes, KL Conrad, DH AF Kilmon, MA Holmes, KL Conrad, DH TI Association of CD23 on the cell surface SO FASEB JOURNAL LA English DT Meeting Abstract C1 Virginia Commonwealth Univ, Richmond, VA USA. NIAID, Flow Cytometry Sect, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1239 EP A1239 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902846 ER PT J AU Koretsky, AP Aoki, I Silva, AC AF Koretsky, AP Aoki, I Silva, AC TI Anatomical, functional, and molecular MRI of the brain SO FASEB JOURNAL LA English DT Meeting Abstract C1 Natl Inst Neurol Disorders & Stroke, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA. RI Aoki, Ichio/G-2529-2011 OI Aoki, Ichio/0000-0002-4429-5053 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1091 EP A1091 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902022 ER PT J AU Kovbasnjuk, A Li, XH Boja, E Fales, H Acheson, DWK Sears, CL Donowitz, M AF Kovbasnjuk, A Li, XH Boja, E Fales, H Acheson, DWK Sears, CL Donowitz, M TI Glycosphingolipid Gb3 as biomarker for invasive colon carcinoma cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Johns Hopkins Sch Med, Baltimore, MD 21205 USA. NHLBI, NIH, Bethesda, MD 20892 USA. Univ Maryland, Baltimore, MD 21201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1200 EP A1200 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902625 ER PT J AU Kuhns, DB Gallin, JI AF Kuhns, DB Gallin, JI TI Induction of monocyte interleukin-8 (IL-8) by fibrinogen - Possible role of the Toll-like receptor pathway SO FASEB JOURNAL LA English DT Meeting Abstract C1 SAIC Fredcrick Inc, Frederick, MD 21702 USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1048 EP A1048 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901782 ER PT J AU Kwon, SY Wei, Q Paterson, BM Carlson, BA Kryukov, GV Lee, HS Martin-Romero, FJ Gladyshev, VN Hatfield, DI Lee, BJ AF Kwon, SY Wei, Q Paterson, BM Carlson, BA Kryukov, GV Lee, HS Martin-Romero, FJ Gladyshev, VN Hatfield, DI Lee, BJ TI Functional studies of Drosophila selenoproteins: selenophosphate synthetase 2 (SPS2), G-rich and BthD. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, BRL, CCR, NIH, Bethesda, MD 20892 USA. NCI, LB, CCR, NIH, Bethesda, MD 20892 USA. Univ Nebraska, Dept Biochem, Lincoln, NE 68583 USA. SENU, Seoul, South Korea. RI Gladyshev, Vadim/A-9894-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A992 EP A992 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901474 ER PT J AU Lancaster, JR Thomas, DD AF Lancaster, JR Thomas, DD TI Cellular consumption of nitric oxide: Kinetics and products SO FASEB JOURNAL LA English DT Meeting Abstract C1 Louisiana State Univ, Hlth Sci Ctr, Dept Physiol, New Orleans, LA 70112 USA. NCI, Radiat Biol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A910 EP A911 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901026 ER PT J AU Landry, JE Streich, FC Heidecker, G Shuh, M AF Landry, JE Streich, FC Heidecker, G Shuh, M TI Constitutive activation of the MAPK pathway by HTLV-I tax SO FASEB JOURNAL LA English DT Meeting Abstract C1 Loyola Univ, New Orleans, LA 70118 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A916 EP A917 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901059 ER PT J AU Le, YY Cui, YH Gong, WH Li, HM Zhang, X Abe, K Sun, RH Van Damme, J Proost, P Wang, JM AF Le, YY Cui, YH Gong, WH Li, HM Zhang, X Abe, K Sun, RH Van Damme, J Proost, P Wang, JM TI TNF alpha up-regulates the expression and function of amyloid beta receptor in murine microgial cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. NCI, Expt Immunol Lab, Frederick, MD 21702 USA. Univ Louvain, Rega Inst, Louvain, Belgium. RI Zhang, Xia/B-8152-2008 OI Zhang, Xia/0000-0002-9040-1486 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1085 EP A1085 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901986 ER PT J AU Lee, JS Weyant, R Corby, P Kritchevsky, SB Harris, TB Newman, AB AF Lee, JS Weyant, R Corby, P Kritchevsky, SB Harris, TB Newman, AB TI Edentulism and nutritional status in a biracial sample of well-functioning community-dwelling elderly. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA 15213 USA. Univ Tennessee, Memphis, TN USA. NIA, Bethesda, MD 20892 USA. RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A979 EP A979 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901410 ER PT J AU Li, CL Klein, JD Wang, WD Knepper, MA Nielsen, S Sands, JM Frokiaer, J AF Li, CL Klein, JD Wang, WD Knepper, MA Nielsen, S Sands, JM Frokiaer, J TI Altered expression of urea transporters in rat kidneys in response to urinary tract obstruction. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Aarhus Univ, Water & Salt Res Ctr, DK-8200 Aarhus, Denmark. Emory Univ, Atlanta, GA 30322 USA. NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A843 EP A843 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900653 ER PT J AU Liu, YS Chen, PL Hutter, D Yang, XL Gorospe, M Davis, RJ AF Liu, YS Chen, PL Hutter, D Yang, XL Gorospe, M Davis, RJ TI Discordance between the binding affinity of MAP kinase subfamily members for MKP-2 and their ability to catalytically activate the phosphatase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA. Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Dept Biochem & Mol Biol, Worcester, MA 01605 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A914 EP A914 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901045 ER PT J AU Mai, V Colbert, L Berrigan, D Lanza, E Perkins, S Schatzkin, A Srinivas, P Hursting, S AF Mai, V Colbert, L Berrigan, D Lanza, E Perkins, S Schatzkin, A Srinivas, P Hursting, S TI Effects of caloric restriction, diet composition, and exercise in a genetic mouse model (MIN) of intestinal cancer. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, DCEG, NEB, Bethesda, MD 20892 USA. NIA, EDB, Bethesda, MD 20892 USA. NCI, DCP, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A974 EP A974 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901383 ER PT J AU Mak, IT Basile, AS Weglicki, WB AF Mak, IT Basile, AS Weglicki, WB TI Elevated oxidative stress in mice infected with murine retrovirus and the effect of moderate Mg-deficiency SO FASEB JOURNAL LA English DT Meeting Abstract C1 George Washington Univ, Med Ctr, Washington, DC 20037 USA. NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1041 EP A1041 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901741 ER PT J AU Martin, KR Kari, FW Barrett, JC French, JE AF Martin, KR Kari, FW Barrett, JC French, JE TI N-acetyl-L-cysteine (NAC) stimulates oxidative stress and cellular proliferation, but decreases apoptosis, in splenocytes from FVB/N mice, and transgenic mice hemizygous and homozygous for v-Ha-ras. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Penn State Univ, Dept Nutr, University Pk, PA 16802 USA. NIEHS, LECM, NIH, Res Triangle Pk, NC 27709 USA. NCI, LBC, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A973 EP A973 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901377 ER PT J AU McCartney-Francis, N Belkaid, Y Jin, WW Wahl, S AF McCartney-Francis, N Belkaid, Y Jin, WW Wahl, S TI TGF-beta deficiency promotes resistance to cutaneous leishmaniasis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDCR, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1071 EP A1071 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901904 ER PT J AU Mendel, I Shevach, EM AF Mendel, I Shevach, EM TI IL-12 sensitizes autoreactive myelin oligodendrocyte glycoprotein (MOG)-specific TCR transgenic (Tg) T cells to activation induced cell death (ACID) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, LI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1059 EP A1059 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901842 ER PT J AU Morimoto, M Morimoto, M Murakami, H Star, R Whitmire, J Urban, JF Gause, WC AF Morimoto, M Morimoto, M Murakami, H Star, R Whitmire, J Urban, JF Gause, WC TI IL-4 producing cells concentrate around encysted nematode larvae in the intestine during a memory Th2 response. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NIDDK, NIH, Bethesda, MD USA. USDA, Beltsville Human Nutr Res Ctr, Beltsville, MD 20705 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1071 EP A1071 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901907 ER PT J AU Murray, MM Horak, H Freeburn, W Haggerty, C Gardner, K AF Murray, MM Horak, H Freeburn, W Haggerty, C Gardner, K TI Selective subnuclear partitioning of BRCA1 and BRCA1-associated proteins in response to genomic damage in ovarian cancer cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Ctr Adv Technol, Pathol Lab, Div Clin Sci,NIH, Gaithersburg, MD 20877 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1203 EP A1203 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902641 ER PT J AU Nie, ZQ Abernethy, DR Soldatove, NM AF Nie, ZQ Abernethy, DR Soldatove, NM TI Immunochemical analysis of human L-type Ca2+ channels showing different inactivation properties. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A959 EP A959 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901297 ER PT J AU Novoselov, SV Rao, M Onoshko, NV Zhi, HJ Kruykov, GV Xiang, YB Weeks, D Hatfield, DL Gladyshev, VN AF Novoselov, SV Rao, M Onoshko, NV Zhi, HJ Kruykov, GV Xiang, YB Weeks, D Hatfield, DL Gladyshev, VN TI Selenoproteins and selenocysteine (Sec) insertion system in the model plant cell system, Chlamydomonas reinhardtii SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA. NCI, BRL, CCR, NIH, Bethesda, MD USA. RI Gladyshev, Vadim/A-9894-2013 NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A992 EP A992 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901476 ER PT J AU Orange, JS Brodeur, SR Jain, A Bonilla, FA Schneider, LC Kretschmer, R Nurko, S Koehler, JR Rasmussen, WL Fergusson, BM Zonnana, J Ramesh, N Ballas, ZK Geha, RS AF Orange, JS Brodeur, SR Jain, A Bonilla, FA Schneider, LC Kretschmer, R Nurko, S Koehler, JR Rasmussen, WL Fergusson, BM Zonnana, J Ramesh, N Ballas, ZK Geha, RS TI Deficiency of natural cytotoxicity in patients with IKK gamma/NEMO mutations SO FASEB JOURNAL LA English DT Meeting Abstract C1 Harvard Univ, Childrens Hosp, Boston, MA 02115 USA. NIH, Bethesda, MD 20892 USA. Hosp ABC, Mexico City, DF, Mexico. Iowa City Vet Adm, Iowa City, IA USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1242 EP A1242 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902859 ER PT J AU Patterson, BH Combs, GF Mary, B Claude, V Patterson, KY Taylor, PR Levander, OA AF Patterson, BH Combs, GF Mary, B Claude, V Patterson, KY Taylor, PR Levander, OA TI Controlled-diet vs. free-living subjects: A comparison of excretion data from two selenium (Se) tracer studies SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA. Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA. USDA, Beltsville, MD 20705 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A995 EP A995 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901492 ER PT J AU Qi, ZH Redha, R Hao, CM Morrow, JD Langenbach, RL Breyer, MD AF Qi, ZH Redha, R Hao, CM Morrow, JD Langenbach, RL Breyer, MD TI Selective targeting of COX1 and COX2 reveals opposite effects on blood pressure and renal function. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Vanderbilt Univ, Nashville, TN 37232 USA. NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1171 EP A1171 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902460 ER PT J AU Qin, SF Chock, PB AF Qin, SF Chock, PB TI Tyrosine phosphatase CD45 regulates hydrogen peroxide-induced calcium mobilization in B cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A915 EP A915 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901049 ER PT J AU Rao, M Kumaraswamy, E Shanmugam, I Carlson, BA Diamond, AN Hatfield, DL AF Rao, M Kumaraswamy, E Shanmugam, I Carlson, BA Diamond, AN Hatfield, DL TI Multiple forms of selenocysteine (Sec) tRNAs may be due to distinct higher order structures. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, BRL, CCR, NIH, Bethesda, MD 20892 USA. Univ Illinois, Dept Human Nutr, Chicago, IL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A992 EP A992 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901475 ER PT J AU Rao, MS AF Rao, MS TI Generation of oligodendrocyte and astrocyte precursors during development SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, Neurosci Lab, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1111 EP A1111 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902135 ER PT J AU Ricketts, SL Carter, JC Thorgeirsson, SS Grisham, JW Coleman, WB AF Ricketts, SL Carter, JC Thorgeirsson, SS Grisham, JW Coleman, WB TI Evaluation of candidate liver tumor suppressor transcripts from human chromosome 11p11.2-p12 in human hepatocellular carcinoma cell lines SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ N Carolina, Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA. NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1105 EP A1105 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902098 ER PT J AU Rossman, MD Thompson, B Frederick, M Cizman, B Monos, D AF Rossman, MD Thompson, B Frederick, M Cizman, B Monos, D CA ACCESS Grp TI Susceptibility to sarcoidosis: Association of HLA Class II alleles with environmental exposures SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Penn, ACCESS Grp, Philadelphia, PA 19104 USA. Clin Trails & Survey Corp, Baltimore, MD USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1072 EP A1072 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901910 ER PT J AU Roth, SM Schrager, MA Riechman, SE Lee, M Metter, EJ Fleg, JL Hurley, BF Ferrell, RE AF Roth, SM Schrager, MA Riechman, SE Lee, M Metter, EJ Fleg, JL Hurley, BF Ferrell, RE TI The IL6 G-174C promoter polymorphism and body composition in adult men and women SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA 15261 USA. Univ Maryland, College Pk, MD 20742 USA. NIA, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A880 EP A881 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900858 ER PT J AU Sarkar, K Shaw, S AF Sarkar, K Shaw, S TI Acute induction of fluid phase endocytosis in IL-4 and GM-CSF treated human monocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1231 EP A1232 PN 2 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902801 ER PT J AU Schwartz, EI Fishbein, K Spencer, R Kobrinsky, E Abernathy, DR Soldatov, NM AF Schwartz, EI Fishbein, K Spencer, R Kobrinsky, E Abernathy, DR Soldatov, NM TI Expression of GFP-tagged human L-type Ca2- channels in transgenic mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A959 EP A959 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901298 ER PT J AU Semnani, RT Liu, AY Nutman, TB AF Semnani, RT Liu, AY Nutman, TB TI Exposure of human dendritic cells to live microfilariae inhibits the production of IL-12 and induces cell death SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. Howard Hughes Med Inst, Res Scholars Program, NIH, Bethesda, MD 20817 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1038 EP A1038 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901726 ER PT J AU Semnani, RT Chaussabel, D McDowell, MA Sabzevari, H Sacks, D Sher, A Nutman, TB AF Semnani, RT Chaussabel, D McDowell, MA Sabzevari, H Sacks, D Sher, A Nutman, TB TI The early response to the infective stage of the filarial parasite Brugia malayi is dominated by inflammatory genes in macrophages SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1038 EP A1038 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901722 ER PT J AU Shaw, M Ortmann, R Shevach, E Sher, A Yap, GS AF Shaw, M Ortmann, R Shevach, E Sher, A Yap, GS TI Genetic analysis of a defect in IL-12 signaling: Susceptibility of B10.Q/J to T-gonii infection SO FASEB JOURNAL LA English DT Meeting Abstract C1 Brown Univ, Dept Mol Microbiol & Immunol, Providence, RI 02912 USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1247 EP A1247 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902887 ER PT J AU Shidham, G McCarthy, ET Sharma, M Schubert, U Kopp, J Henhlein, P Savin, VJ AF Shidham, G McCarthy, ET Sharma, M Schubert, U Kopp, J Henhlein, P Savin, VJ TI Effect of viral protein R (Vpr) on glomerular albumin permeability (Palb) and arachidonic acid (AA) release SO FASEB JOURNAL LA English DT Meeting Abstract C1 Med Coll Wisconsin, Div Nephrol, Milwaukee, WI 53226 USA. Heinrich Pette Inst Expt Virol & Immunol, Hamburg, Germany. NIH, Bethesda, MD 20892 USA. Humboldt Univ, Berlin, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A971 EP A971 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901365 ER PT J AU Singh, BB Liu, XB Ambudkar, IS AF Singh, BB Liu, XB Ambudkar, IS TI CaM regulates Ca2--dependent feedback inhibition of store-operated Ca2+ influx by interaction with a site in the C-terminus of Trp1. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDCR, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD 20874 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A897 EP A897 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900953 ER PT J AU Smeltz, R Chen, J Shevach, EM AF Smeltz, R Chen, J Shevach, EM TI The induction of Th1 cells by TGF-beta 1 is IFN-gamma-dependent, but IL-12/STAT-4-independent SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20892 USA. NIA, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1222 EP A1222 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902747 ER PT J AU Smith, J Khin, EK Zaitseva, EM Freebern, W Dzekunova, I Gardner, K AF Smith, J Khin, EK Zaitseva, EM Freebern, W Dzekunova, I Gardner, K TI Genome wide analysis of protein/DNA interactions SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Div Clin Sci, Pathol Lab, NIH, Gaithersburg, MD USA. NCI, Microarray Facil, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1104 EP A1104 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902092 ER PT J AU Sutherland, VL Barela, A Tompkins, LS Deyholos, M Sharer, K Brooks, H Galbraith, D Koretsky, AP Lynch, RM AF Sutherland, VL Barela, A Tompkins, LS Deyholos, M Sharer, K Brooks, H Galbraith, D Koretsky, AP Lynch, RM TI Identification of glucose-sensing neuroendocrine cells, using a glucokinase promoter driven green fluorescent protein transgenic mouse SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Arizona, Tucson, AZ 85724 USA. NIH, LFMI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A786 EP A786 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900337 ER PT J AU Terris, JM Wang, XY Beutler, K Schooley, J Pamnani, M Knepper, MA AF Terris, JM Wang, XY Beutler, K Schooley, J Pamnani, M Knepper, MA TI Acute and chronic dysregulation of ENaC and other major renal sodium transporters in the two-kidney, one-clip (2K1C) Goldblatt rat SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A843 EP A843 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900654 ER PT J AU Tkaczyk, C Metcalfe, DD Gilfillan, AM AF Tkaczyk, C Metcalfe, DD Gilfillan, AM TI Phospholipase C gamma(1) (PLC gamma(1)) phosphorylation and degranulation of human mast cells (HuMCs) following Fc epsilon RI-aggregation is independent of phosphatidylinositol-3-kinase (PI-3-K). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1241 EP A1241 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902855 ER PT J AU Tkaczyk, C Metcalfe, DD Gilfillan, AM AF Tkaczyk, C Metcalfe, DD Gilfillan, AM TI Role of tyrosine phosphatase-dependent activation of see kinases in degranulation of human mast cells (HuMCs) following Fc epsilon RI-aggregation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Allerg Dis Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1199 EP A1199 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902621 ER PT J AU Troiano, RP Subar, AF Schatzkin, A Kipnis, V Trabulsi, J Ballard-Barbash, R Schoeller, DA AF Troiano, RP Subar, AF Schatzkin, A Kipnis, V Trabulsi, J Ballard-Barbash, R Schoeller, DA TI Energy expenditure determined by doubly labeled water in a large sample of adults was substantially greater than energy intake reported in national dietary surveys SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A750 EP A750 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900134 ER PT J AU Turban, SI Lackhart, H Knepper, MA Masilamani, S AF Turban, SI Lackhart, H Knepper, MA Masilamani, S TI Angiotensin II regulation of renal Na transporter abundances SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A842 EP A842 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900650 ER PT J AU Twigger, S Lu, J Shimoyama, M Pasko, D Long, P Ginster, J Chen, CF Nigam, R Chen, D Kwitek-Black, A Eppig, J Maglott, D Schuler, G Jacob, H Tonellato, PJ AF Twigger, S Lu, J Shimoyama, M Pasko, D Long, P Ginster, J Chen, CF Nigam, R Chen, D Kwitek-Black, A Eppig, J Maglott, D Schuler, G Jacob, H Tonellato, PJ TI The rat genome database SO FASEB JOURNAL LA English DT Meeting Abstract C1 Med Coll Wisconsin, Bioinformat Res Ctr, Milwaukee, WI 53226 USA. Med Coll Wisconsin, Human & Mol Genet Ctr, Milwaukee, WI 53226 USA. Jackson Lab, Bar Harbor, ME 04609 USA. Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A882 EP A882 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900868 ER PT J AU Wade, JB Liu, J Knepper, MA Coleman, RA AF Wade, JB Liu, J Knepper, MA Coleman, RA TI Distribution of 11 beta HSD2 along distal segments of the rat nephron SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Maryland, Sch Med, Baltimore, MD 21201 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A890 EP A890 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593900912 ER PT J AU Wang, J Whitman, MC Natarajan, K Tormo, J Mariuzza, RA Margulies, DH AF Wang, J Whitman, MC Natarajan, K Tormo, J Mariuzza, RA Margulies, DH TI Interaction between NK cell inhibitory receptor and MHC-I ligand: crucial contacts include both H-2D(d) and beta 2m SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, MBS, LI, NIH, Bethesda, MD 20892 USA. Univ Autonoma Madrid, Madrid, Spain. Univ Maryland, Maryland Biotechnol Inst, Ctr Adv Res Biotechnol, Rockville, MD 20850 USA. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1224 EP A1224 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902757 ER PT J AU Wei, RT Phillips, TM Sternberg, EM AF Wei, RT Phillips, TM Sternberg, EM TI Defective secretion of CRH and AVP in the Lewis hypothalamic cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH, Intergrat Neural Immune Program, NIH, Bethesda, MD 20892 USA. OD, ORS, NIH, Div Bioengn & Phys Sci, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1085 EP A1085 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901987 ER PT J AU Weinstein, BM Isogai, S Lawson, ND AF Weinstein, BM Isogai, S Lawson, ND TI Imaging blood vessel development in the zebrafish SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, LMG, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1087 EP A1087 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901999 ER PT J AU Wu, JF Olariu, A Huang, KP Huang, FL AF Wu, JF Olariu, A Huang, KP Huang, FL TI Functional role of neurogranin in the modulation of PKC, PKA, and Ca2+/calmodulin-dependent signalings in NMDA stimulation of hippocampal slices SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, ERRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1180 EP A1180 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902510 ER PT J AU Yim, MB Lee, HI Yim, HS Chock, PB Stadtman, ER AF Yim, MB Lee, HI Yim, HS Chock, PB Stadtman, ER TI Glycated proteins catalyze one-electron redox reactions. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A921 EP A921 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901082 ER PT J AU Zaitseva, EM Smith, J Gardner, K AF Zaitseva, EM Smith, J Gardner, K TI The role of N-terminal sequences of p300 in distal apoptotic death pathways in activated T-lymphocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Pathol Lab, Div Clin Sci, NIH, Gaithersburg, MD 20877 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A964 EP A964 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901326 ER PT J AU Zeng, G Robbins, PF Rosenberg, SA AF Zeng, G Robbins, PF Rosenberg, SA TI Dendritic cells can directly acquire the NY-ESO-1 tumor antigen and cross-present to CTL SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1232 EP A1232 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593902803 ER PT J AU Zhang, JH Wang, SB Danner, RL AF Zhang, JH Wang, SB Danner, RL TI A nitric oxide (NO)-sensitive switch with a Sp1 sensor and an up stream directional element SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. Inst Genom Res, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A912 EP A912 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901034 ER PT J AU Zhang, X Young, HA AF Zhang, X Young, HA TI Inhibition of biological functions of natural killer cells by 15-deoxy-Delta(12,14) 2,14 prostaglandin J(2) through PPAR-gamma-dependent and -independent mechanism SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, CMIS LEI CCR, NIH, Frederick, MD 21702 USA. RI Zhang, Xia/B-8152-2008 OI Zhang, Xia/0000-0002-9040-1486 NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A1082 EP A1082 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901969 ER PT J AU Zhang, Y Dufau, ML AF Zhang, Y Dufau, ML TI Mechanism of luteinizing hormone receptor gene transcriptional regulation by nuclear orphan receptors SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, ERRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 22 PY 2002 VL 16 IS 5 BP A928 EP A928 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 534PC UT WOS:000174593901123 ER PT J AU Andoh, T Chock, PB Chiueh, CC AF Andoh, T Chock, PB Chiueh, CC TI The roles of thioredoxin in protection against oxidative stress-induced apoptosis in SH-SY5Y cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYTOCHROME-C; CASPASE ACTIVATION; LIPID-PEROXIDATION; REDOX REGULATION; REDUCTASE; BCL-2; INHIBITOR; PROTEIN; DEATH; MANGANESE AB Using models of serum deprivation and 1-methyl-4-phenylpyridinium (MPP+), we investigated the mechanism by which thioredoxin (Trx) exerts its antiapoptotic protection in human neuroblastoma cells (SH-SY5Y) and preconditioning-induced neuroprotection. We showed that SH-SY5Y cells are highly sensitive to oxidative stress and responsive to both extracellularly administered and preconditioning-induced Trx. Serum deprivation and MPP+ produced an elevation in the hydroxyl radicals, malondialdehyde and 4-hydroxy-2,3-nonenal (HNE), causing the cells to undergo mitochondria-mediated apoptosis. Trx in the submicromolar range blocked the observed apoptosis via a multiphasic protection mechanism that includes the suppression of cytochrome c release (most likely via the induction of Bcl-2), the inhibition of procaspase-9 and procaspase-3 activation, and the elevated level of Mn-SOD. The reduced form of Trx suppresses the serum-free-induced hydroxyl radicals, lipid peroxidation, and apoptosis, indicating that H2O2 is removed by Trx peroxidase. The participation of Trx in preconditioning-induced neuroprotection is supported by the observation that inhibition of Trx synthesis with antisense oligonucleotides or of Trx reductase drastically reduced the hormesis effect. This effect of Trx-mediated hormesis against oxidative stress-induced apoptosis is striking. It induced a 30-fold shift in LD50 in the MPP+-induced neurotoxicity. C1 NIMH, Clin Sci Lab, Bethesda, MD 20892 USA. NHLBI, Biochem Lab, Bethesda, MD 20892 USA. RP Chiueh, CC (reprint author), NIMH, Clin Sci Lab, Bldg 10,Rm 3D-41, Bethesda, MD 20892 USA. NR 41 TC 108 Z9 120 U1 4 U2 16 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 22 PY 2002 VL 277 IS 12 BP 9655 EP 9660 DI 10.1074/jbc.M110701200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 533UR UT WOS:000174549200008 PM 11751890 ER PT J AU Zhang, F Nakanishi, G Kurebayashi, S Yoshino, K Perantoni, A Kim, YS Jetten, AM AF Zhang, F Nakanishi, G Kurebayashi, S Yoshino, K Perantoni, A Kim, YS Jetten, AM TI Characterization of Glis2, a novel gene encoding a Gli-related, Kruppel-like transcription factor with Transactivation and repressor functions - Roles in kidney development and neurogenesis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ZINC-FINGER PROTEINS; HEDGEHOG-PATCHED-GLI; SONIC-HEDGEHOG; CUBITUS-INTERRUPTUS; MOLECULAR-GENETICS; SIGNALING PATHWAY; DROSOPHILA EMBRYO; MOUSE ZIC1; FAMILY; EXPRESSION AB In this study, we describe the characterization of a gene encoding a novel Kruppel-like protein, named Glis2. Glis2 encodes a relatively proline-rich, basic 55.8-kDa protein. Its five tandem Cys(2)-His(2) zinc finger motifs exhibit the highest homology to those of members of the Gli and Zic subfamilies of Kruppel-like proteins. Confocal microscopic analysis demonstrated that Glis2 localizes to the nucleus. Analysis of the genomic structure of the Glis2 gene showed that it is composed of 6 exons separated by 5 introns spanning a genomic region of more than 7.5 kb. Fluorescence in situ hybridization mapped the mouse Glis2 gene to chromosome 16A3-B1. Northern blot analysis showed that the Glis2 gene encodes a 3.8-kb transcript that is most abundant in adult mouse kidney. By in situ hybridization, expression was localized to somites and neural tube, and during metanephric development predominantly to the ureteric bud, precursor of the collecting duct, and inductor of nephronic tubule formation. One-hybrid analysis using Glis2 deletion mutants identified a novel activation function (AF) at the N terminus. The activation of transcription through this AF domain was totally suppressed by two repressor functions just downstream from the AF. One of the repressor functions is contained within the first zinc finger motif. The level of transcriptional activation and repression varied with the cell line tested, which might be due to differences in cell type-specific expression of co-activators and co-repressors. Our results suggest that Glis2 behaves as a bifunctional transcriptional regulator. Both the activation and repressor functions may play an important role in the regulation of gene expression during embryonic development. C1 NIEHS, NIH, Div Intramural Res, Cell Biol Sect, Res Triangle Pk, NC 27709 USA. NCI, Comparat Carcinogenesis Lab, NIH, Frederick, MD 21702 USA. RP Jetten, AM (reprint author), NIEHS, NIH, Div Intramural Res, Cell Biol Sect, POB 12233, Res Triangle Pk, NC 27709 USA. OI Jetten, Anton/0000-0003-0954-4445 NR 78 TC 35 Z9 36 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 22 PY 2002 VL 277 IS 12 BP 10139 EP 10149 DI 10.1074/jbc.M108062200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 533UR UT WOS:000174549200072 PM 11741991 ER PT J AU Hong, J Zhang, G Dong, F Rechler, MM AF Hong, J Zhang, G Dong, F Rechler, MM TI Insulin-like growth factor (IGF)-binding protein-3 mutants that do not bind IGF-I or IGF-II stimulate apoptosis in human prostate cancer cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BINDING-PROTEIN-3 AUTOCRINE LOOP; LUNG EPITHELIAL-CELLS; BREAST-CANCER; RETINOIC ACID; FACTOR-BETA; PROTEOLYTIC FRAGMENT; LINE PC-3; TARGETED DISRUPTION; NUCLEAR TRANSPORT; HEPARIN-BINDING AB Insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) can stimulate apoptosis and inhibit cell proliferation directly and independently of binding IGFs or indirectly by forming complexes with IGF-I and IGF-II that prevent them from activating the IGF-I receptor to stimulate cell survival and proliferation. To date, IGF-independent actions only have been demonstrated in a limited number of cells that do not synthesize or respond to IGFs. To assess the general importance of IGF-independent mechanisms, we have generated human IGFBP-3 mutants that cannot bind IGF-I or IGF-II by substituting alanine for six residues in the proposed IGF binding site, Ile(56)/Tyr(57)/Arg(75)/Leu(77)/Leu(80)/Leu(81), and expressing the 6m-hIGFBP-3 mutant construct in Chinese hamster ovary cells. Binding of both IGF-I and IGF-II to 6m-hIGFBP-3 was reduced > 80-fold. The nonbinding 6m-hIGFBP-3 mutant still was able to inhibit DNA synthesis in a mink lung epithelial cell line in which inhibition by wild-type hIGFBP-3 previously had been shown to be exclusively IGF-independent. 6m-hIGFBP-3 only can act by IGF-independent mechanisms since it is unable to form complexes with the IGFs that inhibit their action. We next compared the ability of wild-type and 6m-hIGFBP-3 to stimulate apoptosis in serum-deprived PC-3 human prostate cancer cells. PC-3 cells are known to synthesize and respond to IGF-II, so that IGFBP-3 could potentially act by either IGF-dependent or IGF-independent mechanisms. In fact, 6m-hIGFBP-3 stimulated PC-3 cell death and stimulated apoptosis-induced DNA fragmentation to the same extent and with the same concentration dependence as wild-type hIGFBP-3. These results indicate that IGF-independent mechanisms are major contributors to IGFBP-3-induced apoptosis in PC-3 cells and may play a wider role in the antiproliferative and antitumorigenic actions of IGFBP-3. C1 NIDDK, Natl Inst Hlth, Clin Endocrinol Branch, Bethesda, MD 20892 USA. RP Rechler, MM (reprint author), NIDDK, Natl Inst Hlth, Clin Endocrinol Branch, Bldg 10 Rm 8D12, Bethesda, MD 20892 USA. NR 74 TC 120 Z9 123 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 22 PY 2002 VL 277 IS 12 BP 10489 EP 10497 DI 10.1074/jbc.M109604200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 533UR UT WOS:000174549200117 PM 11784719 ER PT J AU Wang, CY Yang, F He, XP Je, HS Zhou, JZ Eckermann, K Kawamura, D Feng, L Shen, L Lu, B AF Wang, CY Yang, F He, XP Je, HS Zhou, JZ Eckermann, K Kawamura, D Feng, L Shen, L Lu, B TI Regulation of neuromuscular synapse development by glial cell line-derived neurotrophic factor and neurturin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NERVE-MUSCLE INTERACTIONS; LONG-TERM POTENTIATION; GDNF-FAMILY; MOTOR-NEURONS; DEVELOPING MOTONEURONS; HIPPOCAMPAL-NEURONS; TRANSMITTER RELEASE; QUANTAL SECRETION; CORTICAL-NEURONS; VISUAL-CORTEX AB Glial cell line-derived neurotrophic factor (GDNF) is known for its potent effect on neuronal survival, but its role in the development and function of synapses is not well studied. Using Xenopus nerve-muscle co-cultures, we show that GDNF and its family member neurturin (NRTN) facilitate the development of the neuromuscular junction (NMJ). Long-term application of GDNF significantly increased the total length of neurites in the motoncurons. GDNF also caused an increase in the number and the size of synaptic vesicle clustering, as demonstrated by synaptobrevin-GFP fluorescent imaging, and FM dye staining. Electrophysiological experiments revealed two effects of GDNF on synaptic transmission at NMJ. First, GDN-F markedly increased the frequency of spontaneous transmission and decreased the variability of evoked transmission, suggesting an enhancement of transmitter secretion. Second, GDNF elicited a small increase in the quantal size, without affecting the average rise and decay times of synaptic currents. Imaging analysis showed that the size of acetylcholine receptor clusters at synapses increased in muscle cells overexpressing GDNF. Neurturin had very similar effects as GDNF. These results suggest that GDNF and NRTN are new neuromodulators that regulate the development of the neuromuscular synapse through both pre- and postsynaptic mechanisms. C1 NICHHD, NIH, Unit Synapse Dev & Plast, Washington, DC 20052 USA. George Washington Univ, Grad Program Genet, Washington, DC 20052 USA. NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. Chinese Acad Sci, Inst Neurosci, Shanghai 200031, Peoples R China. RP Lu, B (reprint author), NICHHD, NIH, Unit Synapse Dev & Plast, Bldg 49,Rm 6A-80,49 Convent Dr,MSC4480, Washington, DC 20052 USA. RI Yang, Feng/C-9530-2011; Lu, Bai/A-4018-2012; OI Je, hyunsoo/0000-0002-2924-5621 NR 69 TC 54 Z9 57 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 22 PY 2002 VL 277 IS 12 BP 10614 EP 10625 DI 10.1074/jbc.M106116200 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 533UR UT WOS:000174549200132 PM 11790765 ER PT J AU Li, XM Yang, YL Ashwell, JD AF Li, XM Yang, YL Ashwell, JD TI TNF-RII and c-IAP1 mediate ubiquitination and degradation of TRAF2 SO NATURE LA English DT Article ID TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; CELL-DEATH; SIGNALING COMPLEX; PROTEIN LIGASE; APOPTOSIS; ACTIVATION; RECEPTOR; MICE; SENSITIVITY AB Tumour necrosis factor-alpha (TNF-alpha) is a proinflammatory mediator that exerts its biological functions by binding two TNF receptors (TNF-RI and TNF-RII), which initiate biological responses by interacting with adaptor and signalling proteins. Among the signalling components that associate with TNF receptors are members of the TNF-R-associated factor (TRAF) family(1,2). TRAF2 is required for TNF-alpha-mediated activation of c-Jun N-terminal kinase (JNK), contributes to activation of NF-kappaB, and mediates anti- apoptotic signals(3,4). TNF-RI and TNF-RII signalling complexes also contain the anti- apoptotic ('inhibitor of apoptosis') molecules c-IAP1 and c-IAP2 (refs 5, 6), which also have RING domain-dependent ubiquitin protein ligase (E3) activity(7). The function of IAPs in TNF-R signalling is unknown. Here we show that binding of TNF-alpha to TNF-RII induces ubiquitination and proteasomal degradation of TRAF2. Although c-IAP1 bound TRAF2 and TRAF1 in vitro, it ubiquitinated only TRAF2. Expression of wild-type c-IAP1, but not an E3-defective mutant, resulted in TRAF2 ubiquitination and degradation. Moreover, E3-defective c-IAP1 prevented TNF-alpha-induced TRAF2 degradation and inhibited apoptosis. These findings identify a physiologic role for c-IAP1 and define a mechanism by which TNF-RII-regulated ubiquitin protein ligase activity can potentiate TNF-induced apoptosis. C1 NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA. RP Ashwell, JD (reprint author), NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA. NR 30 TC 314 Z9 328 U1 1 U2 8 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD MAR 21 PY 2002 VL 416 IS 6878 BP 345 EP 349 DI 10.1038/416345a PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 532NP UT WOS:000174482200049 PM 11907583 ER PT J AU Ashcroft, M Ludwig, RL Woods, DB Copeland, TD Weber, HO MacRae, EJ Vousden, KH AF Ashcroft, M Ludwig, RL Woods, DB Copeland, TD Weber, HO MacRae, EJ Vousden, KH TI Phosphorylation of HDM2 by Akt SO ONCOGENE LA English DT Article DE HDM2; Akt; P53; phosphorylation ID NUCLEOLAR-LOCALIZATION; MDM2 ONCOPROTEIN; P53; PROTEIN; IDENTIFICATION; KINASE; INDUCTION; ACTIVATION; SURVIVAL; PREVENTS AB The HDM2 protein is a key regulator of the tumour suppressor, p53. Control of HDM2 function is critical for normal cell proliferation and stress responses, and it is becoming evident that multiple modifications of HDM2 can regulate its function within cells. In this study we show that HDM2 associated with the serinethreonine kinase, Akt, in response to growth factor stimulation of human primary cells. This association was concurrent with phosphorylation of Akt (at Ser 473), and resulted in elevated expression of HDM2 and enhanced nuclear localization. However, analysis of HDM2 proteins mutated at the consensus Akt recognition sites at serines 166 and 186 indicated that modification at these residues was not sufficient for the increased expression of the protein, which was blocked by the PI3 kinase inhibitor LY294002. Tryptic peptide and mutational analyses revealed evidence for an Akt phosphorylation site in HDM2 additional to the two consensus sites. C1 NCI, FCRDC, Regulat Cell Growth Lab, Frederick, MD 21702 USA. Inst Canc Res, CRC, Ctr Canc Therapeut, Sutton SM2 5NG, Surrey, England. RP Vousden, KH (reprint author), NCI, FCRDC, Regulat Cell Growth Lab, Frederick, MD 21702 USA. NR 37 TC 142 Z9 145 U1 0 U2 3 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 21 PY 2002 VL 21 IS 13 BP 1955 EP 1962 DI 10.1038/sj/onc/1205276 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 538QR UT WOS:000174827000002 PM 11960368 ER PT J AU Arikawa-Hirasawa, E Rossi, SG Rotundo, RL Yamada, Y AF Arikawa-Hirasawa, E Rossi, SG Rotundo, RL Yamada, Y TI Perlecan is essential for localizing AChE to the neuromuscular junction SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDCR, CDBRB, NIH, Bethesda, MD 20892 USA. Univ Miami, Sch Med, Dept Cell Biol & Anat, Miami, FL 33136 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A545 EP A545 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603028 ER PT J AU Aslamkhan, AG Han, YH Zalups, RK Pritchard, JB AF Aslamkhan, AG Han, YH Zalups, RK Pritchard, JB TI Role of the human organic anion transporter subtype 1 (hOAT1) in uptake and toxicity of mercuric thiol conjugates SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharm & Chem, Res Triangle Pk, NC 27709 USA. Mercer Univ, Div Basic Med Sci, Macon, GA 31207 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A459 EP A459 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602543 ER PT J AU Baer, DJ Judd, JT Tracy, R Campbell, WS Brown, E Taylor, PR AF Baer, DJ Judd, JT Tracy, R Campbell, WS Brown, E Taylor, PR TI Antinflammatory and profibrinolytic effects of moderate alcohol consumption by postmenopausal women SO FASEB JOURNAL LA English DT Meeting Abstract C1 USDA ARS, Beltsville Human Nutr Res Ctr, Beltsville, MD USA. Univ Vermont, Colchester, VT USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A239 EP A239 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601327 ER PT J AU Baskar, S Kwak, LW AF Baskar, S Kwak, LW TI Immunotherapy of human follicular lymphoma: Delineation of T cell epitopes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, SAIC Frederick Inc, IRSP, Exptl Transplantat & Immunol, Ft Detrick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A333 EP A333 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601841 ER PT J AU Basu, NK Kole, L Ciotti, M Owens, IS AF Basu, NK Kole, L Ciotti, M Owens, IS TI A novel human chemical defense system in the gastrointestinal tract regulated by PKC mediated phosphorylation and dietary constituents. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. NICHHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A157 EP A157 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600871 ER PT J AU Biragyn, A Ruffini, PA Yang, D Oppenheim, JJ Kwak, LW AF Biragyn, A Ruffini, PA Yang, D Oppenheim, JJ Kwak, LW TI Chemokine receptor mediated targeting of antigen presenting cells with non-immunogenic tumor antigens elicit potent antitumor immunity in vivo: inflammatory chemokines vs. homeostatic chemo-attractants. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Vaccine Res Sect, Expt Transplantat & Immunol Branch, NIH, Frederick, MD 21702 USA. SAIC Frederick, Mol Immunoregulat Lab, Frederick, MD USA. NCI, Mol Immunoregulat Lab, NIH, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A335 EP A335 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601853 ER PT J AU Bitmansour, AD Pitcher, C Douek, DC Maino, VC Picker, LJ AF Bitmansour, AD Pitcher, C Douek, DC Maino, VC Picker, LJ TI Direct ex vivo analysis of human CD4+memory T cell activation requirements at the single clonotype level SO FASEB JOURNAL LA English DT Meeting Abstract C1 Oregon Hlth Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR 97006 USA. NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. Becton Dickinson Immunocytometry Syst, Biosci, San Jose, CA 95131 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A300 EP A300 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601658 ER PT J AU Bleasby, K Breen, CM Pritchard, JB AF Bleasby, K Breen, CM Pritchard, JB TI Cysteine residues in the 1st extracellular loop of the human organic cation transporter hOCT2 are important for membrane localisation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A459 EP A459 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602541 ER PT J AU Borrego, F Kabat, J Sanni, T Coligan, JE AF Borrego, F Kabat, J Sanni, T Coligan, JE TI CD94/NKG2A recycling and transmission of the inhibitory signal are independent processes. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A320 EP A320 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601770 ER PT J AU Bourgeois, C Okazaki, I Cavanaugh, E Nightingale, M Moss, J AF Bourgeois, C Okazaki, I Cavanaugh, E Nightingale, M Moss, J TI Organization of genes for human and mouse mono-ADP-ribosyltransferases. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A550 EP A550 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603056 ER PT J AU Bradbury, JA Athirakul, K Ma, JX Graves, J Miller, L DeGraff, J Quigley, R Coffman, TM Zeldin, DC AF Bradbury, JA Athirakul, K Ma, JX Graves, J Miller, L DeGraff, J Quigley, R Coffman, TM Zeldin, DC TI Targeted disruption of the Cyp2j5 gene causes hypertension and increased proximal tubular transport in mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Duke Univ, Durham, NC 27706 USA. SW Texas State Univ, Dallas, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A146 EP A147 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600812 ER PT J AU Breen, CM Sykes, DB Miller, DS AF Breen, CM Sykes, DB Miller, DS TI Hormonal stimulation of transepithelial organic anion transport in rat choroid plexus (CP) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A461 EP A461 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602555 ER PT J AU Brooks, HL Ageloff, S Terris, J Kwon, TH Michea, L Nielsen, S Knepper, MA AF Brooks, HL Ageloff, S Terris, J Kwon, TH Michea, L Nielsen, S Knepper, MA TI cDNA array analysis identifies vasopressin regulation of 11 beta HSD-2 in rat renal collecting duct SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Arizona, Coll Med, Dept Physiol, Tucson, AZ 85724 USA. NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. Univ Aarhus, Inst Anat, Water & Salt Res Ctr, Aarhus, Denmark. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A416 EP A416 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602304 ER PT J AU Broussard, C Fleischecker, C Chetana, M Mijares, L Lewis, CM Fowlkes, BJ Schwartzberg, P AF Broussard, C Fleischecker, C Chetana, M Mijares, L Lewis, CM Fowlkes, BJ Schwartzberg, P TI Deficiency of the Tec family kinases leads to altered lineage development SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ La Verne, Dept Biol, Verne, CA 91750 USA. NIAID, Cellular & Mol Immunol Lab, Bethesda, MD 20892 USA. NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A696 EP A696 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603864 ER PT J AU Carey, MA Bradbury, JA Gooch, RA Moorman, MP Price, HC Colegrove, CL Rydell, P Langenbach, R Germolec, DR Zeldin, DC AF Carey, MA Bradbury, JA Gooch, RA Moorman, MP Price, HC Colegrove, CL Rydell, P Langenbach, R Germolec, DR Zeldin, DC TI Role of COX-1 and COX-2 in lymphocyte recruitment, cytokine production and lung function in allergic mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A675 EP A676 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603751 ER PT J AU Chattopadhyay, MK Tabor, CW Tabor, H AF Chattopadhyay, MK Tabor, CW Tabor, H TI Absolute requirement of spermidine for growth and S-phase progression in fission yeast SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, Biochem Genet Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A525 EP A525 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602912 ER PT J AU Chay, KO Park, SS Mushinski, JF AF Chay, KO Park, SS Mushinski, JF TI Caspase-mediated degradation of paxillin during apoptosis of Ba/F3 murine pro-B cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A140 EP A141 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600778 ER PT J AU Cherukuri, A Carter, R Levy, S Shoham, T Pierce, SK AF Cherukuri, A Carter, R Levy, S Shoham, T Pierce, SK TI The tetraspanin CD81 regulates the functions of the CD19/CD21 complex from lipid rafts SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, NIH, Rockville, MD 20852 USA. Univ Alabama, Dept Med & Microbiol, Birmingham, AL USA. Stanford Univ, Med Ctr, Dept Med, Stanford, CA 94305 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A715 EP A715 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603970 ER PT J AU Cho, H Kozasa, T Kehrl, JH AF Cho, H Kozasa, T Kehrl, JH TI Developmentally timed expression of RGS5 in blood vessels and RGS5-mediated inhibition of angiotensin II- and endothelin-1 signaling SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Immunoregulat Lab, Bethesda, MD 20892 USA. Univ Illinois, Chicago, IL 60680 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A577 EP A578 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603210 ER PT J AU Choi, CY Kim, YO Park, SJ Kim, Y AF Choi, CY Kim, YO Park, SJ Kim, Y TI Phosphorylation of Groucho by DHIPK2 modulates the corepressor activity of Groucho SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A134 EP A134 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600741 ER PT J AU Choi, WS Kim, YM Comb, C Frohman, MA Beaven, MA AF Choi, WS Kim, YM Comb, C Frohman, MA Beaven, MA TI Phospholipase D1 and D2 regulate different phases of exocytosis in mast cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. Duksung Womens Univ, Coll Pharm, Tobong Gu, Seoul, South Korea. NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA. SUNY Stony Brook, Dept Pharmacol, Stony Brook, NY 11794 USA. SUNY Stony Brook, Ctr Dev Genet, Stony Brook, NY 11794 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A716 EP A717 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603979 ER PT J AU Coligan, JE Borrego, F Brooks, A Kabat, J AF Coligan, JE Borrego, F Brooks, A Kabat, J TI Role that each CD94/NKG2A ITIM motif plays in inhibition of activation signals SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A313 EP A313 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601733 ER PT J AU Corwin, RL Hartman, TJ Maczuga, SA Graubard, BI AF Corwin, RL Hartman, TJ Maczuga, SA Graubard, BI TI Fat intake and bone health in NHANES III. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Penn State Univ, Dept Nutr, University Pk, PA 16802 USA. Penn State Univ, Populat Res Inst, University Pk, PA 16802 USA. NCI, Biostat Branch, DCEG, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 3 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A625 EP A625 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603474 ER PT J AU Cowdery, JS Schroeder, AJ Morse, HC Vogel, SN Bradford, MA AF Cowdery, JS Schroeder, AJ Morse, HC Vogel, SN Bradford, MA TI CpG DNA induces IL-12 p40 gene activation independent of STAT1 activation or production of interferon consensus sequence binding protein (ICSBP). SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Iowa, Coll Med, Dept IM, Iowa City, IA 52246 USA. DVAMC, Iowa City, IA USA. NIAID, NIH, Bethesda, MD 20892 USA. USUHS, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A322 EP A322 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601779 ER PT J AU d'Uscio, LV Milstien, S Katusic, ZS AF d'Uscio, LV Milstien, S Katusic, ZS TI Increased vascular tetrahydrobiopterin production and inducible nitric oxide synthase (iNOS) activity in aortas of apolipoprotein E-deficient mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 Mayo Clin, Rochester, MN 55905 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A434 EP A434 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602405 ER PT J AU Damiani, CL Westin, EH Gibson, LF Piktel, DA Landreth, KS AF Damiani, CL Westin, EH Gibson, LF Piktel, DA Landreth, KS TI C-myb regulates pro-B cell proliferation and differentiation SO FASEB JOURNAL LA English DT Meeting Abstract C1 W Virginia Univ, Dept Microbiol Immunol & Cell Biol, Robert C Byrd Hlth Sci Ctr, Morgantown, WV 26506 USA. NIA, NIH, Baltimore, MD 21224 USA. W Virginia Univ, Dept Pediat, Morgantown, WV 26506 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A351 EP A351 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601942 ER PT J AU Dombrowski, DG Takesono, A Caplen, N Schwartzberg, P AF Dombrowski, DG Takesono, A Caplen, N Schwartzberg, P TI Short interference RNA reduces gene expression and activation in Jurkat T cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHGRI, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A321 EP A321 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601773 ER PT J AU Fan, T Yan, QS Austin, S Ferris, DK Muegge, K AF Fan, T Yan, QS Austin, S Ferris, DK Muegge, K TI Growth defect on Lsh deleted primary embryonal fibroblasts SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, LMI, Frederick, MD 21701 USA. NCI, LLB, Frederick, MD 21701 USA. NCI, SAIC Frederick, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A151 EP A151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600840 ER PT J AU Ferraris, JD Williams, CK Persaud, P Zhang, Z Burg, MB AF Ferraris, JD Williams, CK Persaud, P Zhang, Z Burg, MB TI The TonEBP/OREBP transactivation domain is regulated by hypertonicity-dependent phosphorylation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A56 EP A56 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600314 ER PT J AU Foucras, GJL Diflippantonio, M Ried, T Ben-Sasson, SZ Paul, WE AF Foucras, GJL Diflippantonio, M Ried, T Ben-Sasson, SZ Paul, WE TI Development of a set of cytochrome C/I-E-k-specific T lymphomas SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, Bethesda, MD 20892 USA. NCI, Genet Branch, NIH, Bethesda, MD 20892 USA. Hebrew Univ Jerusalem, Jerusalem, Israel. Hadassah Med Ctr, IL-91120 Jerusalem, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A339 EP A339 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601872 ER PT J AU Fuda, H Lee, YC Shimizu, C Javitt, NB Strott, CA AF Fuda, H Lee, YC Shimizu, C Javitt, NB Strott, CA TI Cholesterol/oxysterol sulfotransferase (SULT2B1): Functional and structural characterization. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, ERRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A535 EP A535 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602972 ER PT J AU Gao, ZG Jacobson, KA AF Gao, ZG Jacobson, KA TI Allosteric modulation of adenosine receptors SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, MRS, LBC, Bethesda, MD 20892 USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A576 EP A576 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603202 ER PT J AU Gavins, FNE Gao, JL Murphy, PM Tailor, A Granger, DN Flower, RJ Perretti, M AF Gavins, FNE Gao, JL Murphy, PM Tailor, A Granger, DN Flower, RJ Perretti, M TI Annexin 1 peptide inhibits ischaemia reperfusion (IR)-induced leukocyte adhesion and emigration: Receptors involved SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ London St Bartholomews Hosp Med Coll, Coll Med, William Harvey Res Inst, London EC1M 6BQ, England. NIAID, Host Def Lab, Bethesda, MD 20892 USA. Louisiana State Univ, Hlth Sci Ctr, Shreveport, LA 71105 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A598 EP A599 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603328 ER PT J AU Ge, H Chuang, E Zhao, SP Temenak, JJ Ching, WM AF Ge, H Chuang, E Zhao, SP Temenak, JJ Ching, WM TI Comparative genomics of Rickettsia prowazekii strains of Madrid E and Breinl by DNA microarray SO FASEB JOURNAL LA English DT Meeting Abstract C1 NMRC, Silver Spring, MD USA. NCI, NIH, Gaithersburg, MD USA. US FDA, CBER, Rockville, MD 20857 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A531 EP A531 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602945 ER PT J AU Goldstein, DS Brentzel, S Dendi, R AF Goldstein, DS Brentzel, S Dendi, R TI Clinical comparison of neturocardiogenic syncope with postural tachycardia syndrome SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A117 EP A117 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600648 ER PT J AU Goldstein, DS Dendi, R Holmes, C AF Goldstein, DS Dendi, R Holmes, C TI Plasma catecholamines in neurocardiogenic syncope and postural tachycardia syndrome SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A117 EP A117 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600647 ER PT J AU Grabowski, KA Coleman, J Espiritu, B Paul, WE Xia, W Clancy, J Huang, H AF Grabowski, KA Coleman, J Espiritu, B Paul, WE Xia, W Clancy, J Huang, H TI Accumulation of robust IL-4 producers in the lung and airway in a murine model of asthma is IL-4 dependent SO FASEB JOURNAL LA English DT Meeting Abstract C1 Loyola Univ, Med Ctr, Dept Med, Maywood, IL 60153 USA. NIAID, NIH, Bethesda, MD 20892 USA. Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A672 EP A672 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603729 ER PT J AU Grammer, AC Heaney, J Hurt, E Staudt, LM Lipsky, PE AF Grammer, AC Heaney, J Hurt, E Staudt, LM Lipsky, PE TI Relationship between the degree of CD40 receptor occupancy on human B cells, activation of signaling pathways and expression of genes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMS, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. NCI, Metab Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A705 EP A705 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603916 ER PT J AU Graves, JP Stumpo, D Tuttle, J Bradbury, JA Miller, L DeGraff, J Blackshear, PJ Zeldin, DC AF Graves, JP Stumpo, D Tuttle, J Bradbury, JA Miller, L DeGraff, J Blackshear, PJ Zeldin, DC TI Identification by insertional mutagenesis of a genomic locus important for the development of the subcommissural organ and congenital hydrocephalus in mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A529 EP A529 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602936 ER PT J AU Greenwell-Wild, T Vazquez-Maldonado, N Peng, G Lei, KJ Jin, WW Orenstein, JM Wahl, SM AF Greenwell-Wild, T Vazquez-Maldonado, N Peng, G Lei, KJ Jin, WW Orenstein, JM Wahl, SM TI Mycobacterium avium inhibition of IL-1 beta in evasion of host defense SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDCR, OIIB, NIH, Bethesda, MD 20892 USA. George Washington Univ, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A305 EP A305 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601687 ER PT J AU Hansen, PB Huang, Y Yang, T Mizel, D Briggs, J Schnermann, J AF Hansen, PB Huang, Y Yang, T Mizel, D Briggs, J Schnermann, J TI Plasma renin activity in adenosine 1 receptor deficient mice: Effect of salt intake and genetic background. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A475 EP A475 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602635 ER PT J AU Hashimoto, S Huang, YN Briggs, JP Schnermann, JB AF Hashimoto, S Huang, YN Briggs, JP Schnermann, JB TI Impaired autoregulation of glomerular filtration rate (GFR) in adenosine 1 receptor-deficient mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A475 EP A475 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602636 ER PT J AU He, LS Grammer, AC Lipsky, PE Lipsky, PE Lipsky, PE AF He, LS Grammer, AC Lipsky, PE Lipsky, PE Lipsky, PE TI Determination of the capacity of TNF receptor associated factor (TRAF)-2 to form hetero- and homo-dimers by fluorscence resonance energy transfer. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMS, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A314 EP A314 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601736 ER PT J AU Jackson, SH Devadas, S Kwon, J Alicea, C Williams, MS AF Jackson, SH Devadas, S Kwon, J Alicea, C Williams, MS TI T cells express an NAD(P)H oxidase that contributes to TcR stimulated generation of reactive oxygen species. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. Amer Red Cross, Holland Lab, Dept Immunol, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A315 EP A316 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601743 ER PT J AU Jennings, NE Lipsky, PE Vazquez, E Fischer, RT Grammer, AC AF Jennings, NE Lipsky, PE Vazquez, E Fischer, RT Grammer, AC TI Engagement of CD154 expressed by human tonsillar B cells induces proximal signaling events and differentiation to immunoglobulin secreting plasma cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMS, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A705 EP A705 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603915 ER PT J AU Johnson, AC Nishi, KH Wilson, MA Nishi, H AF Johnson, AC Nishi, KH Wilson, MA Nishi, H TI Early growth response gene-1 expression induces epidermal growth factor receptor expression during hypoxia SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A63 EP A63 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600352 ER PT J AU Johnson, JD Hess, KL Cook-Mills, JM AF Johnson, JD Hess, KL Cook-Mills, JM TI WEHI-231 apoptotic cell membrane changes that are recognized by the fucoidin receptor do not require protein synthesis SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Cincinnati, Cincinnati, OH 45267 USA. NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A349 EP A349 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601931 ER PT J AU Ju, C Harvey, JD Pohl, LR AF Ju, C Harvey, JD Pohl, LR TI Role of Kupffer cells in the mechanism of tolerance to hapten-protein adducts SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, LMI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A715 EP A715 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603968 ER PT J AU Jutkiewiez, EM Rice, KC Traynor, JR Woods, JH AF Jutkiewiez, EM Rice, KC Traynor, JR Woods, JH TI Differential tolerance to the behavioral effects of SNC80 in rats SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA. NIDDK, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A582 EP A582 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603238 ER PT J AU Katz, JL Chausmer, AL Elmer, GI Low, MJ Rubinstein, M Grandy, DK AF Katz, JL Chausmer, AL Elmer, GI Low, MJ Rubinstein, M Grandy, DK TI Cocaine-induced locomotor activity and cocaine discrimination in dopamine D2 receptor mutant mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 Natl Inst Drug Abuse, Psychobiol Lab, Baltimore, MD 21224 USA. Univ Maryland, Maryland Psychiat Res Ctr, Catonsville, MD 21228 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A194 EP A195 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601084 ER PT J AU Kelly, JA Spolski, R Bollenbacher, J Leonard, WJ AF Kelly, JA Spolski, R Bollenbacher, J Leonard, WJ TI Stat5: Role in CD8+T-cell homeostatsis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, LMI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A330 EP A330 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601826 ER PT J AU Khaled, AR Durum, S AF Khaled, AR Durum, S TI Loss of trophic factor signaling during thymocyte development: On the pathway to death through intracellular alkalinization and Bax activation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A341 EP A341 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601885 ER PT J AU Kim, DK Borrego, F Lieto, L Coligan, JE AF Kim, DK Borrego, F Lieto, L Coligan, JE TI Characterization of the human NKG2A promoter SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A694 EP A694 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603854 ER PT J AU Kipnis, V Subar, A Midthune, D Freedman, L Ballard-Barbash, R Troiano, R Bingham, S Schoeller, D Schatzkin, A Carroll, R AF Kipnis, V Subar, A Midthune, D Freedman, L Ballard-Barbash, R Troiano, R Bingham, S Schoeller, D Schatzkin, A Carroll, R TI Dietary measurement error and its implications: Results of the OPEN biomarker study SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. Bar Ilan Univ, Ramat Gan, Israel. MRC, Dunn Nutr Unit, Cambridge CB4 1XJ, England. Univ Wisconsin, Madison, WI 53706 USA. Texas A&M Univ, College Stn, TX 77843 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A27 EP A27 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600148 ER PT J AU Kole, HK Naramura, M Haines, D Jang, IK Gu, H AF Kole, HK Naramura, M Haines, D Jang, IK Gu, H TI Sustained TCR signaling and severe polyarteritis in mice with c-Cbl/Cbl-b double deficient T cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, NIH, Rockville, MD 20852 USA. Cleveland Clin Fdn, Dept Immunol, Cleveland, OH 44195 USA. NCI, Frederick Canc Res & Dev Ctr, PHL SAIC Frederick, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A697 EP A697 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603868 ER PT J AU Kostic, T Tomic, M Stojilkovic, S AF Kostic, T Tomic, M Stojilkovic, S TI Calcium-independent stimulation of cGMP production by Gs protein-coupled receptors in pituitary cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, ERRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A556 EP A556 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603090 ER PT J AU Leak, LV Petricoin, EF Liotta, LA Jones, M Krutzell, H AF Leak, LV Petricoin, EF Liotta, LA Jones, M Krutzell, H TI Lymphatic endothelium: Protein profiles during quiescence and proliferation SO FASEB JOURNAL LA English DT Meeting Abstract C1 Howard Univ, Washington, DC 20059 USA. US FDA, Div Therapeut Prod, Bethesda, MD 20014 USA. NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. NHLBI, Lab Anim Med & Surg, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A514 EP A514 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602849 ER PT J AU Lee, JH Wu, T Everett, LA Royaux, IE Green, ED Marcus, DC AF Lee, JH Wu, T Everett, LA Royaux, IE Green, ED Marcus, DC TI PDS gene (Pendrin) knockout abolishes transmural voltage but not potassium secretion in the cochlea SO FASEB JOURNAL LA English DT Meeting Abstract C1 Kansas State Univ, Manhattan, KS 66506 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A425 EP A425 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602353 ER PT J AU Li, J Gorospe, M Hutter, D Barnes, J Keyse, SM Liu, YS AF Li, J Gorospe, M Hutter, D Barnes, J Keyse, SM Liu, YS TI Transcriptional induction of MKP-1 in response to stress is associated with histone H3 phosphorylation/acetylation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. Ninewells Hosp, Imperial Canc Res Fund, Mol Pharmacol Unit, Biomed Res Ctr, Dundee DD1 9SY, Scotland. RI Keyse, Stephen/B-9575-2009 OI Keyse, Stephen/0000-0002-5150-8221 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A168 EP A168 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600933 ER PT J AU Liang, W Hoang, Q Curran, PK Fishman, PH AF Liang, W Hoang, Q Curran, PK Fishman, PH TI Differences in endosomal sorting of human beta(1)- and beta(2)-adrenergic receptors after arrestin- and dynamin-dependent internalization SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS, NIH, LMCN, Membrane Biochem Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A150 EP A150 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600830 ER PT J AU Lippincott-Schwartz, J AF Lippincott-Schwartz, J TI Rapid cycling of lipid raft markers between the cell surface and Golgi apparatus and its role in membrane sorting and polarity. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD 20817 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A725 EP A725 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533604027 ER PT J AU Liu, HG Tang, JR Manganiello, VC AF Liu, HG Tang, JR Manganiello, VC TI Regulation of cyclic nucleotide phosphodiesterase 3B gene expression in mouse 3T3-L1 Adipocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, PCCMB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A8 EP A8 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600046 ER PT J AU Lorenz, MGO Liu, ET Singer, D AF Lorenz, MGO Liu, ET Singer, D TI Gene expression profile of mature B- and T-cells using the ImmunoChip SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Ctr Adv Technol, Gaithersburg, MD 20877 USA. Genome Inst Singapore, Singapore, Singapore. NCI, NIH, Bethesda, MD 20892 USA. RI Liu, Edison/C-4141-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A693 EP A693 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603848 ER PT J AU Lumsden, J Ronchese, F Hodes, R AF Lumsden, J Ronchese, F Hodes, R TI B7 costimulation is differentially required for different aspects of T cell activation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Expt Immunol Branch, Bethesda, MD 20892 USA. Malaghan Inst Med Res, Wellington, New Zealand. RI Lumsden, Joanne/B-6475-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A712 EP A712 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603952 ER PT J AU Maasho, K Borrego, F Lieto, L Coligan, JE AF Maasho, K Borrego, F Lieto, L Coligan, JE TI Defining the regulatory factors required for CD94 gene expression. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A694 EP A694 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603853 ER PT J AU McHugh, RS Shevach, EM AF McHugh, RS Shevach, EM TI Depletion of CD4+CD25+ regulatory T cells is necessary, but not sufficient, for induction of organ-specific autoimmunity SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A688 EP A688 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603819 ER PT J AU Medvedev, AE Lentschat, A Wahl, L Golenbock, DT Vogel, SN AF Medvedev, AE Lentschat, A Wahl, L Golenbock, DT Vogel, SN TI Dysregulated LPS-induced TLR4-MyD88 complex formation and IRAK-1 activation in endotoxin-tolerant human monocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA. Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA. Univ Massachusetts, Sch Med, Div Infect Dis & Immunol, Worcester, MA 01605 USA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A287 EP A287 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601589 ER PT J AU Melsaether, AN Lipsky, P Fischer, R Grammer, A AF Melsaether, AN Lipsky, P Fischer, R Grammer, A TI Signaling through sIg and CD40 affects the array of TNF-receptor associated factor (TRAF) family members expressed by human B cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMSD, Autoimmun Branch, NIH, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A705 EP A705 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603914 ER PT J AU Mi, QS Meagher, C Nagel, J Zucker, P Taub, DD Delovitch, TL AF Mi, QS Meagher, C Nagel, J Zucker, P Taub, DD Delovitch, TL TI Gene expression profiling of pancreatic islets during the pathogenesis of type 1 diabetes in NOD mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 John P Robarts Res Inst, London, ON N6G 2V4, Canada. NIA, Immunol Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A329 EP A329 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601820 ER PT J AU Miller, DS Sykes, DB Breen, CM AF Miller, DS Sykes, DB Breen, CM TI Confocal imaging of fluorescein-methotrexate (FL-MTX) transport across intact, isolated rat choroid plexus (CP) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A461 EP A461 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602554 ER PT J AU Min, B Foucras, G Sempowski, G Paul, WE AF Min, B Foucras, G Sempowski, G Paul, WE TI Neonates support "homeostatic" T cell proliferation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, NCI, Bethesda, MD 20892 USA. Duke Univ, Dept Med, Durham, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A341 EP A341 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601887 ER PT J AU Moustafa, ME Carlson, BA El-Saadani, MA Rao, M Feigenbaum, L Hatfield, DL AF Moustafa, ME Carlson, BA El-Saadani, MA Rao, M Feigenbaum, L Hatfield, DL TI Selenocysteine (Sec) tRNA ([Ser]Sec) and selenoprotein levels in transgenic mice expressing See tRNA ([Ser]Sec) with a mutation in the wobble position. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, BRL, CCR, NIH, Bethesda, MD 20892 USA. Univ Alexandria, Fac Sci, Alexandria, Egypt. FCRDC, SAIC, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A605 EP A605 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603364 ER PT J AU Munitic, I D'Oro, U Chacko, G Karpova, T McNally, J Ashwell, JD AF Munitic, I D'Oro, U Chacko, G Karpova, T McNally, J Ashwell, JD TI Enhanced rates of constitutive TCR cycling in zeta-deficient cells: Implications for control of surface receptor levels SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Lab Immune Cell Biol, Bethesda, MD 20892 USA. Chiron SpA, Siena, Italy. NIH, Bethesda, MD 20892 USA. RI Chacko, George/I-4945-2014 OI Chacko, George/0000-0002-2127-1892 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A718 EP A718 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603988 ER PT J AU Murphy, MA Berg, SC Lane, HC Imamichi, T AF Murphy, MA Berg, SC Lane, HC Imamichi, T TI Cell cycle synchronization reagents, actinomycin D (ActD) and Aphidicolin (Aph) induce a high level of thymidine analogue resistance in HIV-1 replication. SO FASEB JOURNAL LA English DT Meeting Abstract C1 SAIC Frederick Inc, Mol Retrovirol Lab, Frederick, MD 21702 USA. NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A296 EP A296 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601638 ER PT J AU Nagineni, C Samuel, W Nagineni, S Pardhasaradhi, K Wiggert, B Detrick, B Hooks, J AF Nagineni, C Samuel, W Nagineni, S Pardhasaradhi, K Wiggert, B Detrick, B Hooks, J TI TGF-beta is a potent inducer of VEGF expression in human retinal pigment epithelial cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI, NIH, Immunol Lab, Bethesda, MD 20892 USA. WRAIR, Washington, DC USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A152 EP A152 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600845 ER PT J AU Paliege, A Huang, YN Mizel, D Yang, TX Bachmann, S Briggs, JP Schnermann, JB AF Paliege, A Huang, YN Mizel, D Yang, TX Bachmann, S Briggs, JP Schnermann, JB TI Effect of the specific NADPH oxidase blocker apocynin on blood pressure and juxtaglomerular protein expression in spontaneously hypertensive rats SO FASEB JOURNAL LA English DT Meeting Abstract C1 Charite, Dept Anat, D-13353 Berlin, Germany. NIDDK, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A431 EP A431 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602391 ER PT J AU Piccirillo, CA Mamura, M Thornton, AM Mizuhara, H Letterio, JJ Shevach, EM AF Piccirillo, CA Mamura, M Thornton, AM Mizuhara, H Letterio, JJ Shevach, EM TI CD4+CD25+-mediated suppression of T cell activation in vitro is independent of TGF-beta 1 production and signalling. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A716 EP A716 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603976 ER PT J AU Pratt, CA Basiotis, P AF Pratt, CA Basiotis, P TI Predictors of diet quality between obese and normal weight individuals with or without hypertension SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, DECA, Bethesda, MD 20892 USA. USDA, Ctr Nutr Policy, Alexandria, VA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A638 EP A638 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603545 ER PT J AU Preasch, PC Chin, J Norvell, JC AF Preasch, PC Chin, J Norvell, JC TI Structural biology of membrane proteins program reannounced SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIGMS, Pharmacol Physiol & Biol Chem Div, Bethesda, MD 20892 USA. NIGMS, Div Cell Biol & Biophys, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A155 EP A156 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600864 ER PT J AU Rao, MS Cai, JL AF Rao, MS Cai, JL TI Properties of neural precursor SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, Neurosci Lab, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A29 EP A29 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600158 ER PT J AU Sayers, TJ Brooks, AD Seki, N Raziuddin, A Ma, WH Blazar, B Elliott, PJ Murphy, WJ AF Sayers, TJ Brooks, AD Seki, N Raziuddin, A Ma, WH Blazar, B Elliott, PJ Murphy, WJ TI The proteasome inhibitor PS-341 sensitizes tumor cells to TRAIL-mediated lysis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, SAIC Frederick, Frederick, MD 21702 USA. NCI, LEI, Frederick, MD 21702 USA. Univ Minnesota, Minneapolis, MN 55455 USA. Millennium Pharmaceut, Cambridge, MA USA. RI Sayers, Thomas/G-4859-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A669 EP A669 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603714 ER PT J AU Schindler, CW Gilman, JP Graczyk, Z Negus, SS Mello, NK Goldberg, SR AF Schindler, CW Gilman, JP Graczyk, Z Negus, SS Mello, NK Goldberg, SR TI Cardiovascular effects of kappa opioid agonists alone and in combination with cocaine in squirrel monkeys. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDA, Intramural Res, NIH, Baltimore, MD 21224 USA. Harvard Univ, McLean Hosp, Sch Med, Belmont, MA 02178 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A584 EP A585 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603251 ER PT J AU Shah, JA Rhee, E Turon, T Davey, D Mendez, S Kirman, J Wu, CY Sacks, DL Seder, RA AF Shah, JA Rhee, E Turon, T Davey, D Mendez, S Kirman, J Wu, CY Sacks, DL Seder, RA TI Vaccination with leishmanial antigen and CpG oligodeoxynucleotides confers long-term protection against Leishmania major infection. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, NIH, Vaccine Res Ctr, Cellular Immunol Sect, Bethesda, MD 20814 USA. NIAID, NIH, Parasit Dis Lab, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A307 EP A307 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601698 ER PT J AU Sharpe, JC Youle, R AF Sharpe, JC Youle, R TI A study of the pro-apoptotic protein Bax in the presence of lipids SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS, NIH, Surg Neurol Branch, Biochem Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A142 EP A142 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600788 ER PT J AU Stolzenberg-Solomon, RZ Pietinen, P Taylor, PR Virtamoc, J Albanes, D AF Stolzenberg-Solomon, RZ Pietinen, P Taylor, PR Virtamoc, J Albanes, D TI A prospective study of medical conditions, anthropometrics, and physical activity and pancreatic cancer in male smokers SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA. NCI, Canc Prevent Studies Branch, Div Clin Sci, Rockville, MD 20852 USA. Natl Publ Hlth Inst, Helsinki, Finland. RI Albanes, Demetrius/B-9749-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A248 EP A248 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601371 ER PT J AU Subar, AF Kipnis, V Troiano, RP Midthune, D Schoeller, DA Bingham, S Sharbaugh, C Trabulsi, J Runswick, S Ballard-Barbash, R Schatzkin, A AF Subar, AF Kipnis, V Troiano, RP Midthune, D Schoeller, DA Bingham, S Sharbaugh, C Trabulsi, J Runswick, S Ballard-Barbash, R Schatzkin, A TI Using intake biomarkers to evaluate the extent of dietary misreporting in a large sample of adults: The observing protein and energy nutrition study SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. Univ Wisconsin, Madison, WI 53706 USA. MRC, Dunn Nutr Unit, Cambridge CB4 1XJ, England. WESTAT Corp, Rockville, MD 20850 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A27 EP A27 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600147 ER PT J AU Thornton, AM Piccirillo, C Shevach, EM AF Thornton, AM Piccirillo, C Shevach, EM TI Cytokine and costimulatory requirements for induction of CD4+CD25+suppressor effector function SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Immunol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A716 EP A716 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603974 ER PT J AU Tingle, MA AF Tingle, MA TI Instrumentation and emerging technologies: NIH funding opportunities SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Natl Ctr Res Resources, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A17 EP A17 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600094 ER PT J AU Ueda, A Kakizaki, S Negishi, M Sueyoshi, T AF Ueda, A Kakizaki, S Negishi, M Sueyoshi, T TI The residue, threonine 350 confers steroid hormone responsiveness to the mouse nuclear receptor CAR SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A146 EP A146 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600810 ER PT J AU Van den Broeke, LT Daschbach, E Andringa, G Berzofsky, JA AF Van den Broeke, LT Daschbach, E Andringa, G Berzofsky, JA TI Dendritic cell induced activation of innate anti-tumor immunity SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Metab Branch, NIH, Mol Immunogenet & Vaccine Res Sect, Bethesda, MD 20892 USA. NINCDS, NIH, Expt Therapeut Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A338 EP A338 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601869 ER PT J AU Villalobos, ARA Miller, DS Renfro, JL AF Villalobos, ARA Miller, DS Renfro, JL TI Active organic anion (OA) transport across the CSF-blood barrier SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ Rochester, Rochester, NY 14642 USA. NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Univ Connecticut, Storrs, CT 06269 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A462 EP A462 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602558 ER PT J AU Wang, Q Li, CC AF Wang, Q Li, CC TI Functional roles of ATP binding motifs and the second region of homology (SRH) in hexamerization of p97/VCP, an AAA-ATPase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, BRL, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A548 EP A548 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603042 ER PT J AU Weng, N Fann, M AF Weng, N Fann, M TI Gene expression profiles of human naive and memory CD8+T cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A346 EP A346 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601915 ER PT J AU Whittaker, P Dunkel, VC Seifried, HE Clarke, JJ San, RHC AF Whittaker, P Dunkel, VC Seifried, HE Clarke, JJ San, RHC TI Evaluation of iron chelators for assessing the mechanism of genotoxicity of iron compounds. SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA, Washington, DC 20204 USA. NCI, Bethesda, MD 20892 USA. BioReliance, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A271 EP A271 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601501 ER PT J AU Wood, MJ Storz, G AF Wood, MJ Storz, G TI Redox regulation of the yeast transcription factor Yap1p SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A553 EP A553 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603071 ER PT J AU Wu, CY Kirman, J Rotte, M Rhee, EG Davey, D Freidag, B Seder, RA AF Wu, CY Kirman, J Rotte, M Rhee, EG Davey, D Freidag, B Seder, RA TI IL-12 is not essential to sustain memory Th1 cells in vivo. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, Cellular Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A330 EP A330 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533601823 ER PT J AU Yang, HS Merrick, W Sonenberg, N Colburn, N AF Yang, HS Merrick, W Sonenberg, N Colburn, N TI Inhibition of translation by a novel tumor suppressor, Pdcd4 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, NIH, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. McGill Univ, Montreal, PQ H3A 2T5, Canada. RI Yang, Hsin-Sheng/A-6419-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A560 EP A561 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603116 ER PT J AU Yang, TX Mizel, D Pasumarthy, A Briggs, JP Schnermann, JB AF Yang, TX Mizel, D Pasumarthy, A Briggs, JP Schnermann, JB TI Role of reactive oxygen species (ROSs) in the osmotic stimulation of COX-2 expression in mIMCD-K2 cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A57 EP A57 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600318 ER PT J AU Yang, XP Bleasby, K Breen, C Miller, D Pritchard, J AF Yang, XP Bleasby, K Breen, C Miller, D Pritchard, J TI Exploring the structure and function of the human organic anion transporter hOAT1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A458 EP A458 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602537 ER PT J AU Yim, JJ Holland, SM AF Yim, JJ Holland, SM TI Toll-like receptor 2 promoter polymorphisms and susceptibility to nontuberculous mycobacterial disease SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Immunopathogenesis Unit, Host Def Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A719 EP A719 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603991 ER PT J AU Youle, RJ AF Youle, RJ TI Bax, mitochondria and apoptosis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS, SNB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A521 EP A521 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602891 ER PT J AU Youn, YH Feng, J Tessarollo, L Ito, K Sieber-Blum, M AF Youn, YH Feng, J Tessarollo, L Ito, K Sieber-Blum, M TI Cardiac neural crest stem cell defect in TrkC null mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 Med Coll Wisconsin, Milwaukee, WI 53226 USA. NCI, Frederick Canc Res & Dev Ctr, Neural Dev Grp, Frederick, MD USA. Osaka Univ, Dept Biol, Osaka 560, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A29 EP A29 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600161 ER PT J AU Yu, MH Jaradat, SA Grossman, LI AF Yu, MH Jaradat, SA Grossman, LI TI Structural characterization and regulatory element analysis of human cytochrome c oxidase subunit VII heart/muscle isoform (COX7AH) SO FASEB JOURNAL LA English DT Meeting Abstract C1 Wayne State Univ, Sch Med, CMMG, Detroit, MI 48201 USA. NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A8 EP A8 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600042 ER PT J AU Yuan, JH Feng, Y Fisher, R Ferris, DK AF Yuan, JH Feng, Y Fisher, R Ferris, DK TI Polo-like kinase and the mitotic DNA damage checkpoint SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, SAIC Frederick, BRL, IRSP, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A524 EP A524 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533602909 ER PT J AU Zeng, G Robbins, PF Rosenberg, SA AF Zeng, G Robbins, PF Rosenberg, SA TI From candidate antigen to CD4+T cell epitopes: A "reverse immunology" approach to cancer vaccine development SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI, Surg Branch, Bethesda, MD 20892 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A667 EP A668 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603707 ER PT J AU Zhang, X Grammer, AC Lipsky, PE AF Zhang, X Grammer, AC Lipsky, PE TI Signaling pathways mediating CD40 induced NF-kappa B activation in human B lymphocytes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH, Autoimmune Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A705 EP A706 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603917 ER PT J AU Zhao, KJ Liu, H AF Zhao, KJ Liu, H TI Regulation of an interferon target gene by the BAF complex SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI, LMI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A151 EP A151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600837 ER PT J AU Zhong, Z Connor, HD Froh, M Mason, RP Bunzendahl, H Lemasters, JJ Thurman, RG AF Zhong, Z Connor, HD Froh, M Mason, RP Bunzendahl, H Lemasters, JJ Thurman, RG TI Extracts of polyphenols from Camellia sinenesis (green tea) prevent primary graft failure after transplantation of fatty livers SO FASEB JOURNAL LA English DT Meeting Abstract C1 Univ N Carolina, Chapel Hill, NC 27599 USA. NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A602 EP A602 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603347 ER PT J AU Zhu, DM Lipsky, RH Marini, AM AF Zhu, DM Lipsky, RH Marini, AM TI Co-activation of the phosphatidylinositol-3-kinase-/Akt signaling pathway by N-methyl-D-aspartate and TrkB receptors in cerebellar granule cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NIAAA, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A106 EP A106 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533600589 ER PT J AU Zhu, JF Guo, LY Min, B Watson, CJ Hu-Li, J Young, HA Tsichlis, PN Paul, WE AF Zhu, JF Guo, LY Min, B Watson, CJ Hu-Li, J Young, HA Tsichlis, PN Paul, WE TI Growth factor independent-1 (Gfi-1) induced by IL-4 regulates Th2 cell proliferation SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID, LI, NIH, Bethesda, MD 20892 USA. NCI, NIH, Frederick, MD 21701 USA. Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 20 PY 2002 VL 16 IS 4 BP A684 EP A685 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 533MG UT WOS:000174533603801 ER PT J AU Boehm, M Bonifacino, JS AF Boehm, M Bonifacino, JS TI Genetic analyses of adaptin function from yeast to mammals SO GENE LA English DT Review DE AP complex; protein trafficking; clathrin ID POLARIZED EPITHELIAL-CELLS; HERMANSKY-PUDLAK-SYNDROME; NEMATODE CAENORHABDITIS-ELEGANS; PIGMENT GRANULE BIOGENESIS; SYNAPTIC VESICLE FORMATION; CLATHRIN-COATED VESICLES; TRANS-GOLGI NETWORK; AP-3 ADAPTER; PROTEIN COMPLEX; INTRACELLULAR-TRANSPORT AB Adaptor protein (AP) complexes are heterotetrameric assemblies of subunits named adaptins. Four AP complexes, termed AP-1. AP-2, AP-3. and AP-4. hake been described in various eukaryotic organisms. Biochemical and morphological evidence indicates that AP complexes play roles in the formation of vesicular transport intermediates and the selection of cargo molecules for inclusion into these intermediates. This understanding is being expanded by the application of genetic interference procedures. Here,we review recent progress in the genetic analysis of the function of AP complexes. focusing on studies that make use of targeted interference or naturally-occurring mutations in various model organisms. (C) 2002 Elsevier Science B.V. All rights reserved. C1 NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. RP Boehm, M (reprint author), NICHHD, Cell Biol & Metab Branch, NIH, Bldg 18T,Room 101, Bethesda, MD 20892 USA. OI Bonifacino, Juan S./0000-0002-5673-6370 NR 83 TC 103 Z9 106 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD MAR 20 PY 2002 VL 286 IS 2 BP 175 EP 186 AR PII S0378-1119(02)00422-5 DI 10.1016/S0378-1119(02)00422-5 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 545RP UT WOS:000175231600002 PM 11943473 ER PT J AU Kralova, J Czerny, T Spanielova, H Ratajova, V Kozmik, Z AF Kralova, J Czerny, T Spanielova, H Ratajova, V Kozmik, Z TI Complex regulatory element within the gamma E- and gamma F-crystallin enhancers mediates Pax6 regulation and is required for induction by retinoic acid SO GENE LA English DT Article DE paired box; DNA binding; transcription; retinoic acid receptor; lens ID MOUSE LENS DEVELOPMENT; PAIRED DOMAIN; DNA-BINDING; TRANSCRIPTIONAL REGULATION; MURINE GAMMA-2-CRYSTALLIN; GENE-EXPRESSION; 5 MEMBERS; ACTIVATION; PROMOTER; RECEPTORS AB The paired domain, DNA-binding domain of Pax6 and other Pax transcription factors, is composed of two subdomains (PAI and RED). each recognizing distinct half-sites of the bipartite binding site in adjacent major grooves of the DNA helix. The alternatively spliced Pax6(5a) isoform containing 14 extra amino acids within the PAI domain recognizes the 5aCON sequence consisting of four interdigitated 5' half-sites of the bipartite consensus sequence. A genome database search for similar tetrameric Pax6(A) recognition sequences led to the identification of a Pax6-binding site in the lens-specific enhancer of the mouse gammaE- and gammaF-crystallin genes. This binding site combines the properties of bipartite and tetrameric recognition sequences and, by mutational analysis, is shown to mediate Pax6-dependent regulation of the gammaE- and gammaF-crystallin promoter constructs both in primary chicken lens cells and in chicken embryo fibroblasts. The Pax6-binding site is adjacent to a previously identified retinoic acid response element and is itself required for retinoic acid induction of the gammaF- and gammaE-crystallin genes, suggesting that Pax proteins and retinoic acid receptors cooperate in transcriptional regulation. In summary, our protein-DNA binding and transactivation studies suggest that gamma-crystallin genes are under the control of a multifunctional enhancer element that mediates Pax6 regulation as well as retinoic acid-mediated induction. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Inst Mol Genet, Prague 16637 6, Czech Republic. Univ Vet Med, Inst Genet & Anim Breeding, A-1210 Vienna, Austria. Dept Genet & Microbiol, Prague 12844 2, Czech Republic. RP Kozmik, Z (reprint author), NIH, Bldg 6,Room 203, Bethesda, MD 20892 USA. RI Spanielova, Hana/G-8908-2014; Kralova, Jarmila/G-3834-2014; Kozmik, Zbynek/G-3581-2014; Kozmik, Zbynek/I-8807-2014 NR 42 TC 28 Z9 30 U1 2 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD MAR 20 PY 2002 VL 286 IS 2 BP 271 EP 282 AR PII S0378-1119(02)00425-0 DI 10.1016/S0378-1119(02)00425-0 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 545RP UT WOS:000175231600011 PM 11943482 ER PT J AU Moss, J DeCastro, R Taveira-DaSilva, A Patronas, NJ AF Moss, J DeCastro, R Taveira-DaSilva, A Patronas, NJ TI Meningiomas in women with lymphangioleiomyomatosis - Reply SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID BRAIN C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NIH, Dept Diagnost Radiol, Bethesda, MD USA. RP Moss, J (reprint author), NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 20 PY 2002 VL 287 IS 11 BP 1398 EP 1398 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 532GB UT WOS:000174465000015 ER PT J AU Lenders, JWM Pacak, K Walther, MM Linehan, WM Mannelli, M Friberg, P Keiser, HR Goldstein, DS Eisenhofer, G AF Lenders, JWM Pacak, K Walther, MM Linehan, WM Mannelli, M Friberg, P Keiser, HR Goldstein, DS Eisenhofer, G TI Biochemical diagnosis of pheochromocytoma - Which test is best? SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LIQUID-CHROMATOGRAPHY; PLASMA METANEPHRINES; ELECTROCHEMICAL DETECTION; URINARY CATECHOLAMINES; METABOLISM; 3,4-DIHYDROXYPHENYLGLYCOL; NOREPINEPHRINE; CURVES AB Context Diagnosis of pheochromocytoma depends on biochemical evidence of catecholamine production by the tumor. However, the best test to establish the diagnosis has not been determined. Objective To determine the biochemical test or combination of tests that provides the best method for diagnosis of pheochromocytoma. Design, Setting, and Participants Multicenter cohort study of patients tested for pheochromocytoma at 4 referral centers between 1994 and 2001. The analysis included 214 patients in whom the diagnosis of pheochromocytoma was confirmed and 644 patients who were determined to not have the tumor, Main Outcome Measures Test sensitivity and specificity, receiver operating characteristic curves, and positive and negative predictive values at different pretest prevalences using plasma free metanephrines, plasma catecholamines, urinary catecholamines, urinary total and fractionated metanephrines, and urinary vanillylmandelic acid. Results Sensitivities of plasma free metanephrines (99% [95% confidence interval {CI}, 96%-100%]) and urinary fractionated metanephrines (97% [95% CI 92%-99%]) were higher than those for plasma catecholamines (84% [95% CI, 78%-89%]), urinary catecholamines (86% [95% CI, 80%-91%]), urinary total metanephrines (77% [95% CI, 68%-85%]), and urinary vanillylmandelic acid (64% [95% CI, 55%-71%]). Specificity was highest for urinary vanillylmandelic acid (95% [95% CI, 93%-97%]) and urinary total metanephrines (93% [95% CI, 89%-97%]); intermediate for plasma free metanephrines (89% [95% CI, 87%-92%]), urinary catecholamines (88% [95% CI, 85%-91%]), and plasma catecholamines (81% [95% CI, 78%-84%]); and lowest for urinary fractionated metanephrines (69% [95% CI, 64%-72%]). Sensitivity and specificity values at different upper reference limits were highest for plasma free metanephrines using receiver operating characteristic curves. Combining different tests did not improve the diagnostic yield beyond that of a single test of plasma free metanephrines. Conclusion Plasma free metanephrines provide the best test for excluding or confirming pheochromocytoma and should be the test of first choice for diagnosis of the tumor. C1 St Radboud Univ, Dept Internal Med, Med Ctr, NL-6500 HB Nijmegen, Netherlands. Univ Florence, Dept Clin Pathophysiol, Florence, Italy. Sahlgrens Univ Hosp, Dept Clin Physiol, S-41345 Gothenburg, Sweden. NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Hypertens Endocrine Branch, NIH, Bethesda, MD 20892 USA. NINCDS, Clin Neuroendocrinol Sect, NIH, Bethesda, MD 20892 USA. RP Lenders, JWM (reprint author), St Radboud Univ, Dept Internal Med, Med Ctr, Geert Grooteplein Zuid 8,POB 9101, NL-6500 HB Nijmegen, Netherlands. RI Lenders, J.W.M./L-4487-2015; OI Mannelli, Massimo/0000-0002-8001-9857 NR 36 TC 534 Z9 577 U1 2 U2 29 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 20 PY 2002 VL 287 IS 11 BP 1427 EP 1434 DI 10.1001/jama.287.11.1427 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 532GB UT WOS:000174465000025 PM 11903030 ER PT J AU Chou, JJ Kaufman, JD Stahl, SJ Wingfield, PT Bax, A AF Chou, JJ Kaufman, JD Stahl, SJ Wingfield, PT Bax, A TI Micelle-induced curvature in a water-insoluble HIV-1 Env peptide revealed by NMR dipolar coupling measurement in stretched polyacrylamide gel SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID PROTEIN-STRUCTURE DETERMINATION; MEMBRANE-PROTEINS; CYTOPLASMIC TAIL; ALIGNMENT; SEQUENCE; BICELLES C1 NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NIAMDS, Prot Express Lab, NIH, Bethesda, MD 20892 USA. RP Bax, A (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RI Chou, James/N-9840-2013 NR 22 TC 154 Z9 158 U1 1 U2 13 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 20 PY 2002 VL 124 IS 11 BP 2450 EP 2451 DI 10.1021/ja017875d PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA 531UM UT WOS:000174435700029 PM 11890789 ER PT J AU Salton, CJ Chuang, ML O'Donnell, CJ Kupka, MJ Larson, MG Kissinger, KV Edelman, RR Levy, D Manning, WJ AF Salton, CJ Chuang, ML O'Donnell, CJ Kupka, MJ Larson, MG Kissinger, KV Edelman, RR Levy, D Manning, WJ TI Gender differences and normal left ventricular anatomy in an adult population free of hypertension - A cardiovascular magnetic resonance study of the Framingham Heart Study Offspring Cohort SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID BODY-SIZE; 3-DIMENSIONAL ECHOCARDIOGRAPHY; EJECTION FRACTION; SYSTOLIC FUNCTION; MASS; DISEASE; AGE; HYPERTROPHY; VOLUMES; FAILURE AB OBJECTIVES We sought to derive gender-specific cardiovascular magnetic resonance (CMR) reference values for normative left ventricular (LV) anatomy and function in a healthy adult population of clinically relevant age. BACKGROUND Cardiovascular magnetic resonance imaging is increasingly applied in the clinical setting, but age-relevant, gender-specific normative values are currently unavailable. METHODS A representative sample of 318 Framingham Heart Study (FHS) Offspring participants free of clinically overt cardiovascular disease underwent CMR examination to determine LV end-diastolic and end-systolic volume (EDV and ESV, respectively), mass, ejection fraction (EF) and linear dimensions (wall thickness, cavity length). Subjects with a clinical history of hypertension or those with a systolic blood pressure greater than or equal to140 mm Hg or diastolic pressure greater than or equal to90 mm Hg at any FHS cycle examination were excluded, leaving 142 subjects (63 men, 79 women; age 57 +/- 9 years). RESULTS All volumetric (EDV, ESV, mass) and unidimensional measures were significantly greater (p < 0.001) in men than in women and remained greater (p < 0.02) after adjustment for subject height. Volumetric measures were greater (p < 0.001) in men than in women after adjustment for body surface area (BSA), but there were increased linear dimensions in women after adjustment for BSA. In particular, end-diastolic dimension indexed to BSA was greater in women (p < 0.001) than in men. There were no gender differences in global LVEF (men = 0.69; women = 0.70). CONCLUSIONS Cardiovascular magnetic resonance measures of LV volumes, mass and linear dimensions differ significantly according to gender and body size. This study provides gender-specific normal CMR reference values, uniquely derived from a population-based sample of persons free of cardiovascular disease and clinical hypertension. These data may serve as a reference to identify LV pathology in the adult population. (J Am Coll Cardiol 2002;39:1055-60) (C) 2002 by the American College of Cardiology Foundation. C1 Beth Israel Deaconess Med Ctr, Charles A Dana Res Inst, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Med, Div Cardiovasc, Harvard Thorndike Lab, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Med, Dept Radiol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol, Boston, MA USA. NHLBI, Framingham Heart Study, Framingham, MA USA. RP Manning, WJ (reprint author), Beth Israel Deaconess Med Ctr, Charles A Dana Res Inst, 330 Brookline Ave, Boston, MA 02215 USA. FU NHLBI NIH HHS [N01-HC-38038] NR 32 TC 182 Z9 185 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 20 PY 2002 VL 39 IS 6 BP 1055 EP 1060 AR PII S0735-1097(02)01712-6 DI 10.1016/S0735-1097(02)01712-6 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 532CB UT WOS:000174453100020 PM 11897450 ER PT J AU Potosky, AL Reeve, BB Clegg, LX Hoffman, RM Stephenson, RA Albertsen, PC Gilliland, FD Stanford, JL AF Potosky, AL Reeve, BB Clegg, LX Hoffman, RM Stephenson, RA Albertsen, PC Gilliland, FD Stanford, JL TI Quality of life following localized prostate cancer treated initially with androgen deprivation therapy or no therapy SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID OF-LIFE; RADICAL PROSTATECTOMY; HORMONAL-THERAPY; OUTCOMES; MEN; SUPPRESSION; RELIABILITY; STAGE AB Many men diagnosed with clinically localized prostate cancer are initially treated conservatively, receiving neither surgery nor radiotherapy for the first year. Treatment patterns and quality-of-life outcomes have not been previously reported for a population-based sample of such men. Methods: A population-based random sample of men (n = 661) from six geographic regions who had been newly diagnosed with clinically localized prostate cancer from 1994 through 1995 were followed for up to 1 year. Eligible subjects received neither surgery nor radiotherapy within 1 year of initial diagnosis. We assessed disease-specific and generic quality-of-life outcomes in men receiving androgen deprivation therapy (ADT) compared with men receiving no therapy. All statistical tests were two-sided. Results: Two hundred and forty-five study patients received ADT and the remaining 416 patients received no therapy. Approximately two thirds of the patients (n = 159) receiving ADT had either baseline Gleason scores greater than six or serum prostate-specific antigen values above 20 ng/mL. Among men who were sexually potent before diagnosis (ADT = 88 patients; no therapy = 223 patients), 80% of those on ADT reported being impotent after 1 year compared with 30% of those receiving no treatment (P <.001). Patients receiving ADT reported more physical discomfort I year after diagnosis than did men who had received no therapy. However, patients receiving ADT, compared with those receiving no therapy, were more likely to be satisfied with their treatment decision (56% pleased versus 45.3%; P = .001). Patients on ADT also experienced a statistically significant decline in vitality, but not in physical function, after adjustment for the confounding factors (P = .05). Conclusion: ADT is a commonly used primary therapy for clinically localized prostate cancer. Therefore, men considering ADT as an initial treatment should be aware that sexual function and some aspects of physical well-being are likely to be affected in the first year following this treatment. C1 NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA. Univ Connecticut, Ctr Hlth, Div Urol, Dept Surg, Farmington, CT USA. Dept Vet Affairs Med Ctr, Med Serv, Albuquerque, NM USA. RP Potosky, AL (reprint author), NCI, Appl Res Program, Div Canc Control & Populat Sci, EPN Rm 4005,6130 Execut Blvd,MSC 7344, Bethesda, MD 20892 USA. FU NCI NIH HHS [N01 CN 67009, N01 PC 67000, N01 PC 67005, N01 PC 67006, N01 PC 67007, N01 PC 67010] NR 25 TC 110 Z9 112 U1 0 U2 2 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 20 PY 2002 VL 94 IS 6 BP 430 EP 437 PG 8 WC Oncology SC Oncology GA 531VF UT WOS:000174437400009 PM 11904315 ER PT J AU Ostrovsky, MA Sergeev, YV Atkinson, DB Soustov, LV Hejtmancik, JF AF Ostrovsky, MA Sergeev, YV Atkinson, DB Soustov, LV Hejtmancik, JF TI Comparison of ultraviolet induced photo-kinetics for lens-derived and recombinant beta-crystallins SO MOLECULAR VISION LA English DT Article ID DESMIN-RELATED MYOPATHY; ALPHA-B-CRYSTALLIN; X-RAY-ANALYSIS; EYE-LENS; MOLECULAR CHAPERONE; GAMMA-CRYSTALLINS; MISSENSE MUTATION; PROTEIN SOLUTIONS; CATARACT; GENE AB Purpose: The photobiology of purified recombinant crystallins has not been studied. Here we examine photo-induced aggregation of purified recombinant mouse betaA3-crystallin (rbetaA3) and compare it with that of betaL-crystallins isolated from bovine lenses. Methods: rbetaA3-Crystallin was expressed in baculovirus-infected Sf9 cells and purified by ion-exchange and gel-filtration chromatography. Protein solutions (pH 7.4) were irradiated at room temperature using a 308 nm excimer laser and light scattering was registered by attenuation of an unabsorbed beam of red light (670 nm). Results: Irradiation of bovine alpha-crystallin, betaL-crystallin, rbetaA3-crystallin and gammaB-crystallin resulted in formation of insoluble aggregates with subsequent light scattering. Different slopes and threshold energies were observed for light scattering by each of these species. Sensitivity to ultraviolet irradiation induced light scattering as determined from threshold energies varied, with gamma-crystallins showing the greatest sensitivity, the betaL- and rbetaA3-crystallins showing an intermediate sensitivity and alpha-crystallins much less sensitive. Low doses (100 J/cm(2)) resulted in irreversible formation of water soluble oligomers but no insoluble aggregates as indicated by changes in light transmission. The photo-behavior of rbA3 was similar to mixed betaL-crystallin and different from that of alpha- and gamma-crystallins. Conclusions: Ultraviolet induced sensitivity of purified recombinant crystallins reflects that of mixed crystallin populations and should provide an indication of the pathogenicity of specific crystallin sequence changes associated with lens aging and hereditary cataract. C1 Russian Acad Sci, Inst Biochem Phys, Moscow 117334, Russia. NEI, NIH, Bethesda, MD 20892 USA. Portland State Univ, Dept Chem, Portland, OR 97207 USA. Russian Acad Sci, Inst Appl Phys, Nizhnii Novgorod 603600, Russia. RP Ostrovsky, MA (reprint author), Russian Acad Sci, Inst Biochem Phys, Kosygin St 4, Moscow 117334, Russia. NR 27 TC 16 Z9 20 U1 1 U2 6 PU MOLECULAR VISION PI ATLANTA PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E, ATLANTA, GA 30322 USA SN 1090-0535 J9 MOL VIS JI Mol. Vis. PD MAR 20 PY 2002 VL 8 IS 10 BP 72 EP 78 PG 7 WC Biochemistry & Molecular Biology; Ophthalmology SC Biochemistry & Molecular Biology; Ophthalmology GA 547UB UT WOS:000175349500001 PM 11951082 ER PT J AU Donovan, PJ Smith, GT AF Donovan, PJ Smith, GT TI X-ray induced mutation in Syrian hamster fetal cells SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE in vivo; 6-thioguanine; mutation; mutagenicity test; somatic cells ID ETHYL-N-NITROSOUREA; GENE-TOX PROGRAM; IONIZING-RADIATION; 6-THIOGUANINE-RESISTANT MUTANTS; MAMMALIAN-CELLS; OVARY CELLS; INDUCTION; MUTAGENESIS; IRRADIATION; SENSITIVITY AB Transabdominal X-rays are a risk factor for childhood leukemia, and X-ray exposure of mouse fetuses has led to increases in both mutations and initiated tumors in offspring. However, fetal sensitivity and dose-response characteristics with regard to transplacental mutagenesis by X-rays have never been quantified. In the current experiment, pregnant Syrian hamsters at day 12 of gestation were irradiated with 300-kV X-rays. Twenty-four hours later, the fetuses were removed and their cells were allowed a 5 day expression time in culture. They were then seeded for colony formation and also for mutation selection by 6-thioguanine (6-TG). Mutation frequency was linear over the entire dose range, 10-600 R. The average induced 6-TG mutant frequency was 4.7 x 10(-7) per R. These results suggest that fetal cells are highly sensitive to induction of mutations by X-rays, and that a no-effect threshold is not likely. The 10 R dose caused a 25-fold increase in mutation frequency over the historical control, 45 x 10(-7) versus 1.8 x 10(-7), an increase per R of 2.5-fold. Increased risk of childhood cancer related to obstetrical transabdominal X-ray has also been estimated at 2.5-fold per R. Thus, our results are consistent with mutation contributing to this effect. Published by Elsevier Science B.V. C1 NCI, Lab Comparat Carcinogenesis, Dept Hlth & Human Serv, Frederick, MD 21702 USA. RP Donovan, PJ (reprint author), NCI, Lab Comparat Carcinogenesis, Dept Hlth & Human Serv, Bldg 538,Room 205E, Frederick, MD 21702 USA. NR 46 TC 2 Z9 3 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD MAR 20 PY 2002 VL 500 IS 1-2 BP 9 EP 15 AR PII S0027-5107(01)00299-8 DI 10.1016/S0027-5107(01)00299-8 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 532VB UT WOS:000174494800002 PM 11890930 ER PT J AU Souliotis, VL Henneman, JR Reed, CD Chhabra, SK Diwan, BA Anderson, LM Kyrtopoulos, SA AF Souliotis, VL Henneman, JR Reed, CD Chhabra, SK Diwan, BA Anderson, LM Kyrtopoulos, SA TI DNA adducts and liver DNA replication in rats during chronic exposure to N-nitrosodimethylamine (NDMA) and their relationships to the dose-dependence of NDMA hepatocarcinogenesis SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE O-6-methylguanine; N7-methylguanine; hepatocarcinogenesis; DNA replication ID ALKYLATING-AGENTS; ESCHERICHIA-COLI; HUMAN CANCER; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; ELECTROCHEMICAL DETECTION; REPAIR METHYLTRANSFERASE; INDUCED TUMORIGENESIS; METHYLATING AGENTS; CHRONIC INGESTION AB Exposure of rats to the hepatocarcinogen N-nitrosodimethylamine (NDMA) (0.2-2.64 ppm in the drinking water) for up to 180 days resulted in rapid accumulation of N7- and O-6-methylguanine in liver and white blood cell DNA, maximum adduct levels being reached within 1-7 days, depending on the dose. The levels of both adducts remained constant up to treatment day 28, subsequently declining slowly to about 40% of maximal levels for the liver and 60% for white blood cells by day 180. In order to elucidate the role of DNA replication in NDMA hepatocarcinogenesis, changes in liver cell labeling index (LI) were also measured on treatment days 21, 120 and 180. Although the time- and dose-dependence of the observed effects were complex, a clear trend towards increased rates of hepatocyte LI, as indicated by BrdU incorporation, with increasing NDMA doses was evident, particularly above I ppm, a concentration above which NDMA hepatocarcinogenicity is known to increase sharply. In contrast, no increase in Kupffer cell DNA replication was found at any of the doses employed, in accordance with the low susceptibility of these cells to NDMA-induced carcinogenesis. No significant increase in the occurrence of necrotic or apoptotic cells was noted under the treatment conditions employed. These results suggest that, in addition to the accumulation of DNA damage, alterations in hepatocyte DNA replication during the chronic NDMA exposure may influence the dose-dependence of its carcinogenic efficacy. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Natl Hellen Res Fdn, Inst Biol Res & Biotechnol, Athens 11635, Greece. NCI, Lab Comparat Carcinogenesis, Div Basic Sci, Frederick, MD 21702 USA. SAIC Frederick Inc, Intramural Res Support Program, Frederick, MD USA. RP Souliotis, VL (reprint author), Natl Hellen Res Fdn, Inst Biol Res & Biotechnol, 48 Vassileos Constantinou Ave, Athens 11635, Greece. NR 69 TC 13 Z9 18 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD MAR 20 PY 2002 VL 500 IS 1-2 BP 75 EP 87 AR PII S0027-5107(01)00301-3 DI 10.1016/S0027-5107(01)00301-3 PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 532VB UT WOS:000174494800008 PM 11890936 ER PT J AU Francischetti, IMB Andersen, JF Ribeiro, JMC AF Francischetti, IMB Andersen, JF Ribeiro, JMC TI Biochemical and functional characterization of recombinant Rhodnius prolixus platelet aggregation inhibitor 1 as a novel lipocalin with high affinity for adenosine diphosphate and other adenine nucleotides SO BIOCHEMISTRY LA English DT Article ID VON-WILLEBRAND-DISEASE; SHEAR-STRESS; ATP-DIPHOSPHOHYDROLASE; VONWILLEBRAND-FACTOR; PFA-100(TM) SYSTEM; DEPENDENT PATHWAY; PROTEIN; ADP; ACTIVATION; PURIFICATION AB The Rhodnius prolixus aggregation inhibitor 1 (RPAI-1) is a novel blood-sucking salivary molecule that binds to ADP and attenuates platelet aggregation. In this report, we determine the binding constants and specificity of RPAI-1 for adenine nucleotides and its functional significance. By the Hummel-Dreyer method of equilibrium gel filtration, we show that RPAI-1 binds ADP with a K-0.5 of 48.6 +/- 12.2 nM. RPAI-1 also displays high-affinity binding to ATP, AMP, Ado, AP4A, and alpha,beta Met ADP; however, RPAI-1 does not bind to inosine, guanosine, uridine, or cytidine. Binding is not modified by EDTA, indicating that Ado structure but not phosphate groups or Call is necessary for binding. By computer simulation, we show that RPAI-1 is more effective in scavenging low but not high concentrations of ADP, in contrast to R. prolixus apyrase. RPAI-1 inhibits in vitro the ADP-dependent platelet-rich plasma aggregation by collagen (COLL), TRAP, PAF, and A23187 but did not block platelet aggregation by ristocetin or phorbol myristate acetate (PMA) and only slightly attenuated that by convulxin. RPAI-1 prolongs the closure time as assessed with PFA-100, when COLL-Epi but not COLL-ADP cartridges are employed. RPAI-1 also affects platelet-mediated hemostasis time and COLL-induced thrombus formation at high shear as assessed with the Clot Signature Analyzer. We conclude that RPAI-1 exerts an antiplatelet effect due to scavenging of low concentrations of ADP in vitro and in vivo. RPAI-1 is the first lipocalin described so far with unique specificity for adenine nucleotides. C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Ribeiro, JMC (reprint author), NIAID, Parasit Dis Lab, NIH, 4 Ctr Dr,Room 4-126,MSC-0425, Bethesda, MD 20892 USA. OI Ribeiro, Jose/0000-0002-9107-0818 NR 48 TC 39 Z9 39 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 19 PY 2002 VL 41 IS 11 BP 3810 EP 3818 DI 10.1021/bi011015s PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 532JR UT WOS:000174471600033 PM 11888300 ER PT J AU Lederman, RJ Guttman, MA Peters, DC Thompson, RB Sorger, JM Dick, AJ Raman, VK McVeigh, ER AF Lederman, RJ Guttman, MA Peters, DC Thompson, RB Sorger, JM Dick, AJ Raman, VK McVeigh, ER TI Catheter-based endomyocardial injection with real-time magnetic resonance imaging SO CIRCULATION LA English DT Article DE magnetic resonance imaging; drugs; ischemia; radiography; catheterization ID MR FLUOROSCOPY; FEASIBILITY; TRACKING AB Background-We tested the feasibility of targeted left ventricular (LV) mural injection using real-time MRI (rtMRI). Methods and Results-A 1.5T MRI scanner was customized with a fast reconstruction engine, transfemoral guiding catheter-receiver coil (GCC), MRI-compatible needle, and tableside consoles. Commercial real-time imaging software was customized to facilitate catheter navigation and visualization of injections at 4 completely refreshed frames per second. The aorta was traversed and the left ventricular cavity was entered under direct rtMRI guidance. Pigs underwent multiple injections with dilute gadolinium-DTPA. All myocardial segments were readily accessed. The active GCC and the passive Stiletto needle injector were readily visualized. More than 50 endomyocardial injections were performed with the aid of rtMRI, 81% were successful with this first-generation prototype. Conclusion-Percutaneous endomyocardial drug delivery is feasible with the aid of rtMRI, which permits precise 3-dimensional localization of injection within the LV wall. C1 NHLBI, Div Intramural Res, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Cardiac Energet Lab, Med Imaging Grp, NIH, Bethesda, MD 20892 USA. RP Lederman, RJ (reprint author), NHLBI, Div Intramural Res, Cardiovasc Branch, NIH, Bldg 10,Room 2c713, Bethesda, MD 20892 USA. RI Thompson, Richard/E-9821-2011 FU Intramural NIH HHS [Z01 HL004608-08] NR 13 TC 87 Z9 91 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 19 PY 2002 VL 105 IS 11 BP 1282 EP 1284 DI 10.1161/01.CIR.0000012425.71261.FC PG 3 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 533NA UT WOS:000174535500005 PM 11901036 ER PT J AU Ho, MWY Yang, XN Carew, MA Zhang, T Hua, L Kwon, YU Chung, SK Adelt, S Vogel, G Riley, AM Potter, BVL Shears, SB AF Ho, MWY Yang, XN Carew, MA Zhang, T Hua, L Kwon, YU Chung, SK Adelt, S Vogel, G Riley, AM Potter, BVL Shears, SB TI Regulation of Ins(3,4,5,6)P-4 signaling by a reversible kinase/phosphatase SO CURRENT BIOLOGY LA English DT Article ID D-MYO-INOSITOL; MYOINOSITOL 3,4,5,6-TETRAKISPHOSPHATE; RAT-LIVER; ENZYME; 1,3,4-TRISPHOSPHATE; TETRAKISPHOSPHATES; HEXAKISPHOSPHATE; 5/6-KINASE; CELLS AB Regulation of Cl- channel conductance by Ins(3,4,5,6)P-4 provides receptor-dependent control over salt and fluid secretion [1], cell volume homeostasis [2], and electrical excitability of neurones and smooth muscle [3]. Ignorance of how Ins(3,4,5,6)P4 is synthesized has long hindered our understanding of this signaling pathway. We now show Ins(3,4,5,6)P4 synthesis by Ins(1,3,4,5,6)P,5 1-phosphatase activity by an enzyme previously characterized [4] as an Ins(3,4,5,6)P-4 1-kinase. Rationalization of these phenomena with a ligand binding model unveils Ins(1,3,4)P-3 as not simply an alternative kinase substrate [4, 5], but also an activator of Ins(1,3,4,5,6)P-5 I-phosphatase. Stable overexpression of the enzyme in epithelial monolayers verifies its physiological role in elevating Ins(3,4,5,6)P4 levels and inhibiting secretion. It is exceptional for a single enzyme to catalyze two opposing signaling reactions (1-kinase/1-phosphatase) under physiological conditions. Reciprocal coordination of these opposing reactions offers an alternative to general doctrine that intracellular signals are regulated by integrating multiple, distinct phosphatases and kinases [6]. C1 Lab Signal Transduct, Inositide Signaling Grp, Res Triangle Pk, NC 27709 USA. NIEHS, Res Triangle Pk, NC 27709 USA. Pohang Univ Sci & Technol, Dept Chem, Div Mol & Life Sci, Pohang 790784, South Korea. Berg Univ Gesamthsch Wuppertal, Fachbereich Biol Chem, D-42097 Wuppertal, Germany. Univ Bath, Dept Pharm & Pharmacol, Wolfson Lab Med Chem, Bath BA2 7AY, Avon, England. RP Shears, SB (reprint author), Lab Signal Transduct, Inositide Signaling Grp, Res Triangle Pk, NC 27709 USA. RI Potter, Barry/A-1845-2012 NR 25 TC 37 Z9 39 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD MAR 19 PY 2002 VL 12 IS 6 BP 477 EP 482 AR PII S0960-9822(02)00713-3 DI 10.1016/S0960-9822(02)00713-3 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 533NC UT WOS:000174535700020 PM 11909533 ER PT J AU Espey, MG Xavier, S Thomas, DD Miranda, KM Wink, DA AF Espey, MG Xavier, S Thomas, DD Miranda, KM Wink, DA TI Direct real-time evaluation of nitration with green fluorescent protein in solution and within human cells reveals the impact of nitrogen dioxide vs. peroxynitrite mechanisms SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE 3-nitrotyrosine; myeloperoxidase; nitric oxide; xanthine oxidase; superoxide ID NITRIC-OXIDE; TYROSINE NITRATION; CATALYZED OXIDATION; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; PHYSIOLOGICAL PH; IN-VIVO; SUPEROXIDE; MYELOPEROXIDASE; KINETICS AB 3-Nitrotyrosyl adducts in proteins have been detected in a wide range of diseases. The mechanisms by which reactive nitrogen oxide species may impede protein function through nitration were examined by using a unique model system, which exploits a critical tyrosyl residue in the fluorophoric pocket of recombinant green fluorescent protein (GFP). Exposure of purified GFP suspended in phosphate buffer to synthetic peroxynitrite in either 0.5 or 5 muM steps resulted in progressively increased 3-nitrotyrosyl immunoreactivity concomitant with disappearance of intrinsic fluorescence (IC50 approximate to 20 muM). Fluorescence from an equivalent amount of GFP expressed within intact MCF-7 tumor cells was largely resistant to this bolus treatment (IC50 > 250 muM). The more physiologically relevant conditions of either peroxynitrite infusion (1 muM/min) or de novo formation by simultaneous, equimolar generation of nitric oxide (NO) and superoxide (e.g., 3-morpholinosydnonimine; NONOates plus xanthine oxidase/hypoxanthine, menadione, or mitomycin C) were examined. Despite robust oxidation of dihydrorhodamine under each of these conditions, fluorescence decrease of both purified and intracellular GFP was not evident regardless of carbon dioxide presence, suggesting that oxidation and nitration are not necessarily coupled. Alternatively, both extra- and intracellular GFP fluorescence was exquisitely sensitive to nitration produced by heme-peroxidase/hydrogen peroxide-catalyzed oxidation of nitrite. Formation of nitrogen dioxide (NO2) during the reaction between NO and the nitroxide 2-phenyl-4,4,5,5-tetramethylimidazole-1-oxyl 3-oxide indicated that NO2 can enter cells and alter peptide function through tyrosyl nitration. Taken together, these findings exemplified that heme-peroxidase-catalyzed formation of NO2 may play a pivotal role in inflammatory and chronic disease settings while calling into question the significance of nitration by peroxynitrite. C1 NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA. RP Espey, MG (reprint author), NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA. RI Miranda, Katrina/B-7823-2009 NR 43 TC 76 Z9 76 U1 3 U2 13 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3481 EP 3486 DI 10.1073/pnas.062604199 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000025 PM 11904413 ER PT J AU Balint, E Phillips, AC Kozlov, S Stewart, CL Vousden, KH AF Balint, E Phillips, AC Kozlov, S Stewart, CL Vousden, KH TI Induction of p57(KIP2) expression by p73 beta SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID BECKWITH-WIEDEMANN-SYNDROME; DEPENDENT KINASE INHIBITOR; C-ABL; P53-RELATED PROTEIN; APOPTOTIC RESPONSE; P53 MUTANTS; DNA-DAMAGE; P73 GENE; FAMILY; DIFFERENTIATION AB The p53-related protein p73 has many functions similar to that of p53 including the ability to induce cell-cycle arrest and apoptosis. Both p53 and p73 function as transcription factors, and p73 activates expression of many genes that also are regulated by p53. Despite their similarities, it is evident that p53 and p73 are not interchangeable functionally, with p73 playing a role in normal growth and development that is not shared by p53. In this paper we describe the ability of p73beta but not p53 to activate expression of the cyclin-dependent kinase inhibitor p57(KIP) and KvLQT1, two genes that are coregulated in an imprinted region of the genome. Our results suggest that p73 may regulate expression of genes through mechanisms that are not shared by p53, potentially explaining the different contributions of p53 and p73 to normal development. C1 NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA. NCI, Canc & Dev Biol Lab, Frederick, MD 21702 USA. RP Vousden, KH (reprint author), NCI, Regulat Cell Growth Lab, Bldg 560,Room 22-96,W 7th St, Frederick, MD 21702 USA. RI Balint, Eva/B-8695-2008 NR 50 TC 26 Z9 26 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3529 EP 3534 DI 10.1073/pnas.062491899 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000033 PM 11891335 ER PT J AU Hathcock, KS Hemann, MT Opperman, KK Strong, MA Greider, CW Hodes, RJ AF Hathcock, KS Hemann, MT Opperman, KK Strong, MA Greider, CW Hodes, RJ TI Haploinsufficiency of mTR results in defects in telomere elongation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LENGTH REGULATION; MOUSE; RNA; CELLS; YEAST; ENDS; MICE AB Telomeres are usually maintained about an equilibrium length, and the set point for this equilibrium differs between species and between strains of a given species. To examine the requirement for telomerase in mediating establishment of a new telomere length equilibrium, we generated interspecies crosses with telomerase mTR knockout mice. In crosses between C57BL/6J (136) and either of two unrelated mouse species, CAST/Ei and SPRET/Ei, telomerase mediated establishment of a new telomere length equilibrium in wild-type mTR(+/+) mice. This new equilibrium was characterized by elongation of the short telomeres of CAST/Ei or SPRET/Ei origin. In contrast, mTR(-/-) offspring of interspecies crosses failed to elongate telomeres. Unexpectedly, haploinsufficiency was observed in mTR(+/-) heterozygous interspecies mice, which had an impaired ability to elongate short SPRET/Ei or CAST/Ei telomeres to the new equilibrium set point that was achieved in wild-type mTR(+/+) mice. These results demonstrate that elongation of telomeres to a new telomere set point requires telomerase and indicate that telomerase RNA may be limiting in vivo. C1 NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. NIA, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA. RP Hodes, RJ (reprint author), NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA16519, P01 CA016519] NR 25 TC 84 Z9 87 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3591 EP 3596 DI 10.1073/pnas.012549799 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000044 PM 11904421 ER PT J AU Lai, ZN Han, I Park, M Brady, RO AF Lai, ZN Han, I Park, M Brady, RO TI Design of an HIV-1 lentiviral-based gene-trap vector to detect developmentally regulated genes in mammalian cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID EMBRYONIC STEM-CELLS; NONDIVIDING CELLS; IN-VIVO; INSERTIONAL MUTAGENESIS; TRANSDUCTION; DELIVERY; EXPRESSION; ZEBRAFISH; REPORTER; LIVER AB The recent development of HIV-1 lentiviral vectors is especially useful for gene transfer because they achieve efficient integration into nondividing cell genomes and successful long-term expression of the transgene. These attributes make the vector useful for gene delivery, mutagenesis, and other applications in mammalian systems. Here we describe two HIV-1-based lentiviral vector derivatives, pZR-1 and pZR-2, that can be used in gene-trap experiments in mammalian cells in vitro and in vivo. Each lentiviral gene-trap vector contains a reporter gene, either p-lactamase or enhanced green fluorescent protein (EGFP), that is inserted into the U3 region of the 3' long terminal repeat. Both of the trap vector's readily integrate into the host genome by using a convenient infection technique. Appropriate insertion of the vector into genes causes EGFP or P-lactamase expression. This technique should facilitate the rapid enrichment and cloning of the trapped cells and provides an opportunity to select subpopulations of trapped cells based on the subcellular localization of reporter genes. Our findings suggest that the reporter gene is driven by an upstream, cell-specific promoter during cell culture and cell differentiation, which further supports the usefulness of lentivirus-based gene-trap vectors. Lentiviral gene-trap vectors appear to offer a wealth of possibilities for the study of cell differentiation and lineage commitment, as well as for the discovery of new genes. C1 Natl Inst Neurol Disorders & Stroke, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Lai, ZN (reprint author), Natl Inst Neurol Disorders & Stroke, Dev & Metab Neurol Branch, NIH, Bldg 10-Room 3D-04, Bethesda, MD 20892 USA. NR 32 TC 13 Z9 14 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3651 EP 3656 DI 10.1073/pnas.062032499 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000054 PM 11891320 ER PT J AU Liu, H Heath, SC Sobin, C Roos, JL Galke, BL Blundell, ML Lenane, M Robertson, B Wijsman, EM Rapoport, JL Gogos, JA Karayiorgou, M AF Liu, H Heath, SC Sobin, C Roos, JL Galke, BL Blundell, ML Lenane, M Robertson, B Wijsman, EM Rapoport, JL Gogos, JA Karayiorgou, M TI Genetic variation at the 22q11 PRODH2/DGCR6 locus presents an unusual pattern and increases susceptibility to schizophrenia SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CARDIO-FACIAL SYNDROME; CHILDHOOD-ONSET SCHIZOPHRENIA; DELETION SYNDROME; CHROMOSOME; LANGUAGE; ADULTS; REGION AB The location of a schizophrenia susceptibility locus at chromosome 22q11 has been suggested by genome-wide linkage studies. Additional support was provided by the observation of a higher-than-expected frequency of 22q11 microdeletions in patients with schizophrenia and the demonstration that approximate to20-30% of individuals with 22q11 microdeletions develop schizophrenia or schizoaffective disorder in adolescence and adulthood. Analysis of the extent of these microdeletions by using polymorphic markers afforded further refinement of this locus to a region of approximate to1.5 Mb. Recently, a high rate of 22q11 microdeletions was also reported for a cohort of 47 patients with Childhood Onset Schizophrenia, a rare and severe form of schizophrenia with onset by age 13. It is therefore likely that this 1.5-Mb region contains one or more genes that predispose to schizophrenia. In three independent samples, we provide evidence for a contribution of the PRODH2/DGCR6locus in 22q11-associated schizophrenia. Vile also uncover an unusual pattern of PRODH2 gene variation that mimics the sequence of a linked pseudogene. Several of the pseudogene-like variants we identified result in missense changes at conserved residues and may prevent synthesis of a fully functional enzyme. Our results have implications for understanding the genetic basis of the 22q11-associated psychiatric phenotypes and provide further insights into the genomic instability of this region. C1 Rockefeller Univ, Human Neurogenet Lab, New York, NY 10021 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Pretoria, Dept Psychiat, ZA-0083 Pretoria, South Africa. Univ Pretoria, Weskoppies Hosp, ZA-0083 Pretoria, South Africa. NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. Univ Cape Town, Dept Psychiat, ZA-7925 Cape Town, South Africa. Univ Cape Town, Valkenberg Hosp, ZA-7925 Cape Town, South Africa. Univ Washington, Div Med Genet, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Columbia Univ, Coll Phys & Surg, Dept Physiol & Cellular Biophys, Ctr Neurobiol & Behav, New York, NY 10032 USA. RP Karayiorgou, M (reprint author), Rockefeller Univ, Human Neurogenet Lab, 1230 York Ave, New York, NY 10021 USA. RI Heath, Simon/J-4138-2012; OI Wijsman, Ellen/0000-0002-2725-6669; Roos, Johannes/0000-0002-0572-1072; Sobin, Christina/0000-0002-2117-2034 FU NCRR NIH HHS [M01 RR000102, M01 RR00102] NR 28 TC 209 Z9 225 U1 2 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3717 EP 3722 DI 10.1073/pnas.042700699 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000066 PM 11891283 ER PT J AU Liu, SQ Liu, WJ Jakubczak, JL Erexson, GL Tindall, KR Chan, R Muller, WJ Adhya, S Garges, S Merlino, G AF Liu, SQ Liu, WJ Jakubczak, JL Erexson, GL Tindall, KR Chan, R Muller, WJ Adhya, S Garges, S Merlino, G TI Genetic instability favoring transversions associated with ErbB2-induced mammary tumorigenesis SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DNA MISMATCH REPAIR; NONPOLYPOSIS COLON-CANCER; TRANSGENIC MICE; G.C->T.A TRANSVERSIONS; NEU ONCOGENE; MUTATION FREQUENCY; PROTO-ONCOGENE; BREAST-CANCER; REPORTER GENE; HUMAN HOMOLOG AB It has been argued that genetic instability is required to generate the myriad mutations that fuel tumor initiation and progression and, in fact, patients with heritable cancer susceptibility syndromes harbor defects in specific genes that normally maintain DNA integrity. However, the vast majority of human cancers arise sporadically, in the absence of deficiencies in known "mutator" genes. We used a cll-based mutation detection assay to show that the mean frequency of forward mutations in primary mammary adenocarcinomas arising in mouse mammary tumor virus-c-erbB2 transgenic mice harboring multiple copies of the A bacteriophage genome was significantly higher than in aged-matched, wild-type mammary tissue. Analysis of the ell mutational spectrum within the mammary tumor genomic DNA demonstrated a >6-fold elevation in transversion mutation frequency, resulting in a highly unusual inversion of the transition/transversion ratio characteristic of normal epithelium; frameshift mutation frequencies were unaltered. Arising oncogenic point mutations within the c-erbB2 transgene of such tumors were predominantly transversions as well. Data from this model system support the notion that elaboration of a mutator phenotype is a consequential event in breast cancer and suggest that a novel DNA replication/repair gene is a relatively early mutational target in c-erbB2-induced mammary tumorigenesis. C1 NCI, Mol Biol Lab, Bethesda, MD 20892 USA. NIEHS, Mol Mutagenesis Grp, Lab Environm Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA. McMaster Univ, Dept Biol, Inst Mol Biol & Biotechnol, Hamilton, ON L8S 4K1, Canada. RP Merlino, G (reprint author), NCI, Mol Biol Lab, Bldg 37, Bethesda, MD 20892 USA. NR 53 TC 18 Z9 18 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3770 EP 3775 DI 10.1073/pnas.52710299 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000075 PM 11867754 ER PT J AU Kodera, T McGaha, TL Phelps, R Paul, WE Bona, CA AF Kodera, T McGaha, TL Phelps, R Paul, WE Bona, CA TI Disrupting the IL-4 gene rescues mice homozygous for the tight-skin mutation from embryonic death and diminishes TGF-beta production by fibroblasts SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID T-CELLS; FIBRILLIN-1 GENE; IFN-GAMMA; INTERLEUKIN-4; MOUSE; GROWTH; DIFFERENTIATION; SCLERODERMA; FIBROSIS; DECAY AB The TSK/TSK mutation is embryonic lethal; embryos have been reported to die at 7-8 days of gestational age. Crossing TSK/+, IL-4+/- mice revealed that disrupting one or both IL-4 alleles allowed survival of 29 and 47%, respectively, of TSK/TSK mice. These mice failed to develop cutaneous hyperplasia but did exhibit the emphysema that is found in TSK/+ mice. We showed that IL-4 stimulation of fibroblasts increased the level of transforming growth factor-beta (TGF-beta) mRNA and that lungs of TSK/+, IL-4-/- mice had substantially less TGF-beta mRNA than lungs of TSK/+, IL-4+/+ mice. Thus IL-4 seems to regulate the expression of TGF-beta in fibroblasts, providing an explanation for the absence of cutaneous hyperplasia in TSK/+, IL-4Ralpha-/- and TSK/+, TGF-beta+/- mice. C1 Mt Sinai Sch Med, Dept Microbiol, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Bona, CA (reprint author), Mt Sinai Sch Med, Dept Microbiol, Box 1124,1 Gustave L Levy Pl, New York, NY 10029 USA. OI McGaha, Tracy/0000-0003-4721-9301 FU NIAID NIH HHS [P01 AI024671, P01AI24671-13] NR 32 TC 82 Z9 84 U1 1 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3800 EP 3805 DI 10.1073/pnas.052709999 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000080 PM 11891315 ER PT J AU Baruch, DI Gamain, B Barnwell, JW Sullivan, JS Stowers, A Galland, GG Miller, LH Collins, WE AF Baruch, DI Gamain, B Barnwell, JW Sullivan, JS Stowers, A Galland, GG Miller, LH Collins, WE TI Immunization of Aotus monkeys with a functional domain of the Plasmodium falciparum variant antigen induces protection against a lethal parasite line SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RED-CELL SURFACE; INFECTED ERYTHROCYTES; EFFICACY TRIAL; MALARIA; VACCINE; CYTOADHERENCE; RECEPTOR; IMMUNITY; IDENTIFICATION; PHENOTYPES AB Immunity to Plasmodium falciparum in African children has been correlated with antibodies to the P. falciparum erythrocyte membrane protein 1 (PfEMP1) variant gene family expressed on the surface of infected red cells. We immunized Aotus monkeys with a subregion of the Malayan Camp variant antigen (MCvar1) that mediates adhesion to the host receptor CD36 on the endothelial surface and present data that PfEMP1 is an important target for vaccine development. The immunization induced a high level of protection against the homologous strain. Protection correlated with the titer of agglutinating antibodies and occurred despite the expression of variant copies of the gene during recurrent waves of parasitemia. A second challenge with a different P. falciparum strain, to which there was no agglutinating activity, showed no protection but boosted the immune response to this region during the infection. The level of protection and the evidence of boosting during infection encourage further exploration of this concept for malaria vaccine development. C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. Ctr Dis Control & Prevent, Div Parasit Dis, Natl Ctr Infect Dis, Atlanta, GA 30341 USA. NIAID, Malaria Vaccine Dev Unit, Parasit Dis Lab, NIH, Rockville, MD 20852 USA. Ctr Dis Control & Prevent, Sci Resources Program, Natl Ctr Infect Dis, Atlanta, GA 30333 USA. RP Baruch, DI (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. OI Gamain, Benoit/0000-0002-8255-2145; Miller, Louis/0000-0003-3420-1284 NR 34 TC 60 Z9 61 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3860 EP 3865 DI 10.1073/pnas.022018399 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000090 PM 11904437 ER PT J AU Dudek, SM Fields, RD AF Dudek, SM Fields, RD TI Somatic action potentials are sufficient for late-phase LTP-related cell signaling SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LONG-TERM POTENTIATION; ELEMENT-BINDING PROTEIN; CAMP-RESPONSIVE ELEMENT; HIPPOCAMPAL PYRAMIDAL CELLS; MEDIATED GENE-EXPRESSION; IMMEDIATE EARLY GENES; SYNAPTIC ACTIVATION; MESSENGER-RNA; MAP KINASE; TRANSCRIPTION FACTORS AB A question of critical importance confronting neuroscientists today is how biochemical signals initiated at a synapse are conveyed to the nucleus. This problem is particularly relevant to the generation of the late phases of long-term potentiation (LTP). Here we provide evidence that some signaling pathways previously associated with late-LTP can be activated in hippocampal CA1 neurons without synaptic activity; somatic action potentials, induced by backfiring the cells, were found to be sufficient for phosphorylation of extracellular signal-regulated kinase-1/2 and CAMP response element-binding protein, as well as for induction of zif268. Furthermore, such antidromic stimulation was adequate to rescue "tagged" synapses (early-LTP) from decay. These results show that a synapse-to-nucleus signal is not necessary for late-phase LTP-associated signaling cascades in the regulation of gene expression. C1 NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA. RP Fields, RD (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bldg 49,Room 5A72,MSC 4495, Bethesda, MD 20892 USA. EM fields@helix.nih.gov RI yu, yan/C-2322-2012; OI Dudek, Serena M./0000-0003-4094-8368 NR 60 TC 67 Z9 71 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 3962 EP 3967 DI 10.1073/pnas.062510599 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000107 PM 11891337 ER PT J AU da Costa, CA Paitel, E Mattson, MP Amson, R Telerman, A Ancolio, K Checler, F AF da Costa, CA Paitel, E Mattson, MP Amson, R Telerman, A Ancolio, K Checler, F TI Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID AMYLOID PRECURSOR PROTEIN; ONSET ALZHEIMERS-DISEASE; TUMOR SUPPRESSION; P53; BAX; PROTEASES; DEATH; GENE; CASPASES; CLEAVAGE AB Presenilins 1 and 2 are two homologous proteins that, when mutated, account for most early onset Alzheimer's disease. Several lines of evidence suggest that, among various functions, presenilins could modulate cell apoptotic responses. Here we establish that the overexpression of presenilin 2 (PS2) and its mutated form Asn-141-lle-PS2 alters the viability of human embryonic kidney (HEK)293 cells as established by combined trypan blue exclusion, sodium 3'-[1-(phenylamino-carbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro)benzene sulfonic acid hydrate assay, and propidium iodide incorporation FACS analyses. The two parent proteins increase the acetyl-DEVD-al-sensitive caspase-3-like activity in both HEK293 cells and Telencephalon specific murine neurons, modulate Sax and bcl-2 expressions, and enhance cytochrome C translocation into the cytosol. We show that overexpression of both wild-type and mutated PS2 increases p53-like immunoreactivity and transcriptional activity. We also establish that wild-type- and mutated PS2-induced caspase activation is reduced by p53 antisense approach and by pifithrin-a, a chemical inhibitor of p53. Furthermore, mouse fibroblasts in which the PS2 gene has been knocked out exhibited strongly reduced p53-transcriptional activity. Finally, we establish that the overexpression of both wild-type and mutated PS2 is accompanied by a drastic reduction of endogenous presenilin 1 (PS1) expression. Interestingly, pifithrin-a diminished endogenous PS2 immunoreactivity, whereas the inhibitor increases PSI expression. Altogether, our data demonstrate that wild-type and familial Alzheimer's disease-linked PS2 trigger apoptosis and down-regulate PSI expression through p53-dependent mechanisms. C1 Inst Pharmacol Mol & Cellulaire, UMR6097 CNRS, F-06560 Valbonne, France. Mol Engines, F-75011 Paris, France. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Checler, F (reprint author), Inst Pharmacol Mol & Cellulaire, UMR6097 CNRS, 660 Route Lucioles, F-06560 Valbonne, France. RI Mattson, Mark/F-6038-2012; alves da Costa, cristine/G-8075-2011; Checler, Frederic/C-1241-2009 OI alves da Costa, cristine/0000-0002-7777-005X; Checler, Frederic/0000-0003-2098-1750 NR 49 TC 104 Z9 105 U1 1 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 2002 VL 99 IS 6 BP 4043 EP 4048 DI 10.1073/pnas.062059899 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 533CC UT WOS:000174511000121 PM 11904448 ER PT J AU Kawamura, M Eisenhofer, G Kopin, IJ Kador, PF Lee, YS Fujisawa, S Sato, S AF Kawamura, M Eisenhofer, G Kopin, IJ Kador, PF Lee, YS Fujisawa, S Sato, S TI Aldose reductase: An aldehyde scavenging enzyme in the intraneuronal metabolism of norepinephrine in human sympathetic ganglia SO AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL LA English DT Article DE aldose reductase; aldehyde reductase; norepinephrine; 3,4-dihydroxyphenylglycol; sympathetic nervous system ID DIABETIC COMPLICATIONS; NEURONAL METABOLISM; MONOAMINE-OXIDASE; PIG BRAIN; CATECHOLAMINE METABOLISM; KETO REDUCTASES; ADRENAL-GLANDS; PC12 CELLS; PLASMA; RATS AB The neurotransmitter norepinephrine is metabolized by monoamine oxidase into an aldehyde intermediate that is further metabolized to the stable glycol derivative, 3,4-dihydroxyphenylglycol (DHPG). In this study, the possible role of aldose reductase in reducing this aldehyde intermediate in human sympathetic neurons has been examined. DHPG is formed when norepinephrine is incubated with aldose reductase in the presence of monoamine oxidase. DHPG metabolism is inhibited by the monoamine oxidase inhibitor, pargyline which prevents the deamination of norepinephrine, and by the aldose reductase inhibitor AL 1576, which inhibits DHPG formation without affecting the deamination of norepinephrine. Although similar formation of DHPG was observed with human liver aldehyde reductase, the production of DHPG was more effective with aldose reductase than aldehyde reductase. Two peaks of reductase activity corresponding to aldose reductase and aldehyde reductase were observed when sympathetic ganglia were chromatofocused. Molecular modeling studies indicate that the energy-minimized structure of 3,4-dihydroxymandelaldehyde bound to aldose reductase is similar to that of glyceraldehyde where the 2' hydroxyl group forms hydrogen bonds with Trp111 and NADPH. These results suggest that aldose reductase may be important in metabolizing the potentially toxic aldehyde intermediate formed from norepinephrine in human sympathetic ganglia, (C) 2002 Elsevier Science B.V All rights reserved. C1 NEI, Lab Ocular Therapeut, NIH, Bethesda, MD 20892 USA. Natl Inst Neurol Disorders & Stroke, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA. Nippon Zoki Pharmaceut Co Ltd, Inst Bioactive Sci, Kobe, Hyogo 6731461, Japan. NIH, Ctr Mol Modeling, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Sato, S (reprint author), NEI, Lab Ocular Therapeut, NIH, 10-10B09,10 Ctr Drive,MSC 1850, Bethesda, MD 20892 USA. NR 51 TC 11 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1566-0702 J9 AUTON NEUROSCI-BASIC JI Auton. Neurosci-Basic Clin. PD MAR 18 PY 2002 VL 96 IS 2 BP 131 EP 139 AR PII S1566-0702(01)00385-X DI 10.1016/S1566-0702(01)00385-X PG 9 WC Neurosciences SC Neurosciences & Neurology GA 536YQ UT WOS:000174729800007 PM 11958479 ER PT J AU Onder, G Penninx, BWJH Balkrishnan, R Fried, LP Chaves, PHM Williamson, J Carter, C Di Bari, M Guralnik, JM Pahor, M AF Onder, G Penninx, BWJH Balkrishnan, R Fried, LP Chaves, PHM Williamson, J Carter, C Di Bari, M Guralnik, JM Pahor, M TI Relation between use of angiotensin-converting enzyme inhibitors and muscle strength and physical function in older women: an observational study SO LANCET LA English DT Article ID SKELETAL-MUSCLE; HEART-FAILURE; HEALTH; PERFORMANCE; DISABILITY; ASSOCIATION; COMMUNITY; CYTOKINES; ENALAPRIL; CACHEXIA AB Background Angiotensin-converting enzyme (ACE) inhibitors prevent decline in physical function in patients with congestive heart failure (CHF). We aimed to see whether ACE inhibitors also prevent reduction in physical performance and in muscle strength in older women who do not have CHF. Methods We assessed 3-year rates of decline in both knee extensor muscle strength and walking speed in 641 women with hypertension who had participated in the Women's Health and Aging Study. Women were stratified into four groups according to type and duration of antihypertensive drug treatment. 61 had used ACE inhibitors continuously, 133 intermittently, 146 never, and 301 had used other hypertensive drugs either continuously or intermittently. Findings Participants who had taken ACE inhibitors continuously had a lower mean 3-year decline in muscle strength of -1.0 kg (SE 1.1) compared with -3.7 (0.5) kg in continuous/intermittent users of other anti hypertensive drugs (p=0.016) and with -3.9 kg in those who had never used antihypertensives (p=0.026). Muscle strength fell by 3.0 kg in 3 years in both continuous and intermittent users of ACE inhibitors (p=0.096). Mean 3-year decline in walking speed in continuous ACE inhibitor users was -1.7 cm/s compared with -13.6 cm/s in intermittent users of ACE inhibitors (p=0.015), -15.7 cm/s in continuous/intermittent users of other anti hypertensive drugs (p=0.002), and -17.9 cm/s in never users of anti hypertensive drugs (p=0.001). Interpretation ACE inhibitor treatment may halt or slow decline in muscle strength in elderly women with hypertension and without CHF. C1 Wake Forest Univ, Baptist Med Ctr, Sticht Ctr Aging, Sect Gerontol & Geriatr,Dept Internal Med,Sch Med, Winston Salem, NC 27157 USA. Univ Cattolica Sacro Cuore, Ctr Med Invecchiamento, Rome, Italy. Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Epidemiol, Baltimore, MD 21205 USA. NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA. RP Onder, G (reprint author), Wake Forest Univ, Baptist Med Ctr, Sticht Ctr Aging, Sect Gerontol & Geriatr,Dept Internal Med,Sch Med, Med Ctr Blvd, Winston Salem, NC 27157 USA. RI Carter, Christy/A-6828-2011; Carter, Christy/E-6630-2011; DI BARI, MAURO/J-1524-2012 FU NIA NIH HHS [5P60 AG 10484-07, N01AG12112] NR 35 TC 140 Z9 143 U1 1 U2 4 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD MAR 16 PY 2002 VL 359 IS 9310 BP 926 EP 930 DI 10.1016/S0140-6736(02)08024-8 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 531AE UT WOS:000174391700011 PM 11918911 ER PT J AU Balfour, JL Kaplan, GA AF Balfour, JL Kaplan, GA TI Neighborhood environment and loss of physical function in older adults: Evidence from the Alameda County Study SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE aged; disabled persons; environment and public health; social class; social environment ID MULTILEVEL ANALYSIS; MAINTAINING MOBILITY; DISABLEMENT PROCESS; SOCIAL-ENVIRONMENT; RISK-FACTORS; LATER LIFE; HEALTH; DISABILITY; PREDICTORS; PEOPLE AB Research suggests that neighborhood environment may influence functional health at an older age. This study examined the association between neighborhood problems and incidence of overall and lower-extremity functional loss. A total of 883 participants in the Alameda County Study who were aged 55 years and older and functionally healthy were questioned in 1994 and 1995 as part of an ongoing cohort study. Participants rated the severity of six neighborhood problems: traffic, noise, crime, trash and litter, lighting, and public transportation. Seventeen percent reported multiple neighborhood problems. Functional loss was measured by self-report of severe difficulty with physical tasks (e.g., climbing stairs, lifting 10 pounds (4.54 kg)). After 1 year, 6.1% developed overall functional loss, and 3.9% developed lower-extremity functional loss. Regression models adjusted for demographic, socioeconomic, health, and behavioral risk factors. Compared with those who reported nonproblem neighborhoods, those who reported multiple-problem neighborhoods were at increased risk of overall functional loss (odds ratio = 2.23, 95% confidence interval: 1.08, 4.60) and lower-extremity functional loss (odds ratio = 3.12, 95% confidence interval: 1.15, 8.51). Neighborhood problems associated with the largest increase in risk were excessive noise, inadequate lighting, and heavy traffic. Older people who reported problematic neighborhood environments had a greater risk of functional deterioration over 1 year compared with those in better neighborhoods. C1 Univ Michigan, Dept Epidemiol, Ctr Social Epidemiol & Populat Hlth, Sch Publ Hlth, Ann Arbor, MI 48104 USA. NIA, Epidemiol Demog & Biometry Program, NIH, Bethesda, MD 20892 USA. RP Balfour, JL (reprint author), Univ Michigan, Dept Epidemiol, Ctr Social Epidemiol & Populat Hlth, Sch Publ Hlth, 1214 S Univ, Ann Arbor, MI 48104 USA. FU NHLBI NIH HHS [T32 HL07365]; NIA NIH HHS [5R37AG11375] NR 68 TC 245 Z9 250 U1 2 U2 24 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 2002 VL 155 IS 6 BP 507 EP 515 DI 10.1093/aje/155.6.507 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 532GE UT WOS:000174465300003 PM 11882524 ER PT J AU Miller, BA Hankey, BF Thomas, TL AF Miller, BA Hankey, BF Thomas, TL TI Impact of sociodemographic factors, hormone receptor status, and tumor grade on ethnic differences in tumor stage and size for breast cancer in US women SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Review DE breast neoplasms; case-control studies; ethnic groups; neoplasm staging; SEER Program; socioeconomic factors ID BLACK-WHITE DIFFERENCES; FACTOR INTERVENTION TRIAL; NON-HISPANIC WHITE; SOCIOECONOMIC-STATUS; RACIAL-DIFFERENCES; SOCIAL-CLASS; PROGNOSTIC FACTORS; UNITED-STATES; CERVICAL-CANCER; AMERICAN WOMEN AB The importance of sociodemographic factors and tumor biomarkers in explaining ethnic differences in tumor stage and size at diagnosis was investigated in over 106,000 female breast cancer patients reported during 1992-1996 from 11 US population-based cancer registries. Japanese and non-Hispanic White women tended to be diagnosed at an earlier stage, with smaller diameter tumors and with a lower tumor grade than women from seven other ethnic groups. Statistical adjustment for individual- and group-level sociodemographic factors produced 50-80% reductions in the odds ratios for distant (vs. localized) stage and larger (vs. <1 cm) tumor size among Black women and Hispanic women. These factors also helped to account for tumor stage and size variation among most other ethnic groups. Consideration of hormone receptor status and tumor grade had little effect on the ethnic patterns. Although small, elevated odds ratios remained for some groups, our results suggest that sociodemographic factors accounted for many of the observed ethnic differences in breast cancer stage and tumor size at the time of diagnosis. Because most of the sociodemographic variables were aggregate measures, it is possible that residual confounding by socioeconomic position could explain the persistence of slightly elevated odds ratios in some ethnic groups. C1 NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Miller, BA (reprint author), NCI, Div Canc Control & Populat Sci, Suite 504,6116 Execut Blvd, Bethesda, MD 20892 USA. NR 112 TC 81 Z9 83 U1 4 U2 6 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 2002 VL 155 IS 6 BP 534 EP 545 DI 10.1093/aje/155.6.534 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 532GE UT WOS:000174465300006 PM 11882527 ER PT J AU Wang, ZY Lubin, JH Wang, LD Zhang, SZ Boice, JD Cui, HX Zhang, SR Conrath, S Xia, Y Shang, B Brenner, A Lei, SW Metayer, C Cao, JS Chen, KW Lei, SJ Kleinerman, RA AF Wang, ZY Lubin, JH Wang, LD Zhang, SZ Boice, JD Cui, HX Zhang, SR Conrath, S Xia, Y Shang, B Brenner, A Lei, SW Metayer, C Cao, JS Chen, KW Lei, SJ Kleinerman, RA TI Residential radon and lung cancer risk in a high-exposure area of Gansu Province, China SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE environment and public health; lung neoplasms; radiation; radon ID INDOOR RADON; WOMEN AB In the general population, evaluation of lung cancer risk from radon in houses is hampered by low levels of exposure and by dosimetric uncertainties due to residential mobility. To address these limitations, the authors conducted a case-control study in a predominantly rural area of China with low mobility and high radon levels. Included were all lung cancer cases diagnosed between January 1994 and April 1998, aged 30-75 years, and residing in two prefectures. Randomly selected, population-based controls were matched on age, sex, and prefecture, Radon detectors were placed in all houses occupied for 2 or more years during the 5-30 years prior to enrollment. Measurements covered 77% of the possible exposure time. Mean radon concentrations were 230.4 Bq/m(3) for cases (n = 768) and 222.2 Bq/m(3) for controls (n = 1,659). Lung cancer risk increased with increasing radon level (p < 0.001). When a linear model was used, the excess odds ratios at 100 Bq/m(3) were 0.19 (95% confidence interval: 0.05, 0.47) for all subjects and 0.31 (95% confidence interval: 0.10, 0.81) for subjects for whom coverage of the exposure interval was 100%. Adjusting for exposure uncertainties increased estimates by 50%. Results support increased lung cancer risks with indoor radon exposures that may equal or exceed extrapolations based on miner data. C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Minist Hlth, Beijing, Peoples R China. Int Epidemiol Inst, Rockville, MD USA. Vanderbilt Univ, Nashville, TN USA. US EPA, Indoor Environm Div, Washington, DC 20460 USA. Minist Publ Hlth, Lab Ind Hyg, Beijing, Peoples R China. RP Lubin, JH (reprint author), NCI, Div Canc Epidemiol & Genet, EPS-8042,6120 Execut Blvd, Bethesda, MD 20892 USA. OI Kleinerman, Ruth/0000-0001-7415-2478 NR 34 TC 69 Z9 79 U1 2 U2 10 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 2002 VL 155 IS 6 BP 554 EP 564 DI 10.1093/aje/155.6.554 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 532GE UT WOS:000174465300008 PM 11882529 ER PT J AU Tayebi, N Andrews, DQ Park, JK Orvisky, E McReynolds, J Sidransky, E Krasnewich, DM AF Tayebi, N Andrews, DQ Park, JK Orvisky, E McReynolds, J Sidransky, E Krasnewich, DM TI A deletion-insertion mutation in the phosphomannomutase 2 gene in an African American patient with congenital disorders of glycosylation-Ia SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE congenital disorders of glycosylation-Ia; African American; phosphomannomutase; insertion-deletion mutation; genotype-phenotype correlation ID DEFICIENT-GLYCOPROTEIN-SYNDROME; SYNDROME TYPE 1A; JAEKEN-SYNDROME; PMM2 MUTATION; CDG-IA; FAMILIES AB Congenital disorders of glycosylation (CDG) are a group of metabolic disorders with multisystemic involvement characterized by abnormalities in the synthesis of N-linked oligosaccharides. The most common form, CDG-Ia, resulting from mutations in the gene encoding the enzyme phosphomannomutase (PMM2), manifests with severe abnormalities in psychomotor development, dysmorphic features and visceral involvement. While this disorder is panethnic, we present the first cases of CDG-Ia identified in an African American family with two affected sisters. The proband had failure to thrive in infancy, hypotonia, ataxia, cerebellar hypoplasia and developmental delay. On examination, she also exhibited strabismus, inverted nipples and an atypical perineal fat distribution, all features characteristic of CDG-Ia. Direct sequencing demonstrated that the patient had a unique genotype, T237M/c.565-571 delAGAGAT insGTGGATTTCC. The novel deletion-insertion mutation, which was confirmed by subcloning and sequencing of each allele, introduces a stop codon 11 amino acids downstream from the site of the deletion. The presence of this deletion-insertion mutation at cDNA position 565 suggests that this site in the PMM2 gene may be a hotspot for chromosomal breakage. Published 2002 Wiley-Liss, Inc.(dagger) C1 NIMH, Clin Neurosci Branch, NIH, Bethesda, MD 20892 USA. Nemours Childrens Clin, Orlando, FL USA. NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA. RP Sidransky, E (reprint author), NIMH, Clin Neurosci Branch, NIH, Bldg 49,Room B1EE16,49 Convent Dr,MSC4405, Bethesda, MD 20892 USA. NR 25 TC 3 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 15 PY 2002 VL 108 IS 3 BP 241 EP 246 DI 10.1002/ajmg.10246 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 528CF UT WOS:000174225900014 PM 11891694 ER PT J AU Bhargava, R Levin, IW AF Bhargava, R Levin, IW TI Effective time averaging of multiplexed measurements: A critical analysis SO ANALYTICAL CHEMISTRY LA English DT Article ID IR AB Multiplexing and time averaging of signal are effective noise reduction protocols applied in many analytical measurement systems. The efficacy of these protocols may be reduced by random occurrences of high-magnitude noise that do not conform to the statistical distribution of noise for all other measurements in the data set. This high-magnitude noise, which may have an insignificant probability of occurrence for a single measurement, almost certainly affects data collected in a multichannel, multiplexed modality, such as Fourier transform infrared (FT-IR) spectroscopic imaging employing focal plane array detectors. To recover time-averaging advantages in these cases, we present a general coaddition method that uses two statistical measures, the mean and median of the ensemble of measurements of a signal, to obtain a better estimate of the true signal than that estimated by time averaging alone. This method, termed median filtered time averaging, is shown to be an effective noise removal procedure for FT-IR imaging data. The effects of noise removal on time averaging and multiplexing are examined theoretically and are demonstrated for hyperspectral infrared microspectroscopic imaging data obtained from human skin biopsies by using a rapid data acquisition procedure. C1 NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Levin, IW (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. OI Bhargava, Rohit/0000-0001-7360-994X NR 16 TC 13 Z9 13 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD MAR 15 PY 2002 VL 74 IS 6 BP 1429 EP 1435 DI 10.1021/ac011153n PG 7 WC Chemistry, Analytical SC Chemistry GA 531KQ UT WOS:000174414900032 PM 11922314 ER PT J AU Ramakrishnan, B Boeggeman, E Qasba, PK AF Ramakrishnan, B Boeggeman, E Qasba, PK TI beta-1,4-galactosyltransferase and lactose synthase: Molecular mechanical devices SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE mechanical device; glycosyltransferases; beta-1,4-galactosyltransferase; alpha-lactalbumin; lactose synthase; conformational change; lectin ID ALPHA-LACTALBUMIN; UDP-GALNAC; BOVINE; GALACTOSYLTRANSFERASE; CDNA; GENE; SPECIFICITY; SYNTHETASE; EXPRESSION; COMPLEX AB Recent structural investigations on the beta-1,4-galactosyltransferase-1 (Gal-T1) and lactose synthase (LS) have revealed that they are akin to an exquisite mechanical device with two well-coordinated flexible loops that are contained within the Gal-T1 catalytic domain. The smaller one has a Trp residue (Trp314) flanked by glycine residues. The larger one comprises amino acid residues 345 to 365. Upon substrate binding, the Trp314 side chain moves to lock the sugar nucleotide in the binding site, while the large loop undergoes a conformational change, masking the sugar nucleotide binding site, and creates (i) the oligosaccharide binding cavity; (ii) a protein-protein interacting site for the enzyme's partner, a-lactalbumin (LA); and (iii) a metal ion binding site. Only in conformation II do Gal-T1 and LA form the LS complex, enabling Gal-T1 to choose the new substrate glucose. LA holds and puts Glc right in the acceptor binding site of Gal-T1, which then maximizes the interactions with Glc, thereby making it a preferred acceptor for the LS reaction. The interaction of LA with Gal-T1 in conformation II also stabilizes the sugar-nucleotide-enzyme complex, kinetically enhancing the sugar transfer, even from the less preferred sugar nucleotides. The conformational change that masks the sugar nucleotide binding site can also be induced by the acceptor alone, thus making it possible for the protein to act as a specific lectin. C1 NCI, Struct Glycobiol Sect, LECB, CCR,NIH, Frederick, MD 21702 USA. NCI, Intramural Res Support Program, SAIC, Lab Expt & Computat Biol,CCR, Frederick, MD 21702 USA. RP Qasba, PK (reprint author), NCI, Struct Glycobiol Sect, LECB, CCR,NIH, Bldg 469,Room 221, Frederick, MD 21702 USA. NR 35 TC 23 Z9 24 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 15 PY 2002 VL 291 IS 5 BP 1113 EP 1118 DI 10.1006/bbrc.2002.6505 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 532GQ UT WOS:000174466300001 PM 11883930 ER PT J AU Stein, P Svoboda, P Stumpo, DJ Blackshear, PJ Lombard, DB Johnson, B Schultz, RM AF Stein, P Svoboda, P Stumpo, DJ Blackshear, PJ Lombard, DB Johnson, B Schultz, RM TI Analysis of the role of RecQ helicases in RNAi in mammals SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GENE; INTERFERENCE; MICE AB The identity of mammalian genes involved in RNA interference (RNAi), the targeted sequence-specific mRNA degradation by double-stranded RNA (dsRNA), is poorly defined. Here we report the analysis of mice with null mutations of Wrn, Blm, and RecQ1 genes that are related to Mut-7 and Qde3, two genes essential for RNAi in Caenorhabditis elegans and quelling in Neurospora, respectively. Our results suggest that Wrn, Blm, and RecQ1 are not involved in sequence-specific mRNA degradation in mammals in response to dsRNA, suggesting potential differences in the mammalian RNAi pathway. (C) 2002 Elsevier Science (USA). C1 Univ Penn, Dept Biol, Philadelphia, PA 19104 USA. Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA. NIEHS, Off Clin Res, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. MIT, Dept Biol, Cambridge, MA 02139 USA. RP Schultz, RM (reprint author), Univ Penn, Dept Biol, 415 S Univ Ave, Philadelphia, PA 19104 USA. RI Svoboda, Petr/G-3890-2012 OI Svoboda, Petr/0000-0002-4370-3705 FU NICHD NIH HHS [HD 22681] NR 9 TC 8 Z9 9 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 15 PY 2002 VL 291 IS 5 BP 1119 EP 1122 DI 10.1006/bbrc.2002.6578 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 532GQ UT WOS:000174466300002 PM 11883931 ER PT J AU Sajan, MP Bandyopadhyay, G Kanoh, Y Standaert, ML Quon, MJ Reed, BC Dikic, I Farese, RV AF Sajan, MP Bandyopadhyay, G Kanoh, Y Standaert, ML Quon, MJ Reed, BC Dikic, I Farese, RV TI Sorbitol activates atypical protein kinase C and GLUT4 glucose transporter translocation/glucose transport through proline-rich tyrosine kinase-2, the extracellular signal-regulated kinase pathway and phospholipase D SO BIOCHEMICAL JOURNAL LA English DT Article DE adipocytes; insulin; 3-kinase; myocytes; phosphatidic acid; phosphatidylinositol ID INSULIN-INDUCED ACTIVATION; RAT ADIPOCYTES; GLUCOSE-TRANSPORTER-4 TRANSLOCATION; HUMAN NEUTROPHILS; PHOSPHATIDYLINOSITOL 3-KINASE; 3T3-L1 ADIPOCYTES; POTENTIAL ROLE; L6 MYOTUBES; ZETA; LAMBDA AB Sorbitol, 'osmotic stress', stimulates GLUT4 glucose transporter translocation to the plasma membrane and glucose transport by a phosphatidylinositol (PI) 3-kinase-independent mechanism that reportedly involves non-receptor proline-rich tyrosine kinase-2 (PYK2) but subsequent events are obscure. In the present study. we found that extracellular signal-regulated kinase (ERK) pathway components, growth-factor-receptor-bound-2 protein. son of sevenless (SOS), RAS, RAF and mitogen-activated protein (MAP) kinase/ERK kinase, MEK(-1), operating downstream of PYK2, were required for sorbitol-stimulated GLUT4 translocation/glucose transport in rat adipocytes. L6 myotubes and 3T3/L1 adipocytes. Furthermore, sorbitol activated atypical protein kinase C (aPKC) through a similar mechanism depending on the PYK2/ERK pathway, independent of PI 3-kinase and its downstream effector. 3-phosphoinositide-dependent protein kinase-1 (PDK-1), Like PYK2/ERK pathway components, aPKCs were required for sorbitol-stimulated GLUT4 translocation/glucose transport. Interestingly, sorbitol stimulated increases in phospholipase D (PLD) activity and generation of phosphatidic acid (PA), which directly activated aPKCs. As with aPKCs and glucose transport. sorbitol-stimulated PLD activity was dependent on the ERK pathway. Moreover, PLD-generated PA was required for sorbitol-induced activation of aPKCs and GLUT4 translocation/glucose transport. Our findings suggest that sorbitol sequentially activates PYK2, the ERK pathway and PLD, thereby increasing PA, which activates aPKCs and GLUT4 translocation. This mechanism contrasts with that of insulin, which primarily uses PI 3-kinase, D3-PO4 polyphosphoinositides and PDK-1 to activate aPKCs. C1 Univ S Florida, James A Haley Vet Hosp, Coll Med, Res Serv, Tampa, FL 33612 USA. Univ S Florida, Coll Med, Dept Internal Med, Tampa, FL 33612 USA. NHLBI, Hypertens Endocrine Branch, NIH, Bethesda, MD 20892 USA. Louisiana State Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Shreveport, LA 71130 USA. Ludwig Inst Canc Res, S-75124 Uppsala, Sweden. RP Farese, RV (reprint author), Univ S Florida, James A Haley Vet Hosp, Coll Med, Res Serv, 13000 Bruce B Downs Blvd, Tampa, FL 33612 USA. RI Quon, Michael/B-1970-2008; Farese, Robert/B-3605-2015; Dikic, Ivan/O-4650-2015; OI Dikic, Ivan/0000-0001-8156-9511; Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707 FU NIDDK NIH HHS [2R01 DK 38079-091A, R01 DK065969] NR 29 TC 40 Z9 41 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON W1N 3AJ, ENGLAND SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 15 PY 2002 VL 362 BP 665 EP 674 DI 10.1042/0264-6021:3620665 PN 3 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 533KV UT WOS:000174529500018 PM 11879194 ER PT J AU Miyata, M Motoki, K Tamura, E Furukawa, M Gonzalez, FJ Yamazoe, Y AF Miyata, M Motoki, K Tamura, E Furukawa, M Gonzalez, FJ Yamazoe, Y TI Relative importance of maternal and embryonic microsomal epoxide hydrolase in 7,12-dimethylbenz[a]anthracene-induced developmental toxicity SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE developmental toxicity; 7,12-dimethylbenz[a]anthracene; microsomal epoxide hydrolase; gene knockout mice; embryo fibroblast; embryo ID DRUG-METABOLIZING-ENZYMES; T-CELL LINE; PHENYTOIN METABOLISM; EXPRESSION; MOUSE; CYP1B1; P450; IDENTIFICATION; HYDROCARBONS; ACTIVATION AB Microsomal epoxide hydrolase (mEH) catalyzes the hydrolysis of epoxide intermediates derived from drugs and environmental chemicals. The response of in vivo (embryo) and it? vitro (embryo fibroblast) tests were analyzed using mEH-null and wild-type mice to determine the relative role of maternal and embryonic mEH in the developmental toxicity induced by 7,12-dimethylbenz[a]anthracene (DMBA). Embryos derived from DMBA-treated [50 mg/kg, daily from gestational day (GD) 11 to GD 15] dams were analyzed, Although weight (P = 0.0009) and crown-rump length (P = 0.0003) of wild-type fetuses on GD IS were significantly lower than those of mEH-null fetuses, respectively, no significant difference was found between mEH-null and heterozygous fetuses of mEH-null dams. Cell viability was decreased to 50% in wild-type mouse embryo fibroblasts (MEFs) treated with 3 M DMBA, but no significant decrease was found in mEH-null MEFs. DMBA-3,4-diol produced a significant decrease in cell viability and suppressed the proliferation of wild-type MEFs at a 10-fold lower concentration than did DMBA. Although mEH protein was expressed in liver microsomes from wild-type embryos (GD 15), DMBA-3,4-diol was not detected among the DMBA metabolites. However, it was detected in the serum of wild-type pregnant mice treated with DMBA, but not in that of mEH-null mice. These results suggest that maternal mEH plays a major role in DMBA-induced developmental toxicity, and embryonic mEH is less involved in the toxicity. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Tohoku Univ, Grad Sch Pharmaceut Sci, Div Durg Metab & Mol Toxicol, Aoba Ku, Sendai, Miyagi 9800845, Japan. NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. RP Miyata, M (reprint author), Tohoku Univ, Grad Sch Pharmaceut Sci, Div Durg Metab & Mol Toxicol, Aoba Ku, Sendai, Miyagi 9800845, Japan. NR 33 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 15 PY 2002 VL 63 IS 6 BP 1077 EP 1084 AR PII S0006-2952(02)00847-X DI 10.1016/S0006-2952(02)00847-X PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 558NB UT WOS:000175972600007 PM 11931840 ER PT J AU Lorberbaum, JP Newman, JD Horwitz, AR Dubno, JR Lydiard, RB Hamner, MB Bohning, DE George, MS AF Lorberbaum, JP Newman, JD Horwitz, AR Dubno, JR Lydiard, RB Hamner, MB Bohning, DE George, MS TI A potential role for thalamocingulate circuitry in human maternal behavior SO BIOLOGICAL PSYCHIATRY LA English DT Article DE maternal behavior; infant crying; brain imaging; functional magnetic resonance imaging; human; auditory perception ID MEDIAL PREOPTIC AREA; RIGHT-HEMISPHERE; LACTATING RATS; PERIPEDUNCULAR NUCLEUS; PERIAQUEDUCTAL GRAY; AUDITORY-CORTEX; BRAIN ACTIVITY; FEMALE RATS; C-FOS; LESIONS AB Background: Little is known about the regional brain basis of human. maternal behavior. To understand this better, we have been examining brain activity in mothers listening to infant cries. Methods: We measured functional Magnetic Resonance Imaging brain activity in healthy, breastfeeding first-time mothers with young infants while they listened to infant cries, white noise control sounds, and a rest condition. Based on the thalamocingulate theory of maternal behavior and pilot work, we hypothesized that the cingulate, medial thalamus, medial prefrontal cortex, and right orbitofrontal cortex would display more activity with infant cries than with white noise (comparison 1) and would uniquely activate with the cries, meaning that these regions would display activity with cry minus rest but not with white noise minus rest (comparison 2). Results: In hypothesized regions, the group displayed more activity in the medial thalamus, medial prefrontal and right orbitofrontal cortices with both comparisons. The anterior and posterior cingulate cortex displayed more activity only with comparison 1. In non-hypothesized brain regions, several other structures thought important in rodent maternal behavior displayed activity with both comparisons including the midbrain, hypothalamus, dorsal and ventral striatum, and vicinity of the lateral septal region. Conclusions: Our results partially support our hypotheses and are generally consistent with neuroanatomical studies of rodent maternal behavior. (C) 2002 Society of Biological Psychiatry. C1 Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA. Ralph H Johnson VA Med Ctr, Charleston, SC USA. NICHHD, Bethesda, MD USA. RP Lorberbaum, JP (reprint author), Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA. FU NINDS NIH HHS [R01 NS 40259] NR 77 TC 175 Z9 177 U1 3 U2 16 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 2002 VL 51 IS 6 BP 431 EP 445 DI 10.1016/S0006-3223(01)01284-7 PG 15 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 537CD UT WOS:000174739000001 PM 11922877 ER PT J AU Berman, RM Sanacora, G Anand, A Roach, LM Fasula, MK Finkelstein, CO Wachen, RM Oren, DA Heninger, GR Charney, DS AF Berman, RM Sanacora, G Anand, A Roach, LM Fasula, MK Finkelstein, CO Wachen, RM Oren, DA Heninger, GR Charney, DS TI Monoamine depletion in unmedicated depressed subjects SO BIOLOGICAL PSYCHIATRY LA English DT Article DE major depression; alpha-methly-para-tyrosine; tryptophan depletion; catecholamine; indoleamine ID ANTIDEPRESSANT-INDUCED REMISSION; HEALTHY-HUMAN SUBJECTS; TRYPTOPHAN DEPLETION; CATECHOLAMINE DEPLETION; SEROTONIN; RESPONSES; MOOD; VULNERABILITY; MECHANISM; DISORDER AB Background: Although significant evidence suggests that diminished monoamine function is associated with clinical depression, catecholamine or indoleamine depletion alone has not been associated with significant mood changes in unmedicated depressed subjects or never-depressed control subjects. This study assesses the integrated role of these monoamine systems in depressed patients. Methods: Unmedicated depressed subjects underwent a 2-week, double-blind, random-ordered crossover study consisting of the following active and control conditions respectively: indoleamine (via tryptophan depletion) plus catecholamine (via alpha-methyl paratyrosine administration) depletion and, separately, indoleamine plus sham (via diphenhydramine administration) catecholamine depletion. Tert subjects completed both conditions; two subjects were withdrawn. after active testing and one after control testing. Results: Mean Hamilton Depression Rating Scale (HDRS) scores decreased progressively throughout the study days (baseline 26.7 points +/- 1.7 SEM and termination 20.0 +/- 2.4, active depletion; baseline 26.1 points +/- 2.3 SEM and termination 23.2 +/- 2.6, control testing) but did not differ between groups. Only three patients demonstrated 20% or greater increases from baseline HDRS at any point during the observation clays. Conclusions: Overall, results show that simultaneous disruptions of indoleamine and catecholamine function do not exacerbate symptoms in unmedicated depressed subjects, thus lending further support to the notion that monoamines regulate mood in actively depressed patients via indirect mechanisms. (C) 2002 Society of Biological Psychiatry. C1 Connecticut Mental Hlth Ctr, Abraham Ribicoff Ctr Clin Neurosci Res Unit, New Haven, CT 06519 USA. Dept Psychiat, Affect Disorders Program, West Haven, CT USA. Vet Affairs Connecticut Healthcare Syst, West Haven, CT USA. Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06519 USA. NIMH, Washington, DC 20032 USA. RP Berman, RM (reprint author), Pfizer Inc, Pfizer Global Res & Dev, Eastern Point Rd, Groton, CT 06430 USA. RI Anand, Amit/D-4232-2013 NR 26 TC 20 Z9 22 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 2002 VL 51 IS 6 BP 469 EP 473 DI 10.1016/S0006-3223(01)01285-9 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 537CD UT WOS:000174739000005 PM 11922881 ER PT J AU Bodine, DM AF Bodine, DM TI Thalassemia gene therapy looks good at one year SO BLOOD LA English DT Article C1 NHGRI, Bethesda, MD 20892 USA. RP Bodine, DM (reprint author), NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 2002 VL 99 IS 6 BP 1883 EP 1883 PG 1 WC Hematology SC Hematology GA 530KA UT WOS:000174355800002 ER PT J AU Kitazono, M Rao, VK Robey, R Aikou, T Bates, S Fojo, T Goldsmith, ME AF Kitazono, M Rao, VK Robey, R Aikou, T Bates, S Fojo, T Goldsmith, ME TI Histone deacetylase inhibitor FR901228 enhances adenovirus infection of hematopoietic cells SO BLOOD LA English DT Article ID MEDIATED GENE-TRANSFER; LONG-TERM CULTURE; RECOMBINANT ADENOVIRUS; VECTOR; TRANSDUCTION; RECEPTOR; VIVO; ELIMINATION; EFFICIENCY; EXPRESSION AB Adenovirus infection of hematopoietic cells frequently requires high virus concentrations and long incubation times to obtain moderate infection levels because these cells have tow levels of Coxsackie and adenovirus receptor (CAR) and alpha(nu) integrin. The effect of treatment with FR901228 (depsipeptide), a histone deacetylase inhibitor in phase 2 clinical trials, was studied in K582 cells, granulocyte-colony-stimulating factor-mobilized peripheral blood mononuclear cells (PBMCs), and CD34(+) peripheral blood stem cells (PBSCs). FR901228 Increased CAR and alpha(nu) integrin RNA levels and histone H3 acetylation. FR901228 treatment before adenovirus infection was associated with at least a 10-fold increase in transgene expression from a beta-galactosidase-expressing adenoviral vector. More than 80% of the PBMCs or CD34(+) PBSCs from 7 different donors were beta-galactosidase-positive after adenovirus infection with a multiplicity of infection of 10 for 60 minutes. Increased CAR, alpha(nu) integrin, and acetylated histone H3 levels were observed in PBMCs from a patient treated with FR901228. These studies suggest that FR901228 can increase the efficiency of adenoviral infection in hematopoietic cells. C1 NCI, Canc Therapeut Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Kagoshima Univ, Dept Surg 1, Fac Med, Kagoshima 890, Japan. RP Fojo, T (reprint author), NCI, Canc Therapeut Branch, Ctr Canc Res, NIH, Bldg 10,Rm 12C103,MSC 1910,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 29 TC 32 Z9 37 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 2002 VL 99 IS 6 BP 2248 EP 2251 DI 10.1182/blood.V99.6.2248 PG 4 WC Hematology SC Hematology GA 530KA UT WOS:000174355800053 PM 11877306 ER PT J AU Notarangelo, LD Mazza, C Giliani, S D'Aria, C Gandellini, F Ravelli, C Locatelli, MG Nelson, DL Ochs, HD Notarangelo, LD AF Notarangelo, LD Mazza, C Giliani, S D'Aria, C Gandellini, F Ravelli, C Locatelli, MG Nelson, DL Ochs, HD Notarangelo, LD TI Missense mutations of the WASP gene cause intermittent X-linked thrombocytopenia SO BLOOD LA English DT Article ID WISKOTT-ALDRICH-SYNDROME; SYNDROME PROTEIN AB Mutations of the WASP gene have been previously shown to be responsible for classical Wiskott-Aldrich syndrome, isolated X-linked thrombocytopenia, and severe, congenital X-linked neutropenia. We report herewith 2 families in which affected males had a history of intermittent thrombocytopenia with consistently reduced platelet volume, in the absence of other major clinical features, and carried missense mutations of the WASP gene that allowed substantial protein expression. This observation broadens the spectrum of clinical phenotypes associated with WASP gene defects, and it indicates the need for molecular analysis In males with reduced platelet volume, regardless of the platelet number. C1 Univ Brescia, Dept Pediat, Ist Med Mol Angelo Nocivelli, Brescia, Italy. NCI, Metab Branch, NIH, Bethesda, MD 20892 USA. Univ Washington, Dept Pediat, Seattle, WA 98195 USA. RP Notarangelo, LD (reprint author), Univ Brescia, Spedali Civili, Dept Pediat, I-25123 Brescia, Italy. RI Notarangelo, Luigi/F-9718-2016 OI Notarangelo, Luigi/0000-0002-8335-0262 NR 13 TC 51 Z9 54 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 2002 VL 99 IS 6 BP 2268 EP 2269 DI 10.1182/blood.V99.6.2268 PG 2 WC Hematology SC Hematology GA 530KA UT WOS:000174355800059 PM 11877312 ER PT J AU Zhou, Y Gwadry, FG Reinhold, WC Miller, LD Smith, LH Scherf, U Liu, ET Kohn, KW Pommier, Y Weinstein, JN AF Zhou, Y Gwadry, FG Reinhold, WC Miller, LD Smith, LH Scherf, U Liu, ET Kohn, KW Pommier, Y Weinstein, JN TI Transcriptional regulation of mitotic genes by camptothecin-induced DNA damage: Microarray analysis of dose- and time-dependent effects SO CANCER RESEARCH LA English DT Article ID CANCER CELL-LINES; EXPRESSION PATTERNS; MOLECULAR PHARMACOLOGY; TOPOISOMERASE-I; CYCLIN B1; G(2) CHECKPOINT; KINASE; P53; APOPTOSIS; ARREST AB cDNA microarray technology can be used to establish associations between characteristic gene expression patterns and molecular responses to drug therapy. In this study, we used cDNA microarrays of 1694 cancer-related genes to monitor the gene expression consequences of the treatment of HCT116 colon cancer cells with the topoisomerase I inhibitor camptothecin (CPT). To obtain a more homogeneous cellular response, we synchronized the cells in S-phase using aphidicolin (APH) before CPT treatment. Brief incubation with 20 and 1000 nM CPT caused reversible and irreversible G(2) arrest, respectively, and the patterns of gene expression change (with reference to untreated controls) were strikingly different at the two concentrations. Thirty-three genes, mainly divided into three groups, showed characteristic changes in the first 20 h as a consequence of treatment. Northern blots performed for five of these genes (each under eight experimental conditions) were quite consistent with the microarray results (average correlation coefficient, 0.86). Several p53-activated stress response genes were up-regulated after treatment with 1000 nM CPT or prolonged exposure to APH, but it seemed that the up-regulation did not directly cause cell cycle arrest because the up-regulation induced by prolonged treatment with APH did not prevent cell cycle progression after removal of APH. In contrast, cell cycle-dependent up-regulation of a group of mitosis-related genes was delayed or blocked after CPT treatments. The interrupted up-regulation of this group of genes was directly associated with G(2) arrest. In addition, we observed down-regulation of gene expression in cells that were recovering from cell cycle delay. The observations reported here suggest a fundamental difference at the gene expression level between the molecular mechanism of reversible G(2) delay that follows mild DNA damage and the mechanism of permanent G(2) arrest that follows more extensive DNA damage. C1 NCI, Mol Pharmacol Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NCI, Microarray Facil, Ctr Adv Technol, Div Clin Sci,NIH, Bethesda, MD 20892 USA. NCI, Off Director, Div Clin Sci, NIH, Bethesda, MD 20892 USA. RP Weinstein, JN (reprint author), NCI, Mol Pharmacol Lab, Div Basic Sci, NIH, Bldg 37-5D-02,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA. RI Liu, Edison/C-4141-2008; Miller, Lance/A-5633-2009 NR 47 TC 88 Z9 102 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 2002 VL 62 IS 6 BP 1688 EP 1695 PG 8 WC Oncology SC Oncology GA 533ZM UT WOS:000174560200018 PM 11912141 ER PT J AU Chang, BL Zheng, SQL Hawkins, GA Isaacs, SD Wiley, KE Turner, A Carpten, JD Bleecker, ER Walsh, PC Trent, JM Meyers, DA Isaacs, WB Xu, JF AF Chang, BL Zheng, SQL Hawkins, GA Isaacs, SD Wiley, KE Turner, A Carpten, JD Bleecker, ER Walsh, PC Trent, JM Meyers, DA Isaacs, WB Xu, JF TI Joint effect of HSD3B1 and HSD3B2 genes is associated with hereditary and sporadic prostate cancer susceptibility SO CANCER RESEARCH LA English DT Article ID 3-BETA-HYDROXYSTEROID DEHYDROGENASE GENE; DOMINANT INHERITANCE; EPITHELIAL-CELLS; LOCUS; CHROMOSOME; EXPRESSION; INTERLEUKIN-4; INDUCTION; SWEDEN; LINES AB 3beta-hydroxysteroid dehydrogenases (HSD3Bs), encoded by the HSD3B gene family at 1p13, have long been hypothesized to have a major role in prostate cancer susceptibility. The recent reports of a prostate cancer linkage at Ip13 provided additional evidence that HSD3B genes may be prostate cancer susceptibility genes. To evaluate the possible role of HSD3B genes in prostate cancer, we screened a panel of DNA samples collected from 96 men with or without prostate cancer for sequence variants in the putative promoter region, exons, exon-intron junctions, and 3'-untranslated region of HSD3B1 and HSD3B2 genes by direct sequencing. Eleven single nucleotide polymorphisms (SNPs) were identified, four of which, including a missense change (B1-N367T), were informative. These four SNPs were further genotyped in a total of 159 hereditary prostate cancer probands, 245 sporadic prostate cancer cases, and 222 unaffected controls. Although a weak association between prostate cancer risk and a missense SNP (B1-N367T) was found, stronger evidence for association was found when the joint effect of the two genes was considered. Men with the variant genotypes at either B1-N367T or B2-c7519g had a significantly higher risk to develop prostate cancer, especially the hereditary type of prostate cancer. Most importantly, the subset of hereditary prostate cancer probands, whose families provided evidence for linkage at 1p13, predominantly contributed to the observed association. Additional studies are warranted to confirm these findings. C1 Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Gen, Winston Salem, NC 27157 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD 21287 USA. NHGRI, NIH, Bethesda, MD 20892 USA. RP Xu, JF (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Gen, Med Ctr Blvd, Winston Salem, NC 27157 USA. FU NCI NIH HHS [CA58236] NR 34 TC 57 Z9 61 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 2002 VL 62 IS 6 BP 1784 EP 1789 PG 6 WC Oncology SC Oncology GA 533ZM UT WOS:000174560200032 PM 11912155 ER PT J AU Anaissie, EJ Stratton, SL Dignani, MC Summerbell, RC Rex, JH Monson, TP Spencer, T Kasai, M Francesconi, A Walsh, TJ AF Anaissie, EJ Stratton, SL Dignani, MC Summerbell, RC Rex, JH Monson, TP Spencer, T Kasai, M Francesconi, A Walsh, TJ TI Pathogenic Aspergillus species recovered from a hospital water system: A 3-year prospective study SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 40th Interscience Conference on Antimicrobial Agents and Chemotherapy CY SEP 17-21, 2000 CL TORONTO, CANADA ID BONE-MARROW TRANSPLANTATION; INVASIVE ASPERGILLOSIS; CUTANEOUS ASPERGILLOSIS; RANDOM AMPLIFICATION; FUNGAL-INFECTIONS; FILAMENTOUS FUNGI; POLYMORPHIC DNA; FUMIGATUS; EPIDEMIOLOGY; NIGER AB Nosocomial aspergillosis, a life-threatening infection in immunocompromised patients, is thought to be caused primarily by Aspergillus organisms in the air. A 3-year prospective study of the air, environmental surfaces, and water distribution system of a hospital in which there were known cases of aspergillosis was conducted to determine other possible sources of infection. Aspergillus species were found in the hospital water system. Significantly higher concentrations of airborne aspergillus propagules were found in bathrooms, where water use was highest (2.95 colony-forming units [cfu]/m(3)) than in patient rooms (0.78 cfu/m(3;) P = .05) and in hallways (0.61 cfu/m(3); P = .03). A correlation was found between the rank orders of Aspergillus species recovered from hospital water and air. Water from tanks yielded higher counts of colony-forming units than did municipal water. An isolate of Aspergillus fumigatus recovered from a patient with aspergillosis was genotypically identical to an isolate recovered from the shower wall in the patient's room. In addition to the air, hospital water systems may be a source of nosocomial aspergillosis. C1 Univ Arkansas Med Sci, Arkansas Canc Res Ctr, Myeloma & Transplantat Res Ctr, Little Rock, AR 72205 USA. Univ Arkansas Med Sci, John L McClellan Mem Vet Hosp, Little Rock, AR 72205 USA. Cent Bur Schimmelcultures, NL-3740 AG Baarn, Netherlands. Univ Texas, Houston Med Sch, Ctr Infect Dis, Houston, TX USA. NCI, Immunocompromised Host Sect, NIH, Bethesda, MD 20892 USA. RP Anaissie, EJ (reprint author), Univ Arkansas Med Sci, Arkansas Canc Res Ctr, Myeloma & Transplantat Res Ctr, 4301 W Markham,Mail Slot 776, Little Rock, AR 72205 USA. OI Dignani, Maria Cecilia/0000-0002-7446-6183 NR 50 TC 131 Z9 138 U1 3 U2 6 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR 15 PY 2002 VL 34 IS 6 BP 780 EP 789 DI 10.1086/338958 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 525BL UT WOS:000174047300007 PM 11850861 ER PT J AU Kang, JG Hamiche, A Wu, C AF Kang, JG Hamiche, A Wu, C TI GAL4 directs nucleosome sliding induced by NURF SO EMBO JOURNAL LA English DT Article DE chromatin; nucleosome; NURF; remodeling; transcription ID CHROMATIN-REMODELING COMPLEX; YEAST SWI/SNF COMPLEX; HEAT-SHOCK FACTOR; SWI-SNF COMPLEX; HISTONE OCTAMER; TRANSCRIPTION FACTOR; FACILITATED BINDING; POSITIONED NUCLEOSOMES; TRANS-DISPLACEMENT; IN-VITRO AB The Drosophila nucleosome remodeling factor (NURF) is an imitation switch (ISWI)-containing chromatin remodeling complex that can catalyze nucleosome repositioning at promoter regions to regulate access by the transcription machinery. Mononucleosomes reconstituted in vitro by salt dialysis adopt an ensemble of translational positions on DNA templates. NURF induces bi-directional 'sliding' of these nucleosomes to a subset of preferred positions. Here we show that mononucleosome sliding catalyzed by NURF bears similarity to nucleosome movement induced by elevated temperature. Moreover, we demonstrate that the GAL4 DNA-binding domain can extend NURF-induced nucleosome movement on a GAL4-E4 promoter, expanding the stretch of histone-free DNA at GAL4 recognition sites. The direction of NURF-induced nucleosome movement can be significantly modulated by asymmetric placement of tandem GAL4 sites relative to the nucleosome core particle. As such, sequence-specific, transcription factor-directed nucleosome sliding is likely to have substantial influence on promoter activation. C1 NCI, Mol Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Wu, C (reprint author), NCI, Mol Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37,Room 6068, Bethesda, MD 20892 USA. NR 65 TC 36 Z9 36 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD MAR 15 PY 2002 VL 21 IS 6 BP 1406 EP 1413 DI 10.1093/emboj/21.6.1406 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 531CR UT WOS:000174398900017 PM 11889046 ER PT J AU Sun, WH Coleman, TR DePamphilis, ML AF Sun, WH Coleman, TR DePamphilis, ML TI Cell cycle-dependent regulation of the association between origin recognition proteins and somatic cell chromatin SO EMBO JOURNAL LA English DT Article DE cell cycle; DNA replication; initiation; origin recognition proteins; Xenopus ID REPLICATION LICENSING SYSTEM; XENOPUS EGG EXTRACTS; MINICHROMOSOME MAINTENANCE PROTEINS; DNA-REPLICATION; SACCHAROMYCES-CEREVISIAE; MAMMALIAN NUCLEI; SIMIAN VIRUS-40; SPERM CHROMATIN; BUDDING YEAST; MCM PROTEINS AB Previous studies have suggested that cell cycle-dependent changes in the affinity of the origin recognition complex (ORC) for chromatin are involved in regulating initiation of DNA replication. To test this hypothesis, chromatin lacking functional ORCs was isolated from metaphase hamster cells and incubated in Xenopus egg extracts to initiate DNA replication. Intriguingly, Xenopus ORC rapidly bound to hamster somatic chromatin in a Cdc6-dependent manner and was then released, concomitant with initiation of DNA replication. Once pre-replication complexes (pre-RCs) were assembled either in vitro or in vivo, further binding of XlORC was inhibited. Neither binding nor release of XlORC was affected by inhibitors of either cyclin-dependent protein kinase activity or DNA synthesis. In contrast, inhibition of pre-RC assembly, either by addition of Xenopus geminin or by depletion of XlMcm proteins, augmented ORC binding by inhibiting ORC release. These results demonstrate a programmed release of XlORC from somatic cell chromatin as it enters S phase, consistent with the proposed role for ORC in preventing re-initiation of DNA replication during S phase. C1 NICHHD, NIH, Bethesda, MD 20892 USA. NIMH, Bethesda, MD 20892 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. RP DePamphilis, ML (reprint author), NICHHD, NIH, Bldg 6-416, Bethesda, MD 20892 USA. NR 60 TC 39 Z9 40 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD MAR 15 PY 2002 VL 21 IS 6 BP 1437 EP 1446 DI 10.1093/emboj/21.6.1437 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 531CR UT WOS:000174398900020 PM 11889049 ER PT J AU Greene, EC Mizuuchi, K AF Greene, EC Mizuuchi, K TI Dynamics of a protein polymer: the assembly and disassembly pathways of the MuB transposition target complex SO EMBO JOURNAL LA English DT Article DE DNA transposition; fluorescence resonance energy transfer; green fluorescent protein; MuB ID DNA STRAND-TRANSFER; BACTERIOPHAGE-MU; B-PROTEIN; PHAGE-MU; SITE; RECOMBINATION; IMMUNITY; TETRAMER; CLEAVAGE; ATPASE AB MuB assembles into a polymer on DNA in the presence of ATP and is directly involved in the selection of an appropriate site on the Escherichia coli chromosome for the insertion of the bacteriophage Mu genome. We have developed an assay using fluorescently tagged proteins to monitor the polymeric state of MuB via fluorescence resonance energy transfer. We show that polymer assembly is initiated by the formation of an ATP-MuB complex. MuB then self-associates into a protomer before binding to DNA. Upon binding to DNA, a dramatic increase in energy transfer is observed, suggesting a conformational change within MuB. Polymer disassembly is much slower than assembly and is greatly stimulated by the MuA transposase. Additionally, MuB is readily exchanged between polymers, and ATP hydrolysis is directly coupled to polymer disassembly. Our data support a model in which a combination of rapid polymer assembly, MuA-mediated disassembly, followed by rapid reassembly of the polymer allows MuB to sample multiple DNA targets until an appropriate site is located for the insertion of the bacteriophage genome. C1 NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Mizuuchi, K (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NR 24 TC 18 Z9 18 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD MAR 15 PY 2002 VL 21 IS 6 BP 1477 EP 1486 DI 10.1093/emboj/21.6.1477 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 531CR UT WOS:000174398900024 PM 11889053 ER PT J AU Liu, J Kadiiska, MB Corton, JC Qu, W Waalkes, MP Mason, RP Liu, YP Klaassen, CD AF Liu, J Kadiiska, MB Corton, JC Qu, W Waalkes, MP Mason, RP Liu, YP Klaassen, CD TI Acute cadmium exposure induces stress-related gene expression in wild-type and metallothionein-I/II-null mice SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE cadmium; acute toxicity; metallothionein-null mice; cDNA microarray; AP-1; JNK; radical production; free radicals ID LUNG EPITHELIAL-CELLS; MESSENGER-RNA EXPRESSION; FREE-RADICAL FORMATION; IN-VIVO EVIDENCE; KNOCK-OUT MICE; OXIDATIVE STRESS; INDUCED HEPATOTOXICITY; RAT LUNG; MAMMALIAN-CELLS; HEME OXYGENASE AB This study examined the effect of acute cadmium on stress-related gene expression and free radical production in wild-type and metallothionein-I/II-null (MT-null) mice. Atlas Toxicology arrays showed that acute cadmium (40 mumol/kg as CdCl2, ip for 3 h) markedly increased the expression of genes encoding heat-shock proteins, heme oxygenase-1, and genes in response to DNA damage/repair. The expression of genes encoding cytochrome P450 enzymes, UDP-glucuronosyltransferases, Mn-superoxide dismutase, and catalase was suppressed by cadmium. MT-null mice were more sensitive than wild-type mice to cadmium-induced, stress-related gene expression, in accord with greater activation of transcription factor AP-1 and phosphorylated JNK and ERK. To evaluate free radical production, mice were simultaneously given the spin trap agent, N-tert-butyl-alpha-phenylnitrone (PBN, 250 mg in DMSO/kg, ip) with cadmium, and livers were removed 30 min later for PBN-trapped radical extraction with chloroform: methanol (2: 1), and detected with electron spin resonance (ESR). Cadmium treatment caused detectable ESR signals for PBN adducts as well as lipid peroxidation in the liver similarly in both wild-type and MT-null mice. Thus, the mechanism of acute cadmium toxicity involves multiple facets including oxidative damage and aberrant gene expression, and absence of NIT exacerbates Cd-induced aberrant gene expression. (C) 2002 Elsevier Science Inc. C1 NIEHS, NCI, Comparat Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. CIIT Ctr Hlth Res, Res Triangle Pk, NC USA. Univ Kansas, Med Ctr, Kansas City, KS 66103 USA. RP Liu, J (reprint author), NIEHS, NCI, Comparat Carcinogenesis Lab, Mail Drop F0-09, Res Triangle Pk, NC 27709 USA. FU NIEHS NIH HHS [ES-01142] NR 53 TC 49 Z9 52 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD MAR 15 PY 2002 VL 32 IS 6 BP 525 EP 535 AR PII S0891-5849(01)00826-7 DI 10.1016/S0891-5849(01)00826-7 PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 530ZT UT WOS:000174390300005 PM 11958953 ER PT J AU Li, JW Lin, QS Wang, WD Wade, P Wong, JM AF Li, JW Lin, QS Wang, WD Wade, P Wong, JM TI Specific targeting and constitutive association of histone deacetylase complexes during transcriptional repression SO GENES & DEVELOPMENT LA English DT Article DE nuclear hormone receptor; chromatin; corepressor; histone deacetylase; chromatin immunoprecipitation assay ID NUCLEAR RECEPTOR COREPRESSORS; THYROID-HORMONE RECEPTOR; N-COR; CHROMATIN; SMRT; REPLICATION; SUPERFAMILY; MSIN3A; HDAC3 AB Specific recruitment of corepressor complexes containing histone deacetylases (HDAC) by transcription factors is believed to play an essential role in transcriptional repression. Recent studies indicate that repression by unliganded nuclear hormone receptors and by the Mad family of repressors requires distinct HDAC-containing corepressor complexes. In this work, we show that unliganded TR specifically recruits only the closely related N-CoR and SMRT-HDAC3 complexes, whereas the Mad1 recruits only the Sin3-HDAC1/2 complex. Significantly, both the Sin3 and Mi-2/NURD complexes also exhibit constitutive association with chromatin and contribute to chromatin deacetylation in a nontargeted fashion. These results suggest that HDAC complexes can contribute to gene repression by two distinct mechanisms as follows: (1) specific targeting by repressors and (2) constitutive association with chromatin. C1 Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. NIA, NIH, Genet Lab, Baltimore, MD 21224 USA. Emory Univ, Dept Pathol, Atlanta, GA 30322 USA. RP Wong, JM (reprint author), Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. FU NICHD NIH HHS [5K22HD01238-02] NR 29 TC 90 Z9 94 U1 0 U2 8 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR 15 PY 2002 VL 16 IS 6 BP 687 EP 692 DI 10.1101/gad.962502 PG 6 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA 533EM UT WOS:000174516500005 PM 11914274 ER EF