FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Sanz-Ortega, J Saez, MC Sierra, E Torres, A Balibrea, JL Hernando, F Sanz-Esponera, J Merino, MJ AF Sanz-Ortega, J Saez, MC Sierra, E Torres, A Balibrea, JL Hernando, F Sanz-Esponera, J Merino, MJ TI 3p21, 5q21, and 9p21 allelic deletions are frequently found in normal bronchial cells adjacent to non-small-cell lung cancer, while they are unusual in patients with no evidence of malignancy SO JOURNAL OF PATHOLOGY LA English DT Article DE lung; non-small-cell; carcinoma; microdissection; genetics; loss of heterozygosity ID APC/MCC GENE 5Q21; PRENEOPLASTIC LESIONS; FORMER SMOKERS; HETEROZYGOSITY; CARCINOMA; PROGRESSION; P53; POPULATIONS; MUTATION; LOSSES AB Molecular cytogenetic and loss of heterozygosity (LOH) analyses of non-small-cell lung cancer (NSCLC) have shown frequent allelic deletions in a variety of chromosomes, such as 1p, 3p, 5q, 8p, 9p, 11p, 11q, and 17p. Allelic loss at 3p21, 9p21, and 5q21 has also been reported in premalignant epithelial lesions of the bronchus and in normal bronchial cells. These findings suggest that a tissue field of somatic genetic alterations precedes the histopathological phenotypic changes of carcinoma. LOH at chromosomal regions 3p21, 5q21, 9p21, and 17p (TP53) was looked for in the peritumoural normal bronchial cells from 30 archival surgically resected tumours. Microdissected normal bronchial cells from 20 benign cytological smears were also added to the study. Matched populations of lymphocytes, tumour cells, and normal bronchial cells adjacent to the tumour were microdissected from, paraffin-embedded tissues, while matched populations of normal bronchial cells and inflammatory cells were microdissected from benign cytological smears (bronchial brushings). Polymerase chain reaction (PCR) amplification was performed utilizing the specific markers D5S346, D3S1300, D9S157, D9S171, and TP53. Within the NSCLC tumour cells, LOH was more frequently found at the 5q21: locus (72% of the informative cases), the 3p21 locus (47%), 9p21 (48%.), and 17p (33%.). Within the peritumoural normal bronchial cells, LOH at 5q21 was found in 37.5%, of the cases, 22%, showed LOH at 3p21, 27%, at 9p21, and U-Mi, at 17p (TP53). LOH was also detected in one case, in normal bronchial cells obtained from cytological smears at one locus (5q21). In conclusion, normal bronchial mucosa adjacent to NSCLC has frequent allelic losses at 3p21, 5q2l, and 9p21, while LOH at these loci is unusual in normal bronchial cells obtained from cytological smears from patients with no evidence of malignancy. LOH at these loci may be present before the onset of the malignant growth. LOH studies may supplement the histopathological evaluation of bronchial cells to detect genotypic alterations in both cytological and biopsy specimens. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Hosp San Carlos, Dept Anat Patol, Madrid 28040, Spain. NIH, NCI, Pathol Lab, Bethesda, MD USA. RP Sanz-Ortega, J (reprint author), Hosp San Carlos, Dept Anat Patol, Martin Lagos SN, Madrid 28040, Spain. RI Sanz, Julian/G-5276-2013 NR 24 TC 15 Z9 16 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0022-3417 J9 J PATHOL JI J. Pathol. PD NOV PY 2001 VL 195 IS 4 BP 429 EP 434 DI 10.1002/path.987 PG 6 WC Oncology; Pathology SC Oncology; Pathology GA 490NG UT WOS:000172057500005 PM 11745674 ER PT J AU Toretsky, JA Zitomersky, NL Eskenazi, AE Voigt, RW Strauch, ED Sun, CC Huber, R Meltzer, SJ Schlessinger, D AF Toretsky, JA Zitomersky, NL Eskenazi, AE Voigt, RW Strauch, ED Sun, CC Huber, R Meltzer, SJ Schlessinger, D TI Glypican-3 expression in Wilms tumor and hepatoblastoma SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article DE glypican-3; insulin-like growth factor 2; Wilms tumor; hepatoblastoma ID BECKWITH-WIEDEMANN-SYNDROME; BEHMEL OVERGROWTH SYNDROME; GROWTH FACTOR-II; GPC3 GENE; CANCER AB Background: Glypican-3 (GPC3) is a heparan sulfate proteoglycan. When it is disrupted, it causes the X-linked gigantism-overgrowth Simpson-Golabi-Behmel syndrome. Its involvement in growth control is consistent with recent reports that it can bind to growth factors, possibly including insulin-like growth factor 2. Further, it has been hypothesized that it may function as a tumor suppressor gene in breast and ovarian carcinomas and mesotheliomas. Patients and Methods: RNA and protein were extracted from Wilms tumor and hepatoblastoma tissue samples and GPC3 levels were measured in these extracts by Northern blotting, reverse transcription polymerase chain reaction, and immunoblotting. Results: In contrast to published results with carcinomas, high levels of GPC3 expression were found in Wilms tumor and hepatoblastoma. Low or undetectable expressions of this gene were found in normal tissue surrounding the tumor. Conclusions: Increased expression of GPC3 in Wilms tumor and hepatoblastoma suggests a growth-promoting or neutral activity for this gene product rather than a growth-suppressive effect. C1 Univ Maryland, Med Ctr, Dept Pediat, Sch Med, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Mol & Cell Biol Grad Program, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Greenebaum Canc Ctr, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA. Baltimore VA Med Ctr, Baltimore, MD USA. NIA, Baltimore, MD 21224 USA. RP Toretsky, JA (reprint author), Univ Maryland, Med Ctr, Dept Pediat, Sch Med, 22 S Greene St,Room N5E16, Baltimore, MD 21201 USA. FU NCI NIH HHS [R01 CA78843]; NICHD NIH HHS [N01-HD8-3283] NR 13 TC 56 Z9 59 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1077-4114 J9 J PEDIAT HEMATOL ONC JI J. Pediatr. Hematol. Oncol. PD NOV PY 2001 VL 23 IS 8 BP 496 EP 499 DI 10.1097/00043426-200111000-00006 PG 4 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA 494PB UT WOS:000172290100006 PM 11878776 ER PT J AU Albandar, JM DeNardin, AM Adesanya, MR Diehl, SR Winn, DM AF Albandar, JM DeNardin, AM Adesanya, MR Diehl, SR Winn, DM TI Associations between serum antibody levels to periodontal pathogens and early-onset periodontitis SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE periodontal diseases/pathogenesis; periodontal diseases/immunology; antibodies; Actinobacillus actinomycetemcomitans; Porphyromonas gingivalis; Prevotella intermedia; Campylobacter rectus; Eikenella corrodens; Fusobacterium nucleatum; follow-up studies; blacks; periodontitis, early-onset/etiology; periodontitis, early-onset/pathogenesis ID G SUBCLASS CONCENTRATIONS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; PORPHYROMONAS-GINGIVALIS; YOUNG-ADULTS; JUVENILE PERIODONTITIS; IMMUNOGLOBULIN ALLOTYPES; DISEASE; RESPONSES; SMOKING; RACE AB Background: The role of antibodies to periodontal microorganisms in the development of periodontal tissue destruction is still unclear. The aim of this study was to investigate the association between serum levels of IgG, IgA, and IgM antibodies to 6 periodontal microorganisms and clinical subtypes of varying severity of early-onset periodontitis (EOP) in young African American adults. Methods: The study group consisted of 159 African Americans aged 19 to 25 years (mean 22 years) and included 97 cases with EOP and 62 controls with no clinical signs of EOP. These subjects were selected from a nationally representative sample of adolescents who received an oral examination as part of the National Survey of Oral Health of United States Children in 1986-1987. The group was examined clinically a second time 6 years later and blood samples were collected. Serum levels of IgG, IgA, and IgM reactive to Actinobacillas actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Campylobacter rectus, Eikenella corrodens, and Fusobacterium nucleatum were assessed. Results: Serum levels of IgG and IgA antibody reactive to P gingivalis and A. actinomycetemcomitans and IgA antibody to P intermedia were significantly higher in generalized EOP cases compared to healthy controls. IgM antibody levels did not show any significant associations with EOP for any of the 6 bacterial species tested. There were no significant differences in antibody levels between controls and the 13 subjects in our study who were classified with localized EOP. Conclusions: The findings suggest that antibodies to P gingivalis, P intermedia, and A. actinomycetemcomitans may play a significant role in the pathogenesis of EOP. Substantial longitudinal studies that monitor antibody levels and avidity prior to disease onset, during progression, and following clinical intervention will be necessary to fully understand the role of this component of the immune response in protection versus tissue destruction and the potential use in EOP risk assessment and disease management. C1 Temple Univ, Sch Dent, Dept Periodontol, Philadelphia, PA 19140 USA. Univ Buffalo, Dept Oral Biol, Buffalo, NY USA. NIDCR, Craniofacial Epidemiol & Genet Branch, Bethesda, MD USA. RP Temple Univ, Sch Dent, Dept Periodontol, 3223 N Broad St, Philadelphia, PA 19140 USA. EM jalbandar@dental.temple.edu OI Albandar, Jasim M./0000-0001-7801-3811 NR 35 TC 35 Z9 41 U1 1 U2 2 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 USA SN 0022-3492 EI 1943-3670 J9 J PERIODONTOL JI J. Periodont. PD NOV PY 2001 VL 72 IS 11 BP 1463 EP 1469 DI 10.1902/jop.2001.72.11.1463 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 496TC UT WOS:000172411700001 PM 11759856 ER PT J AU Fritsche, E Baek, SJ King, LM Zeldin, DC Eling, TE Bell, DA AF Fritsche, E Baek, SJ King, LM Zeldin, DC Eling, TE Bell, DA TI Functional characterization of cyclooxygenase-2 polymorphisms SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID SINGLE-NUCLEOTIDE POLYMORPHISMS; HUMAN COLON-CANCER; ADENOMATOUS POLYPOSIS; COLORECTAL-CANCER; EXPRESSION; CARCINOMA; COX-2; SYNTHASE-2; GENE; CELLS AB Cyclooxygenases (COX)-1 and -2 are the key enzymes in the conversion of arachidonic acid to prostaglandins. COX-2 appears to play an emerging role in inflammation and carcinogenesis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are used for the treatment of numerous diseases and reduce the risk of developing colorectal cancer. Polymorphisms in the COX-2 gene could alter enzyme expression, function, and/or the response to NSAIDs. Therefore, they could modify individual risks for developing cancer and other diseases or the occurrence of side effects or sensitivity toward selective or nonselective COX inhibitors. We sequenced the COX-2 gene of 72 individuals and identified rare polymorphisms in the promoter and the coding region. A COX-2 molecular model was used to locate the coding region polymorphisms relative to functional sites in the protein, and the COX-2 V511A polymorphism was very near to the active site. This variant protein was expressed, and function was evaluated, but no difference was detected in metabolism of the COX-2 substrates, arachidonic acid, linoleic acid, and 2-arachidonyl glycerol, compared with the wild type. The K-m values for arachidonic acid showed no differences between the COX-2 wild type and V511A mutant. Inhibition with selective or nonselective COX inhibitors was essentially the same for the two enzymes. The absence of functionally important polymorphisms in the COX-2 gene may suggest that there has been selective pressure against those single nucleotide polymorphisms because of the critical role of this enzyme in maintenance of homeostasis. C1 NIEHS, Lab Computat Biol & Risk Anal, Res Triangle Pk, NC 27709 USA. NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. NIEHS, Pulm Pathobiol Lab, Res Triangle Pk, NC 27709 USA. RP Bell, DA (reprint author), NIEHS, Lab Computat Biol & Risk Anal, POB 12233, Res Triangle Pk, NC 27709 USA. OI Baek, Seung/0000-0001-7866-7778 NR 39 TC 83 Z9 92 U1 0 U2 1 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 2001 VL 299 IS 2 BP 468 EP 476 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 485PU UT WOS:000171764100009 PM 11602656 ER PT J AU Miller, DS AF Miller, DS TI Nucleoside phosphonate interactions with multiple organic anion transporters in renal proximal tubule SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID MULTIDRUG-RESISTANCE; CLINICAL PHARMACOKINETICS; NUCLEOTIDE ANALOGS; SECRETION; ADEFOVIR; LOCALIZATION; CIDOFOVIR; DRUGS; CYTOTOXICITY; EXPRESSION AB The interactions of two antiviral, acyclic nucleoside phosphonates, adefovir and cidofovir, with xenobiotic transporters was studied in intact killifish (Fundulus heteroclitus) renal proximal tubules by using fluorescent substrates, confocal microscopy, and quantitative image analysis. Both drugs reduced in a concentration-dependent manner the transport of fluorescein on the classical organic anion system and transport of fluorescein-methotrexate on multidrug resistance-associated protein 2 (Mrp2). Neither drug inhibited transport of a fluorescent cyclosporin A derivative on P-glycoprotein. Inhibition of Mrp2-mediated transport was abolished by 50 muM p-aminohippurate, indicating that adefovir and cidofovir entered the cells at the basolateral membrane on the classical organic anion transport system (OAT1). Comparison of the inhibitory potencies of the nucleoside phosphonates with other substrates and inhibitors showed them to be moderate inhibitors of OAT1- and Mrp2-mediated transport. C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. RP Miller, DS (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, MD F2-03, Res Triangle Pk, NC 27709 USA. NR 34 TC 57 Z9 59 U1 0 U2 2 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 2001 VL 299 IS 2 BP 567 EP 574 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 485PU UT WOS:000171764100021 PM 11602668 ER PT J AU Brandt, MR Furness, MS Rice, KC Fischer, BD Negus, SS AF Brandt, MR Furness, MS Rice, KC Fischer, BD Negus, SS TI Studies of tolerance and dependence with the delta-opioid agonist SNC80 in rhesus monkeys responding under a schedule of food presentation SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID DIFFERENTIAL CROSS-TOLERANCE; RECEPTOR-MEDIATED PHENOMENA; DISCRIMINATIVE STIMULUS; (+)-4-<(ALPHA-R)-ALPHA-((2S,5R)-4-ALLYL-2,5-DIMETHYL-1-PIPERAZINYL)-3-ME THOXYBE.; ALPHA-ACETYLMETHADOL; DOWN-REGULATION; MU-RECEPTOR; MORPHINE; RAT; BW373U86 AB Tolerance and dependence after acute or chronic administration of the selective delta -opioid agonist SNC80 were assessed in rhesus monkeys (Macaca mulatta) responding under a schedule of food presentation. SNC80 dose dependently decreased response rates. These effects waned after 5 h. When administered as an acute 24-h pretreatment, SNC80 (1.0-10.0 mg/kg) produced tolerance as evidenced by dose-dependent rightward shifts in the SNC80 dose-effect curve. Pretreatments of 3.2 or 10.0 mg/kg SNC80 increased the SNC80 ED50 by 4- or 25-fold, respectively. Tolerance to acute SNC80 was also time-dependent as evidenced by increased ED50 values when administered as a 5-h (14-fold), 24-h (25-fold), or 3-day (11-fold) pretreatment. The SNC80 dose-effect curve was similar to control after a 7-day pretreatment. The selective delta -antagonist naltrindole (1.0 mg/kg) partially blocked tolerance to acute SNC80. Chronic SNC80 (1.0-10.0 mg/kg/day) also produced dose-dependent rightward shifts in the SNC80 dose-effect curve. Chronic SNC80 was more effective than acute SNC80 in producing tolerance. Moreover, tolerance to chronic SNC80 waned more slowly than to acute SNC80. Acute or chronic SNC80 (10.0 mg/kg/day) also produced cross-tolerance to the rate-decreasing effects of other delta -agonists (SNC162 and SNC243A) but not to mu- (morphine) or kappa (U-50,488)-agonists. Changes in response rates or behavioral signs of withdrawal were not observed after the administration of opioid antagonists (i.e., naltrindole or naltrexone) in monkeys treated with SNC80. These data suggest that a pharmacologically selective tolerance develops to delta -agonists after both acute and chronic administration of SNC80 with little or no dependence. C1 Harvard Univ, McLean Hosp, Sch Med, Alcohol & Drug Abuse Res Ctr, Belmont, MA 02178 USA. NIDDKD, Med Chem Lab, NIH, Bethesda, MD 20892 USA. RP Negus, SS (reprint author), Harvard Univ, McLean Hosp, Sch Med, Alcohol & Drug Abuse Res Ctr, 115 Mill St, Belmont, MA 02178 USA. FU NIDA NIH HHS [KO5-DA00101, P50-DA04059, R01-DA11460, T32-DA0752] NR 40 TC 36 Z9 38 U1 0 U2 1 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 2001 VL 299 IS 2 BP 629 EP 637 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 485PU UT WOS:000171764100028 PM 11602675 ER PT J AU Goold, CP Usdin, TB Hoare, SRJ AF Goold, CP Usdin, TB Hoare, SRJ TI Regions in rat and human parathyroid hormone (PTH) 2 receptors controlling receptor interaction with PTH and with antagonist ligands SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID PHOTOAFFINITY CROSS-LINKING; TUBEROINFUNDIBULAR PEPTIDE; 39 RESIDUES; (PTH)/PTH-RELATED PEPTIDE; EXTRACELLULAR LOOP; CHIMERIC RECEPTORS; PROTEIN-RECEPTOR; AGONIST-BINDING; AMINO-TERMINUS; SELECTIVITY AB The parathyroid hormone (PTH) 2 receptor is potently activated by tuberoinfundibular peptide (TIP39). Rat and human PTH2 receptors differ considerably in their PTH responsiveness. PTH weakly stimulates cAMP accumulation via the rat receptor, and here we show it did not detectably increase intracellular calcium ([Ca2+](i)) and bound with low affinity (450 nM). For the human PTH2 receptor PTH was a full agonist for increasing cAMP, a partial agonist for increasing [Ca2+](i), and bound with high affinity (18 nM). In addition, the antagonists PTH(7-34) and TIP(7-39) bound with 10- to 49-fold lower affinity to the rat receptor. We investigated the molecular basis of differential PTH and antagonist interaction with human and rat PTH2 receptors by using chimeric human/rat PTH2 receptors. PTH cAMP-signaling efficacy (E-max) was determined by extracellular loop (EL) 1 and a region including EL2 and EL3. The N-terminal domain determined PTH binding selectivity at the inactive receptor state. Multiple regions throughout the receptor are required for the PTH-PTH2 receptor complex to adopt a high-affinity active state: inserting the rat receptor's N-terminal domain, EL1 or EL2/3, into the human receptor increased PTH's EC50 and reciprocal exchanges did not reduce EC50. This suggests the global receptor conformation prevents the rat receptor from adopting a high-affinity state when in complex with PTH. N-terminal ligand truncation, producing the antagonists PTH(7-34) and TIP(7-39), altered ligand interaction with the membrane-embedded domain of the receptor, eliminating EL2/3 as a specificity determinant and lowering binding affinity. These insights should contribute to the development of a high-affinity PTH2 receptor antagonist, for investigating the receptor's physiological role. C1 NIMH, Cell Biol Unit, Genet Lab, Bethesda, MD 20892 USA. RP Hoare, SRJ (reprint author), Neurocrine Biosci, 10555 Sci Ctr Dr, San Diego, CA 92121 USA. NR 39 TC 16 Z9 17 U1 0 U2 2 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 2001 VL 299 IS 2 BP 678 EP 690 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 485PU UT WOS:000171764100034 PM 11602681 ER PT J AU Ventura, ON Kieninger, M Denis, PA Cachau, RE AF Ventura, ON Kieninger, M Denis, PA Cachau, RE TI Density functional computational thermochemistry: Isomerization of sulfine and its enthalpy of formation SO JOURNAL OF PHYSICAL CHEMISTRY A LA English DT Article ID CORRELATED MOLECULAR CALCULATIONS; GAUSSIAN-BASIS SETS; CHEMISTRY; ENERGY; EXCHANGE; RADICALS; BASICITY; ACCURATE; CH2=S=O; OXIDES AB Density functional (DFT), second-order perturbation theory (MP2), and coupled-cluster [(CCSD(T)] calculations using Pople's basis sets up to 6-311++G(3df,2pd) and Dunning's correlation consistent basis sets have been employed to determine the enthalpy of formation of sulfine, CH2SO, 1, using the isodesmic reaction CH2S + SO2 reversible arrow CH2SO + SO. Previous calculations showed an inconsistency between the enthalpy of formation obtained using this methodology, Delta (f)H(298.15)degrees (1) = -52 +/- 10 kJ/mol, and the value obtained employing the isomerization reaction CH2SO (1) reversible arrow HC(=O)SH (2) if Benson's estimate for the enthalpy of formation of isomer 2 (thioformic acid) was employed. This result was particularly vexing, since the computed enthalpy of formation of I was reasonably in agreement with Benson's own estimate. In this paper we extended our previous study using the reactions HC(=O)-XH + RH reversible arrow H2CO + R-XH with R = H, Me, Et, Pr, and i-Pr. X was either sulfur, to obtain the enthalpy of formation of 2, or oxygen, to assess the errors to be expected in the use of these reactions for the evaluation of Delta H-f degrees. The result, Delta (f)H(298.15)degrees (2) = -121 +/- 8 kJ/mol, arrived at after a critical assessment of B3LYP, MP2, and CCDSD(T) results, is in complete agreement with the value of - 126 +/- 4 kJ/mol estimated by Benson. This implies that the isomerization reaction cannot be employed for the determination of the enthalpy of formation of sulfine. We ascribe this inadequacy to the errors introduced due to the change in the oxidation state of sulfur. C1 UDELAR, Fac Quim, DEQUIFIM, CCPG, Montevideo 11800, Uruguay. NCI, Frederick Biomed Supercomp Ctr, Ft Detrick, MD 21702 USA. RP Ventura, ON (reprint author), UDELAR, Fac Quim, DEQUIFIM, CCPG, Gral Flores 2124,CC 1157, Montevideo 11800, Uruguay. OI Denis, Pablo/0000-0003-3739-5061 NR 37 TC 17 Z9 17 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1089-5639 J9 J PHYS CHEM A JI J. Phys. Chem. A PD NOV 1 PY 2001 VL 105 IS 43 BP 9912 EP 9916 DI 10.1021/jp004374q PG 5 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 489YG UT WOS:000172020100014 ER PT J AU Ventura, ON Kieninger, M Denis, PA AF Ventura, ON Kieninger, M Denis, PA TI Density functional computational thermochemistry: Isomerization of sulfine and its enthalpy of formation. SO JOURNAL OF PHYSICAL CHEMISTRY B LA English DT Meeting Abstract C1 UDELAR, Fac Quim, DEQUIFIM, CCPG, Montevideo 11800, Uruguay. NCI, Frederick Biomed Supercomp Ctr, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1089-5647 J9 J PHYS CHEM B JI J. Phys. Chem. B PD NOV 1 PY 2001 VL 105 IS 43 BP 23A EP 23A PG 1 WC Chemistry, Physical SC Chemistry GA 489YH UT WOS:000172020200052 ER PT J AU Clay, JR AF Clay, JR TI Moderately alkaline intracellular pH causes spontaneous electrical activity in squid giant axons SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract CT Scientific Meeting of the Physiological-Society CY SEP 05-07, 2001 CL UNIV BRISTOL, BRISTOL, ENGLAND SP Physiolog Soc HO UNIV BRISTOL C1 NINDS, NIH, Bethesda, MD 20892 USA. Marine Biol Lab, Woods Hole, MA 02543 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3751 EI 1469-7793 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD NOV PY 2001 VL 536 SU S BP 120P EP 121P PG 2 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 606ZP UT WOS:000178766200145 ER PT J AU Paydarfar, D Forger, DB Clay, JR AF Paydarfar, D Forger, DB Clay, JR TI Control of transitions between repetitive firing and quiescence by stochastic stimulation of squid axons with membrane bistability SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract CT Scientific Meeting of the Physiological-Society CY SEP 05-07, 2001 CL UNIV BRISTOL, BRISTOL, ENGLAND SP Physiolog Soc HO UNIV BRISTOL ID OSCILLATOR C1 Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA 01655 USA. Univ Massachusetts, Sch Med, Dept Physiol, Worcester, MA 01655 USA. NYU, Courant Inst Math Sci, New York, NY 10012 USA. NINDS, NIH, Bethesda, MD 20892 USA. Marine Biol Lab, Woods Hole, MA 02543 USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3751 EI 1469-7793 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD NOV PY 2001 VL 536 SU S BP 120P EP 120P PG 1 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 606ZP UT WOS:000178766200144 ER PT J AU Jenkins, JF Prows, C Dimond, E Monsen, R Williams, J AF Jenkins, JF Prows, C Dimond, E Monsen, R Williams, J TI Recommendations for educating nurses in genetics SO JOURNAL OF PROFESSIONAL NURSING LA English DT Article DE genetics; nursing curriculum; continuing education; faculty training ID HEREDITARY HEMOCHROMATOSIS; HEALTH; MANAGEMENT AB With the ongoing and increasingly rapid pace of genetic discoveries, nurses must be able to incorporate genetic knowledge into their everyday practices of promoting the genetic health of individuals, families, and communities. Although development of genetic health knowledge is in its infancy, nurses are currently expected to integrate information about genetic risks, testing, and treatments for clients throughout the clients' entire lifespan. All nurses must have an understanding of the relationship between genetics and health to appropriately identify and address genetic concerns in their clients. To fulfill these roles, nurses need to improve their knowledge base in genetics. This article provides recommendations for genetics curriculum in continuing and entry-level nursing education programs. These recommendations are outcomes of a research project involving genetics nurse experts as well as nurses new to the area of genetics, and a consensus workshop of nursing faculty involved in curriculum changes subsequent to an intensive genetics continuing education program. Nursing educators are beginning to recognize the importance of education of all nurses about genetics. If, however, all educators do not accept this responsibility, nurses will be left behind in designing and offering health care for the 21st century. (C) 2001 by W.B. Saunders Company. C1 NCI, NIH, Bethesda, MD 20889 USA. Cincinnati Childrens Hosp, Cincinnati, OH USA. Univ Iowa, Iowa City, IA 52242 USA. RP Jenkins, JF (reprint author), NCI, NIH, Bldg 8,Room 5101, Bethesda, MD 20889 USA. NR 42 TC 23 Z9 24 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 8755-7223 J9 J PROF NURS JI J. Prof. Nurs. PD NOV-DEC PY 2001 VL 17 IS 6 BP 283 EP 290 DI 10.1053/jpnu.2001.28186 PG 8 WC Nursing SC Nursing GA 494LL UT WOS:000172284000007 PM 11712113 ER PT J AU Derijk, RH Schaaf, MJM Turner, G Datson, NA Vreugdenhil, E Cidlowski, J De Kloet, ER Emery, P Sternberg, EM Detera-Wadleigh, SD AF Derijk, RH Schaaf, MJM Turner, G Datson, NA Vreugdenhil, E Cidlowski, J De Kloet, ER Emery, P Sternberg, EM Detera-Wadleigh, SD TI A human glucocorticoid receptor gene variant that increases the stability of the glucocorticoid receptor beta-isoform mRNA is associated with rheumatoid arthritis SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE rheumatoid arthritis; systemic lupus erythematosus; glucocorticoid receptor; ATTA motif ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; MESSENGER-RNA DEGRADATION; AU-RICH ELEMENTS; EXPRESSION; RESISTANCE; CORTICOSTEROIDS; POLYMORPHISMS; SENSITIVITY; SEQUENCE; CORTISOL AB Objective. To study the occurrence and function of polymorphism in the human glucocorticoid receptor (hGR) gene in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Methods. We used single stranded conformation polymorphism (SSCP) and direct sequencing to study the hGR gene in 30 patients with RA, 40 with SLE, and 24 controls. A newly identified polymorphism was transfected in COS-1 cells and the stability of the mRNA containing the polymorphism was tested using real-time PCR. Results. A polymorphism in the hGR gene in exon9 beta, in an "ATTTA" motif, was found to be significantly associated with RA. Introduction of this polymorphism in the hGRb mRNA was found to significantly increase stability in vitro compared to the wild-type sequence. Conclusion. Our findings show an association between RA and a previously unreported polymorphism in the hGR gene. This polymorphism increased stability of hGR beta mRNA, which could contribute to an altered glucocorticoid sensitivity since the hGR beta is thought to function as an inhibitor of hGR alpha activity. C1 Rijngeest Grp, NL-2342 AJ Oegstgeest, Netherlands. Leiden Univ, Leiden, Netherlands. NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. Univ Leeds, Leeds, W Yorkshire, England. NIMH, Sect Neuroendocrine Immunol & Behav, Neural Immune Program, NIH, Bethesda, MD 20892 USA. NIMH, Unit Gene Mapping & Express, Clin Neurogenet Branch, NIH, Bethesda, MD 20892 USA. RP Derijk, RH (reprint author), Rijngeest Grp, Endegeesterstraatweg 5, NL-2342 AJ Oegstgeest, Netherlands. NR 41 TC 166 Z9 174 U1 0 U2 2 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO, ONTARIO M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD NOV PY 2001 VL 28 IS 11 BP 2383 EP 2388 PG 6 WC Rheumatology SC Rheumatology GA 489BQ UT WOS:000171972500004 PM 11708406 ER PT J AU Petzke, F Khine, A Williams, D Groner, K Clauw, DJ Gracely, RH AF Petzke, F Khine, A Williams, D Groner, K Clauw, DJ Gracely, RH TI Dolorimetry performed at 3 paired tender points highly predicts overall tenderness SO JOURNAL OF RHEUMATOLOGY LA English DT Letter ID PRESSURE PAIN THRESHOLD; GENERAL-POPULATION; FIBROMYALGIA; PREVALENCE C1 Georgetown Univ, Med Ctr, Chron Pain & Fatigue Res Ctr, Washington, DC 20007 USA. Natl Inst Dent & Craniofacial Res, Clin Measurement & Mech Unit, Pain & Neurosensory Mech Branch, NIH, Bethesda, MD 20892 USA. RP Petzke, F (reprint author), Georgetown Univ, Med Ctr, Chron Pain & Fatigue Res Ctr, Washington, DC 20007 USA. RI Williams, David/A-1180-2007 NR 9 TC 46 Z9 46 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO, ONTARIO M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD NOV PY 2001 VL 28 IS 11 BP 2568 EP 2569 PG 2 WC Rheumatology SC Rheumatology GA 489BQ UT WOS:000171972500046 PM 11708444 ER PT J AU Dawson, DA AF Dawson, DA TI Alcohol and mortality from external causes SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Article ID UNITED-STATES; CONSUMPTION; INJURIES; SUICIDE; RATES; METAANALYSIS; ASSOCIATION; PHYSICIANS; DRINKING; HOMICIDE AB Objective: The aim of this study was to examine the relationship between alcohol consumption, considering both volume of intake and drinking pattern, and the risk of death from external causes. Method: A prospective study of mortality from external causes was conducted using data from the 1988 National Health Interview Survey linked with the National Death Index for 1988 through 1995. During the 7.5-year follow-up interval, there were 155 deaths from external causes among the 42,910 adults 18 years of age and over included in the sample. Proportional hazards models were used to adjust for censoring due to competing causes of death and for the effects of potentially confounding background variables including age, gender, marital status, education, smoking and poor health at baseline. Results: Relative to lifetime abstainers and infrequent drinkers, the risk of death from external causes increased directly with volume of intake, exhibiting a logarithmic-shaped risk curve. There was no evidence of reduced risk among light or moderate drinkers. When usual quantity and frequency were examined, the only drinkers at significantly increased risk were those who drank less than once a month but usually drank 5+ drinks (or, to a lesser extent, 3+ drinks) and those who drank at least twice a week and usually drank 2+ drinks. Former drinkers also were at increased risk. Age strongly affected the drinking pattern parameters. Conclusions: Quantity and frequency of drinking are proxies for in-the-event risks associated with alcohol intake and their cumulative effect on mortality risk. The results are discussed with particular attention to the role of factors that may affect the association between usual quantity of drinks consumed and the in-the-event risk of mortality from external causes. C1 NIAAA, NIH, Bethesda, MD 20892 USA. RP Dawson, DA (reprint author), NIAAA, NIH, Willco Bldg,Suite 514,6000 Execut Blvd,MSC 7003, Bethesda, MD 20892 USA. NR 25 TC 21 Z9 21 U1 0 U2 2 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA C/O DEIRDRE ENGLISH, 607 ALLISON RD, PISCATAWAY, NJ 08854-8001 USA SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD NOV PY 2001 VL 62 IS 6 BP 790 EP 797 PG 8 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA 517JU UT WOS:000173608000012 PM 11838916 ER PT J AU James, RS Sharp, WS Bastain, TM Lee, PP Walter, JM Czarnolewski, M Castellanos, FX AF James, RS Sharp, WS Bastain, TM Lee, PP Walter, JM Czarnolewski, M Castellanos, FX TI Double-blind, placebo-controlled study of single-dose amphetamine formulations in ADHD SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE attention-cleficit/hyperactivity disorder; dextroamphetamine; Adderall (R); psychostimulants ID DEFICIT HYPERACTIVITY DISORDER; METHYLPHENIDATE; CHILDREN; DEXTROAMPHETAMINE; NONRESPONDERS AB Objective: To compare the efficacy and time course of single morning doses of Adderall (R), extended-release, and immediate-release dextroamphetamine sulfate. Method: Thirty-five children with attention-deficit/hyperactivity disorder, combined type, were given Adderall, immediate-release dextroamphetamine, dextroamphetamine Spansuless, and placebo in a randomized, double-blind, crossover study. Behavior ratings, locomotor activity measurements, and academic measures were obtained over a period of 8 weeks. Results: All three drugs exhibited robust efficacy versus placebo on nearly all measures. The effects of dextroamphetamine Spansules were less robust in the morning, particularly compared with Adderall, but they lasted 3 to 6 hours longer, depending on the measure. Although parent behavior ratings and locomotor activity showed improvements up to 12 hours after single doses of all three drugs, the number of math problems attempted and completed correctly 4 hours after dosing were only robustly increased by Spansules. Conclusions: Both immediate-release amphetamines demonstrated earlier onset of effects, but dextroamphetamine Spansules showed more sustained effects that were present on a wider range of measures. C1 NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. RP Castellanos, FX (reprint author), NYU, Ctr Child Study, 577 1St Ave, New York, NY 10016 USA. NR 24 TC 43 Z9 46 U1 3 U2 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 2001 VL 40 IS 11 BP 1268 EP 1276 DI 10.1097/00004583-200111000-00006 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 485KE UT WOS:000171752900006 PM 11699800 ER PT J AU DiGiovanna, JJ AF DiGiovanna, JJ TI Isotretinoin effects on bone SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article; Proceedings Paper CT Conference on Isotretinoin: State of the Art CY JUN 20-22, 1999 CL NEW YORK, NEW YORK ID POSTERIOR LONGITUDINAL LIGAMENT; SKELETAL RADIOGRAPHIC CHANGES; PREMATURE EPIPHYSEAL CLOSURE; TERM ETRETINATE THERAPY; LOW-DOSE ISOTRETINOIN; 13-CIS-RETINOIC ACID; HYPERVITAMINOSIS-A; HYPEROSTOSIS; CALCIFICATION; OSSIFICATION AB Isotretinoin has demonstrated efficacy in a wide range of disorders. The beneficial effects of the drug, however, arc limited by its adverse effects on the bone. Children exposed to high doses are at risk for premature epiphyseal closure, while adults on long-term therapy have an increased tendency to develop hyperstosis and other changes of the bone. The knowledge of these effects, in conjunction with continued surveillance, are necessary for expert management and call ensure many years of efficacious treatment with minimal toxicity. C1 Brown Univ, Rhode Isl Hosp, Sch Med, Dept Dermatol,Div Dermatopharmacol, Providence, RI 02903 USA. NCI, Basic Res Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP DiGiovanna, JJ (reprint author), Brown Univ, Rhode Isl Hosp, Sch Med, Dept Dermatol,Div Dermatopharmacol, JBS-1,593 Eddy St, Providence, RI 02903 USA. NR 31 TC 48 Z9 48 U1 0 U2 3 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 NOV PY 2001 VL 45 IS 5 BP S176 EP S182 DI 10.1067/mjd.2001.113721 PG 7 WC Dermatology SC Dermatology GA 487CJ UT WOS:000171855800038 PM 11606950 ER PT J AU Alfano, MC Horowitz, AM AF Alfano, MC Horowitz, AM TI Professional and community efforts to prevent morbidity and mortality from oral cancer SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article AB Background. Oral and pharyngeal cancers cause significant morbidity and mortality, yet there has been little improvement survival rates in the past 30 years. Because early diagnoses significantly increase survival rates, the authors summa rize several approaches to educating and mobilizing the dental profession and the public about this problem. Clinicians are invited to initiate similar programs to catalyze change in their own communities. Methods. The authors found that many, approaches have been used to. define the,.problem and initiate change. These include surveys, focus groups, development of consortia, media programs, flyers, leaflets, prescription pads, legislation and professional Results. In Maryland in 1996, only 20 perment of adults reported receving ari oral cancer examination, and most oral cancers, ere diagnosed at late stages by physicians, not dentists. Results of the public educational campaigns in the regions of New York/New Jersey and Maryland have not been form evaluated, but there is a developing consensus that oral cancer diagnostic practices regions with active educational programs are increasing. Conclusions. Coalitions or partnerships among and organizations from government, academia, private practice, industry, the general community and the media can affect awareness about oral cancer prevention and early detection on a regional asis awareness of oral cancer prevention and early detection on a regional basis. Clinical Implications. By increasing awareness of oral cancer among the dental profession and the public, earlier diagnosis of these cancers with consequent improved cure is likely. Providing oral cancer diagnostic services as a routine part of an oral examination also may motivate patients to visit the dentist at least once year. C1 NYU, Coll Dent, New York, NY 10010 USA. NIDCD, NIH, Bethesda, MD USA. RP Alfano, MC (reprint author), NYU, Coll Dent, 345 E 24th St, New York, NY 10010 USA. NR 18 TC 12 Z9 12 U1 1 U2 2 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD NOV PY 2001 VL 132 SU S BP 24S EP 29S PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 495ZY UT WOS:000172371300006 PM 11803649 ER PT J AU Horowitz, AM AF Horowitz, AM TI Perform a death defying act - The 90-second oral cancer examination SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article C1 Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA. RP Horowitz, AM (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Bldg 45,Room 3AN-44B, Bethesda, MD 20892 USA. NR 3 TC 11 Z9 11 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD NOV PY 2001 VL 132 SU S BP 36S EP 40S PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 495ZY UT WOS:000172371300008 ER PT J AU Dwyer, JT Garceau, AO Evans, M Li, DL Lytle, L Hoelscher, D Nicklas, TA Zive, M AF Dwyer, JT Garceau, AO Evans, M Li, DL Lytle, L Hoelscher, D Nicklas, TA Zive, M TI Do adolescent vitamin-mineral supplement users have better nutrient intakes than nonusers? Observations from the CATCH tracking study SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID HEALTH INTERVIEW SURVEY; CARDIOVASCULAR HEALTH; DIETARY-INTAKE; UNITED-STATES; CHILDREN; STUDENTS; TRIAL AB Objective Describe whether users of vitamin-mineral supplements differed from nonusers in micronutrient intakes or in nutrition awareness. Design Cross-sectional, observational study. Subjects One thousand five hundred thirty-two students now in grade 8, who participated in the Third Child and Adolescent Trial for Cardiovascular Health tracking study and who also provided a single 24-hour dietary recall. Statistical analyses performed Mixed-model analysis of covariance was used to ascertain if supplement users had higher vitamin and mineral intakes from food sources, and to examine if supplement users had better nutrition awareness than nonusers. Results The 24-hour recall showed that 17.6% of the students reported using vitamin-mineral supplements. Users reported a mean of 1.4 supplements, of which 47% were multivitamin or multimineral preparations, 37% were single nutrients, and 16% were combinations. White persons and residents of Minnesota and California were more likely to be supplement users. Users had higher micronutrient intakes from food sources for 16 of the 20 nutrients studied after adjusting for gender, race/ethnicity, site, treatment condition, and within-school variability. Users had higher scores on a health behavior survey for food choice and slightly but not significantly higher nutrition knowledge scores. Conclusions Vitamin-mineral supplement use is prevalent among eighth-grade students. Users have higher nutrient intakes from foods, higher total intakes for several micronutrients, higher nutrition awareness, and differ in their demographic characteristics from nonusers. C1 Tufts Univ, Sch Med, Boston, MA 02111 USA. Tufts Univ, Sch Nutr Sci & Policy, Boston, MA 02111 USA. WESTAT Corp, Rockville, MD 20850 USA. Tufts Univ New England Med Ctr, Frances Stern Nutr Ctr, Watertown, MA USA. New England Res Inst, Watertown, MA 02172 USA. NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. NHLBI, Bethesda, MD 20892 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Univ Texas, Sch Publ Hlth, Houston, TX USA. Baylor Coll Med, Childrens Nutr Res Ctr, Waco, TX USA. Tulane Univ, Sch Publ Hlth & Trop Med, Dept Community Hlth Sci, New Orleans, LA USA. Univ Calif San Diego, Div Community Pediat, San Diego, CA 92103 USA. RP Dwyer, JT (reprint author), Tufts Univ, New England Med Ctr Hosp, 750 Washington St,Box 783, Boston, MA 02111 USA. OI Dwyer, Johanna/0000-0002-0783-1769 FU NHLBI NIH HHS [HL-398880, HL 39852, HL 399927, HL-30870, HL-399906] NR 27 TC 38 Z9 40 U1 0 U2 11 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 NOV PY 2001 VL 101 IS 11 BP 1340 EP 1346 DI 10.1016/S0002-8223(01)00321-2 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 499BU UT WOS:000172551800014 PM 11716315 ER PT J AU Roth, SM Ivey, FM Martel, GF Lemmer, JT Hurlbut, DE Siegel, EL Metter, EJ Fleg, JL Fozard, JL Kostek, MC Wernick, DM Hurley, BF AF Roth, SM Ivey, FM Martel, GF Lemmer, JT Hurlbut, DE Siegel, EL Metter, EJ Fleg, JL Fozard, JL Kostek, MC Wernick, DM Hurley, BF TI Muscle size responses to strength training in young and older men and women SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE aging; MRI; muscle mass; resistance training; sarcopenia ID PHYSICAL-ACTIVITY; LEG MUSCLE; AGE; HYPERTROPHY; ADAPTATIONS; ACTIVATION; QUALITY; PEOPLE; GENDER; FORCE AB OBJECTIVES: To examine the possible influences of age and gender on muscle volume responses to strength training (ST). DESIGN: Prospective intervention study. SETTING: University of Maryland Exercise Science and Wellness Research Laboratories. PARTICIPANTS: Eight young men (age 20-30 years), six young women (age 20-30 years), nine older men (age 65-75 years), and ten older women (age 65-75 years). INTERVENTION: A 6-month whole-body ST program that exercised all major muscle groups of the upper and lower body 3 days/week. MEASUREMENTS: Thigh and quadriceps muscle volumes and mid-thigh muscle cross-sectional area (CSA) were assessed by magnetic resonance imaging before and after the ST program. RESULTS: Thigh and quadriceps muscle volume increased significantly in all age and gender groups as a result of ST (P < .001), with no significant differences between the groups. Modest correlations were observed between both the change in quadriceps versus the change in total thigh muscle volume (r = 0.65; P < .001) and the change in thigh muscle volume versus the change in mid-thigh CSA (r = 0.76, P < .001). CONCLUSIONS: The results indicate that neither age nor gender affects muscle volume response to whole-body ST. Muscle volume, rather than muscle CSA, is recommended for studying muscle mass responses to ST. C1 Univ Maryland, Dept Kinesiol, College Pk, MD 20742 USA. Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA. Univ Maryland, Sch Med, Div Gerontol, Baltimore, MD 21201 USA. Univ Maryland Eastern Shore, Dept Phys Therapy, Princess Anne, MD USA. Tufts Univ, Jean Mayer USDA HNRC Aging, Boston, MA 02111 USA. Baltimore VA Med Ctr, Dept Radiol, Baltimore, MD USA. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. Florida Gerontol Res & Training Serv, Palm Harbor, FL USA. RP Hurley, BF (reprint author), Univ Maryland, Dept Kinesiol, College Pk, MD 20742 USA. RI Fozard, James Leonard/B-3660-2009; OI Roth, Stephen/0000-0002-7841-3695 FU NIA NIH HHS [AG-00268, AG-05893, AG-42148] NR 26 TC 60 Z9 62 U1 3 U2 15 PU BLACKWELL SCIENCE 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 NOV PY 2001 VL 49 IS 11 BP 1428 EP 1433 DI 10.1046/j.1532-5415.2001.4911233.x PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 490MF UT WOS:000172055100003 PM 11890579 ER PT J AU Guralnik, JM Ferrucci, L Balfour, JL Volpato, S Di Iorio, A AF Guralnik, JM Ferrucci, L Balfour, JL Volpato, S Di Iorio, A TI Progressive versus catastrophic loss of the ability to walk: Implications for the prevention of mobility loss SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE disability; functional status; mobility; aging; chronic disease ID OLDER PERSONS; FUNCTIONAL OUTCOMES; HIP FRACTURE; DISABILITY; HOSPITALIZATION; PREDICTORS; PATTERNS; DECLINE; ADULTS; TRIAL AB OBJECTIVES: Loss of mobility is an important functional outcome that can have devastating effects on quality of life and the ability of older persons to remain independent in the community. Although a large amount of research has been done on risk factors for disability onset, little work has focused on the pace of disability progression. This study characterizes the development of severe walking disability over time and evaluates risk factors and subsequent mortality as they relate to mobility disability with progressive or catastrophic onset. DESIGN: Population-based prospective cohort study with annual follow-up assessments for up to 7 years SETTING: Three communities of the Established Populations for Epidemiologic Studies of the Elderly. PARTICIPANTS: There were 5,355 persons not disabled at baseline and the first follow-up who had adequate data available to classify mobility disability during subsequent follow-ups. MEASUREMENTS: Severe mobility disability was defined as the need for help from a person to walk across a room or inability to walk across a room. Those developing severe mobility disability were classified as having progressive mobility disability if they had been unable to walk half a mile in either of the prior 2 years. They were classified as having catastrophic mobility disability if they reported having been able to walk half a mile in two previous annual interviews. RESULTS: The overall incidence of severe mobility disability was 11.6 cases/1,000 person years. Those age 85 and older or having three or ii-tore chronic conditions at baseline were significantly more likely to develop progressive disability than catastrophic disability. Stroke, hip fracture, and cancer occurring during follow-up were associated with very high risk of severe mobility disability. For stroke and hip fracture, the risk was twice as high for catastrophic disability as for progressive disability, but this difference did not reach statistical significance. Risk for catastrophic disability from cancer was significantly greater than for progressive disability. Half of catastrophic disability subjects had stroke, hip fracture, or cancer in the year immediately preceding this disability. Incident heart attack did not predict severe mobility disability. Among those who developed severe mobility disability, type of disability did not influence subsequent survival for the first 3 years, but beyond 3 years those with catastrophic disability had a relative risk of death of 0.4 (95% confidence interval 0.2-0.9) compared with those with progressive disability. CONCLUSION: The observation that risk factors and mortality outcomes were both different for progressive and catastrophic mobility disability supports the value of ascertaining the pace of disability development as a useful characterization of disability. Further progress in developing prevention and treatment strategies may be made by taking the pace of disability development into account. C1 NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA. INRCA Geriatr Dept, Florence, Italy. Univ Chieti, Inst Geriatr Med, Chieti, Italy. RP Guralnik, JM (reprint author), NIA, Lab Epidemiol Demog & Biometry, 7201 Wisconsin Ave,Suite 3C-309, Bethesda, MD 20892 USA. RI VOLPATO, STEFANO/H-2977-2014 OI VOLPATO, STEFANO/0000-0003-4335-6034 FU NIA NIH HHS [N01-AG-0-2105, N01-AG-0-2106, N01-AG-0-2107] NR 30 TC 73 Z9 85 U1 6 U2 11 PU BLACKWELL SCIENCE 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 NOV PY 2001 VL 49 IS 11 BP 1463 EP 1470 DI 10.1046/j.1532-5415.2001.4911238.x PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 490MF UT WOS:000172055100008 PM 11890584 ER PT J AU Christensen, K Frederiksen, H Hoffman, HJ AF Christensen, K Frederiksen, H Hoffman, HJ TI Genetic and environmental influences on self-reported reduced hearing in the old and oldest old SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE hearing impairment; genetics; epidemiology; twins; heritability ID AGE; PREVALENCE; POPULATION; TWINS; ADULTS; IMPAIRMENT; THRESHOLDS; DEAFNESS AB OBJECTIVES: The aim of the present twin study was to estimate the relative importance of genetic and environmental factors in variation in self-reported reduced hearing among the old and the oldest old. DESIGN: Self-reported hearing abilities of older twins assessed at intake interview in a population-based longitudinal survey. SETTING: Denmark. PARTICIPANTS: Twins age 75 and older identified in the population-based Danish Twin Registry in 1995. An interview was conducted with 77% of 3,099 individuals in the stud), population. In 1997 and 1999, a follow-up contact to the survivors was made and an additional 2,778 twins, age 70-76, were included in the study. MEASUREMENTS: Reduced hearing was assessed by the same question in all interview waves. Heritability (proportion of the population variance attributable to genetic variation) was estimated using structural-equation analyses. RESULTS: The prevalence of self-reported reduced hearing corresponded to previous studies and showed the expected age and sex dependence. Concordance rates, odds ratios, and correlations were consistently higher for monozygotic twin pairs than for dizygotic twin pairs in all age and sex categories, indicating heritable effects. Structural-equation analyses revealed a substantial heritability for self-reported reduced hearing of 40% (95% Cl = 19-53%). The remaining variation could be attributed to individuals' nonfamilial environments. CONCLUSION: We found that genetic factors play an important role in self-reported reduced hearing in both men and women age 70 and older. Because self-reports of reduced hearing involve misclassification, this estimate of the genetic influence on hearing disabilities is probably conservative. Hence, genetic and environmental factors play a substantial role in reduced hearing among the old and oldest old. This suggests that clinical epidemiological studies of age-related hearing loss should include not only information on environmental exposures but also on family history of hearing loss and, if possible, biological samples for future studies of candidate genes for hearing loss. C1 Danish Twin Registry, Inst Publ Hlth, DK-5000 Odense C, Denmark. Danish Ctr Demog Res, Odense, Denmark. Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA. RP Christensen, K (reprint author), Danish Twin Registry, Inst Publ Hlth, Sdr Blvd 23A St, DK-5000 Odense C, Denmark. RI Christensen, Kaare/C-2360-2009 OI Christensen, Kaare/0000-0002-5429-5292 FU NIA NIH HHS [P01-AG08761] NR 32 TC 49 Z9 56 U1 1 U2 3 PU BLACKWELL SCIENCE 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 NOV PY 2001 VL 49 IS 11 BP 1512 EP 1517 DI 10.1046/j.1532-5415.2001.4911245.x PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 490MF UT WOS:000172055100015 PM 11890591 ER PT J AU Simonsick, EM Montgomery, PS Newman, AB Bauer, DC Harris, T AF Simonsick, EM Montgomery, PS Newman, AB Bauer, DC Harris, T TI Measuring fitness in healthy older adults: The health ABC long distance corridor walk SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE fitness testing; older; validation ID CHRONIC HEART-FAILURE; 6-MINUTE WALK; KNEE OSTEOARTHRITIS; TREADMILL WALKING; EXERCISE CAPACITY; ELDERLY SUBJECTS; DISEASE; REPRODUCIBILITY; PERFORMANCE; POPULATION AB OBJECTIVES: The Health ABC Long Distance Corridor Walk (LDCW) was designed to extend the testing range of self-paced walking tests of fitness for older adults by including a warm-up and timing performance over 400 meters. This study compares performance on the LDCW and 6-minute walk to determine whether the LDCW encourages greater participant effort. DESIGN: Subjects were administered the LDCW and 6-minute walk during a single visit. Test order alternated between subjects, and a 15-minute rest was given between tests, SETTING: The Baltimore Veterans Affairs Medical Center. PARTICIPANTS: Twenty volunteers age 70 to 78. MEASUREMENTS: The LDCW, consisting of a 2-minute warm-up walk followed by a 400-meter walk and a 6-minute walk test were administered using a 20-meter long course in an unobstructed hallway. Heart rate (HR) and blood pressure (BP) were recorded at rest and before and after all walks. RESULTS: All 20 subjects walked a faster pace over 400 meters than for 6 minutes, in which the mean distance covered was 402 meters. From paired t-tests, walking speed was faster (mean difference = 0.23 m/sec; P < .001), and ending FIR (mean difference = 7.6 bpm; P < .001) and systolic BP (mean difference = 8.3 mmHg; P = .024) were greater for the 400-meter walk than for the 6-minute walk. Results were independent of test order and subject fitness level. CONCLUSIONS: Providing a warm-up walk and using a target distance instead of time encouraged subjects to work closer to their maximum capacity. This low-cost alternative to treadmill testing can be used in research and clinical settings to assess fitness and help identify early functional decline in older adults. C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Pittsburgh, Dept Med, Div Geriatr Med, Pittsburgh, PA USA. Vet Adm Med Ctr, Dept Geriatr, Baltimore, MD 21218 USA. NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA. RP Simonsick, EM (reprint author), NIA, Ctr Gerontol Res, 5600 Nathan Shock Dr,Box 06, Baltimore, MD 21224 USA. RI Agaliotis, Maria/G-5334-2012; Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 NR 25 TC 128 Z9 131 U1 3 U2 15 PU BLACKWELL SCIENCE 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 NOV PY 2001 VL 49 IS 11 BP 1544 EP 1548 DI 10.1046/j.1532-5415.2001.4911247.x PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 490MF UT WOS:000172055100021 PM 11890597 ER PT J AU Berger, A AF Berger, A TI Palliative care in long-term-care facilities - A comprehensive model SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Editorial Material C1 NIH, Ctr Clin, Bethesda, MD 20892 USA. RP Berger, A (reprint author), NIH, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA. NR 9 TC 4 Z9 4 U1 3 U2 3 PU BLACKWELL SCIENCE 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 NOV PY 2001 VL 49 IS 11 BP 1570 EP 1571 DI 10.1046/j.1532-5415.2001.4911257.x PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 490MF UT WOS:000172055100027 PM 11890603 ER PT J AU Yasnoff, WA Overhage, JM Humphreys, BL LaVenture, M AF Yasnoff, WA Overhage, JM Humphreys, BL LaVenture, M TI A national agenda for public health informatics: Summarized recommendations from the 2001 AMIA Spring Congress SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB The AMIA 2001 Spring Congress brought together members of the the public health and informatics communities to develop a national agenda for public health informatics. Discussions of funding and governance; architecture and infrastructure; standards and vocabulary; research, evaluation, and best practices; privacy, confidentiality, and security; and training and workforce resulted in 74 recommendations with two key themes-that all stakeholders need to be engaged in coordinated activities related to public health information architecture, standards, confidentiality, best practices, and research; and that informatics training is needed throughout the public health workforce. Implementation of this consensus agenda will help promote progress in the application of information technology to improve public health. C1 US Ctr Dis Control & Prevent, Atlanta, GA USA. Indiana Univ, Indianapolis, IN 46204 USA. Natl Lib Med, Bethesda, MD USA. Minnesota Dept Hlth, Minneapolis, MN USA. RP Yasnoff, WA (reprint author), CDC, Mailstop K-36, Atlanta, GA 30333 USA. OI Overhage, Joseph/0000-0003-0223-0195 NR 10 TC 44 Z9 46 U1 1 U2 4 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PD NOV-DEC PY 2001 VL 8 IS 6 BP 535 EP 545 PG 11 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA 493YW UT WOS:000172251900002 PM 11687561 ER PT J AU Irvine, T Stetten, GD Sachdev, V Zetts, AD Jones, M Mori, Y Ramsperger, C Castellucci, JB Kenny, A Panza, JA von Ramm, OT Sahn, DJ AF Irvine, T Stetten, GD Sachdev, V Zetts, AD Jones, M Mori, Y Ramsperger, C Castellucci, JB Kenny, A Panza, JA von Ramm, OT Sahn, DJ TI Quantification of aortic regurgitation by real-time 3-dimensional echocardiography in a chronic animal model: Computation of aortic regurgitant volume as the difference between left and right ventricular stroke volumes SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY LA English DT Article; Proceedings Paper CT 10th Annual Scientific Sessions of the American-Society-of-Echocardiography CY JUN 13-16, 1999 CL WASHINGTON, D.C. SP Amer Soc Echocardiog ID FLOW CONVERGENCE REGION; IMAGED VENA-CONTRACTA; MITRAL REGURGITATION; IN-VITRO; EJECTION FRACTION; IMAGING-SYSTEM; DOPPLER; RECONSTRUCTION; VALIDATION; ULTRASOUND AB Background: The accuracy of conventional 2-dimensional echocardiographic and Doppler techniques for the quantification of valvular regurgitation remains controversial. In this study, we examined the ability of real-time 3-dimensional (RT3D) echocardiography to quantify aortic regurgitation by computing aortic regurgitant volume as the difference between 3D echocardiographic-determined left and right ventricular stroke volumes in a chronic animal model. Methods. Three to 6 months before the study, 6 sheep underwent surgical incision of one aortic valve cusp to create aortic regurgitation. During the subsequent open chest study session, a total of 25 different steady-state hemodynamic conditions were examined. Electromagnetic (EM) flow probes were placed around the main pulmonary artery and ascending aorta and balanced against each other to provide reference right and left ventricular stroke volume (RVSV and LVSV) data. RT3D imaging was performed by epicardial placement of a matrix array transducer on the volumetric ultrasound system, originally developed at the Duke University Center for Emerging Cardiovascular Technology. During each hemodynamic steady state, the left and right ventricles were scanned in rapid succession and digitized image loops stored for subsequent measurement of end-diastolic and end-systolic volumes. Left and right ventricular stroke volumes and aortic regurgitant volumes were then calculated and compared with reference EM-derived values. Results. There was good correlation between RT3D left and right ventricular stroke volumes and reference data (r = 0.83, y = 0.94x + 2.6, SEE = 9.86 mL and r = 0.63, y = 0.8x - 1.0, SEE - 5.37 mL, respectively). The resulting correlation between 3D- and EM-derived aortic regurgitant volumes was at an intermediate level between that for LVSV and that for RVSV (r = 0.80, y = 0.88x + 7.9, SEE = 10.48 mL). RT3D tended to underestimate RVSV (mean difference -4.7 +/- 5.4 mL per beat, compared with -0.03 +/- 9.7 mL per beat for the left ventricle). There was therefore a small overestimation of aortic regurgitant volume (4.7 +/- 10.4 mL per beat). Conclusion: Quantification of aortic regurgitation through the computation of ventricular stroke volumes by RT3D is feasible and shows good correlation with reference flow data. This method should also be applicable to the quantification of other valvular lesions or single site intracardiac shunts where a difference between right and left ventricular cavity stroke volumes is produced. C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Duke Univ, Durham, NC USA. NHLBI, Bethesda, MD 20892 USA. Freeman Rd Hosp, Newcastle Upon Tyne NE7 7DN, Tyne & Wear, England. RP Sahn, DJ (reprint author), Oregon Hlth Sci Univ, L608,3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. NR 33 TC 12 Z9 13 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0894-7317 J9 J AM SOC ECHOCARDIOG JI J. Am. Soc. Echocardiogr. PD NOV PY 2001 VL 14 IS 11 BP 1112 EP 1118 DI 10.1067/mje.2001.115660 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 491JW UT WOS:000172106100012 PM 11696837 ER PT J AU Zivadinovic, D Vidovic, S Matic, G Andjus, RK AF Zivadinovic, D Vidovic, S Matic, G Andjus, RK TI Hyperthermic stress affects the thermal modulation of glucocorticoid-receptor affinity SO JOURNAL OF THERMAL BIOLOGY LA English DT Article DE glucocorticoid receptor; hormone-receptor affinity; hyperthermia ID HEAT-SHOCK-PROTEIN; RAT-LIVER; LACTATE-DEHYDROGENASE; FUNCTIONAL-PROPERTIES; TEMPERATURE; BINDING; HSP70; PH AB In vitro binding of a steroid hormone (triamcinolone acetonide) to hepatic glucocorticoid receptors was studied in liver cytosols prepared from untreated control rats and rats sacrificed after being exposed in vivo to whole body hyperthermia (41 or 42 degreesC). Positive temperature modulation of glucocorticoid-receptor affinity (decrease of affinity with increasing temperature) was well expressed in all preparations. In preparations from hyperthermic rats, alterations of a possible functional (adaptive) significance have been recorded: the amplitude of positive thermal modulation was reduced, and its lower-temperature limit shifted towards higher temperatures. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Univ Belgrade, Ctr Multidisciplinary Studies, YU-11060 Belgrade, Yugoslavia. Univ Banja Luka, Fac Med, Dept Biol & Human Genet, Banja Luka 78000, Bosnia & Herceg. Inst Biol Res, YU-11060 Belgrade, Yugoslavia. RP Zivadinovic, D (reprint author), NICHHD, ERRB, N111,Bldg 49,Room 6B-23,49 Convent Dr,MSC 4510, Bethesda, MD 20892 USA. OI Matic, Gordana/0000-0002-0142-1056 NR 37 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4565 J9 J THERM BIOL JI J. Therm. Biol. PD NOV PY 2001 VL 26 IS 6 BP 575 EP 584 DI 10.1016/S0306-4565(01)00003-1 PG 10 WC Biology; Zoology SC Life Sciences & Biomedicine - Other Topics; Zoology GA 491KG UT WOS:000172107100006 ER PT J AU Karck, M Tanaka, S Bolling, SF Simon, A Su, TP Oeltgen, PR Haverich, A AF Karck, M Tanaka, S Bolling, SF Simon, A Su, TP Oeltgen, PR Haverich, A TI Myocardial protection by ischemic preconditioning and delta-opioid receptor activation in the isolated working rat heart SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID HIBERNATION INDUCTION TRIGGERS; K-ATP CHANNELS; NATURAL HIBERNATION; POTASSIUM CHANNELS; PRESERVATION; NALOXONE; LINK AB Objective: delta -Opioid receptors are involved in the cardioprotective effect of ischemic preconditioning. This study was designed (1) to assess the protective capacities of ischemic preconditioning and the synthetic delta -opioid receptor agonist D-Ala(2)-D-Leu(5) enkephalin (DADLE) in a functionally oriented experimental model of ischemia. and reperfusion and (2) to assess whether the effects of both protective measures are similarly blocked by naloxone, a nonspecific delta -opioid receptor antagonist. Methods: Sixty-four isolated working rat hearts were subjected to 45 minutes of hypothermic ischemia at 30 degreesC followed by 25 minutes of normothermic reperfusion. Rats were pretreated with DADLE (1 mg/kg body weight intravenously), naloxone (3 mg/k-g body weight intravenously), or a combination thereof within 60 minutes before onset of isolated heart perfusion. During the preischemic perfusion period, 8 hearts per group were preconditioned by one cycle of 5 minutes of normothermic global ischemia and subsequent reperfusion whereas another 8 served as nonpreconditioned controls. The postischemic functional recovery of hearts and their creatine kinase leakage were determined. Results: Pretreatment with DADLE and ischemic preconditioning improved the postischemic recovery of aortic flow when compared with nonpreconditioning (57.7% +/- 4.0% and 60.8% +/- 4.3% vs 40.0% +/- 4.2% of preischemic baseline value, P < .001). Combined pretreatment with DADLE before ischemic preconditioning afforded additional aortic flow recovery compared with pretreatment with DADLE alone (68.6% +/- 3.3% vs 57.7% +/- 4.0% of preischemic baseline value; P =.038). With combined pretreatment, early postischemic creatine kinase release was lower than control in hearts without pretreatment (0.48 +/- 0.11 vs 0.80 +/- 0.12 IU/5 minutes per heart; P =.001). Naloxone abolished the beneficial functional effects of pretreatment with DADLE and ischemic preconditioning. Conclusions: Pharmacologic activation of delta -opioid receptors affords improvement of functional protection in isolated working rat hearts similar to that conferred by classic ischemic preconditioning. The combination of both pretreatments reduces ischemic cellular damage and further adds to postischemic functional recovery. These changes are reversed by naloxone, an observation providing evidence that ischemic preconditioning involves signaling through opioid receptors. C1 Hannover Med Sch, Dept Thorac & Cardiovasc Surg, D-30623 Hannover, Germany. Univ Michigan Hosp, Sect Cardiac Surg, Ann Arbor, MI 48109 USA. Natl Inst Drug Abuse, Addict Res Ctr, Baltimore, MD 21224 USA. Univ Kentucky, Coll Med, Dept Pathol, Lexington, KY USA. RP Karck, M (reprint author), Hannover Med Sch, Dept Thorac & Cardiovasc Surg, D-30623 Hannover, Germany. NR 30 TC 20 Z9 23 U1 0 U2 1 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 NOV PY 2001 VL 122 IS 5 BP 986 EP 992 DI 10.1067/mtc.2001.116950 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA 493VV UT WOS:000172244900021 PM 11689805 ER PT J AU Walther, MM Pautler, S AF Walther, MM Pautler, S TI Re: von Hippel-Lindau disease: Renal tumors less than 3 cm. can metastasize SO JOURNAL OF UROLOGY LA English DT Letter C1 NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA. RP Walther, MM (reprint author), NCI, Urol Oncol Branch, NIH, Bldg 10,Room 2B-43,10 Ctr Dr, Bethesda, MD 20892 USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0022-5347 J9 J UROLOGY JI J. Urol. PD NOV PY 2001 VL 166 IS 5 BP 1837 EP 1837 DI 10.1016/S0022-5347(05)65694-7 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA 481YC UT WOS:000171547200064 PM 11586243 ER PT J AU Vorberg, I Chan, K Priola, SA AF Vorberg, I Chan, K Priola, SA TI Deletion of beta-strand and alpha-helix secondary structure in normal prion protein inhibits formation of its protease-resistant isoform SO JOURNAL OF VIROLOGY LA English DT Article ID FOLLICULAR DENDRITIC CELLS; CREUTZFELDT-JAKOB-DISEASE; SCRAPIE-ASSOCIATED FORM; NEURO-BLASTOMA CELLS; CULTURED-CELLS; TRANSGENIC MICE; NEUROBLASTOMA-CELLS; MASS-SPECTROMETRY; SPECIES BARRIERS; PRP 27-30 AB A fundamental event in the pathogenesis of transmissible spongiform encephalopathies (TSE) is the conversion of a normal, proteinase K-sensitive, host-encoded protein, PrP-sen, into its protease-resistant isoform, PrP-res. During the formation of PrP-res, PrP-sen undergoes conformational changes that involve an increase of P-sheet secondary structure. While previous studies in which PrP-sen deletion mutants were expressed in transgenic mice or scrapie-infected cell cultures have identified regions in PrP-sen that are important in the formation of PrP-res, the exact role of PrP-sen secondary structures in the conformational transition of PrP-sen to PrP-res has not yet been defined. We constructed PrP-sen mutants with deletions of the first beta -strand, the second beta -strand, or the first alpha -helix and tested whether these mutants could be converted to PrP-res in both scrapie-infected neuroblastoma cells (Sc+-MNB cells) and a cell-free conversion assay. Removal of the second beta -strand or the first a-helix significantly altered both processing and the cellular localization of PrP-sen, while deletion of the first beta -strand had no effect on these events. However, all of the mutants significantly inhibited the formation of PrP-res in Sc+-MNB cells and had a greatly reduced ability to form protease-resistant PrP in a cell-free assay system. Thus, our results demonstrate that deletion of the beta -strands and the first alpha -helix of PrP-sen can fundamentally affect PrP-res formation and/or PrP-sen processing. C1 NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA. RP Priola, SA (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA. NR 67 TC 28 Z9 30 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10024 EP 10032 DI 10.1128/JVI.75.21.10024-10032.2001 PG 9 WC Virology SC Virology GA 480DZ UT WOS:000171447900002 PM 11581371 ER PT J AU Race, R Raines, A Raymond, GJ Caughey, B Chesebro, B AF Race, R Raines, A Raymond, GJ Caughey, B Chesebro, B TI Long-term subclinical carrier state precedes scrapie replication and adaptation in a resistant species: Analogies to bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease in humans SO JOURNAL OF VIROLOGY LA English DT Article ID TRANSMISSIBLE MINK ENCEPHALOPATHY; CHRONIC WASTING DISEASE; PRION PROTEIN; DIFFERENT STRAINS; HAMSTER SCRAPIE; AGENT; MICE; SHEEP; SUSCEPTIBILITY; PATHOGENESIS AB Cattle infected with bovine spongiform encephatopathy (BSE) appear to be a reservoir for transmission of variant Creutzfeldt-Jakob disease (vCJD) to humans. Although just over 100 people have developed clinical vCJD, millions have probably been exposed to the infectivity by consumption of BSE-infected beef. It is currently not known whether some of these individuals will develop disease themselves or act as asymptomatic carriers of infectivity which might infect others in the future. We have studied agent persistence and adaptation after cross-species infection, using a model of mice inoculated with hamster scrapie strain 263K. Although mice inoculated with hamster scrapie do not develop clinical disease after inoculation with 10 million hamster infectious doses, hamster scrapie infectivity persists in brain and spleen for the life span of the mice. In the present study, we were surprised to find a I-year period postinfection with hamster scrapie where there was no evidence for replication of infectivity in mouse brain. In contrast, this period of inactive persistence was followed by a period of active replication of infectivity as well as adaptation of new strains of agent capable of causing disease in mice. In most mice, neither the early persistent phase nor the later replicative phase could be detected by immunoblot assay for protease-resistant prion protein (PrP). If similar asymptomatic carriers of infection arise after exposure of humans or animals to BSE, this could markedly increase the danger of additional spread of BSE or vCJD infection by contaminated blood, surgical instruments, or meat. If such subclinical carriers were negative for protease-resistant PrP, similar to our mice, then the recently proposed screening of brain, tonsils, or other tissues of animals and humans by present methods such as immunobtotting or immunohistochemistry might be too insensitive to identify these individuals. C1 NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT 59840 USA. RP Chesebro, B (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, 903 S 4th St, Hamilton, MT 59840 USA. EM bchesebro@nih.gov NR 25 TC 109 Z9 109 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 NOV PY 2001 VL 75 IS 21 BP 10106 EP 10112 DI 10.1128/JVI.75.21.10106-10112.2001 PG 7 WC Virology SC Virology GA 480DZ UT WOS:000171447900009 PM 11581378 ER PT J AU Glushakova, S Munch, J Carl, S Greenough, TC Sullivan, JL Margolis, L Kirchhoff, F AF Glushakova, S Munch, J Carl, S Greenough, TC Sullivan, JL Margolis, L Kirchhoff, F TI CD4 down-modulation by human immunodeficiency virus type 1 Nef correlates with the efficiency of viral replication and with CD4(+) T-cell depletion in human lymphoid tissue ex vivo SO JOURNAL OF VIROLOGY LA English DT Article ID LONG-TERM SURVIVOR; SURFACE CD4; INFECTION; HIV-1; EXPRESSION; GENE; LYMPHOCYTES; ACTIVATION; ALLELES; PROTEIN AB The human immunodeficiency virus type 1 (HIV-1) Nef protein is an important virulence factor. Nef has several functions, including down-modulation of CD4 and class I major histocompatibility complex cell surface expression, enhancement of virion infectivity, and stimulation of viral replication in peripheral blood mononuclear cells. Nef also increases HIV-1 replication in human lymphoid tissue (HLT) ex vivo. We analyzed recombinant and primary nef alleles with highly divergent activity in different in vitro assays to clarify which of these Nef activities are functionally linked. Our results demonstrate that Nef activity in CD4 downregulation correlates significantly with the efficiency of HIV-1 replication and with the severity of CD4(+) T-celI depletion in HLT. In conclusion, HIV-1 Nef variants with increased activity in CD4 down-modulation would cause severe depletion of CD4(+) T cells in lymphoid tissues and accelerate AIDS progression. C1 NICHHD, Lab Mol & Cellular Biophys, NIH, Bethesda, MD 20892 USA. Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA. Univ Erlangen Nurnberg, Inst Clin & Mol Virol, D-91054 Erlangen, Germany. RP Margolis, L (reprint author), Univ Ulm Klinikum, Abt Virol, Albert Einstein Allee 11, D-89081 Ulm, Germany. NR 31 TC 81 Z9 81 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10113 EP 10117 DI 10.1128/JVI.75.21.10113-10117.2001 PG 5 WC Virology SC Virology GA 480DZ UT WOS:000171447900010 PM 11581379 ER PT J AU Lifson, JD Rossio, JL Piatak, M Parks, T Li, L Kiser, R Coalter, V Fisher, B Flynn, BM Czajak, S Hirsch, VM Reimann, KA Schmitz, JE Ghrayeb, J Bischofberger, N Nowak, MA Desrosiers, RC Wodarz, D AF Lifson, JD Rossio, JL Piatak, M Parks, T Li, L Kiser, R Coalter, V Fisher, B Flynn, BM Czajak, S Hirsch, VM Reimann, KA Schmitz, JE Ghrayeb, J Bischofberger, N Nowak, MA Desrosiers, RC Wodarz, D TI Role of CD8(+) lymphocytes in control of simian immunodeficiency virus infection and resistance to rechallenge after transient early antiretroviral treatment SO JOURNAL OF VIROLOGY LA English DT Article ID T-CELL DEPLETION; RHESUS MACAQUES; IMMUNE-RESPONSES; HIV-INFECTION; HETEROLOGOUS CHALLENGE; MONOCLONAL-ANTIBODY; VIRAL REPLICATION; PLASMA VIREMIA; SIV INFECTION; PROTECTION AB Transient antiretroviral treatment with tenofovir, (R)-9-(2-phosphonylmethoxypropyl) adenine, begun shortly after inoculation of rhesus macaques with the highly pathogenic simian immunodeficiency virus (SIV) isolate SIVsmE660, facilitated the development of SIV-specific lymphoproliferative responses and sustained effective control of the infection following drug dis continuation. Animals that controlled plasma viremia following transient postinoculation treatment showed substantial resistance to subsequent intravenous rechallenge with homologous (SIVsmE660) and highly heterologous (SIVmac239) SIV isolates, up to more than 1 year later, despite the absence of measurable neutralizing antibody. In some instances, resistance to rechallenge was observed despite the absence of detectable SIV-specific binding antibody and in the face of SIV lymphoproliferative responses that were low or undetectable at the time of challenge. In vivo monoclonal antibody depletion experiments demonstrated a critical role for CD8(+) lymphocytes in the control of viral replication; plasma viremia rose by as much as five log units after depletion of CD8(+) cells and returned to predepletion levels (as low as <100 copy Eq/ml) as circulating CD8(+) cells were restored. The extent of host control of replication of highly pathogenic SIV strains and the level of resistance to heterologous rechallenge achieved following transient postinoculation treatment compared favorably to the results seen after SIVsmE660 and SIVmac239 challenge with many vaccine strategies. This impressive control of viral replication was observed despite comparatively modest measured immune responses, less than those often achieved with vaccination regimens. The results help establish the underlying feasibility of efforts to develop vaccines for the prevention of AIDS, although the exact nature of the protective host responses involved remains to be elucidated. C1 NCI, Retroviral Pathogenesis Lab, AIDS Vaccine Program, SAIC Frederick, Ft Detrick, MD 21702 USA. NCI, Vaccine Support Lab, AIDS Vaccine Program, SAIC Frederick, Ft Detrick, MD 21702 USA. NCI, Anim Sci Branch, Bethesda, MD 20892 USA. Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Southborough, MA 01772 USA. NIAID, Mol Microbiol Lab, NIH, Rockville, MD 20852 USA. Centocor Inc, Malvern, PA 19355 USA. Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02215 USA. Gilead Sci Inc, Foster City, CA 94404 USA. Inst Adv Study, Program Theoret Biol, Princeton, NJ 08540 USA. RP Lifson, JD (reprint author), NCI, Retroviral Pathogenesis Lab, AIDS Vaccine Program, SAIC Frederick, Bldg 535,5th Floor, Ft Detrick, MD 21702 USA. RI Nowak, Martin/A-6977-2008 FU NCI NIH HHS [N01-CO-56000]; NCRR NIH HHS [R01 RR 13150, R24 RR 160001] NR 46 TC 214 Z9 218 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10187 EP 10199 DI 10.1128/JVI.75.21.10187-10199.2001 PG 13 WC Virology SC Virology GA 480DZ UT WOS:000171447900018 PM 11581387 ER PT J AU Hu, Y Lee, J McCart, JA Xu, H Moss, B Alexander, HR Bartlett, DL AF Hu, Y Lee, J McCart, JA Xu, H Moss, B Alexander, HR Bartlett, DL TI Yaba-like disease virus: An alternative replicating poxvirus vector for cancer gene therapy SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT VACCINIA VIRUS; THYMIDINE KINASE; EXPRESSION VECTORS; ANTIGEN; MODEL; ADENOVIRUS; PROMOTERS; MELANOMA; TANAPOX; CELLS AB Vaccinia virus is being investigated as a replicating vector for tumor-directed gene therapy. However, the majority of cancer patients have preformed immunologic reactivity against vaccinia virus, as a result of smallpox vaccination, which may limit its use as a vector. The Yaba-like disease (YLD) virus was investigated here as an alternative, replicating poxvirus for cancer gene therapy. We have demonstrated that the YLD virus does not cross-react with vaccinia virus antibodies, and it replicates efficiently in human tumor cells. YLD virus can be expanded and purified to high titer in CV-1 cells under conditions utilized for vaccinia virus. The YLD virus RNA polymerase was able to express genes regulated by a synthetic promoter designed for use in orthopoxviruses. We sequenced, the YLD virus TK gene and created a shuttle plasmid, which allowed the recombination of the green fluorescent protein (GFP) gene into the YLD virus. In a murine model of ovarian cancer, up to 38% of cells in the tumor expressed the GFP transgene 12 days after intraperitoneal virus delivery. YLD virus has favorable characteristics as a vector for cancer gene therapy, and this potential should be explored further. C1 NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. RP Bartlett, DL (reprint author), NCI, Surg Branch, NIH, Bldg 10,Rm 2B16,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 36 TC 28 Z9 28 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10300 EP 10308 DI 10.1128/JVI.75.21.10300-10308.2001 PG 9 WC Virology SC Virology GA 480DZ UT WOS:000171447900029 PM 11581398 ER PT J AU Roden, RBS Day, PM Bronzo, BK Yutzy, WH Yang, YQ Lowy, DR Schiller, JT AF Roden, RBS Day, PM Bronzo, BK Yutzy, WH Yang, YQ Lowy, DR Schiller, JT TI Positively charged termini of the L2 minor capsid protein are necessary for papillomavirus infection SO JOURNAL OF VIROLOGY LA English DT Article ID VIRUS-LIKE PARTICLES; BOVINE PAPILLOMAVIRUS; L1; CELLS; DNA; NEUTRALIZATION; BINDING; PSEUDOVIRIONS; GENERATION; EXPRESSION AB Coexpression of bovine papillomavirus L1 with L2 mutants lacking either eight N-terminal or nine C-terminal amino acids that encode positively charged domains resulted in wild-type levels of viral genome encapsidation. Despite wild-type binding to the cell surface, the resulting virions were noninfectious. An L2 mutant encoding a scrambled version of the nine C-terminal residues restored infectivity, in contrast to an L2 mutant encoding a scrambled version of the N-terminal residues. C1 Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21205 USA. NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA. RP Roden, RBS (reprint author), Johns Hopkins Univ, Dept Pathol, Room 656,Ross REs Bldg,720 Rutland Ave, Baltimore, MD 21205 USA. FU NIAID NIH HHS [P01 AI48203-01, P01 AI048203] NR 26 TC 44 Z9 50 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10493 EP 10497 DI 10.1128/JVI.75.21.10493-10497.2001 PG 5 WC Virology SC Virology GA 480DZ UT WOS:000171447900050 PM 11581419 ER PT J AU Skiadopoulos, MH Surman, SR Riggs, JM Collins, PL Murphy, BR AF Skiadopoulos, MH Surman, SR Riggs, JM Collins, PL Murphy, BR TI A chimeric human-bovine parainfluenza virus type 3 expressing measles virus hemagglutinin is attenuated for replication but is still immunogenic in rhesus monkeys SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT VACCINIA VIRUS; PARALYTIC POLIOMYELITIS; MATERNAL ANTIBODY; PROTECTIVE TITERS; FUSION PROTEIN; LIVE; STRAINS; IMMUNIZATION; CANDIDATE; MACAQUES AB The chimeric recombinant virus rHPIV3-N-B, a version of human parainfluenza virus type 3 (HPIV3) that is attenuated due to the presence of the bovine PIV3 nucleocapsid (N) protein open reading frame (ORF) in place of the HPIV3 ORF, was modified to encode the measles virus hemagglutinin (RA) inserted as an additional, supernumerary gene between the HPIV3 P and M genes. This recombinant, designated rHPIV3-N(B)HA, replicated like its attenuated rHPIV3-N-B parent virus in vitro and in the upper and lower respiratory tracts of rhesus monkeys, indicating that the insertion of the measles virus RA did not further attenuate rHPIV3-N-B in,vitro or in vivo. Monkeys immunized with rHPIV3-N(B)HA developed a vigorous immune response to both measles virus and HPIV3, with serum antibody titers to both measles virus (neutralizing antibody) and HPIV3 (hemagglutination inhibiting antibody) of over 1:500. An attenuated HPIV3 expressing a major protective antigen of measles virus provides a method for immunization against measles by the intranasal route, a route that has been shown with HPIV3 and respiratory syncytial virus vaccines to be relatively refractory to the neutralizing and immunosuppressive effects of maternally derived virus-specific serum antibodies. It should now be possible to induce a protective immune response against measles virus in 6-month-old infants, an age group that in developing areas of the world is not responsive to the current measles virus vaccine. C1 NIAID, Resp Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA. RP Skiadopoulos, MH (reprint author), NIAID, Resp Viruses Sect, Infect Dis Lab, NIH, Room 100,Bldg 7,7 Ctr Dr,MSC 0720, Bethesda, MD 20892 USA. NR 55 TC 21 Z9 22 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10498 EP 10504 DI 10.1128/JVI.75.21.10498-10504.2001 PG 7 WC Virology SC Virology GA 480DZ UT WOS:000171447900051 PM 11581420 ER PT J AU Veazey, RS Gauduin, MC Mansfield, KG Tham, IC Altman, JD Lifson, JD Lackner, AA Johnson, RP AF Veazey, RS Gauduin, MC Mansfield, KG Tham, IC Altman, JD Lifson, JD Lackner, AA Johnson, RP TI Emergence and kinetics of simian immunodeficiency virus-specific CD8(+) T cells in the intestines of macaques during primary infection SO JOURNAL OF VIROLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; CYTOTOXIC LYMPHOCYTES-T; PRIMARY IMMUNE-RESPONSE; RHESUS-MONKEYS; DISEASE PROGRESSION; PERIPHERAL-BLOOD; SIV INFECTION; CEREBROSPINAL-FLUID; PATHOGENIC SIV; PLASMA VIREMIA AB In this report, three Mamu-A*01(+) rhesus macaques were examined to compare the emergence of simian immunodeficiency virus (SIV)-specific CD8(+) T cells in the intestines and blood in early SIV infection using a major histocompatibility complex class I tetramer complexed with the Gag(181-189) peptide. Fourteen days after intravenous inoculation with SIVmac251, large numbers of SrV Gag(181-189)-specific CD8(+) T cells were detected in the intestinal mucosa (3.1 to 11.5% of CD3(+) CD8(+) lymphocytes) as well as in the blood (3.1 to 13.4%) of all three macaques. By 21 days postinoculation, levels of tetramer-binding cells had dropped in both the intestines and blood. At day 63, however, levels of SIV Gag(181-189)- specific CD8(+) T cells in the intestines had rebounded in all three macaques to levels that were higher (8.6 to 18.7%) than those at day 21. In contrast, percentages of tetramer-binding cells in the peripheral blood remained comparatively stable (2.5 to 4.5%) at this time point. In summary, SFV Gag(181-189)-specific CD8(+) T cells appeared in both the intestinal mucosa and peripheral blood at a comparable rate and magnitude in primary SIV infection. Given that the intestine is a major site of early viral replication as well as the site where most of the total body lymphocyte pool resides, these data indicate that it is also an early and important site of development of antiviral immune responses. C1 Tulane Univ, Tulane Reg Primate Res Ctr, Covington, LA 70433 USA. Harvard Univ, Sch Med, New England Reg Primate Res Ctr, Southborough, MA 01772 USA. Emory Univ, Sch Med, Emory Vaccine Ctr Yerkes, Atlanta, GA 30322 USA. NCI, SAIC, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Infect Dis Unit, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA 02129 USA. RP Veazey, RS (reprint author), Tulane Univ, Tulane Reg Primate Res Ctr, 18703 3 Rivers Rd, Covington, LA 70433 USA. FU NCI NIH HHS [N01-CO-56000]; NCRR NIH HHS [P51 RR000168, RR00168, K26 RR000168]; NIAID NIH HHS [AI45314, AI49080, R01 AI049080]; NICHD NIH HHS [HD36310]; NIDDK NIH HHS [DK50550, R01 DK050550] NR 39 TC 51 Z9 53 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10515 EP 10519 DI 10.1128/JVI.75.21.10515-10519.2001 PG 5 WC Virology SC Virology GA 480DZ UT WOS:000171447900054 PM 11581423 ER PT J AU Malkevich, N Womack, C Pandya, P Grivel, JC Fauci, AS Margolis, L AF Malkevich, N Womack, C Pandya, P Grivel, JC Fauci, AS Margolis, L TI Human immunodeficiency virus type 1 (HIV-1) non-B subtypes are similar to HIV-1 subtype B in that coreceptor specificity is a determinant of cytopathicity in human lymphoid tissue infected ex vivo SO JOURNAL OF VIROLOGY LA English DT Article ID CELL DEPLETION; AIDS; PROGRESSION; USAGE; PHENOTYPE; DISEASE AB We sought to determine the relationship between virus-mediated CD4(+) T-lymphocyte cytopathicity,and viral coreceptor preference among various human immunodeficiency virus type 1 (HIV-1) subtypes in an ex vivo-infected human lymphoid, tissue model. Oar data show that all R5 HIV-1 infections resulted in mild depletion of CD4(+) T lymphocytes, whereas all X4 HIV-1 infections caused severe depletion of CD4(+) T lymphocytes regardless of their subtype origin. Thus, at least for the viruses within subtypes A, B, C, and E that were tested, coreceptor specificity is a critical factor that determines the ability of HIV-1 to deplete CD4(+) T cells in human lymphoid tissue infected ex vivo. C1 NICHHD, Lab Cellular & Mol Biophys, NIH, Bethesda, MD 20892 USA. NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. RP Womack, C (reprint author), NICHHD, Lab Cellular & Mol Biophys, NIH, Bldg 10,Rm 6A11, Bethesda, MD 20892 USA. NR 19 TC 11 Z9 11 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10520 EP 10522 DI 10.1128/JVI.75.21.10520-10522.2001 PG 3 WC Virology SC Virology GA 480DZ UT WOS:000171447900055 PM 11581424 ER PT J AU Ben-Arieh, SV Zimerman, B Smorodinsky, NI Yaacubovicz, M Schechter, C Bacik, I Gibbs, J Bennink, JR Yewdell, JW Coligan, JE Firat, H Lemonnier, F Ehrlich, R AF Ben-Arieh, SV Zimerman, B Smorodinsky, NI Yaacubovicz, M Schechter, C Bacik, I Gibbs, J Bennink, JR Yewdell, JW Coligan, JE Firat, H Lemonnier, F Ehrlich, R TI Human cytomegalovirus protein US2 interferes with the expression of human HFE, a nonclassical class I major histocompatibility complex molecule that regulates iron homeostasis SO JOURNAL OF VIROLOGY LA English DT Article ID HEREDITARY HEMOCHROMATOSIS; TRANSFERRIN RECEPTOR; ENDOPLASMIC-RETICULUM; ANTIGEN PRESENTATION; HUMAN ADENOVIRUSES; HEPATITIS-C; CELLS; GENE; ASSOCIATION; METABOLISM AB HFE is a nonclassical class I major histocompatibility complex (MHC) molecule that is mutated in the autosomal recessive iron overload disease hereditary hemochromatosis. There is evidence linking HFE with reduced iron uptake by the transferrin receptor (TfR). Using a panel of HFE and TfR monoclonal antibodies to examine human HFE (hHFE) -expressing cell lines, we demonstrate the expression of stable and fully glycosylated TfR-free and TfR-associated hHFE/beta 2m complexes. We show that both the stability and assembly of hHFE complexes can be modified by the human cytomegalovirus (HCMV) viral protein US2, known to interfere with the expression of classical class I MHC molecules. HCMV US2, but not US11, targets FIFE molecules for degradation by the proteasome. Whether this interference with the regulation of iron metabolism by a viral protein is a means of potentiating viral replication remains to be determined. The reduced expression of classical class I MHC and FIFE complexes provides the virus with an efficient tool for altering cellular metabolism and escaping certain immune responses. C1 Tel Aviv Univ, George S Wise Fac Life Sci, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel. NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. Inst Pasteur, Unite Immunite Cellulaire Antivirale, Paris, France. RP Ehrlich, R (reprint author), Tel Aviv Univ, George S Wise Fac Life Sci, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 48 TC 47 Z9 48 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 21 BP 10557 EP 10562 DI 10.1128/JVI.75.21.10557-10562.2001 PG 6 WC Virology SC Virology GA 480DZ UT WOS:000171447900062 PM 11581431 ER PT J AU Parker, CE Deterding, LJ Hager-Braun, C Binley, JM Schulke, N Katinger, H Moore, JP Tomer, KB AF Parker, CE Deterding, LJ Hager-Braun, C Binley, JM Schulke, N Katinger, H Moore, JP Tomer, KB TI Fine definition of the epitope on the gp41 glycoprotein of human immunodeficiency virus type 1 for the neutralizing monoclonal antibody 2F5 SO JOURNAL OF VIROLOGY LA English DT Article ID INTERMOLECULAR DISULFIDE BOND; HIV-1 GP41; ENVELOPE GLYCOPROTEIN; VACCINE; INDUCTION; GP120; RESPONSES; VARIANTS; PEPTIDE; FUSION AB Matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS), in combination with proteolytic. protection assays, has been used to identify the functional epitope on human immunodeficiency virus envelope glycoprotein gp41 for the broadly neutralizing and-gp41 human monoclonal antibody 2F5. In this protection assay-based procedure, a soluble gp140 protein with a stabilizing intermolecular disulfide bond between the gp120 and gp41 subunits (SOS gp140) was affinity bound to immobilized 2F5 under physiological; conditions. A combination of proteolytic enzymatic cleavages was then performed to remove unprotected residues. Residues of SOS gp140 protected by their binding to 2F5 were then identified based on their molecular weights as determined by direct MALDI-MS of the immobilized antibody beads. The epitope, NEQELLELDKWASLWN, determined by this MALDI-MS protection assay approach consists of 16 amino acid residues near the C terminus of gp41. It is significantly longer than the ELDKWA core epitope previously determined for 2F5 by peptide enzyme-linked immunosorbent. assay. This new knowledge of the structure of the 2F5 epitope may facilitate the design of vaccine antigens intended to induce antibodies with the breadth and potency of action of the 2F5 monoclonal antibody. C1 NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA. Cornell Univ, Joan & Sanford I Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA. Progen Pharmaceut Inc, Tarrytown, NY 10591 USA. Univ Agr & Forestry, Inst Appl Microbiol, A-1190 Vienna, Austria. RP Parker, CE (reprint author), Univ N Carolina, Sch Med, Dept Biochem & Biophys, CB7260, Chapel Hill, NC 27599 USA. RI Tomer, Kenneth/E-8018-2013 FU NIAID NIH HHS [R01 AI39420, R01 AI039420, R01 AI045463, R01 AI45463, UO1 AI49764] NR 61 TC 139 Z9 145 U1 3 U2 21 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 22 BP 10906 EP 10911 DI 10.1128/JVI.75.22.10906-10911.2001 PG 6 WC Virology SC Virology GA 483TV UT WOS:000171652700033 PM 11602730 ER PT J AU Bloom, ME Best, SM Hayes, SF Wells, RD Wolfinbarger, JB McKenna, R Agbandje-McKenna, M AF Bloom, ME Best, SM Hayes, SF Wells, RD Wolfinbarger, JB McKenna, R Agbandje-McKenna, M TI Identification of Aleutian mink disease parvovirus capsid sequences mediating antibody-dependent enhancement of infection, virus neutralization, and immune complex formation SO JOURNAL OF VIROLOGY LA English DT Article ID FELINE PANLEUKOPENIA VIRUS; BACULOVIRUS VECTOR SYSTEM; B-CELL EPITOPES; CANINE PARVOVIRUS; ENTERITIS VIRUS; FUNCTIONAL IMPLICATIONS; 3-DIMENSIONAL STRUCTURE; MONOCLONAL-ANTIBODIES; KIDNEY-CELLS; ADULT MINK AB Aleutian mink disease parvovirus (ADV) causes a persistent infection associated with circulating immune complexes, immune complex disease, hypergammaglobulinemia, and high levels of antiviral antibody. Although antibody can neutralize ADV infectivity in Crandell feline kidney cells in vitro, virus is not cleared in,vivo, and capsid-based vaccines have proven uniformly ineffective. Antiviral antibody also enables ADV to infect macrophages, the target cells for persistent infection, by Fc-receptor-mediated antibody-dependent enhancement (ADE). The antibodies involved in these unique aspects of ADV pathogenesis may have specific targets on the ADV capsid. Prominent differences exist between the structure of ADV and other, more-typical parvoviruses, which can be accounted for by short peptide sequences in the flexible loop regions of the capsid proteins. In order to determine whether these short sequences are targets for antibodies involved in ADV pathogenesis, we studied heterologous antibodies against several peptides present in the major capsid protein, VP2. Of these antibodies, a polyclonal rabbit antibody to peptide VP2:428-446 was the most interesting. The anti-VP2:428-446 antibody aggregated virus particles into immune complexes, mediated ADE, and neutralized virus infectivity in vitro. Thus, antibody against this short peptide can be implicated in key facets of ADV pathogenesis. Structural modeling suggested that surface-exposed residues of VP2:428-446 are readily accessible for antibody binding. The observation that antibodies against a single target peptide in the ADV capsid can mediate both neutralization and ADE may explain the failure of capsid-based vaccines. C1 NIAID, Rocky Mt Lab, Persistent Viral Dis Lab, Hamilton, MT 59840 USA. NIAID, Rocky Mt Microscopy Branch, Persistent Viral Dis Lab, Hamilton, MT 59840 USA. Univ Florida, Coll Med, Inst Brain,Ctr Struct Biol, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA. RP Bloom, ME (reprint author), NIAID, Rocky Mt Lab, Persistent Viral Dis Lab, MT 59840, Hamilton, MT 59840 USA. NR 64 TC 27 Z9 31 U1 0 U2 10 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 22 BP 11116 EP 11127 DI 10.1128/JVI.75.22.11116-11127.2001 PG 12 WC Virology SC Virology GA 483TV UT WOS:000171652700054 PM 11602751 ER PT J AU Szajner, P Weisberg, AS Moss, B AF Szajner, P Weisberg, AS Moss, B TI Unique temperature-sensitive defect in vaccinia virus morphogenesis maps to a single nucleotide substitution in the A30L gene SO JOURNAL OF VIROLOGY LA English DT Article ID CLEAVAGE AB Marker rescue experiments demonstrated that the genetic lesion of a previously isolated vaccinia virus temperature-sensitive mutant which forms multilayered envelope structures with lucent interiors and foci of viroplasm with dense centers mapped to the A30L open reading frame. A single base change, resulting in a nonconservative Ser-to-Phe substitution at residue 17, was associated with degradation of the A30L protein at elevated temperatures. C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. George Washington Univ, Dept Genet, Grad Program, Washington, DC 20052 USA. RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, 4 Ctr Dr,MSC 0445, Bethesda, MD 20892 USA. NR 6 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 22 BP 11222 EP 11226 DI 10.1128/JVI.75.22.11222-11226.2001 PG 5 WC Virology SC Virology GA 483TV UT WOS:000171652700065 PM 11602762 ER PT J AU Fujisawa, R McAtee, FJ Favara, C Hayes, SF Portis, JL AF Fujisawa, R McAtee, FJ Favara, C Hayes, SF Portis, JL TI N-terminal cleavage fragment of Glycosylated Gag is incorporated into murine oncornavirus particles SO JOURNAL OF VIROLOGY LA English DT Article ID LEUKEMIA-VIRUS; CELL-MEMBRANE; POLYPROTEINS; SEQUENCE; PROTEINS; VIRIONS; IDENTIFICATION; MUTANTS; UNIQUE AB Glycosylated Gag (Glycogag) is a transmembrane protein encoded by murine and feline oncornaviruses. While the protein is dispensible for virus replication, Glycogag-null mutants of a neurovirulent murine oncornavirus are slow to spread in vivo and exhibit a loss of pathogenicity. The function of this protein in the virus life cycle, however, is not understood. Glycogag is expressed at the plasma membrane of infected cells but has not been detected in virions. In the present study we have reexamined this issue and have found an N-terminal cleavage fragment of Glycogag which was pelleted by high-speed centrifugation and sedimented in sucrose density gradients at the same bouyant density as virus particles. Its association with virions was confirmed by velocity sedimentation through iodixanol, which effectively separated membrane microvesicles from virus particles. Furthermore, the apparent molecular weight of the virion-associated protein was different from that of the protein extracted from the plasma membrane, suggesting some level of specificity or selectivity of incorporation. C1 NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, Hamilton, MT 59840 USA. NIAID, Rocky Mt Labs, Microscopy Branch, Hamilton, MT 59840 USA. RP Portis, JL (reprint author), NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, 903 S 4th St, Hamilton, MT 59840 USA. NR 22 TC 11 Z9 11 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 2001 VL 75 IS 22 BP 11239 EP 11243 DI 10.1128/JVI.75.22.11239-11243.2001 PG 5 WC Virology SC Virology GA 483TV UT WOS:000171652700068 PM 11602765 ER PT J AU Soules, MR Sherman, S Parrott, E Rebar, R Santoro, N Utian, W Woods, N AF Soules, MR Sherman, S Parrott, E Rebar, R Santoro, N Utian, W Woods, N TI Executive summary - Stages of Reproductive Aging Workshop (STRAW) SO JOURNAL OF WOMENS HEALTH & GENDER-BASED MEDICINE LA English DT Editorial Material C1 Univ Washington, Div Reprod Endocrinol & Infertil, Seattle, WA 98195 USA. Amer Soc Reprod Med, Birmingham, AL USA. NIA, NIH, Bethesda, MD 20892 USA. NICHHD, Reprod Med Gynecol Program, NIH, Bethesda, MD 20892 USA. Albert Einstein Coll Med, Div Reprod Endocrinol & Infertil, Bronx, NY 10467 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. N Amer Menopause Soc, Cleveland, OH USA. Univ Washington, Sch Nursing, Seattle, WA 98195 USA. RP Soules, MR (reprint author), Univ Washington, Div Reprod Endocrinol & Infertil, Seattle, WA 98195 USA. NR 3 TC 138 Z9 142 U1 1 U2 8 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 NOV PY 2001 VL 10 IS 9 BP 843 EP 848 DI 10.1089/152460901753285732 PG 6 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 500LY UT WOS:000172630100004 PM 11747678 ER PT J AU Baker, SG Kramer, BS AF Baker, SG Kramer, BS TI Good for women, good for men, bad for people: Simpson's paradox and the importance of sex-specific analysis in observational studies SO JOURNAL OF WOMENS HEALTH & GENDER-BASED MEDICINE LA English DT Article AB Even if a medial intervention has a beneficial effect in both men and women, an observational study that combines data from men and women can lead to the incorrect conclusion that treatment has a harmful effect. This is an example of Simpson's paradox, which although uncommon in practice, does, in fact, occur (Wainer H. Simpson's paradox. Chance 1999;12:43). More importantly, it is likely that in an observational study, a related result will occur, namely, ignoring sex in the analysis will lead to biased results. To better understand why Simpson's paradox and the related result occur, we present a graphic explanation. C1 NCI, Biometry Res Grp, Div Canc Prevent, EPN 3131,NIH, Bethesda, MD 20892 USA. NIH, Off Dis Prevent & Med Applicat Res, Bethesda, MD 20892 USA. RP Baker, SG (reprint author), NCI, Biometry Res Grp, Div Canc Prevent, EPN 3131,NIH, 6130 Execut Blvd,MSC 7354, Bethesda, MD 20892 USA. RI bowman, marjorie/F-7235-2013 OI bowman, marjorie/0000-0002-1945-9212 NR 6 TC 14 Z9 14 U1 1 U2 8 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 NOV PY 2001 VL 10 IS 9 BP 867 EP 872 DI 10.1089/152460901753285769 PG 6 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 500LY UT WOS:000172630100007 PM 11747681 ER PT J AU Meneilly, GS McIntosh, CHS Pederson, RA Habener, JF Gingerich, R Egan, JM Elahi, D AF Meneilly, GS McIntosh, CHS Pederson, RA Habener, JF Gingerich, R Egan, JM Elahi, D TI Glucagon-like peptide-1 (7-37) augments insulin-mediated glucose uptake in elderly patients with diabetes SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID RAT SKELETAL-MUSCLE; GLYCOGEN-SYNTHASE; GLP-I; MELLITUS; HORMONE; AMIDE; GLP-1(7-36)AMIDE; HEPATOCYTES; METABOLISM; ADIPOCYTES AB Background. Glucagon-Like peptide-1 (GLP-1) is an intestinal insulinotropic hormone that augments glucose-induced insulin secretion in patients with type 2 diabetes. It has also been proposed that a substantial component of the glucose-lowering effects of GLP-1 occurs because this hormone enhances insulin-mediated glucose disposal. However, interpretations of the studies have been controversial. This study determines the effect of GLP-1 on insulin-mediated glucose disposal in elderly patients with type 2 diabetes. Methods. Studies were conducted on 8 elderly patients with type 2 diabetes (age range, 76 +/- 1 years; body mass index, 28 +/- 1 kg/m(2)). Each subject underwent two 180-minute euglycemic (insulin infusion rate, 40 mU/m(2)/min) insulin clamps in random order. Glucose production (Ra) and disposal (Rd) rates were measured using tritiated. glucose methodology. In one study, glucose and insulin alone were infused. In the other study, a primed-continuous infusion of GLP-1 was administered at a final rate of 1.5 pmol . ka(-1) . min(-1) from 30 to 180 minutes. Results. Glucose values were similar between the control and GLP-1 infusion studies. 120- to 180-minute insulin values appeared to be higher during the GLP-1 infusion study (control, 795 +/- 63 pmol/l; GLP-1, 1140 +/- 275 pmol/l; p = not significant [NS]). The higher insulin values were largely due to 2 subjects who had substantial insulin responses to GLP-1 despite euglycemia and hyperinsulinemia. The 120- to 180-minute insulin values were similar in the other 6 subjects (Control, 746 +/- 35 pmol/l; GLP-1, 781 +/- 41 pmol/l; p = NS). Basal (control, 2.08 +/- 0.05 mg/kg/min; GLP-1, 2.13 +/- 0.04 mg/kg/min; p = NS) and 120- to 180-minute (control, 0.50 +/- 0.18 mg/kg/min; GLP-1, 0.45 +/- 0.14 mg/kg/min; p = NS) Ra was similar between studies. The 120- to 180-minute Rd values were higher during the GLP-1 infusion studies (control. 4.73 +/- 0.39 mg/kg/min; GLP-1, 5.52 +/- 0.43 mg/kg/min; p < 0.1). When the 2 subjects who had significant insulin responses to GLP-1 during the euglycemic clamp were excluded, the 120- to 180-minute Rd values were still higher in the GLP-1 infusion study (control, 5.22 +/- 0.32 mg/kg/min; GLP-1, 6.05 +/- 037 mg/kg/min; p < .05). Conclusions. We conclude that GLP-1 may enhance insulin sensitivity in elderly patients with diabetes. C1 Univ British Columbia, Dept Med, Vancouver, BC V5Z 1M9, Canada. Univ British Columbia, Dept Physiol, Vancouver, BC V5Z 1M9, Canada. Harvard Univ, Sch Med, Howard Hughes Med Inst, Mol Endocrinol Lab, Boston, MA 02115 USA. Linco Res, St Charles, MO USA. NIA, Lab Clin Physiol, Gerontol Res Ctr, NIH, Baltimore, MD USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. RP Meneilly, GS (reprint author), Vancouver Hosp & Hlth Sci Ctr, Room S169,UBC Site,2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada. NR 26 TC 20 Z9 20 U1 0 U2 1 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD NOV PY 2001 VL 56 IS 11 BP M681 EP M685 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 489LG UT WOS:000171992400010 PM 11682575 ER PT J AU Dalakas, MC Semino-Mora, C Leon-Monzon, M AF Dalakas, MC Semino-Mora, C Leon-Monzon, M TI Mitochondrial alterations with mitochondrial DNA depletion in the nerves of AIDS patients with peripheral neuropathy induced by 2 ' 3 '-dideoxycytidine (ddC) SO LABORATORY INVESTIGATION LA English DT Article ID ZIDOVUDINE-INDUCED MYOPATHY; 2',3'-DIDEOXYCYTIDINE DDC; ANTIRETROVIRAL-THERAPY; MUSCLE MITOCHONDRIA; NUCLEOSIDE ANALOGS; TOXIC NEUROPATHY; ANIMAL-MODEL; RISK-FACTORS; DISEASE; CELLS AB The 2'3'-dideoxycytidine (ddC), a nonazylated dideoxynucleoside analog used for the treatment of AIDS, causes a dose-dependent, painful, sensorimotor axonal peripheral neuropathy in up to 30% of the patients. To investigate the cause of the neuropathy, we performed morphological and molecular studies on nerve biopsy specimens from well-selected patients with ddC-neuropathy and from control subjects with disease, including patients with AIDS-related neuropathy never treated with ddC. Because ddC, in vitro, inhibits the replication of mitochondrial DNA (mtDNA), we counted the number of normal and abnormal mitochondria in a 0.04 mm(2) cross-sectional area of the nerves and quantified the copy numbers of mtDNA by competitive PCR in all specimens. A varying degree of axonal degeneration was present in all nerves. Abnormal mitochondria with enlarged size, excessive vacuolization, electron-dense concentric inclusions and degenerative myelin structures were prominent in the ddC-neuropathy and accounted for 55% +/- 2.5% of all counted mitochondria in the axon and Schwann cells, compared with 9% +/- 0.7% of the controls (p < 0.001). Significantly (p < 0.005) reduced copy numbers, with as high as 80% depletion, of the mtDNA was demonstrated in the nerves of the ddC-treated patients compared with the controls. We conclude that ddC induces a mitochondrial neuropathy with depletion of the nerve's mtDNA. The findings are consistent with the ability of ddC to selectively inhibit the gamma -DNA polymerase in neuronal cell lines. Toxicity to mitochondria of the peripheral nerve is a new cause of acquired neuropathy induced by exogenous toxins and may be the cause of neuropathy associated with the other neurotoxic antiretroviral drugs or toxic-metabolic conditions. C1 NINCDS, Neuromuscular Dis Sect, NIH, Bethesda, MD 20892 USA. RP Dalakas, MC (reprint author), NINCDS, Neuromuscular Dis Sect, NIH, Bldg 10,Room 4N248, Bethesda, MD 20892 USA. NR 42 TC 129 Z9 133 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD NOV PY 2001 VL 81 IS 11 BP 1537 EP 1544 PG 8 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA 495QH UT WOS:000172351500006 PM 11706061 ER PT J AU Srinivas, PR Kramer, BS Srivastava, S AF Srinivas, PR Kramer, BS Srivastava, S TI Trends in biomarker research for cancer detection SO LANCET ONCOLOGY LA English DT Review ID CELL LUNG-CANCER; GENE-EXPRESSION; MICROSATELLITE ALTERATIONS; COLORECTAL-CANCER; PLASMA DNA; EXFOLIATIVE CYTOLOGY; MISMATCH REPAIR; SERIAL ANALYSIS; METHYLATION; MUTATIONS AB A key challenge in cancer control and prevention is detection of the disease as early as possible, enabling effective interventions and therapies to contribute to reduction in mortality and morbidity. Biomarkers are important as molecular signposts of the physiological state of a cell at a specific time. Active genes, their respective protein products, and other organic chemicals made by the cell create these signposts. As a normal cell progresses through the complex process of transformation to a cancerous state, biomarkers could prove vital for the identification of early cancer and people at risk of developing cancer. We discuss current research into the genetic and molecular signatures of cells, including microsatellite instability, hypermethylation and single-nucleotide polymorphisms. The use of genomic and proteomic high-throughput technology platforms to facilitate detection of early cancer by means of biomarkers, and issues on the analysis, validation, and predictive value of biomarkers based on these technologies are also discussed. We report on recent advances in identifying sources of biomarkers that can be accessed by non-invasive techniques, such as buccal-cell isolates, as well as traditional sources such as serum or plasma. We also focus on the work of the Early Detection Research Network at the National Cancer Institute, harnessing expertise from leading national and international institutions, to identify and validate biomarkers for the detection of precancerous and cancerous cells in assessing risk of cancer. The network also has a role in linking discovery to process development, resulting in early detection tests and clinical assessment. C1 Natl Canc Inst, Div Canc Prevent, Canc Biomarkers Res Grp, Rockville, MD 20852 USA. NIH, Off Med Applicat Res, Bethesda, MD USA. RP Srivastava, S (reprint author), Natl Canc Inst, Div Canc Prevent, Canc Biomarkers Res Grp, 6130 Execut Blvd,Room EPN 330F, Rockville, MD 20852 USA. NR 47 TC 180 Z9 198 U1 7 U2 73 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1470-2045 J9 LANCET ONCOL JI Lancet Oncol. PD NOV PY 2001 VL 2 IS 11 BP 698 EP 704 DI 10.1016/S1470-2045(01)00560-5 PG 7 WC Oncology SC Oncology GA 525UL UT WOS:000174092400023 PM 11902541 ER PT J AU Lam, DH Aplan, PD AF Lam, DH Aplan, PD TI NUP98 gene fusions in hematologic malignancies SO LEUKEMIA LA English DT Review DE NUP98; acute leukemia; myelodysplastic syndrome; 11p15.5 translocations ID NUCLEAR-PORE COMPLEX; ACUTE MYELOID-LEUKEMIA; INV(11)(P15Q22) CHROMOSOME-TRANSLOCATION; CHRONIC MYELOGENOUS LEUKEMIA; ACUTE LYMPHOCYTIC-LEUKEMIA; HOX HOMEOBOX GENES; RNA HELICASE GENE; MYELODYSPLASTIC SYNDROME; NUP98/HOXA9 FUSION; NUCLEOPORIN NUP98 AB Acute leukemia Is associated with a wide spectrum of recurrent, non-random chromosomal translocations. Molecular analysis of the genes involved In these translocations has led to a better understanding of both the causes of chromosomal rearrangements as well as the mechanisms of leukemic transformation. Recently, a number of laboratories have cloned translocations involving the NUP98 gene on chromosome 11p15.5, from patients with acute myelogenous leukemia (AML), myelodysplastic syndrome (MDS), chronic myelogenous leukemia (CIVIL), and T cell acute lymphoblastic leukemia (T-ALL). To date, at least eight different chromosomal rearrangements involving NUP98 have been identified. The resultant chimeric transcripts encode fusion proteins that juxtapose the N-terminal GLFG repeats of NUP98 to the C-terminus of the partner gene. Of note, several of these translocations have been found In patients with therapy-related acute myelogenous leukemia (t-AML) or myelodysplastic syndrome (t-MDS), suggesting that genotoxic chemotherapeutic agents may play an important role in generating chromosomal rearrangements involving NUP98. C1 Natl Canc Inst, Dept Genet, Med Branch, Div Clin Sci,Adv Technol Ctr, Gaithersburg, MD 20877 USA. Roswell Pk Canc Inst, Dept Immunol, Buffalo, NY 14263 USA. RP Aplan, PD (reprint author), Natl Canc Inst, Dept Genet, Med Branch, Div Clin Sci,Adv Technol Ctr, 8717 Grovemont Circle, Gaithersburg, MD 20877 USA. RI Aplan, Peter/K-9064-2016 NR 82 TC 66 Z9 74 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD NOV PY 2001 VL 15 IS 11 BP 1689 EP 1695 PG 7 WC Oncology; Hematology SC Oncology; Hematology GA 488CQ UT WOS:000171918100004 PM 11681408 ER PT J AU Yongbi, MN Fera, F Mattay, VS Frank, JA Duyn, JH AF Yongbi, MN Fera, F Mattay, VS Frank, JA Duyn, JH TI Simultaneous BOLD/perfusion measurement using dual-echo FAIR and UNFAIR: sequence comparison at 1.5T and 3.0T SO MAGNETIC RESONANCE IMAGING LA English DT Article DE FAIR-UNFAIR; simultaneous BOLD/CBF; 3.0T; FOCI pulses ID INVERSION FOCI PULSES; MAGNETIC-RESONANCE; MR PERFUSION; CBF AB Functional MRI (fMRI) studies designed for simultaneously measuring Blood Oxygenation Level Dependent (BOLD) and Cerebral Blood Flow (CBF) signal often employ the standard Flow Alternating Inversion Recovery (FAIR) technique. However, some sensitivity is lost in the BOLD data due to inherent T1 relaxation. We sought to minimize the preceding problem by employing a modified UN-inverted FAIR (UNFAIR) technique, which (in theory) should provide identical CBF signal as FAIR with minimal degradation of the BOLD signal. UNFAIR BOLD maps acquired from human subjects (n = 8) showed significantly higher mean z-score of similar to 17% (p < 0.001), and number of activated voxels at 1.5T. On the other hand, the corresponding FAIR perfusion maps were superior to the UNFAIR perfusion maps as reflected in a higher mean z-score of similar to8% (p = 0.013), and number of activated voxels. The reduction in UNFAIR sensitivity for perfusion is attributed to increased motion sensitivity related to its higher background signal, and, T2 related losses from the use of an extra inversion pulse. Data acquired at 3.0T demonstrating similar trends are also presented. (C) 2001 Elsevier Science Inc. All rights reserved. C1 NINCDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA. NIMH, Clin Brain Disorder Branch, NIH, Bethesda, MD 20892 USA. CNR, Inst Expt Med & Biotechnol, Cosenza, Italy. NIH, Ctr Clin, Lab Diagnost Radiol Res, Bethesda, MD 20892 USA. RP Yongbi, MN (reprint author), NINCDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA. RI Duyn, Jozef/F-2483-2010 NR 15 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PD NOV PY 2001 VL 19 IS 9 BP 1159 EP 1165 DI 10.1016/S0730-725X(01)00436-2 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 505DA UT WOS:000172895200002 PM 11755725 ER PT J AU Hu, TCC Pautler, RG MacGowan, GA Koretsky, AP AF Hu, TCC Pautler, RG MacGowan, GA Koretsky, AP TI Manganese-enhanced MRI of mouse heart during changes in inotropy SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE calcium influx; cardiac MRI; dobutamine; diltiazem; imaging inotropy ID PERFUSED RAT-HEART; CONTRAST AGENTS; DIPYRIDOXYL DIPHOSPHATE; CA CHANNELS; CARDIAC MRI; QUANTIFICATION; MNDPDP; MOTION; MNCL2; MN AB Recently the dual properties of manganese ion (Mn2+) as an MRI contrast agent and a calcium analogue to enter excitable cells has been used to mark specific cells in brain and as a potential intracellular cardiac contrast agent. Here the hypothesis that in vivo manganese-enhanced MRI(MEMRI) can detect changes in inotropy in the mouse heart has been tested. T-1-weighted images were acquired every minute during an experimental time course of 75 min. Varying doses of Mn2+ (3.3-14.0 nmoles/min/g BW) were infused during control and altered inotropy with dobutamine (positive inotropy due to increased calcium influx) and the calcium channel blocker diltiazem (negative inotropy). Infusion of MnCl2 led to a significant increase in signal enhancement in mouse heart that saturated above 3.3 +/- 0.1 nmoles/min/g BW Mn2+ infusion. At the highest Mn2+ dose infused there was a 41-47% increase in signal intensity with no alteration in cardiac function as measured by MRI-determined ejection fractions. Dobutamine increased both the steady-state level of enhancement and the rate of MRI signal enhancement. Diltiazem decreased both the steady-state level of enhancement and the rate of MRI signal enhancement. These results are consistent with the model that Mn2+-induced enhancement of cardiac signal is indicative of the rate of calcium influx into the heart. Thus, the simultaneous measurement of global function and calcium influx using MEMRI may provide a useful method of evaluating in vivo responses to inotropic therapy. Published 2001 Wiley-Liss, Inc.(dagger). C1 NINCDS, In Vivo NMR Res Ctr, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA. Carnegie Mellon Univ, Pittsburgh NMR Ctr Biomed Res, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Dept Chem, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Med Ctr, Cardiovasc Inst, Pittsburgh, PA USA. CALTECH, Beckman Inst, Biol Imaging Ctr, Pasadena, CA 91125 USA. RP Koretsky, AP (reprint author), NINCDS, In Vivo NMR Res Ctr, Lab Funct & Mol Imaging, NIH, 10 Ctr Dr,Room B1D-69B,MSC 1060,9000 Rockville Pi, Bethesda, MD 20892 USA. RI Koretsky, Alan/C-7940-2015 OI Koretsky, Alan/0000-0002-8085-4756 FU NHLBI NIH HHS [HL03826, HL40354] NR 31 TC 93 Z9 98 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD NOV PY 2001 VL 46 IS 5 BP 884 EP 890 DI 10.1002/mrm.1273.abs PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 486MG UT WOS:000171821100007 PM 11675639 ER PT J AU Caravan, P Greenfield, MT Bulte, JWM AF Caravan, P Greenfield, MT Bulte, JWM TI Molecular factors that determine Curie spin relaxation in dysprosium complexes SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE dysprosium; Curie spin; relaxation; T-2 contrast agent; water exchange; inner-sphere; out-sphere; human serum; albumin ID LANTHANIDE IONS LN(3+); WATER EXCHANGE-RATE; O-17 NMR; GADOLINIUM(III) COMPLEXES; DYNAMICS SIMULATION; NUCLEAR-RELAXATION; AQUEOUS-SOLUTION; CONTRAST AGENTS; MECHANISM; MS-325 AB Dysprosium complexes can serve as transverse relaxation (T-2) agents for water protons through chemical exchange and the Curie spin relaxation mechanism. Using a pair of matched dysprosium(ill) complexes, Dy-L1 (contains one inner-sphere water) and Dy-L2 (no inner-sphere water), it is shown that the transverse relaxation of bulk water is predominantly an inner-sphere effect. The kinetics of water exchange at Dy-L1 were determined by O-17 NMR. Proton transverse relaxation by Dy-L1 at high fields is governed primarily through a large chemical shift difference between free and bound water. Dy-L1 forms a noncovalent adduct with human serum albumin which dramatically lengthens the rotational correlation time, tau (R), causing the dipole-dipole component of the Curie spin mechanism to become significant and transverse relaxivity to increase by 3-8 times that of the unbound chelate. These findings aid in the design of new molecular species as efficient r(2) agents. Published 2001 Wiley-Liss, Inc.(dagger). C1 EPIX Med Inc, Cambridge, MA 02142 USA. NIH, Lab Diagnost Radiol Res, CC, Bethesda, MD 20892 USA. RP Caravan, P (reprint author), EPIX Med Inc, 71 Rogers St, Cambridge, MA 02142 USA. EM pcaravan@epixmed.com RI Bulte, Jeff/A-3240-2008 OI Bulte, Jeff/0000-0003-1202-1610 NR 27 TC 26 Z9 26 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD NOV PY 2001 VL 46 IS 5 BP 917 EP 922 DI 10.1002/mrm.1277.abs PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 486MG UT WOS:000171821100011 PM 11675643 ER PT J AU Walsh, PJ Wang, Y Campbell, CE De Boeck, G Wood, CM AF Walsh, PJ Wang, Y Campbell, CE De Boeck, G Wood, CM TI Patterns of nitrogenous waste excretion and gill urea transporter mRNA expression in several species of marine fish SO MARINE BIOLOGY LA English DT Article ID TOADFISH OPSANUS-BETA; EARLY-LIFE STAGES; GULF TOADFISH; MOLECULAR CHARACTERIZATION; RAINBOW-TROUT; CYCLE ENZYMES; AMMONIA; METABOLISM; ELASMOBRANCH AB Many prior studies of nitrogenous waste excretion in marine fish have examined excretion patterns for short time periods, and with relatively coarse sampling schemes (e.g., an initial and a final sample point). Recent studies of a ureotelic marine fish (the gulf toadfish, Opsanus beta) have demonstrated that urea excretion in this species occurs in brief but massive bursts, lasting from 0.5 to 3 h, and often only once per day. The present study sought to determine if prior sampling protocols may have underestimated the amount of urea being excreted by marine fish. A survey of 16 marine species (the teleosts: Myoxocephalus octo-decemspinosus, Scophthalamus aquosa, Cyclopterus lumpus, Lophius americanus, Aprodon cortezianus, Cymatogaster aggregatus, Parophrys vetulis, Microstomus pacificus, Hippoglossoides elassodon, Bathyagonus nigripinnus, Ophiodon elongatus, Hemilepidatus spinosus, Icelinus terrius; the elasmobranch: Raja rhina; and the hagfish: Eptatretus stoutii) was undertaken for ammonia-N and urea-N excretion using a long sampling period (48 h) and hourly sample collection. Apart from the obvious exception of an elasmobranch, ammonia excretion was confirmed to be predominant in marine fish, with urea excretion constituting between 1.4 and 23.8% of the total of ammonia plus urea excreted. Notably, no pulses of urea excretion were detected. Despite the relatively low level of urea excretion, expression of urea transporter-like mRNA (detected using the toadfish urea transporter, tUT, cDNA as a probe) was discovered in gills of many of the species surveyed for nitrogen excretion patterns, although no signal was detected in the hagfish. These results suggest that urea excretion takes place through a specific transport pathway. Finally, more detailed analysis of nitrogen excretion in one of the surveyed species, the plainfin midshipman (Porichthys notatus) demonstrates that "total" nitrogen excretion estimated by summing ammonia and urea excretion underestimates true total nitrogen excretion by 37-51%. C1 Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, NIEHS Marine & Freshwater Biomed Sci Ctr, Div Marine Biol & Fisheries, Miami, FL 33149 USA. Bamfield Marine Stn, Bamfield, BC V0R 1B0, Canada. Mt Desert Isl Biol Lab, Salsbury Cove, ME 04672 USA. McMaster Univ, Dept Biol, Hamilton, ON L8S 4K1, Canada. RP Walsh, PJ (reprint author), Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, NIEHS Marine & Freshwater Biomed Sci Ctr, Div Marine Biol & Fisheries, 4600 Rickenbacker Causeway, Miami, FL 33149 USA. RI De Boeck, Gudrun/A-1938-2015 OI De Boeck, Gudrun/0000-0003-0941-3488 NR 33 TC 34 Z9 36 U1 0 U2 7 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0025-3162 J9 MAR BIOL JI Mar. Biol. PD NOV PY 2001 VL 139 IS 5 BP 839 EP 844 PG 6 WC Marine & Freshwater Biology SC Marine & Freshwater Biology GA 503HR UT WOS:000172793500004 ER PT J AU Kudoh, T Dawid, IB AF Kudoh, T Dawid, IB TI Zebrafish mab21l2 is specifically expressed in the presumptive eye and tectum from early somitogenesis onwards SO MECHANISMS OF DEVELOPMENT LA English DT Article DE zebrafish mab21l2; presumptive eye; midbrain; presumptive tectum ID HOMEOBOX GENE; MIDBRAIN; HINDBRAIN; BOUNDARY; ENCODES; MAB-21; BRAIN AB Random screening for tissue specific genes in zebrafish by in situ hybridization led us to isolate a gene which showed highly restricted expression in the developing eyes and midbrain at somitogenesis stages. This gene was very similar to mouse and human mab21l2. The characteristic expression pattern of mab21l2 facilitates a detailed description of the morphogenesis of the eves and midbrain in the zebrafish. In the eye field, mab21l2 expression illustrates the transformation of the eye field to form two separate eyes in the anterior neural plate. Mab21l2 staining in the cyclopic mutants, cyc and oep, exhibited incomplete splitting of the eye primodium. In the midbrain, mab21l2 is expressed in the tectum, and its expression follows the expansion of the tectal region. In mutants affecting the mid-hindbrain boundary (MHB), mab21l2 expression is affected differentially. In the noi/pax2.1 mutant, mab21l2 is down-regulated and the size of the tectum remains small, whereas in the ace/fgf8 mutant, mab21l2 expression persists although the shape of the tectum is altered. Crown Copyright (C) 2001 Published by Elsevier Science Ireland Ltd. All rights reserved. C1 NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. RP Dawid, IB (reprint author), NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. NR 14 TC 17 Z9 18 U1 0 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 NOV PY 2001 VL 109 IS 1 BP 95 EP 98 DI 10.1016/S0925-4773(01)00505-6 PG 4 WC Developmental Biology SC Developmental Biology GA 493JA UT WOS:000172217800011 PM 11677058 ER PT J AU Schulz, RJ Deye, JA AF Schulz, RJ Deye, JA TI Through the preoccupation with new technical developments, physicists have lost sight of the realities of cancer care and statistics SO MEDICAL PHYSICS LA English DT Editorial Material C1 Yale Univ, New Haven, CT 06520 USA. NCI, Radiat Res Programs, Bethesda, MD 20892 USA. RP Schulz, RJ (reprint author), Yale Univ, New Haven, CT 06520 USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER INST PHYSICS PI MELVILLE PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1, MELVILLE, NY 11747-4501 USA SN 0094-2405 J9 MED PHYS JI Med. Phys. PD NOV PY 2001 VL 28 IS 11 BP 2185 EP 2187 DI 10.1118/1.1415073 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 496KY UT WOS:000172395800001 PM 11764020 ER PT J AU Dinc, M Tchugunova, Y Dinc, S Cinarli, B Atasever, T Oz, M AF Dinc, M Tchugunova, Y Dinc, S Cinarli, B Atasever, T Oz, M TI Decreased osteocalcin levels in patients with chronic obstructive pulmunary disease using long-term inhaled beclomethasone dipropionate SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID CORTICOSTEROID-INDUCED OSTEOPOROSIS; AIR-FLOW OBSTRUCTION; PULMONARY-DISEASE; SERUM OSTEOCALCIN; BONE TURNOVER; ORAL PREDNISOLONE; CALCIUM-METABOLISM; CONTROLLED TRIAL; BUDESONIDE; MARKERS AB Inhaled corticosteroids have been used in the treatment of chronic obstructive pulmonary disease (COPD) for many years. However the adverse effects of corticosteroids on bone formation may require special consideration in these patients. This study was undertaken to investigate the effects of long-term inhaled beclomethasone dipropionate treatment on the biochemical markers of bone formation. For this purpose, serum osteocalcin, alkaline phosphatase, free calcium, and inorganic phosphate levels were measured in 65 male COPD patients. Patients in the control group (n = 30) had not taken oral or inhaled corticosteroids for at least 1 year. Only those patients using beclomethasone with metered-dose inhalers were included in the treatment group (n = 35). The mean age of the control group was 61.63 +/- 1.84 (mean +/- SEM). In the treatment group, the mean age was 59.10 +/- 2.29 and patients in this group had taken beclomethasone for an average time of 23.94 +/- 2.72 months (for at least 12 months) at an average concentration of 1,142.0 +/- 79.64 mug/d. The mean serum osteocalcin levels in the control group and treatment group were 7.03 +/- 0.19 ng/mL and 3.74 +/- 0.12 ng/mL, respectively. Comparison of values between groups indicates that serum osteocalcin levels in patients using beclomethasone were significantly lower than that of patients in the control group. Serum alkaline phosphatase levels were 167.96 +/- 1.49 U/L and 168.17 +/- 1.60 U/L for the control and treatment groups, respectively, There was no statistically significant difference among these values (Student's t test; P > .05). The mean values of total serum calcium and inorganic phosphate were not statistically different between the groups (P > .05). These results indicate that long-term inhaled beclomethasone treatment in COPD patients may induce significant changes in osteocalcin levels and require close monitoring for osteoporotic changes. Copyright (C) 2001 by W.B. Saunders Company. C1 Loeb Res Inst, Ottawa, ON K1Y 4E9, Canada. Gazi Univ, Dept Nucl Med, Ankara, Turkey. Ataturk Ctr Pulm Dis & Thorac Surg, Ankara, Turkey. RP NIDA, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Oz, Murat/E-2148-2012 NR 51 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0026-0495 EI 1532-8600 J9 METABOLISM JI Metab.-Clin. Exp. PD NOV PY 2001 VL 50 IS 11 BP 1336 EP 1339 DI 10.1053/meta.2001.27231 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 490XE UT WOS:000172078300013 PM 11699053 ER PT J AU Marshall, MA Jankovic, D Maher, VE Sher, A Berzofsky, JA AF Marshall, MA Jankovic, D Maher, VE Sher, A Berzofsky, JA TI Mice infected with Schistosoma mansoni develop a novel non-T-lymphocyte suppressor population which inhibits virus-specific CTL induction via a soluble factor SO MICROBES AND INFECTION LA English DT Article DE CTL; suppression; schistosomiasis; viral inununity; eosinophil ID GROWTH-FACTOR-BETA; RECOMBINANT VACCINIA VIRUS; HEPATITIS-B INFECTION; NON-PARASITE ANTIGEN; HELMINTH INFECTION; ANTITUMOR IMMUNITY; CELL RESPONSES; GRANULOMA-FORMATION; CYTOKINE PRODUCTION; DOWN-REGULATION AB We previously observed that Schistosoma mansoni-infected mice were deficient in their ability to mount a CTL response to unrelated viral antigens and to clear a vaccinia viral infection. Here, we explore the mechanism of that deficiency. Mixing experiments showed that splenocytes from S. mansoni-infected mice actively suppress stimulation in vitro of both viral-peptide specific CTL in spleen cells from virus-infected mice, and allospecific CTL. The mechanism of suppression involves at least in part a soluble factor, in that it can occur across a 0.4+mum membrane which prohibits direct cell contact. However, the inhibition is not alleviated by blocking with antibodies to IL-4, IL-10 or TGF-beta. Fractionation of the splenocyte population from S. mansoni-infected mice shows that the suppression is mediated by a non-B, non-T cell that expresses CD16 and Mac-1, but not Fc epsilonR or NK1.1. This represents a novel suppressor population that is distinct from the Fc epsilon RI+ populations of non-B, non-T cells in the spleens of S. mansoni-infected mice that provide a major source of IL-4 in these animals. Similar cells in schistosome-infected humans could affect susceptibility to other infections or responsiveness to vaccines. Published by editions scientifiques et medicales Elsevier SAS. C1 NCI, NIH, Mol Immunogenet & Vaccine Res Sect, Metab Branch, Bethesda, MD 20892 USA. NIAID, NIH, Immunobiol Sect, Parasit Dis Lab, Bethesda, MD 20892 USA. RP Berzofsky, JA (reprint author), NCI, NIH, Mol Immunogenet & Vaccine Res Sect, Metab Branch, Bldg 10,Room 6B-12, Bethesda, MD 20892 USA. NR 52 TC 19 Z9 19 U1 0 U2 0 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 NOV PY 2001 VL 3 IS 13 BP 1051 EP 1061 DI 10.1016/S1286-4579(01)01499-X PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 494XV UT WOS:000172311900001 PM 11709285 ER PT J AU Singh, VK Moskovitz, J Wilkinson, BJ Jayaswal, RK AF Singh, VK Moskovitz, J Wilkinson, BJ Jayaswal, RK TI Molecular characterization of a chromosomal locus in Staphylococcus aureus that contributes to oxidative defence and is highly induced by the cell-wall-active antibiotic oxacillin SO MICROBIOLOGY-SGM LA English DT Article DE PilB; oxidative stress; MsrA; antibiotic stress ID METHIONINE SULFOXIDE REDUCTASE; IN-VIVO; ALPHA-1-PROTEINASE INHIBITOR; STRESS RESPONSE; GENE; RESIDUES; PROTEINS; IDENTIFICATION; EXPRESSION; CLONING AB Previous studies employing two-dimensional gel electrophoresis and N-terminal protein sequencing have shown elevated synthesis of the enzyme methionine sulfoxide reductase (MsrA) in Staphylococcus aureus in response to cell-wall-active antibiotics. In the present study, the S. aureus msrA gene was cloned, overexpressed, purified as His-tagged MsrA and shown to have methionine sulfoxide reductase activity. The transcription of msrA was studied by assaying fl-galactosidase activity in an msrA promoter:: lacZ fusion strain and by Northern blot analysis. Transcription of msrA was increased by oxacillin; but not by a variety of other stresses including H2O2. Northern blot analysis revealed that the size of the msrA transcript was 2.3 kb, considerably larger than the 531 nt msrA ORF. The msrA transcription start site was mapped 25 nt upstream of the msrA start codon. Computer analysis from database sequences indicated at least three additional ORFs downstream of msrA. The deduced amino acid sequences of two of these three ORFs showed significant sequence homologies to PilB, and enzyme IIA of the phosphotransferase system, respectively. The third ORF could not be identified by homology searches. Northern blot hybridization with probes specific to the msrA downstream region indicated that the S. aureus msrA was transcribed as part of a polycistronic message. Interestingly, purified S. aureus PilB was shown to possess similar to 28-fold higher methionine sulfoxide reductase activity than the MsrA. An insertional knockout mutation in the first gene of this operon resulted in increased susceptibility of the mutant to H2O2 compared to the parent strain, but not to oxacillin. C1 Illinois State Univ, Dept Biol Sci, Microbiol Grp, Normal, IL 61790 USA. NHLBI, Biochem Lab, NIH, Bethesda, MD 20982 USA. RP Jayaswal, RK (reprint author), Illinois State Univ, Dept Biol Sci, Microbiol Grp, Normal, IL 61790 USA. FU NIAID NIH HHS [1R15 AI43027-01] NR 34 TC 40 Z9 42 U1 0 U2 1 PU SOC GENERAL MICROBIOLOGY PI READING PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AE, BERKS, ENGLAND SN 1350-0872 J9 MICROBIOL-SGM JI Microbiology-(UK) PD NOV PY 2001 VL 147 BP 3037 EP 3045 PN 11 PG 9 WC Microbiology SC Microbiology GA 492YR UT WOS:000172195600016 PM 11700354 ER PT J AU Rathore, D Kumar, S Lanar, DE McCutchan, TF AF Rathore, D Kumar, S Lanar, DE McCutchan, TF TI Disruption of disulfide linkages of the Plasmodium falciparum circumsporozoite protein: effects on cytotoxic and antibody responses in mice SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE malaria; DNA vaccine; sporozoites ID T-CELL EPITOPES; MALARIA SPOROZOITES; LYMPHOCYTE EPITOPE; VIRAL PROTEIN; DNA VACCINE; CS PROTEIN; IN-VITRO; IMMUNIZATION; RECOGNITION; IMMUNOGENICITY AB The circumsporozoite protein is a predominant surface antigen present on Plasmodium sporozoites. In Plasmodium falciparum circumsporozoite protein (PfCSP), two cysteine residues (396 and 401) are present adjacent to two overlapping cytotoxic T-lymphocyte epitopes of the protein and are involved in the formation of disulfide bridges. We investigated the role of these cysteines on the cellular and antibody responses towards the CS protein because disruption of disulfide linkages and the presence of cysteine residues in the flanking region of an epitope has been shown to significantly alter the immune responses to various proteins, Mice were immunized with variant forms of PfCSP DNA vaccine plasmids where these cysteine residues were individually mutated to alanine. The plasmid vaccines induced antigen specific antibody and cytotoxic T lymphocyte responses. While no alterations of cysteine influenced the CTL responses to P. falciparum CS protein, vaccine pVRCS4, containing an altered cysteine at position 401, dramatically improved the antibody response to the carboxyl-terminal region of the protein. This work indicates that sequence alterations of genes in an anti-malarial vaccine could enhance the response towards the native protein. Given the fact that long term natural immunity to the pathogen has not been documented, it may be important to challenge the immune system with non-native proteins. (C) 2001 Published by Elsevier Science B.V. C1 NIAID, Growth & Dev Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. USN, Med Res Ctr, Malaria Program, Silver Spring, MD 20910 USA. Walter Reed Army Inst Res, Silver Spring, MD 20910 USA. RP McCutchan, TF (reprint author), NIAID, Growth & Dev Sect, Parasit Dis Lab, NIH, Room 126,Bldg 4,4 Ctr Dr,MSC 0425, Bethesda, MD 20892 USA. RI Lanar, David/B-3560-2011 NR 53 TC 5 Z9 6 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD NOV PY 2001 VL 118 IS 1 BP 75 EP 82 DI 10.1016/S0166-6851(01)00369-3 PG 8 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA 500RZ UT WOS:000172641700008 PM 11704275 ER PT J AU Shan, XC Balakir, R Criado, G Wood, JS Seminario, MC Madrenas, J Wange, RL AF Shan, XC Balakir, R Criado, G Wood, JS Seminario, MC Madrenas, J Wange, RL TI ZAP-70-independent Ca2+ mobilization and Erk activation in Jurkat T cells in response to T-Cell antigen receptor ligation SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN-KINASE-C; KAPPA-B ACTIVATION; CD3 CROSS-LINKING; SIGNAL-TRANSDUCTION; TYROSINE KINASE; ADAPTER PROTEINS; GENETIC-EVIDENCE; EXCHANGE FACTOR; FAMILY KINASES; RAS ACTIVATION AB The tyrosine kinase ZAP-70 has been implicated as a critical intermediary between T-cell antigen receptor (TCR) stimulation and Erk activation on the basis of the ability of dominant negative ZAP-70 to inhibit TCR-stimulated Erk activation, and the reported inability of anti-CD3 antibodies to activate Erk in ZAP-70-negative Jurkat cells. However, Erk is activated in T cells receiving a partial agonist signal, despite failing to activate ZAP-70. This discrepancy led us to reanalyze the ZAP-70-negative Jurkat T-cell line P116 for its ability to support Erk activation in response to TCR/CD3 stimulation. Erk was activated by CD3 cross-linking in P116 cells. However, this response required a higher concentration of anti-CD3 antibody and was delayed and transient compared to that in Jurkat T cells. Activation of Raf-1 and MEK-1 was coincident with Erk activation. Remarkably, the time course of Ras activation was comparable in the two cell lines, despite proceeding in the absence of LAT tyrosine phosphorylation in the P116 cells. CD3 stimulation of P116 cells also induced tyrosine phosphorylation of phospholipase C-gamma1 (PLC gamma1) and increased the intracellular Ca2+ concentration. Protein kinase C (PKC) inhibitors blocked CD3-stimulated Erk activation in P116 cells, while parental Jurkat cells were refractory to PKC inhibition. The physiologic relevance of these signaling events is further supported by the finding of PLC gamma1 tyrosine phosphorylation, Erk activation, and CD69 upregulation in P116 cells on stimulation with superantigen and antigen-presenting cells. These results demonstrate the existence of two pathways leading to TCR-stimulated Erk activation in Jurkat T cells: a ZAP-70-independent pathway requiring PKC and a ZAP-70-dependent pathway that is PKC independent. C1 NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA. Univ Western Ontario, John P Robarts Res Inst, London, ON N6A 5K8, Canada. Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 5K8, Canada. Univ Western Ontario, Dept Med, London, ON N6A 5K8, Canada. RP Wange, RL (reprint author), NIA, Cellular & Mol Biol Lab, NIH, 5600 Nathan Shock Dr,MSC-12, Baltimore, MD 21224 USA. EM wanger@grc.nia.nih.gov NR 64 TC 33 Z9 33 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 NOV PY 2001 VL 21 IS 21 BP 7137 EP 7149 DI 10.1128/MCB.21.21.7137-7149.2001 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 480WQ UT WOS:000171486900002 PM 11585897 ER PT J AU Niimi, T Nagashima, K Ward, JM Minoo, P Zimonjic, DB Popescu, NC Kimura, S AF Niimi, T Nagashima, K Ward, JM Minoo, P Zimonjic, DB Popescu, NC Kimura, S TI claudin-18, a novel downstream target gene for the T/EBP/NKX2.1 homeodomain transcription factor, encodes lung- and stomach-specific isoforms through alternative splicing SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TIGHT-JUNCTION STRANDS; THYROTROPIN RECEPTOR GENE; ENHANCER-BINDING PROTEIN; FACTOR-I; MOLECULAR PHYSIOLOGY; MORPHOGENESIS; PROMOTER; EXPRESSION; MOUSE; TTF-1 AB T/EBP/NKX2.1, a member of the NKX family of homeodomain-containing transcription factors, regulates the expression of a number of genes in lung and thyroid. Here we describe the isolation and characterization of a novel target gene, termed claudin-18, that is down-regulated in the lungs of T/ebp/Nkr2.1-null mouse embryos. The gene product exhibits an amino acid sequence similar to those of the claudin multigene family of proteins that constitute tight junction strands in epithelial cells. The gene was localized by fluorescence in situ hybridization to mouse chromosome 9 at region 9E3-F1 and to human chromosome 3 at region 3q21-23. The claudin-18 gene has two promoters, each with its own unique exon I that is spliced to common exons 2 through 5. Alternative usage of these promoters leads to production of lung and stomach-specific transcripts. The downstream lung-specific promoter contains two T/EBP/NKX2.1 binding sites responsible for trans activation of the gene by T/EBP/NKX2.1 in lung cells. Only claudin-18 was down-regulated in T/ebp/Nkr2.1-null embryo lungs among 11 claudin transcripts examined. Furthermore, the claudin-18 transcript has an alternative 12-bp insertion derived from the 5' end of intron 4, which produces a C-terminally truncated isoform in lung and stomach. Immunohistochemistry demonstrated complete membrane localization of claudin-18 with small focal dots in the lung and stomach epithelial cells. Immunogold electron microscopy analysis revealed that claudin-18 is concentrated at the cell-cell borders of epithelial cells. These unique features suggest a potentially important role for claudin-18 in the structure and function of tight junctions in lung and stomach. C1 NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. NCI, SAIC Frederick, EM Facil Image Anal Lab, Frederick, MD 21702 USA. NCI, Vet & Tumor Pathol Sect, Off Lab Anim Resources, Frederick, MD 21702 USA. Univ So Calif, Sch Med, Womens & Childrens Hosp, Dept Pediat, Los Angeles, CA 90033 USA. RP Kimura, S (reprint author), NCI, Lab Metab, NIH, Bldg 37,Rm 3E-24, Bethesda, MD 20892 USA. NR 47 TC 77 Z9 79 U1 1 U2 4 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 NOV PY 2001 VL 21 IS 21 BP 7380 EP 7390 DI 10.1128/MCB.21.21.7380-7390.2001 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 480WQ UT WOS:000171486900024 ER PT J AU Nicot, C Mahieux, R Pise-Masison, C Brady, J Gessain, A Yamaoka, S Franchini, G AF Nicot, C Mahieux, R Pise-Masison, C Brady, J Gessain, A Yamaoka, S Franchini, G TI Human T-Cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappa B pathway and modulation of coactivator usage SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HTLV-I; V-MYB; MEDIATED ACTIVATION; MOLECULAR-CLONING; BINDING-PROTEIN; MICE LACKING; DNA-BINDING; MIM-1 GENE; KINASE; EXPRESSION AB The proto-oncogene c-myb is essential for a controlled balance between cell growth and differentiation. Aberrant c-Myb activity has been reported for numerous human cancers, and enforced c-Myb transcription can transform cells of lymphoid origin by stimulating cellular proliferation and inhibiting apoptotic pathways. Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of I kappaB alpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1 beta), and lipopolysaccharide, also inhibited c-Myb transcription. These results uncover a new link between extracellular signaling and c-Myb-dependent transcription. The mechanism underlying NF-kappaB-mediated repression was identified as sequestration of the coactivators CBP/p300 by Re1A. Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind Re1A retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. C1 NCI, Canc Res Ctr, BRL, Sect Anim Models & Retroviral Vaccines, Bethesda, MD 20892 USA. NCI, Canc Res Ctr, Basic Res Lab, Sect Virus & Tumor Biol, Bethesda, MD 20892 USA. Inst Pasteur, Unite Epidemiol & Physiopathol Virus Oncogenes, F-75724 Paris, France. Tokyo Med & Dent Univ, Dept Microbiol, Bunkyo Ku, Tokyo 1138519, Japan. RP Nicot, C (reprint author), NCI, Canc Res Ctr, BRL, Sect Anim Models & Retroviral Vaccines, 41 Lib Dr,Bldg 41,Room C303, Bethesda, MD 20892 USA. NR 68 TC 28 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 NOV PY 2001 VL 21 IS 21 BP 7391 EP 7402 DI 10.1128/MCB.21.21.7391-7402.2001 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 480WQ UT WOS:000171486900025 PM 11585920 ER PT J AU Khaled, AR Moor, AN Li, AQ Ferris, DK Muegge, K Fisher, RJ Fliegel, L Durum, SK AF Khaled, AR Moor, AN Li, AQ Ferris, DK Muegge, K Fisher, RJ Fliegel, L Durum, SK TI Trophic factor withdrawal: p38 mitogen-activated protein kinase activates NHE1, which induces intracellular alkalinization SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID NA+/H+ EXCHANGER NHE1; RECEPTOR-DEFICIENT MICE; T-CELL PROLIFERATION; MAP KINASES; IN-VIVO; SIGNAL-TRANSDUCTION; CYTOKINE RECEPTORS; CULTURED-CELLS; FLOW-CYTOMETRY; GROWTH-FACTORS AB Trophic factor withdrawal induces cell death by mechanisms that are incompletely understood. Previously we reported that withdrawal of interleukin-7 (IL-7) or IL-3 produced a rapid intracellular alkalinization, disrupting mitochondrial metabolism and activating the death protein Bax. We now observe that this novel alkalinization pathway is mediated by the pH regulator NHE1, as shown by the requirement for sodium, blocking by pharmacological inhibitors or use of an NHE1-deficient cell line, and the altered phosphorylation of NHE1 Alkalinization also required the stress-activated p38 mitogen-activated protein kinase (MAPK). Inhibition of p38 MAPK activity with pharmacological inhibitors or expression of a dominant negative kinase prevented alkalinization. Activated p38 MAPK directly phosphorylated the C terminus of NHE1 within a 40-amino-acid region. Analysis by mass spectroscopy identified four phosphorylation sites on NHE1, Thr 717, Ser 722, Ser 725, and Ser 728. Thus, loss of trophic cytokine signaling induced the p38 MAPK pathway, which phosphorylated NHE1 at specific sites, inducing intracellular alkalinization. C1 NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick,Ctr Canc Res, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Leukocyte Biol, Ctr Canc Res, Frederick, MD 21702 USA. Univ Alberta, Dept Biochem, Edmonton, AB, Canada. RP Durum, SK (reprint author), NCI, Sect Cytokines & Immun, Bldg 560,Rm 31-71, Frederick, MD 21702 USA. EM durums@mail.ncifcrf.gov RI Fisher, Robert/B-1431-2009 FU NCI NIH HHS [N01-CO-56000] NR 61 TC 118 Z9 122 U1 1 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 NOV PY 2001 VL 21 IS 22 BP 7545 EP 7557 DI 10.1128/MCB.21.22.7545-7557.2001 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 485CW UT WOS:000171736800002 PM 11604491 ER PT J AU Kim, BS Savinova, OV Reedy, MV Martin, J Lun, Y Gan, L Smith, RS Tomarev, SI John, SWM Johnson, RL AF Kim, BS Savinova, OV Reedy, MV Martin, J Lun, Y Gan, L Smith, RS Tomarev, SI John, SWM Johnson, RL TI Targeted disruption of the myocilin gene (Myoc) suggests that human glaucoma-causing mutations are gain of function SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID OPEN-ANGLE GLAUCOMA; NAIL-PATELLA SYNDROME; TRABECULAR MESHWORK; MOLECULAR-CLONING; TIGR MUTATION; EXPRESSION; OLFACTOMEDIN; PROTEIN; FAMILY; IDENTIFICATION AB Glaucoma is a heterogeneous eye disease and a major cause of blindness worldwide. Recently, primary open angle glaucoma (POAG)-associated mutations have been found in the trabecular meshwork inducible glucocorticoid response gene (TIGR), also known as the myocilin gene (MYOC), at the GLC1A locus on chromosome 1q21-q31. These mutations occurred in a subset of patients with juvenile- and adult-onset POAG and exhibited autosomal dominant inheritance. Ocular expression and its involvement in POAG suggest that TIGR/MYOC may have a role(s) in regulating intraocular pressure (IOP). Here, we report the generation and analysis of mice heterozygous and homozygous for a targeted null mutation in Myoc. Our study shows that Myoc mutant mice are both viable and fertile. Our in vivo findings further demonstrate that Myoc is not required for normal IOP or normal ocular morphology. The lack of a discernable phenotype in both Myoc-heterozygous and Myoc-null mice suggests that haploinsufficiency is not a critical mechanism for POAG in individuals with mutations in MYOC. Instead, disease-causing mutations in humans likely act by gain of function. C1 Univ Texas, MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA. Univ Texas, MD Anderson Canc Ctr, Program Genes & Dev, Houston, TX 77030 USA. Jackson Lab, Bar Harbor, ME 04609 USA. Howard Hughes Med Inst, Bar Harbor, ME 04609 USA. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Tufts Univ, Sch Med, Dept Ophthalmol, Boston, MA 02111 USA. Univ Rochester, Ctr Aging & Dev Biol, Rochester, NY 14642 USA. RP Johnson, RL (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Box 117, Houston, TX 77030 USA. FU NEI NIH HHS [5F32EY06945, EY0702420, EY123113, F32 EY006945] NR 36 TC 142 Z9 150 U1 0 U2 6 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 NOV PY 2001 VL 21 IS 22 BP 7707 EP 7713 DI 10.1128/MCB.21.22.7707-7713.2001 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 485CW UT WOS:000171736800017 PM 11604506 ER PT J AU Berkeley, JL Gomeza, J Wess, J Hamilton, SE Nathanson, NM Levey, AI AF Berkeley, JL Gomeza, J Wess, J Hamilton, SE Nathanson, NM Levey, AI TI M-1 muscarinic acetylcholine receptors activate extracellular signal-regulated kinase in CA1 pyramidal neurons in mouse hippocampal slices SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID LONG-TERM POTENTIATION; PROTEIN-COUPLED RECEPTORS; METHYL-D-ASPARTATE; RAT HIPPOCAMPUS; MAP KINASE; KNOCKOUT MICE; TYROSINE KINASES; PC12 CELLS; PHOSPHORYLATION; PATHWAYS AB Activation of extracellular signal-regulated kinases (ERK) Is crucial for many neural functions, including learning, memory, and synaptic plasticity. As muscarinic acetylcholine receptors (mAChR) modulate many of the same higher brain functions as ERK, we examined mAChR-mediated ERK activation in mouse hippocampal slices. The cholinergic agonist carbachol caused an atropine-sensitive ERK activation in the dendrites and somata CAI pyramidal neurons. To determine the responsible mAChR subtype, we combined pharmacologic and genetic approaches. Pretreatment with M-1 antagonists inhibited ERK activation. Furthermore, mAChR-induced ERK activation was absent in slices from M-1 knockout mice. ERK activation was normal in slices derived from other mAChR subtype knockouts (M-2, M-3, and M-4), although these other subtypes are expressed in many of the same neurons. Thus, we demonstrate divergent functions for the different mAChR subtypes. We conclude that M-1 is responsible for mAChR-mediated ERK activation, providing a mechanism by which M-1 may modulate learning and memory. C1 Emory Univ, Dept Neurol, WMB 6000, Atlanta, GA 30322 USA. NIDDKD, NIH, Bethesda, MD 20892 USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA. RP Levey, AI (reprint author), Emory Univ, Dept Neurol, WMB 6000, 1639 Pierce Dr, Atlanta, GA 30322 USA. RI Levey, Allan/F-2104-2011; OI Levey, Allan/0000-0002-3153-502X; Berkeley, Jennifer/0000-0001-8164-282X FU NINDS NIH HHS [R01 NS26920, R01 NS30454] NR 51 TC 62 Z9 74 U1 0 U2 0 PU ACADEMIC PRESS INC 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 NOV PY 2001 VL 18 IS 5 BP 512 EP 524 DI 10.1006/mcne.2001.1042 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 498QN UT WOS:000172522100006 PM 11922142 ER PT J AU Avedisov, SN Rogozin, IB Koonin, EV Thomas, BJ AF Avedisov, SN Rogozin, IB Koonin, EV Thomas, BJ TI Rapid evolution of a cyclin A inhibitor gene, roughex, in Drosophila SO MOLECULAR BIOLOGY AND EVOLUTION LA English DT Article DE roughex; cell cycle inhibitor; cyclin A; evolution; Drosophila ID DEPENDENT-KINASE INHIBITOR; NONSYNONYMOUS SUBSTITUTION; MOLECULAR EVOLUTION; POSITIVE SELECTION; EVOLVING GENES; PROTEIN; MELANOGASTER; RATES; G(1); G1 AB The recent sequencing of the complete genome of the fruit fly Drosophila melanogaster has yielded about 30% of the predicted genes with no obvious counterparts in other organisms. These rapidly evolving genes remain largely unexplored. Here, we present evidence for a striking variability in an important Drosophila cell cycle regulator encoded by the gene roughex (rux) in closely related fly species. The unusual level of Rux protein variability indicates that there are very low overall constraints on amino acid substitutions. Despite the lack of sequence similarity, certain common features, including the presence of a C-terminal nuclear localization signal and a functionally important N-terminal RXL cyclin-binding motif, exist between Rux and cyclin-dependent kinase inhibitors of the Cip/Kip family. These results indicate that even some genes involved in key regulatory processes in eukaryotes evolve at extremely high rates. C1 NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Avedisov, SN (reprint author), VA Engelhardt Mol Biol Inst, 32 Vavilov St, Moscow 117984, Russia. NR 53 TC 8 Z9 8 U1 0 U2 1 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 NOV PY 2001 VL 18 IS 11 BP 2110 EP 2118 PG 9 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA 489NY UT WOS:000171998900013 PM 11606707 ER PT J AU Dhanvantari, S Zhang, CF Lou, H Loh, YP AF Dhanvantari, S Zhang, CF Lou, H Loh, YP TI Carboxypeptidase E, a prohormone sorting receptor, is sorted to the regulated secretory pathway by anchoring to lipid rafts SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, LDN, NIH, Bethesda, MD 20892 USA. RI Dhanvantari, Savita/B-5362-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 21 BP 4A EP 5A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500022 ER PT J AU Dykstra, ML Pierce, SK AF Dykstra, ML Pierce, SK TI Epstein-Barr Virus coopts lipid rafts to regulate BCR signaling and the intracellular targeting of antigen SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIAID, LIG, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 19 BP 4A EP 4A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500020 ER PT J AU Kumar, M Kenworthy, AK Verma, A Roth, MG Zimmerberg, J AF Kumar, M Kenworthy, AK Verma, A Roth, MG Zimmerberg, J TI Microdomain topology in membrane fusion by influenza hemagluttinin - The ring raft hypothesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, Cellular & Mol Biophys Lab, Bethesda, MD 20892 USA. NIH, NICHD, CBMB, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75235 USA. NIH, Mol & Cellular Biophys Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 18 BP 4A EP 4A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500019 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 that links RNA transcription to nuclear export SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Emory Univ, Atlanta, GA 30322 USA. NICHHD, CBMB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 42 BP 8A EP 8A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500043 ER PT J AU Zheng, YL Li, BS Amin, ND Pant, HC AF Zheng, YL Li, BS Amin, ND Pant, HC TI Cdk5/p25 inhibitory peptide (CIP) derived from p35 regulates Tau protein phosphorylation in transfected cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NINDS, LNC, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 57 BP 11A EP 11A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500058 ER PT J AU Brodie, C Blass, M Melamed, D Zrachia, A Blumberg, PM Kobiler, D Lustig, S AF Brodie, C Blass, M Melamed, D Zrachia, A Blumberg, PM Kobiler, D Lustig, S TI Phosphorylation of PKCdelta on specific tyrosine residues regulates its ability to activate pro- and anti-apoptotic pathways SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Bar Ilan Univ, IL-52900 Ramat Gan, Israel. NCI, NIH, MMTP, LCCTP, Bethesda, MD 20892 USA. Israel Inst Biol Res, IL-70450 Ness Ziona, Israel. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 89 BP 17A EP 17A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500090 ER PT J AU Sharma, P Veeranna, V Kulkarni, AB Ahn, N Pant, HC AF Sharma, P Veeranna, V Kulkarni, AB Ahn, N Pant, HC TI Regulation of the MAP kinase pathway by cyclin dependent kinase 5 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Natl Inst Immunol, EGE Lab, New Delhi 110067, India. NINCDS, Neurochem Lab, NIH, Bethesda, MD USA. Natl Inst Dent & Craniofacial Res, Funct Genom Unit, Gene Targeting Facil, NIH, Bethesda, MD USA. Univ Colorado, Dept Biochem, Boulder, CO 80309 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 93 BP 17A EP 17A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500094 ER PT J AU Skupsky, R Nossal, R AF Skupsky, R Nossal, R TI Phosphoinositide cycles as triggers in cell signaling SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Maryland, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. NIH, NICHD, LIMB, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 102 BP 19A EP 19A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500103 ER PT J AU Kruman, II Cardozo-Pelaez, F Kumaravel, TS Stedeford, TJ Lohani, A Evans, M Sanchez-Ramos, JR Mattson, MP AF Kruman, II Cardozo-Pelaez, F Kumaravel, TS Stedeford, TJ Lohani, A Evans, M Sanchez-Ramos, JR Mattson, MP TI Folate deficiency is neurotoxic and potentiates oxidative stress by impairing DNA repair in models of Alzheimer's disease SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA, Neurosci Lab, Baltimore, MD 21224 USA. Univ S Florida, Dept Neurol, Tampa, FL 33620 USA. NIA, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA. RI Mattson, Mark/F-6038-2012; Sanchez-Ramos, Juan/A-1188-2009 OI Sanchez-Ramos, Juan/0000-0002-3391-7857 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 137 BP 25A EP 25A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500138 ER PT J AU Damer, CK Szydlowski, EG Tifft, KE AF Damer, CK Szydlowski, EG Tifft, KE TI Dictyostelium discoideum copines: A family of C2 domain-containing proteins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Vassar Coll, Poughkeepsie, NY 12604 USA. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 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 NOV PY 2001 VL 12 SU S MA 151 BP 27A EP 27A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500152 ER PT J AU Shen, DW Chauhan, S Su, A Pai-Panandiker, A Liang, XJ Gottesman, MM AF Shen, DW Chauhan, S Su, A Pai-Panandiker, A Liang, XJ Gottesman, MM TI Reduced expression and disorganization of actin and dynamin II are associated with a defect in endocytosis in human cisplatin-resistant cell lines SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Cell Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 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 NOV PY 2001 VL 12 SU S MA 177 BP 32A EP 32A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500178 ER PT J AU Bai, RL Covell, DG Liu, CF Ghosh, AK Hamel, E AF Bai, RL Covell, DG Liu, CF Ghosh, AK Hamel, E TI (-)-doliculide, a new macrocyclic depsipeptide enhancer of actin assembly SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Screening Technol Branch, DTP, DCTD, Frederick, MD 21701 USA. Univ Illinois, Dept Chem, Chicago, IL 60680 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 183 BP 33A EP 33A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500184 ER PT J AU Conti, MA Du, YB Liu, CY Adelstein, RS AF Conti, MA Du, YB Liu, CY Adelstein, RS TI The effect of deletion of nonmuscle myosin II-A during mouse development SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Lab Mol Cardiol, Bethesda, MD 20892 USA. NHLBI, Transgen Facil, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 190 BP 34A EP 34A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500191 ER PT J AU Hu, AH Wang, F Sellers, JR AF Hu, AH Wang, F Sellers, JR TI Mutations in human nonmuscle myosin IIA found in patients with May-Hegglin Anomaly and Fechtner Syndrome result in impaired enzymatic function SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA, NIH, Bethesda, MD 20892 USA. NHLBI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 188 BP 34A EP 34A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500189 ER PT J AU Kishi, H Takeda, K Yu, ZX Ferrans, VJ Adelstein, RS AF Kishi, H Takeda, K Yu, ZX Ferrans, VJ Adelstein, RS TI Decreased cardiac myocyte proliferation in nonmuscle myosin II-B-ablated mouse embryos SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Lab Mol Cardiol, Bethesda, MD 20892 USA. NIH, Pathol Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 189 BP 34A EP 34A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500190 ER PT J AU Takeda, K Yu, ZX Kishi, H Ferrans, VJ Adelstein, RS AF Takeda, K Yu, ZX Kishi, H Ferrans, VJ Adelstein, RS TI Increased apoptosis in brain and heart of nonmuscle myosin II-B-ablated mouse embryos SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, LMC, Bethesda, MD 20892 USA. NHLBI, Pathol Sect, Bethesda, MD 20892 USA. NHLBI, Mol Cardiol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 191 BP 34A EP 35A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500192 ER PT J AU Buxton, DB Golomb, E Adelstein, RS AF Buxton, DB Golomb, E Adelstein, RS TI Butyrate induces expression of nonmuscle myosin heavy chain IIC (NMHC-IIC) in neuroblastoma cells and macrophages SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Mol Cardiol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 192 BP 35A EP 35A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500193 ER PT J AU Davis, JS Hassanzadeh, S Winitsky, S Wen, H Epstein, ND AF Davis, JS Hassanzadeh, S Winitsky, S Wen, H Epstein, ND TI A spatial gradient of myosin regulatory light chain phosphorylation is critical to the complex pattern of cardiac contraction SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, Cardiol Branch, Mol Physiol Sect, Bethesda, MD USA. NHLBI, Cardiac Energet Lab, Bethesda, MD USA. RI Wen, Han/G-3081-2010 OI Wen, Han/0000-0001-6844-2997 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 194 BP 35A EP 35A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500195 ER PT J AU Golomb, E Conti, MA Preston, Y Bromberg, Y Zuckerman, JD Goldin, E Takeda, K Yu, ZX Ferrans, VJ Buxton, D Adelstein, RS AF Golomb, E Conti, MA Preston, Y Bromberg, Y Zuckerman, JD Goldin, E Takeda, K Yu, ZX Ferrans, VJ Buxton, D Adelstein, RS TI Myosin II-C: A third cytoskeletal myosin II SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, LMC, Bethesda, MD 20892 USA. Natl Inst Hlth, Pathol Sect, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 193 BP 35A EP 35A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500194 ER PT J AU Carroll, S Herrera, AH Horowits, R AF Carroll, S Herrera, AH Horowits, R TI A novel model for the initiation of myofibril assembly SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 218 BP 39A EP 40A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500219 ER PT J AU Shu, S Uyeda, TQP Korn, ED AF Shu, S Uyeda, TQP Korn, ED TI Studies on the functional properties of the coiled-coil helical tails of class II myosins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Cell Biol Lab, Bethesda, MD 20892 USA. Natl Inst Adv Ind Sci & Technol, Gene Discovery Res Ctr, Osaka, Japan. NIH, NHLBI, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 227 BP 41A EP 41A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500228 ER PT J AU Gao, CY Negash, S Zelenka, PS AF Gao, CY Negash, S Zelenka, PS TI A role for CDK5 in corneal epithelial cell adhesion and migration SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI, LMDB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 242 BP 44A EP 44A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500243 ER PT J AU Galbraith, JA Terasaki, M AF Galbraith, JA Terasaki, M TI Two photons are better than one: Intracellular wounding with a two photon microscope SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NINDS, Neurobiol Lab, Bethesda, MD 20892 USA. Univ Connecticut, Ctr Hlth, Farmington, CT 06032 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 268 BP 49A EP 49A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500269 ER PT J AU Herrmann, H Wedig, T Muecke, N Tran, S Langowski, J Steinert, P Burkhard, P Aebi, U AF Herrmann, H Wedig, T Muecke, N Tran, S Langowski, J Steinert, P Burkhard, P Aebi, U TI Molecular and Biophysical Characterization of "unit-length filaments" (ULFs) assembled from wild-type in comparison to a temperature-sensitive human vimentin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 German Canc Res Ctr, D-69120 Heidelberg, Germany. NIH, Skin Biol Lab, Bethesda, MD USA. Univ Basel, Biozentrum, M E Mueller Inst, Basel, Switzerland. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 299 BP 55A EP 55A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500300 ER PT J AU Muecke, N Wedig, T Buerer, A Marekov, L Steinert, PM Langowski, J Aebi, U Herrmann, H AF Muecke, N Wedig, T Buerer, A Marekov, L Steinert, PM Langowski, J Aebi, U Herrmann, H TI Characterization of physiological "assembly-starter-units" of vimentin: The phosphate buffer system SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 German Canc Res Ctr, D-6900 Heidelberg, Germany. Univ Basel, Biozentrum, M E Mueller Inst, Basel, Switzerland. NIH, NIAMS, Bethesda, MD 20892 USA. RI Langowski, Jorg/A-1843-2011 OI Langowski, Jorg/0000-0001-8600-0666 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 300 BP 55A EP 55A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500301 ER PT J AU Steinert, PM Muecke, N Buerer, A Aebi, U Marekov, L Herrmann, H AF Steinert, PM Muecke, N Buerer, A Aebi, U Marekov, L Herrmann, H TI Investigating the association state of headless intermediate filament proteins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIAMS, Skin Biol Lab, Bethesda, MD 20892 USA. Univ Basel, Biozentrum, Div Biophys & Macromol, Basel, Switzerland. Univ Basel, Biozentrum, M E Mueller Inst, Basel, Switzerland. Univ Basel, Biozentrum, Basel, Switzerland. Deutsch Krebsforschungszentrum, Div Cell Biol, Heidelberg, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 298 BP 55A EP 55A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500299 ER PT J AU Dhanvantari, S Arnaoutova, I Snell, CR Steinbach, PJ Hammond, K Caputo, GA London, E Loh, YP AF Dhanvantari, S Arnaoutova, I Snell, CR Steinbach, PJ Hammond, K Caputo, GA London, E Loh, YP TI Molecular modeling and biochemical studies of a sorting receptor, carboxypeptidase E: Evidence for a transmembrane orientation in secretory granules SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, LDN, Bethesda, MD 20892 USA. Novartis Inst Med Sci, London WC1E 6BN, England. NIH, Ctr Mol Modeling, Ctr Informat Technol, Bethesda, MD USA. SUNY Albany, Dept Biochem & Cell Biol, Albany, NY 12222 USA. RI Dhanvantari, Savita/B-5362-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 366 BP 67A EP 68A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500367 ER PT J AU Aleman, C Liang, XJ Taylor, B Aszalos, A Gottesman, MM AF Aleman, C Liang, XJ Taylor, B Aszalos, A Gottesman, MM TI The effect of P-glycoprotein on cell membrane fluidity and membrane potential using a tetracycline-inducible system SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Cell Biol Lab, Bethesda, MD 20910 USA. NCI, Bethesda, MD 20892 USA. NCI, FACS Core Lab, Bethesda, MD USA. NCI, Cell Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 373 BP 69A EP 69A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500374 ER PT J AU Puri, N Roche, PA AF Puri, N Roche, PA TI NSF-mediated SNARE "priming" is required for regulated exocytosis from RBL mast cells SO MOLECULAR BIOLOGY OF THE CELL 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 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 NOV PY 2001 VL 12 SU S MA 382 BP 70A EP 71A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500383 ER PT J AU Verma, A Coorssen, JR Yin, SR Poustka, A Blank, PS Backlund, P Zimmerberg, J AF Verma, A Coorssen, JR Yin, SR Poustka, A Blank, PS Backlund, P Zimmerberg, J TI Identification of the calcium-binding proteins regulating the membrane fusion steps of exocytosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, LCMB, Bethesda, MD 20892 USA. Univ Calgary, Calgary, AB T2N 4N1, Canada. Max Planck Inst Mol Genet, NIH, NICHD, D-14195 Berlin, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 378 BP 70A EP 70A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500379 ER PT J AU Hepp, R Cabaniols, JP Roche, P AF Hepp, R Cabaniols, JP Roche, P TI Regulation of SNAP-25 phosphorylation during exocytosis SO MOLECULAR BIOLOGY OF THE CELL 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 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 NOV PY 2001 VL 12 SU S MA 384 BP 71A EP 71A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500385 ER PT J AU Gao, MG Peters, PJ Gaschet, J Ambach, A van Donselaar, E Traverse, JF Bos, E Wolffe, EJ Hsu, VW AF Gao, MG Peters, PJ Gaschet, J Ambach, A van Donselaar, E Traverse, JF Bos, E Wolffe, EJ Hsu, VW TI Characterization of coated vesicles that participate in endocytic recycling SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Netherlands Canc Inst, Amsterdam, Netherlands. NIAID, Bethesda, MD 20892 USA. RI Gaschet, Joelle/F-6761-2013 OI Gaschet, Joelle/0000-0003-2154-1255 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 392 BP 72A EP 72A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500393 ER PT J AU Kim, T Tao-Cheng, JH Eiden, LE Loh, YP AF Kim, T Tao-Cheng, JH Eiden, LE Loh, YP TI Chromogranin A, a master "on/off" switch controlling dense-core secretory granule biogenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, Dev Neurobiol Lab, Bethesda, MD 20892 USA. NIH, NINDS, EM Facil, Bethesda, MD 20892 USA. NIH, NIMH, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 394 BP 73A EP 73A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500395 ER PT J AU Kumar, M Kenworthy, AK Roth, MG Zimmerberg, J AF Kumar, M Kenworthy, AK Roth, MG Zimmerberg, J TI Raft association plays an important role in Influenza Hemagglutinin-mediated fusion SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, LCMB, Bethesda, MD 20892 USA. NIH, NICHD, CBMB, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75235 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 401 BP 74A EP 74A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500402 ER PT J AU Mittal, A Leikina, E Chernomordik, LV Bentz, JE AF Mittal, A Leikina, E Chernomordik, LV Bentz, JE TI Monitoring single cell fusion kinetics from automated video fluorescence microscopy SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Drexel Univ, Dept Biosci & Biotechnol, Philadelphia, PA 19104 USA. NIH, NICHD, Lab Cellular & Mol Biophys, Sect Membrane Biol, Bethesda, MD 20892 USA. RI Mittal, Aditya/E-3087-2010 OI Mittal, Aditya/0000-0002-4030-0951 NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 404 BP 74A EP 75A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500405 ER PT J AU Puri, A Ablan, SD Rawat, SS Martin, T KewalRamani, VN Rein, AR Blumenthal, R AF Puri, A Ablan, SD Rawat, SS Martin, T KewalRamani, VN Rein, AR Blumenthal, R TI Are glycosphingolipid-enriched domains in the plasma membrane portals for entry of enveloped viruses? SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, CCR, NIH, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, HIV DRP, NIH, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 402 BP 74A EP 74A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500403 ER PT J AU Shor, J Curran, PK Fishman, PH AF Shor, J Curran, PK Fishman, PH TI Targeting beta-adrenergic receptor subtypes to caveolae: Differences between endogenous and heterologously expressed beta(1)- but not beta(2)-adrenergic receptors SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS, Membrane Biochem Sect, LMCN, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 443 BP 81A EP 82A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500444 ER PT J AU Hinshaw, JE Zhang, PJ AF Hinshaw, JE Zhang, PJ TI Three dimensional reconstruction of dynamin in the constricted state SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, LCBB, NIDDK, Bethesda, MD 20892 USA. NIH, NCI, LB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 450 BP 83A EP 83A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500451 ER PT J AU Misra, S Puertollano, R Bonifacino, JS Hurley, JH AF Misra, S Puertollano, R Bonifacino, JS Hurley, JH TI Structural basis of acidic/dileucine-motif-based sorting by GGA proteins SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NICHHD, NIH, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 462 BP 85A EP 85A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500463 ER PT J AU Novoradovskaya, N Perou, C Pesich, R Aprelikova, O Sotiriou, C Fero, M Brown, P Botstein, D Braman, J AF Novoradovskaya, N Perou, C Pesich, R Aprelikova, O Sotiriou, C Fero, M Brown, P Botstein, D Braman, J TI Universal human and mouse reference RNA for microarrays SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Stratagene, La Jolla, CA 92130 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Stanford Univ, Stanford, CA 94305 USA. NCI, NIH, Gaithersburg, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 2 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 NOV PY 2001 VL 12 SU S MA 531 BP 98A EP 98A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500531 ER PT J AU Dyer, KD Moreau, JM Rosenberg, HF AF Dyer, KD Moreau, JM Rosenberg, HF TI Transcriptional regulation of mouse eosinophil associated ribonuclease 2 (mEAR2) by intronic enhancer elements: Common regulatory features of mouse EAR genes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIAID, Bethesda, MD 20892 USA. NIAID, Host Def Lab, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 537 BP 99A EP 99A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500537 ER PT J AU Nielsen, JA Hudson, LD Armstrong, RC AF Nielsen, JA Hudson, LD Armstrong, RC TI Nuclear organization in differentiating oligodendrocytes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NIH, NINDS, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 539 BP 99A EP 99A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500539 ER PT J AU Demidenko, ZN Badenhorst, P Jones, T Bi, XL Mortin, MA AF Demidenko, ZN Badenhorst, P Jones, T Bi, XL Mortin, MA TI Regulated nuclear export of the homeodomain transcription factor Prospero SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Biochem Lab, Bethesda, MD 20892 USA. NIH, NCI, Mol Cell Biol Lab, Bethesda, MD USA. RI Bi, Xiaolin/C-7038-2014 OI Bi, Xiaolin/0000-0003-2837-9457 NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 612 BP 112A EP 113A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500612 ER PT J AU Zhao, M Gold, L Ginsgerg, AM Liang, LF Dean, J AF Zhao, M Gold, L Ginsgerg, AM Liang, LF Dean, J TI Conserved furin site is not required for ZP3 participation in the extracellular egg coat SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIDDK, Cellular & Dev Biol Lab, Bethesda, MD 20892 USA. NIH, NIDDK, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 618 BP 113A EP 114A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500618 ER PT J AU Sinha, D Zigler, S Wheelock, R O'Brien, TP Gongora, C AF Sinha, D Zigler, S Wheelock, R O'Brien, TP Gongora, C TI Functional significance of cannabinoid receptor in macrophage-like cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21287 USA. NEI, LMOD, NIH, Bethesda, MD 20892 USA. NICHHD, LMGR, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 661 BP 121A EP 122A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500661 ER PT J AU Virata, MLA Yang, HYT Iadarola, MJ FitzGerald, DJ AF Virata, MLA Yang, HYT Iadarola, MJ FitzGerald, DJ TI Neuropeptide FF receptors: Regulation of its mRNAs and development of a NPFF receptor-specific toxin conjugate SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Mol Biol Lab, Biotherapy Sect, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Pain & Neurosensory Mechanisms Branch, Neuronal Gene Express Unit, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 659 BP 121A EP 121A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500659 ER PT J AU Lavoie, B Wolstenholme, JT Hyman, SE AF Lavoie, B Wolstenholme, JT Hyman, SE TI Ania4 - a dopamine-induced gene that shares high homology with doublecortin-like kinase, a microtubule-associated protein SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS, Mol Plast Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 665 BP 122A EP 122A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500665 ER PT J AU Rabadan-Diehl, C Aguilera, G AF Rabadan-Diehl, C Aguilera, G TI Regulation of vasopressin V1b receptor involves translational mechanisms and an internal ribosome entry site (IRES) in the 5 ' untranslated region SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 664 BP 122A EP 122A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500664 ER PT J AU Wang, YJ Szabo, K Haft, CR Trejo, J AF Wang, YJ Szabo, K Haft, CR Trejo, J TI Sorting nexin 1 associates with protease-activated receptor-1 and regulates downregulation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ N Carolina, Chapel Hill, NC 27515 USA. Natl Inst Diabet & Kidney Dis, Diabet Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 670 BP 123A EP 123A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500670 ER PT J AU Ewen, BS Gasper, PW Hoover, EA Pontzer, CM AF Ewen, BS Gasper, PW Hoover, EA Pontzer, CM TI Mathematical modeling of FeLV-induced erythroid aplasia SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Maryland, College Pk, MD 20882 USA. NIA, RRB, Bethesda, MD 20892 USA. Colorado State Univ, Ft Collins, CO 80523 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 706 BP 130A EP 130A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500706 ER PT J AU Wu, C AF Wu, C TI ATP-dependent chromatin remodeling complexes for transcription SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 711 BP 131A EP 131A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500711 ER PT J AU Panchision, DM Pickel, JM Studer, L Lee, SH Turner, PA Hazel, TG McKay, RDG AF Panchision, DM Pickel, JM Studer, L Lee, SH Turner, PA Hazel, TG McKay, RDG TI Sequential actions of BMP receptors control neural stem cell identity, proliferation and differentiation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS, NIH, Bethesda, MD 20892 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 726 BP 134A EP 134A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500726 ER PT J AU Duckett, CS AF Duckett, CS TI Novel modulators of the apoptotic cell death pathway SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Canc Res Ctr, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 732 BP 135A EP 135A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500732 ER PT J AU Fearnhead, HO AF Fearnhead, HO TI Oncogene-dependent caspase activation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. RI Fearnhead, Howard/D-4826-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 735 BP 135A EP 135A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500735 ER PT J AU Zhang, N Fan, HT Guo, XZ AF Zhang, N Fan, HT Guo, XZ TI p15(INK4B) gene methylation in malignant hematopoietic diseases SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GuangHua Hosp, Guangzhou 510080, Peoples R China. NCI, Lab Populat Genet, Bethesda, MD 20892 USA. Jinan Univ, Jinan, Peoples R China. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 768 BP 142A EP 142A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500768 ER PT J AU Hang, J Cavenagh, M Joseph, J Tan, SH Dasso, M AF Hang, J Cavenagh, M Joseph, J Tan, SH Dasso, M TI Localization and function of vertebrate SUMO proteases SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, LGRD, SCCR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 780 BP 144A EP 144A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500780 ER PT J AU Choi, KS Park, HJ Kim, BC Kim, SJ AF Choi, KS Park, HJ Kim, BC Kim, SJ TI Role of MAP kinases and their cross-talks in TGF-beta 1-induced apoptosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Ajou Univ, Sch Med, Inst Med Sci, Suwon 442749, South Korea. NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 800 BP 147A EP 147A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500800 ER PT J AU Rodgers, EE Kearns, BG Donaldson, JG Theibert, AB AF Rodgers, EE Kearns, BG Donaldson, JG Theibert, AB TI In vivo interactions of centaurin alpha with PtdIns(3,4,5)P-3, Arf6 and actin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Alabama, Birmingham, AL 35294 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 816 BP 150A EP 150A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500816 ER PT J AU McNeil, EL Klinger, CA Stewart, BL Sellers, JR King-Smith, C AF McNeil, EL Klinger, CA Stewart, BL Sellers, JR King-Smith, C TI Pigment granules from fish retinal pigment epithelial (RPE) cells undergo plus-end directed motility in assays using the characean alga, Nitella axillaris SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 St Josephs Univ, Dept Biol, Philadelphia, PA 19131 USA. NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 897 BP 165A EP 165A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500897 ER PT J AU Galbraith, CG Sheetz, MP AF Galbraith, CG Sheetz, MP TI Force-dependent reinforcement of integrin-cytoskeletal linkages by vinculin recruitment SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, CDBRB, Bethesda, MD 20892 USA. Columbia Univ, Dept Biol Sci, New York, NY 10027 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 929 BP 171A EP 171A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372500929 ER PT J AU Pendrak, ML Thomas, WJ Roberts, DD AF Pendrak, ML Thomas, WJ Roberts, DD TI Biochemical characterization of two distinct fibronectin receptors in Candida albicans SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 1 PU 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 NOV PY 2001 VL 12 SU S MA 1039 BP 191A EP 191A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501039 ER PT J AU Strunnikova, NV Csaky, KG AF Strunnikova, NV Csaky, KG TI Evaluation of role of human retinal pigment epithelial cell (ARPE-19) SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NEI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1063 BP 196A EP 196A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501063 ER PT J AU Jackson, CL Smirnova, E AF Jackson, CL Smirnova, E TI Roles of the Sec7 domain ARF exchange factors in membrane traffic and organelle structure SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, Cell Biol & Metab Branch, Bethesda, MD 20892 USA. RI Jackson, Catherine/A-3421-2013 OI Jackson, Catherine/0000-0002-0843-145X NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1129 BP 208A EP 208A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501129 ER PT J AU Merritt, SA Hirschberg, K Phair, R Lippincott-Schwartz, J AF Merritt, SA Hirschberg, K Phair, R Lippincott-Schwartz, J TI Analysis of cargo transport in cells without microtubules reveals a role for Golgi 'fragmentation' in re-establishing normal secretory trafficking kinetics SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Alabama, Sch Med, Birmingham, AL 35294 USA. NICHHD, NIH, Bethesda, MD USA. Bioinformat Serv, Bethesda, MD USA. NICHHD, CBMB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1133 BP 208A EP 209A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501133 ER PT J AU Brown, FD Donaldson, JG AF Brown, FD Donaldson, JG TI EFA6 induces the formation of Arf6-and actin-dependent ventral ruffles SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1159 BP 213A EP 213A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501159 ER PT J AU Arnaoutova, HP Donaldson, JG Loh, PY AF Arnaoutova, HP Donaldson, JG Loh, PY TI Recycling of a prohormone sorting receptor, carboxypeptidase E, between plasma membrane and Golgi is ARF6-dependent SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD 20892 USA. NHLBI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1181 BP 217A EP 217A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501181 ER PT J AU Dundr, M Hu, Q Rothblum, LI Phair, RD Misteli, T AF Dundr, M Hu, Q Rothblum, LI Phair, RD Misteli, T TI Dynamics of the RNA polymerase I transcription machinery in living cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. Weis Ctr Res, Danville, PA USA. BioInformat Serv, Bethesda, MD USA. NCI, NIH, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1214 BP 223A EP 223A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501214 ER PT J AU Prufer, K Barsony, J AF Prufer, K Barsony, J TI Nuclear import and export mechanisms for the vitamin D receptor and the retinoid X receptor SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 1230 BP 225A EP 226A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501230 ER PT J AU Wu, YT Marsh, JW AF Wu, YT Marsh, JW TI Selective transcription and modulation of resting T cell activity by preintegration HIV DNA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, LMB, NHMH, Bethesda, MD 20892 USA. NIH, LMB, NIMH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 1225 BP 225A EP 225A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501225 ER PT J AU Moreau, JM Rosenberg, HF AF Moreau, JM Rosenberg, HF TI Differential expression of mouse eosinophil-associated ribonucleases in response to challenge with viral pathogens SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1235 BP 226A EP 226A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501234 ER PT J AU Rouzaud, F Hearing, VJ AF Rouzaud, F Hearing, VJ TI Regulation of extension gene expression by alpha MSH and ASP in marine melanocytes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Cell Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1252 BP 229A EP 229A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501250 ER PT J AU Haak, LL Stevens, B Porta, S Yuan, YQ Gallo, V Fields, RD AF Haak, LL Stevens, B Porta, S Yuan, YQ Gallo, V Fields, RD TI Oligedendrocytes express P1 and P2 purinergic receptors SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Lab Cell Synapt Neurophysiol, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1306 BP 239A EP 239A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501304 ER PT J AU Smith, GH Boulanger, CA AF Smith, GH Boulanger, CA TI Mammary stem cell repertoire: Transplantation of clonal epithelial populations SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, BRL, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1329 BP 243A EP 243A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501327 ER PT J AU Lee, TH Kim, SU Yu, SL Dho, SH Han, YH Kim, S Kwon, H Kang, SW Kwon, KS Rhee, SG Yu, DY AF Lee, TH Kim, SU Yu, SL Dho, SH Han, YH Kim, S Kwon, H Kang, SW Kwon, KS Rhee, SG Yu, DY TI Oxidative stress response in red blood cells from peroxiredoxin II-deficient mice SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Korea Res Inst Biosci & Biotechnol, Lab Anim Dev Biotechnol, Yusung Gu, Taejon 305333, South Korea. Korea Res Inst Biosci & Biotechnol, Proteome Res Lab, Taejon 305333, South Korea. NHLBI, Lab Cell Signaling, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1333 BP 244A EP 244A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501331 ER PT J AU Iwata, T Zhang, Q Nishiyama, T Mashima, Y Sergeev, Y Noda, S Imamura, Y Kudoh, J Umeda, S Shimizu, N AF Iwata, T Zhang, Q Nishiyama, T Mashima, Y Sergeev, Y Noda, S Imamura, Y Kudoh, J Umeda, S Shimizu, N TI Cloning and characterization of amine oxidase (AOC2) specifically expressed in retina SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Natl Tokyo Med Ctr, Natl Ctr Sensory Organs, Tokyo 1528902, Japan. Keio Univ, Sch Med, Dept Ophthalmol, Tokyo 108, Japan. NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD USA. Tokai Univ, Sch Hlth Sci, Dept Nursing, Hiratsuka, Kanagawa 25912, Japan. Keio Univ, Sch Med, Dept Biol Mol, Tokyo 108, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1349 BP 247A EP 247A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501347 ER PT J AU Snapp, EL Lippincott-Schwartz, J AF Snapp, EL Lippincott-Schwartz, J TI Remodeling of the endoplasmic reticulum ultrastructure in living cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Cell Biol & Metab Branch, Bethesda, MD 20892 USA. NIH, NICHD, CBMB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1351 BP 247A EP 247A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501349 ER PT J AU Partridge, JJ Latterich, M Indig, FE AF Partridge, JJ Latterich, M Indig, FE TI Intracellular distribution and protein interactions of VCP/p97 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, LCB, CCR, Bethesda, MD 20892 USA. Diversa Corp, San Diego, CA 92121 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 1354 BP 248A EP 248A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501352 ER PT J AU Huizing, M Anikster, Y Boissy, RE Toro, JR Gahl, WA AF Huizing, M Anikster, Y Boissy, RE Toro, JR Gahl, WA TI Hermansky-Pudlak syndrome: A model for intracellular membrane formation and trafficking SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, Bethesda, MD 20892 USA. Univ Cincinnati, Coll Med, Dept Dermatol, Cincinnati, OH 45221 USA. NIH, NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 1366 BP 250A EP 250A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501364 ER PT J AU Qian, SB Bennink, JR Yewdell, JW AF Qian, SB Bennink, JR Yewdell, JW TI Directional degradation of polyubiquitinated substrates by 26S proteasomes in mammalian cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, LVD, NIH, Bethesda, MD 20892 USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1370 BP 251A EP 251A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501368 ER PT J AU Jamur, MC Grodzki, AC Berenstein, EH Hamawy, MM Siraganian, RP Oliver, C AF Jamur, MC Grodzki, AC Berenstein, EH Hamawy, MM Siraganian, RP Oliver, C TI Purification and characterization of a committed mast cell precursor from bone marrow SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Cell & Mol Biol & Pathogen Bioagents, BR-05508 Sao Paulo, Brazil. NIDCR, Oral Infect & Immun Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1390 BP 254A EP 254A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501388 ER PT J AU Uniyal, S Cialacu, V Singer, A Chan, BMC AF Uniyal, S Cialacu, V Singer, A Chan, BMC TI Strain differences in the expression and function of a5b1 integrin in thymocyte development SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Robarts Res Inst, London, ON N6A 5C1, Canada. NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1393 BP 255A EP 255A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501391 ER PT J AU Becker, M Walker, D McNally, JG Baumann, CT Hager, GL AF Becker, M Walker, D McNally, JG Baumann, CT Hager, GL TI Dynamic behavior of transcription factors on a natural promoter in living cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, NIH, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1458 BP 267A EP 267A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501455 ER PT J AU Garcia, MJC Sipes, JM Krutzsch, HC Annis, D Mosher, DF Roberts, DD AF Garcia, MJC Sipes, JM Krutzsch, HC Annis, D Mosher, DF Roberts, DD TI Differential role of alpha 4 beta 1 integrin as a thrombospondin-1 receptor in human umbilical vein and microvascular endothelial cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Lab Pathol, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. Univ Wisconsin, Madison, WI 53706 USA. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1464 BP 268A EP 268A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501461 ER PT J AU Li, BS Zheng, YL Kulkarni, AB Pant, HC AF Li, BS Zheng, YL Kulkarni, AB Pant, HC TI Regulation of Akt activity by Cdk5 through phosphadylinositol 3-dependent kinase signaling pathway SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NIH, Funcat Genom Unit, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1491 BP 273A EP 273A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501488 ER PT J AU Arudchandran, A Crouch, RJ AF Arudchandran, A Crouch, RJ TI An overlapping MCB/SCB sequence regulates cell cycle transcription of RNH2L (RNase H2) in Saccharomyces cerevisiae SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, Mol Genet Lab, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1517 BP 278A EP 278A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501514 ER PT J AU Brichkina, AI Bulavin, DV Tararova, ND Savelieva, IA Pospelov, VA Pospelova, TV AF Brichkina, AI Bulavin, DV Tararova, ND Savelieva, IA Pospelov, VA Pospelova, TV TI The G1/S cell cycle arrest in E1A/19kDa transformants after gamma-irradiation and serum starvation depends on selective suppression of cyclinE-Cdk2 activity SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Russian Acad Sci, Inst Cytol, Dept Cell Culture, St Petersburg 194064, Russia. Russian Acad Sci, Inst Cytol, St Petersburg 194064, Russia. NIH, Div Basic Sci, Bethesda, MD USA. Russian Acad Sci, Inst Cytol, Lab Mol Basis Cell Differentiat, St Petersburg 194064, Russia. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1520 BP 278A EP 278A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501517 ER PT J AU Song, CC Li, CC AF Song, CC Li, CC TI Characteristics of ATPase activity of VCP, an AAA protein involved in ubiquitin proteasome pathway SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, SAIC Frederick, Basic Res Lab, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1525 BP 279A EP 279A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501522 ER PT J AU Redon, CE Pilch, DR Lowndes, NF Bonner, WM AF Redon, CE Pilch, DR Lowndes, NF Bonner, WM TI Histone H2A serine 129 is necessary for yeast survival during topoisomerase I mediated SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, CCR, LMP, Bethesda, MD 20892 USA. Imperial Canc Res Fund, Clare Hall Labs, Cell Div Cycle Lab, S Mimms EN6 3LD, Herts, England. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1544 BP 282A EP 282A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501540 ER PT J AU Vassilenko, KP Butylin, PA Arnaoutov, AM Nickolsky, NN AF Vassilenko, KP Butylin, PA Arnaoutov, AM Nickolsky, NN TI The tyrosine kinase Src are involved in the activation of signal transducer and activator of transcription 1 by hyperosmolarity SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Russian Acad Sci, Inst Cytol, Lab Cell Cycle Physiol, St Petersburg 194064, Russia. NICHHD, SCCR, LGRD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 1541 BP 282A EP 282A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501537 ER PT J AU Vijayachandra, K Lee, J Glick, AB AF Vijayachandra, K Lee, J Glick, AB TI A role for Smad3 in the senescence response of mouse keratinocytes to transforming growth factor beta SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Cellular Carcinogenesis & Tumor Promot Lab, NCI, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1547 BP 283A EP 283A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501543 ER PT J AU Remmert, K Olszewski, TE Bowers, B Dimitrova, M Ginsburg, A Zigmond, SH Hammer, JA AF Remmert, K Olszewski, TE Bowers, B Dimitrova, M Ginsburg, A Zigmond, SH Hammer, JA TI Acanthamoeba CARMIL forms a tight complex with capping protein that can cap the barbed end of actin filaments SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Cell Biol Lab, Bethesda, MD USA. NIH, Biochem Lab, Bethesda, MD USA. Univ Penn, Dept Biol, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1586 BP 289A EP 290A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501582 ER PT J AU Liu, X Korn, ED AF Liu, X Korn, ED TI Effect of substitution of the tail and light chain on the actin-activated ATPase activity of Acanthamoeba myosin IC SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Cell Biol Lab, Bethesda, MD 20892 USA. NIH, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1609 BP 293A EP 293A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501605 ER PT J AU Battelle, BA Kempler, KE Yamashita, R Sellers, JR AF Battelle, BA Kempler, KE Yamashita, R Sellers, JR TI Myosin III from Limulus autophosphorylates SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Florida, Whitney Lab, St Augustine, FL 32080 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1614 BP 294A EP 294A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501610 ER PT J AU DeGiorgis, JA Schneider, EW George, P Reese, TS Bearer, EL AF DeGiorgis, JA Schneider, EW George, P Reese, TS Bearer, EL TI Association of a non-muscle myosin II with axoplasmic organelles SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Brown Univ, Dept Pathol & Med, Biomed Ctr, Providence, RI 02912 USA. NIH, NINDS, Neurobiol Lab, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1611 BP 294A EP 294A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501607 ER PT J AU Wu, XFS Wang, F Sellers, JR Rao, K Copeland, NG Jenkins, NA Hammer, JA AF Wu, XFS Wang, F Sellers, JR Rao, K Copeland, NG Jenkins, NA Hammer, JA TI Identification of a multicomponent, Exon F- and Rab27a-dependent linkage driving the interaction of myosin Va with melanosomes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Cell Biol Lab, Bethesda, MD USA. NIH, Mol Cardiol Lab, Bethesda, MD USA. NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1618 BP 295A EP 295A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501614 ER PT J AU Labno, CM Lewis, CM Broussard, C Kamberos, NK Schwartzberg, PL Burkhardt, JK AF Labno, CM Lewis, CM Broussard, C Kamberos, NK Schwartzberg, PL Burkhardt, JK TI Tec kinases itk and rlk participate in actin remodeling in T cell-APC interactions SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Chicago, Dept Pathol, Chicago, IL 60637 USA. Univ Chicago, Dept Pathol, Comm Immunol, Chicago, IL 60637 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1636 BP 298A EP 298A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501632 ER PT J AU Wei, QZ Adelstein, RS AF Wei, QZ Adelstein, RS TI Regulation of the Rho GTPase and p53 pathways by ectopic expression of Pitx2a in HeLa cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Mol Cardiol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1641 BP 299A EP 299A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501637 ER PT J AU Galbraith, JA Hutchins, HK Gallant, PE AF Galbraith, JA Hutchins, HK Gallant, PE TI An active role for the cytoskeleton tn the repair process: Actin-myosin mediated contraction of transected axons SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NINDS, Neurobiol Lab, Bethesda, MD 20892 USA. Marine Biol Lab, Woods Hole, MA 02543 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 EI 1939-4586 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 2001 VL 12 SU S MA 1648 BP 300A EP 301A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501644 ER PT J AU Miura, K Jacques, KM Stauffer, S Kubosaki, A Zhu, KJ Resau, J Zheng, Y Randazzo, PA AF Miura, K Jacques, KM Stauffer, S Kubosaki, A Zhu, KJ Resau, J Zheng, Y Randazzo, PA TI ARAP1, a point of convergence for phosphoinositide, Arf and Rho signaling, regulates both membrane and actin cytoskeleton remodeling SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Oral Infect & Immun Branch, Bethesda, MD USA. Univ Tennessee, Hlth Sci Ctr, Dept Mol Sci, Knoxville, TN 37996 USA. Van Andel Res Inst, Grand Rapids, MI USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 1657 BP 302A EP 302A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501653 ER PT J AU Carabeo, R Grieshaber, S Fischer, E Hackstadt, T AF Carabeo, R Grieshaber, S Fischer, E Hackstadt, T TI Actin remodeling and microvillar hypertrophy during attachment and entry of Chlamydia trachomatis into Hela cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1796 BP 327A EP 327A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501792 ER PT J AU Fields, KA Dooley, CA Mead, DJ Hackstadt, T AF Fields, KA Dooley, CA Mead, DJ Hackstadt, T TI The Chlamydia trachomatis type III secretion apparatus is present and functional during early-cycle development SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, Rocky Mt Labs, Intracellular Parasites Lab, Hamilton, MT 59840 USA. NR 0 TC 0 Z9 0 U1 2 U2 2 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 NOV PY 2001 VL 12 SU S MA 1797 BP 327A EP 327A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501793 ER PT J AU Grieshaber, SS Swanson, J Hackstadt, T AF Grieshaber, SS Swanson, J Hackstadt, T TI Determination of ionic conditions within the Chlamydia trachomatis inclusion using membrane permeant ratiometric probes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, LICP, NIH, Hamilton, MT 59840 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1795 BP 327A EP 327A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501791 ER PT J AU Verma, A Kumar, M Zimmerberg, J AF Verma, A Kumar, M Zimmerberg, J TI Visualisation of influenza hemagglutinin at the cell surface using immunoelectronmicroscopy SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, LCMB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 1824 BP 332A EP 332A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501820 ER PT J AU Viard, M Parolini, I Fecchi, K Ramoni, C Sargiacomo, M Ablan, S Wang, JM Blumenthal, R AF Viard, M Parolini, I Fecchi, K Ramoni, C Sargiacomo, M Ablan, S Wang, JM Blumenthal, R TI The role of membrane raft microdomains and signal transduction in human immunodeficiency virus envelope protein-mediated fusion with host cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Frederick, MD 21701 USA. Ist Super Sanita, I-00161 Rome, Italy. NCI, CCR, NIH, Frederick, MD 21702 USA. RI parolini, Isabella/J-9955-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1823 BP 332A EP 332A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501819 ER PT J AU Winderbaum, JH Cole, NB Suchy, SF Hellsten, E Nussbaum, RL AF Winderbaum, JH Cole, NB Suchy, SF Hellsten, E Nussbaum, RL TI Characterization of the PtdIns(4,5)P2 5-phosphatase, Inpp5b SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, HHMI, NHGRI, GDRB, Bethesda, MD 20892 USA. NIH, GDRB, NHGRI, Bethesda, MD 20892 USA. NIH, NHGRI, Bethesda, MD 20892 USA. RI Fernandez, Jamie/I-5256-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1832 BP 333A EP 334A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501828 ER PT J AU Cherukuri, A Carter, R Levy, S Pierce, SK AF Cherukuri, A Carter, R Levy, S Pierce, SK TI The CD19/CD21 complex: Regulating the B cell antigen receptor within lipid rafts SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, LIG, NIH, Rockville, MD 20852 USA. Univ Alabama, Birmingham, AL USA. Stanford Univ, Sch Med, Stanford, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1841 BP 335A EP 335A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501837 ER PT J AU Sohn, HW Grammer, AC Pierce, SK AF Sohn, HW Grammer, AC Pierce, SK TI Actin cytoskeleton is required for the translocation of CD40 and the recruitment of TRAF2 into the lipid rafts on human B cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, NIH, LIG, Rockville, MD 20852 USA. NIAMS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1839 BP 335A EP 335A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501835 ER PT J AU Sugimoto, H Sugahara, M Foelsch, H Koide, Y Tanaka, N Mullins, C Nakamura, N Ohno, H AF Sugimoto, H Sugahara, M Foelsch, H Koide, Y Tanaka, N Mullins, C Nakamura, N Ohno, H TI Importance of tyrosine-recognition by mu 1B in basolateral sorting in polarized epithelial cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Kanazawa Univ, Inst Canc Res, Div Mol Membrane Biol, Kanazawa, Ishikawa 9200394, Japan. Yale Univ, Sch Med, Dept Cell Biol, New Haven, CT 06510 USA. Yale Univ, Sch Med, Ludwig Inst Canc Res, New Haven, CT USA. NIH, NICHHD, Cell Biol & Metab Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1845 BP 336A EP 336A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501841 ER PT J AU Polishchuk, RS Lippincott-Schwarz, J AF Polishchuk, RS Lippincott-Schwarz, J TI In vivo dynamics of apical and basolateral cargo proteins between Golgi and plasma membrane SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, CBMB, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1860 BP 338A EP 339A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501856 ER PT J AU Chen, XL Olausson, T Al-Hasani, H Smith, U Cushman, SW AF Chen, XL Olausson, T Al-Hasani, H Smith, U Cushman, SW TI Phosphorylation and translocation of GLUT4-Akt2 fusion proteins in rat adipose cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIDDK, EDMNS, DB, Bethesda, MD 20892 USA. Gothenburg Univ, Lundberg Lab Diabet Res, S-41124 Gothenburg, Sweden. Univ Cologne, Ctr Mol Med, Cologne, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1906 BP 347A EP 347A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501902 ER PT J AU Kee, SH Steinert, PM Jang, SI AF Kee, SH Steinert, PM Jang, SI TI Regulation of E-cadherin cleavages in keratinocytes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIAMS, Skin Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1913 BP 348A EP 348A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501909 ER PT J AU Mabon, SA Misteli, T AF Mabon, SA Misteli, T TI Differential recruitment of splicing factors to alternatively spliced transcripts in vivo SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1934 BP 352A EP 352A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501930 ER PT J AU Elbi, C Baumann, CT Misteli, T Hager, GL AF Elbi, C Baumann, CT Misteli, T Hager, GL TI Targeting of the aryl hydrocarbon receptor to subnuclear foci that correspond to active sites of transcription SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Lab Receptor Biol & Gene Express, NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 1936 BP 353A EP 353A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501932 ER PT J AU Ferraris, JD Williams, CK Zhang, Z Avritt, MD Wittie, MA Burg, MB AF Ferraris, JD Williams, CK Zhang, Z Avritt, MD Wittie, MA Burg, MB TI TonEBP/OREBP contains a transactivation domain (TAD) that is regulated by tonicity (high extracellular NaCl) SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, LKEM, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1942 BP 354A EP 354A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501938 ER PT J AU Mueller, WG Walker, D Hager, GL McNally, JG AF Mueller, WG Walker, D Hager, GL McNally, JG TI Large-scale chromatin decondensation and recondensation regulated by transcription from a natural promoter SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1958 BP 357A EP 357A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501954 ER PT J AU Baek, SJ Horowitz, JM Eling, TE AF Baek, SJ Horowitz, JM Eling, TE TI Transcriptional regulation of the human NSAID activated gene (NAG-1) is mediated by Sp1, Sp3, and COUP-TF1 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS, LMC, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Raleigh, NC 27695 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 1983 BP 361A EP 361A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372501979 ER PT J AU Panchision, DM Pickel, JM Studer, L Lee, SH Turner, PA Hazel, TG McKay, RDG AF Panchision, DM Pickel, JM Studer, L Lee, SH Turner, PA Hazel, TG McKay, RDG TI BMP receptors act sequentially to control neural stem cell identity, proliferation and differentiation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NINDS, Mol Biol Lab, Bethesda, MD 20892 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2008 BP 366A EP 366A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502004 ER PT J AU Gopal, TV Winitsky, S Hassanzadeh, S Epstein, N AF Gopal, TV Winitsky, S Hassanzadeh, S Epstein, N TI A novel subpopulation of adult skeletal muscle cells differentiates into beating cardiomyocytes in vitro SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2017 BP 367A EP 367A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502013 ER PT J AU Brzostowski, JA Parent, C Johnson, C Kimmel, AR AF Brzostowski, JA Parent, C Johnson, C Kimmel, AR TI G alpha 9: A heterotrimeric G protein that functions as a novel general inhibitor of developmental signaling pathways in Dictyostelium discoideum SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIDDK, LCDB, Bethesda, MD 20982 USA. NIH, NCI, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2031 BP 370A EP 370A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502027 ER PT J AU Wallace, WC Wei, WL Luo, JJ Wallace, M Norton, D Kusiak, J AF Wallace, WC Wei, WL Luo, JJ Wallace, M Norton, D Kusiak, J TI The extracellular fragment of amyloid precursor protein produced by beta-secretase induces neuronal apoptosisatase SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIA, Cellular & Mol Biol Lab, Rockville, MD 20852 USA. NIA, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2062 BP 376A EP 376A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502058 ER PT J AU Chandran, JS Zaal, KJM Lu, ZM Ralston, E AF Chandran, JS Zaal, KJM Lu, ZM Ralston, E TI Changes in ER exit site distribution during muscle differentiation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2086 BP 380A EP 380A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502082 ER PT J AU Combs, CA Balaban, RS AF Combs, CA Balaban, RS TI Imaging metabolic activity using ED-FRAP: Application to dehydrogenase activation in cardiac myocytes SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Light Microscopy Facil, Bethesda, MD 20892 USA. NIH, Cardiac Energet Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 2100 BP 382A EP 382A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502096 ER PT J AU Balaban, RS Bose, S French, SA Territo, PR AF Balaban, RS Bose, S French, SA Territo, PR TI Work-related cytosolic signaling between cardiac sarcoplasmic-reticulum (SR) and mitochondria: Role of Ca2+ SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2101 BP 383A EP 383A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502097 ER PT J AU Zhang, CX Baffi, J Csaky, KG AF Zhang, CX Baffi, J Csaky, KG TI Cell death in human retinal pigmented epithelium involves apoptosis-inducing factor and no caspase activation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 3 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 NOV PY 2001 VL 12 SU S MA 2127 BP 387A EP 387A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502123 ER PT J AU Hirayama, T Ogushi, K Wada, A Moss, J AF Hirayama, T Ogushi, K Wada, A Moss, J TI Induction of human beta-defensin-2 in human colon adenocarcinoma cell, Caco-2 by Salmonella enteritidis FliC (flagella filament protein) SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Nagasaki Univ, Inst Trop Med, Nagasaki 8258253, Japan. NHLBI, PCCMB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2134 BP 388A EP 389A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502130 ER PT J AU Malide, D Chen, WS Calvo, P Bennink, J Yewdell, J AF Malide, D Chen, WS Calvo, P Bennink, J Yewdell, J TI A novel influenza A virus mitochondrial protein (DAMP) that induces cell death: a morphological approach SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 2 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 NOV PY 2001 VL 12 SU S MA 2187 BP 398A EP 398A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502183 ER PT J AU Dmitrieva, NI Bulavin, DV Fornace, AJ Burg, MB AF Dmitrieva, NI Bulavin, DV Fornace, AJ Burg, MB TI Hypertonicity-induced G2 arrest in renal inner medullary collecting duct (IMCD) cells is protective and requires p38 kinase SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI, LKEM, Bethesda, MD 20892 USA. NCI, Div Basic Sci, Bethesda, MD 20892 USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2241 BP 407A EP 407A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502237 ER PT J AU Yong-Gonzalez, V Strunnikov, A AF Yong-Gonzalez, V Strunnikov, A TI Analysis of protein factors that affect Condensin targeting to chromatin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHD, Unit Chromosome Struct & Funt, LGRD, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2247 BP 408A EP 408A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502242 ER PT J AU Agarwal, R Cohen-Fix, O AF Agarwal, R Cohen-Fix, O TI Pds1 is a novel substrate of Cdc28 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK, LMCB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2254 BP 409A EP 409A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502249 ER PT J AU Tan, SH Arnaoutov, AM Boutell, C Everett, R Dasso, M AF Tan, SH Arnaoutov, AM Boutell, C Everett, R Dasso, M TI Herpes simplex virus protein ICP0 blocks progression through mitosis: Studies in Xenopus egg extracts SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, SCCR, LGRD, NIH, Bethesda, MD 20892 USA. Univ Glasgow, Inst Virol, Glasgow G11 5JR, Lanark, Scotland. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 2259 BP 410A EP 410A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502254 ER PT J AU Cho, H Kehrl, JH AF Cho, H Kehrl, JH TI Does RGS14 regulate heterotrimeric G-protein-mediated centrosome function? SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Immunoregulat Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2264 BP 411A EP 411A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502259 ER PT J AU Danino, D Hinshaw, JE AF Danino, D Hinshaw, JE TI Dynamin self-assembly in the presence of nucleotides SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2273 BP 413A EP 413A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502268 ER PT J AU Basanez, G Brandt, TA Hardwick, JM Zimmerberg, J AF Basanez, G Brandt, TA Hardwick, JM Zimmerberg, J TI Apoptogenic forms of Bcl-x(L) permeabilize pure lipid bilayers through a mechanism sensitive to membrane curvature SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NICHHD, Lab Cellular & Mol Biophys, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Publ Hlth, Dept Mol Microbiol Immunol, Baltimore, MD 21218 USA. Johns Hopkins Univ, Sch Publ Hlth, Dept Pharmacol & Mol Sci, Baltimore, MD 21218 USA. Johns Hopkins Univ, Sch Publ Hlth, Dept Neurol, Baltimore, MD 21218 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2296 BP 417A EP 417A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502291 ER PT J AU Suchy, SF Nussbaum, RL AF Suchy, SF Nussbaum, RL TI PIP2 5-phosphatase deficiency in Lowe syndrome affects actin polymerization SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHGRI, GDRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2238 BP 425A EP 425A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502333 ER PT J AU Cruz-Monserrate, Z Pettit, GR Fenical, WH Hamel, E AF Cruz-Monserrate, Z Pettit, GR Fenical, WH Hamel, E TI Interactions of antimitotic peptides with tubulin: Induction of aberrant oligomerization and polymerization reactions SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, Screening Technol Branch, DTP, DCTD, Frederick, MD 21701 USA. Arizona State Univ, Canc Res Inst, Tempe, AZ 85287 USA. Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA. RI Cruz-Monserrate, Zobeida/H-2290-2013; Cruz, Zobeida/J-2714-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 2369 BP 430A EP 430A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502364 ER PT J AU Zambito, AM Wolff, J AF Zambito, AM Wolff, J TI Immune characterization of alpha- and beta- tubulin isoelectric variants SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Univ Udine, DPMSC, I-33100 Udine, Italy. NIDDK, LBG, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2367 BP 430A EP 430A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502362 ER PT J AU Dabydeen, DA Florence, GJ Paterson, I Hamel, E AF Dabydeen, DA Florence, GJ Paterson, I Hamel, E TI A quantitative evaluation of the effects of inhibitors of tubulin assembly on assembly induced by discodermolide, epothilone B, and paclitaxel SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, DCTD, DTP, Screening Technol Branch, Frederick, MD 21701 USA. Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2375 BP 431A EP 431A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502370 ER PT J AU Jung, MK Hessian, KO Chaplin, JH Verdier-Pinard, P Flynn, BL Hamel, E AF Jung, MK Hessian, KO Chaplin, JH Verdier-Pinard, P Flynn, BL Hamel, E TI Analysis of the antitubulin activities of thiophene, benzofuran and indole derivatives SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, SAIC Frederick, Frederick, MD 21702 USA. NCI, DCTD, DTP, Screening Technol Branch, Frederick, MD 21702 USA. Australian Natl Univ, Dept Chem, Canberra, ACT, Australia. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2376 BP 431A EP 431A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502371 ER PT J AU Bugnard, E Winters, CA Ralston, E AF Bugnard, E Winters, CA Ralston, E TI Relative changes in centrosomal protein distribution during muscle differentiation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NINDS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2413 BP 438A EP 438A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502408 ER PT J AU Takesono, A Schwartzberg, PL AF Takesono, A Schwartzberg, PL TI Involvement of Tec kinases in chemokine signaling in T cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2436 BP 442A EP 442A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502431 ER PT J AU Harrison, RE Balla, T Schreiber, AD Grinstein, S AF Harrison, RE Balla, T Schreiber, AD Grinstein, S TI Microtubules promote optimal accumulation of 3 ' phosphoinositides and pseudopod formation during Fc gamma receptor-mediated phagocytosis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Hosp Sick Children, Toronto, ON M5G 1X8, Canada. NIH, Endocrinol & Reprod Res Branch, Bethesda, MD 20892 USA. Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2493 BP 452A EP 453A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502488 ER PT J AU Lukyanov, DV Kagansky, AM Strunnikov, A AF Lukyanov, DV Kagansky, AM Strunnikov, A TI Purification and identification of proteins interacting with Scc2 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2499 BP 453A EP 454A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502493 ER PT J AU Whittard, JD Akiyama, SK AF Whittard, JD Akiyama, SK TI Positive regulation of cell-cell and cell-substrate adhesion by protein kinase A SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Natl Inst Hlth, Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2557 BP 464A EP 464A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502551 ER PT J AU Kovbasnjuk, ON Li, XH Lavine, G Fales, H Edidin, MA Donowitz, M AF Kovbasnjuk, ON Li, XH Lavine, G Fales, H Edidin, MA Donowitz, M TI Role of lipid microdomains (LM) in Shiga toxin 1 uptake into Caco-2 cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA. NHLBI, LBC, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 2580 BP 468A EP 468A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502574 ER PT J AU Kenworthy, AK Nichols, BJ Bekiranov, S Kumar, M Zimmerberg, J Bunnell, S Samelson, LE Chiu, V Philips, MR Lippincott-Schwartz, J AF Kenworthy, AK Nichols, BJ Bekiranov, S Kumar, M Zimmerberg, J Bunnell, S Samelson, LE Chiu, V Philips, MR Lippincott-Schwartz, J TI Large-scale lateral diffusion measurements of plasma membrane proteins reveal uncorrelated diffusion of lipid raft markers SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD, CBMB, NIH, Bethesda, MD 20892 USA. MRC, London W1N 4AL, England. Rockefeller Univ, New York, NY 10021 USA. NIH, NICHD, Bethesda, MD 20892 USA. NIH, NCI, Bethesda, MD 20892 USA. NYU, New York, NY USA. NYU, Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 2592 BP 471A EP 471A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502586 ER PT J AU Fletcher, PL Fletcher, MD Fainter, LK Lucas, SM Martin, BM AF Fletcher, PL Fletcher, MD Fainter, LK Lucas, SM Martin, BM TI Scorpion venom-induced exocrine pancreatic secretion involves unique signaling events associated with the actin/microfilament cytoskeleton SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 E Carolina Univ, Brody Sch Med, Greenville, NC 27858 USA. Inst Butantan, Sao Paulo, Brazil. NIMH, Unit Mol Struct, Bethesda, MD USA. RI Lucas, Sylvia/L-8777-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2616 BP 475A EP 475A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502610 ER PT J AU McKee, ML Yun, C FitzGerald, DJ AF McKee, ML Yun, C FitzGerald, DJ TI Expression and secretion of enzymatically inactive pseudomonas exotoxin A (ntPE) by CHO cells SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, LMB, Biotherapy Sect, Bethesda, MD 20892 USA. Seoul Natl Univ, Sch Agr Biotechnol, Seoul, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 2 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 NOV PY 2001 VL 12 SU S MA 2672 BP 485A EP 485A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502666 ER PT J AU Kim, SJ Hegde, RS AF Kim, SJ Hegde, RS TI The molecular mechanism of prion protein biogenesis SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2678 BP 486A EP 486A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502672 ER PT J AU Park, GT Morasso, MI AF Park, GT Morasso, MI TI Bone morphogenetic protein-2 (BMP-2) transactivates the distal-less 3 (Dlx3) homeodomain gene through binding of Smad1 and Smad4 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIAMS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2697 BP 489A EP 490A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502691 ER PT J AU Ledee, DR Zelenka, PS AF Ledee, DR Zelenka, PS TI Identification of two cDNAs, ID1 and FABP, up-regulated upon lens cell differentiation SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NEI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2699 BP 490A EP 490A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502693 ER PT J AU Parada, LA Misteli, T AF Parada, LA Misteli, T TI Proximal positioning of translocated and normal chromosomes in the interphase nucleus SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NCI, Bethesda, MD 20892 USA. NIH, NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 2001 VL 12 SU S MA 2708 BP 491A EP 492A PG 2 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502702 ER PT J AU Catez, F Misteli, T Bustin, M AF Catez, F Misteli, T Bustin, M TI HMGN chromosomal proteins modulate the binding of histone H1 to chromatin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. NCI, NIH, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. RI Bustin, Michael/G-6155-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 2001 VL 12 SU S MA 2717 BP 493A EP 493A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502711 ER PT J AU Ten Hagen, KG Tran, D AF Ten Hagen, KG Tran, D TI Cloning and characterization of the gene family encoding the UDP-GalNAc : polypeptide N-acetylgalactosaminyltransferases from Drosophila melanogaster SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, NIDDK, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2785 BP 506A EP 506A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502778 ER PT J AU Shakarian, AM Joshi, M Ghedin, M Dwyer, DM AF Shakarian, AM Joshi, M Ghedin, M Dwyer, DM TI Molecular dissection of the functional domains of a unique, tartrate-resistant surface membrane acid phosphatase in the primitive human pathogen Leishmania donovani SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 Salva Regina Univ, Dept Biol & Biomed Sci, Newport, RI 02840 USA. NIAID, Parasit Dis Lab, Cell Biol Sect, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2862 BP 520A EP 520A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502855 ER PT J AU Sakai, T Larsen, M Iehara, N Clark, K Hoffman, MP Yamada, KM AF Sakai, T Larsen, M Iehara, N Clark, K Hoffman, MP Yamada, KM TI T7-SAGE: Serial analysis of gene expression utilizing high-fidelity T7-based mRNA amplification for microanalysis of gene expression SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH, Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 12 SU S MA 2870 BP 521A EP 521A PG 1 WC Cell Biology SC Cell Biology GA 496AL UT WOS:000172372502863 ER PT J AU Deroo, BJ Archer, TK AF Deroo, BJ Archer, TK TI Glucocorticoid receptor activation of the I kappa B alpha promoter within chromatin SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID TUMOR VIRUS PROMOTER; LONG TERMINAL REPEAT; BREAST-CANCER CELLS; GENE-EXPRESSION; POSITIONED NUCLEOSOMES; HYPERSENSITIVE REGION; TRANSCRIPTION FACTORS; VIVO; INDUCTION; IMMUNOSUPPRESSION AB The glucocorticoid receptor (GR) is a ligand-activated transcription factor that induces expression of many genes. The GR has been useful for understanding how chromatin structure regulates steroid-induced transcription in model systems. However, the effect of glucocorticoids on chromatin structure has been examined on few endogenous mammalian promoters. We investigated the effect of glucocorticoids on the in vivo chromatin structure of the glucocorticoid-responsive I kappaB alpha gene promoter, the inhibitor of the ubiquitous transcription factor, nuclear factor kappa B (NF kappaB). Glucocorticoids inhibit NF kappaB activity in some tissues by elevating the levels Of I kappaB alpha. We found that glucocorticoids activated the I kappaB alpha promoter in human T47D/A1-2 cells containing the GR. We then investigated the chromatin structure of the I kappaB alpha promoter in the absence and presence of glucocorticoids with the use of micrococcal nuclease, restriction enzyme, and deoxyribonuclease (DNasel) analyses. In untreated cells, the promoter assembles into regularly positioned nucleosomes, and glucocorticoid treatment did not alter nucleosomal position. Restriction enzyme accessiblity studies indicated that the I kappaB alpha promoter is assembled as phased nucleosomes that adopt an "open" chromatin architecture in the absence of hormone. However, glucocorticoids may be required for transcription factor binding, because DNaseI footprinting studies suggested that regulatory factors bind to the promoter upon glucocorticoid treatment. C1 NIEHS, Chromatin & Gene Express Sect, NIH, Res Triangle Pk, NC 27709 USA. Univ Western Ontario, Dept Biochem, London, ON N6A 4L6, Canada. RP Archer, TK (reprint author), NIEHS, Chromatin & Gene Express Sect, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 45 TC 41 Z9 46 U1 0 U2 1 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 NOV PY 2001 VL 12 IS 11 BP 3365 EP 3374 PG 10 WC Cell Biology SC Cell Biology GA 495TV UT WOS:000172357200006 PM 11694573 ER PT J AU Gamcsik, MP Kasibhatla, MS Adams, DJ Flowers, JL Colvin, OM Manikumar, G Wani, M Wall, ME Kohlhagen, G Pommier, Y AF Gamcsik, MP Kasibhatla, MS Adams, DJ Flowers, JL Colvin, OM Manikumar, G Wani, M Wall, ME Kohlhagen, G Pommier, Y TI Dual role of glutathione in modulating camptothecin activity: Depletion potentiates activity, but conjugation enhances the stability of the topoisomerase I-DNA cleavage complex SO MOLECULAR CANCER THERAPEUTICS LA English DT Article ID CELLULAR-RESISTANCE; BILIARY-EXCRETION; ANTITUMOR-ACTIVITY; P-GLYCOPROTEIN; CELLS; DRUG; CPT-11; CYTOTOXICITY; METABOLITES; DERIVATIVES AB Depletion of glutathione (GSH) in MCF-7 and MDA-MB-231 cell lines by pretreatment with the GSH synthesis inhibitor buthionine sulfoximine potentiated the activity of 10,11-methylenedioxy-20(S)-camptothecin, SN-38 [7-ethyl-10-hydroxy-20(S)-camptothecin], topotecan, and 7-chloromethyl-10,11-methylenedioxy-20(S)camptothecin (CMMDC). The greatest potentiation was observed with the alkylating camptothecin CMMDC. Buthionine sulfoximine pretreatment also increased the number of camptothecin-induced DNA-protein crosslinks, indicating that GSH affects the mechanism of action of camptothecin. We also report that GSH interacts with CMMDC to form a stable conjugate, 7-(glutathionylmethyl)-10,11-methylenedioxy-20(S)- camptothecin (GSMMDC), which is formed spontaneously in buffered solutions and in MCF-7 cells treated with CMMDC. GSMMDC was synthesized and found to be nearly as active as 10,11-methylenedioxy-20(S)-camptothecin in a topoisomerase (topo) mediated DNA nicking assay. The resulting topo I cleavage complexes were remarkably stable. In cell culture, GSMMDC displayed potent growth-inhibitory activity against U937 and P388 leukemia cell lines. GSMMDC was not active against a topo I-deficient P388 cell line, indicating that topo I is its cellular target. Peptide-truncated analogues of GSMMDC were prepared and evaluated. All three derivatives [7-(gamma-glutamylcysteinylmethyl)-10,11-methylenedioxy-20(S)- camptothecin, 7-(cysteinylglycylmethyl)-10,11-methylenedioxy-20(S)-camptothecin, and 7-(cysteinylmethyl)-10,11-methylenedioxy-20(S)- camptothecin] displayed topo I and, cell growth-inhibitory activity. These results suggest that 7-peptidyl derivatives represent a new class of camptothecin analogues. C1 Duke Univ, Dept Med, Ctr Comprehens Canc, Durham, NC 27710 USA. Res Triangle Inst, Res Triangle Pk, NC 27709 USA. NCI, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA. RP Gamcsik, MP (reprint author), Duke Univ, Dept Med, Ctr Comprehens Canc, Box 3843,MSRB 301,Res Dr, Durham, NC 27710 USA. FU NCI NIH HHS [CA68697] NR 41 TC 16 Z9 17 U1 2 U2 7 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1535-7163 J9 MOL CANCER THER JI Mol. Cancer Ther. PD NOV PY 2001 VL 1 IS 1 BP 11 EP 20 PG 10 WC Oncology SC Oncology GA 606LW UT WOS:000178736300003 PM 12467234 ER PT J AU Bienstock, RJ Barrett, JC AF Bienstock, RJ Barrett, JC TI KAI1, a prostate metastasis' suppressor: Prediction of solvated structure and interactions with binding partners; Integrins, cadherins, and cell-surface receptor proteins SO MOLECULAR CARCINOGENESIS LA English DT Article DE membrane protein modeling; KAI1; prostate cancer; transmembrane-4; tetraspan protein; integrin-binding protein ID SECONDARY STRUCTURE PREDICTION; PHOTOSYNTHETIC REACTION-CENTER; KAI1/CD82 GENE-EXPRESSION; MHC CLASS-II; TRANSMEMBRANE-4 SUPERFAMILY; ANGSTROM RESOLUTION; CRYSTAL-STRUCTURE; CRYSTALLOGRAPHIC REFINEMENT; SEQUENCE ALIGNMENTS; SUBSTITUTION TABLES AB the solution structure of the transmembrane-4 superfamily protein KAI1, a recently identified prostate cancer metastasis suppressor gene that encodes a 267-amino acid protein, was modeled. The structure of this four-helical transmembrane protein was developed by defining and modeling sections individually. A complete three-dimensional structure for the solvated protein was developed by combining the Individually modeled sections. The four-helix transmembrane bundle structure was predicted combining information from several methods including Fourier transform analysis of residue variability for helix orientation. The structure of the KAI1 large extracellular domain was modeled based on the solved crystal structure of the extracellular domain of another tetraspanin superfamily protein member, CD81 (hepatitis C virus envelope E2 glycoprotein receptor). This is a novel protein fold consisting of five alpha helices held together by two disulfide bonds for which the CD81 protein is the first solved representative. Molecular dynamics studies were performed to test stability and to relax the total model KAI1 structure's solution. The resulting KAI1 structural model should be a useful tool for predicting modes of self-association and associations with other TM4SF proteins, integrins, cadherins, and other KAI1 binding partners. Mutations for probing the interactions of KAI1 with antibodies and with other binding partners are suggested. Published 2001 Wiley-Liss, Inc.dagger C1 NIEHS, NIH, Comp Sci Lab, Res Triangle Pk, NC 27709 USA. NIEHS, NIH, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. RP Bienstock, RJ (reprint author), NIEHS, NIH, Comp Sci Lab, POB 12233,Mail Drop FO-O11, Res Triangle Pk, NC 27709 USA. NR 95 TC 57 Z9 59 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD NOV PY 2001 VL 32 IS 3 BP 139 EP 153 DI 10.1002/mc.1073 PG 15 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA 490DU UT WOS:000172035800004 PM 11746826 ER PT J AU Zhou, YJ Chen, M Cusack, NA Kimmel, LH Magnuson, KS Boyd, JG Lin, W Roberts, JL Lengi, A Buckley, RH Geahlen, RL Candotti, F Gadina, M Changelian, PS O'Shea, JJ AF Zhou, YJ Chen, M Cusack, NA Kimmel, LH Magnuson, KS Boyd, JG Lin, W Roberts, JL Lengi, A Buckley, RH Geahlen, RL Candotti, F Gadina, M Changelian, PS O'Shea, JJ TI Unexpected effects of FERM domain mutations on catalytic activity of Jak3: Structural implication for Janus kinases SO MOLECULAR CELL LA English DT Article ID PROTEIN-TYROSINE KINASES; MICE LACKING JAK3; PSEUDOKINASE DOMAIN; BINDING-SITE; ACTIVATION; SRC; PHOSPHORYLATION; INHIBITORS; TERMINUS; COMPLEX AB Janus kinases comprise carboxyterminal kinase, pseudokinase, SH2-like, and N-terminal FERM domains. We identified three patient-derived mutations in the FERM domain of Jak3 and investigated the functional consequences of these mutations. These mutations inhibited receptor binding and also abrogated kinase activity, suggesting interactions between the FERM and kinase domains. In fact, the domains were found to physically associate, and coexpression of the FERM domain enhanced activity of the isolated kinase domain. Conversely, staurosporine, which alters kinase domain structure, disrupted receptor binding, even though the catalytic activity of Jak3 is dispensable for receptor binding. Thus, the Jak FERM domain appears to have two critical functions: receptor interaction and maintenance of kinase integrity. C1 NIAMSD, Lymphocyte Cell Biol Sect, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. Pfizer Inc, Global Res & Dev, Dept Immunol, Groton, CT 06340 USA. Duke Univ, Sch Med, Dept Pediat, Durham, NC 27710 USA. Purdue Univ, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47907 USA. RP O'Shea, JJ (reprint author), NIAMSD, Lymphocyte Cell Biol Sect, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. OI Geahlen, Robert/0000-0001-8400-2924 NR 35 TC 90 Z9 92 U1 2 U2 3 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTES AVE,, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD NOV PY 2001 VL 8 IS 5 BP 959 EP 969 DI 10.1016/S1097-2765(01)00398-7 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 494YA UT WOS:000172312400006 PM 11741532 ER PT J AU Muller, J Ory, S Copeland, T Piwnica-Worms, H Morrison, DK AF Muller, J Ory, S Copeland, T Piwnica-Worms, H Morrison, DK TI C-TAK1 regulates Ras signaling by phosphorylating the MAPK scaffold, KSR1 SO MOLECULAR CELL LA English DT Article ID ACTIVATED PROTEIN-KINASE; PLASMA-MEMBRANE; HUMAN CDC25C; SUPPRESSOR; IDENTIFICATION; SERINE-216; LOCALIZATION; TRANSDUCTION; BINDING; MAMMALS AB Kinase suppressor of Ras (KSR) is a conserved component of the Ras pathway that interacts directly with MEK and MAPK. Here we show that KSR1 translocates from the cytoplasm to the cell surface in response to growth factor treatment and that this process is regulated by Cdc25C-associated kinase 1 (C-TAK1). C-TAK1 constitutively associates with mammalian KSR1 and phosphorylates serine 392 to confer 14-3-3 binding and cytoplasmic sequestration of KSR1 in unstimulated cells. In response to signal activation, the phosphorylation state of S392 is reduced, allowing the KSR1 complex to colocalize with activated Ras and Raf-1 at the plasma membrane, thereby facilitating the phosphorylation reactions required for the activation of MEK and MAPK. C1 NCI, Regulat Cell Growth Lab, Ctr Canc Res, Frederick, MD 21702 USA. Washington Univ, Sch Med, Howard Hughes Med Inst, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA. RP NCI, Regulat Cell Growth Lab, Ctr Canc Res, Frederick, MD 21702 USA. EM dmorrison@ncifcrf.gov RI Ory, Stephane/E-9947-2010; Piwnica-Worms, Helen/C-5214-2012 OI Ory, Stephane/0000-0003-4359-1157; NR 38 TC 190 Z9 194 U1 0 U2 6 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 1097-2765 EI 1097-4164 J9 MOL CELL JI Mol. Cell PD NOV PY 2001 VL 8 IS 5 BP 983 EP 993 DI 10.1016/S1097-2765(01)00383-5 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 494YA UT WOS:000172312400008 PM 11741534 ER PT J AU Uphyrkina, O Johnson, WE Quigley, H Miquelle, D Marker, L Bush, M O'Brien, SJ AF Uphyrkina, O Johnson, WE Quigley, H Miquelle, D Marker, L Bush, M O'Brien, SJ TI Phylogenetics, genome diversity and origin of modern leopard, Panthera pardus SO MOLECULAR ECOLOGY LA English DT Article DE evolution; microsatellites; mitochondrial DNA; Panthera pardus; subspecies ID CAT FELIS-CATUS; GENETIC-VARIATION; MITOCHONDRIAL-DNA; NUCLEOTIDE-SEQUENCES; HUMAN-POPULATIONS; MOLECULAR CLOCK; COMBINING DATA; TREES; MICROSATELLITES; EVOLUTION AB Leopards, Panthera pardus, are widely distributed across southern Asia and sub-Saharan Africa. The extent and phylogeographic patterns of molecular genetic diversity were addressed in a survey of 77 leopards from known geographical locales representing 13 of the 27 classical trinomial subspecies. Phylogenetic analysis of mitochondrial DNA sequences (727 bp of NADH5 and control region) and 25 polymorphic microsatellite loci revealed abundant diversity that could be partitioned into a minimum of nine discrete populations, tentatively named here as revised subspecies: P. pardus pardus, P. p. nimr, P. p. saxicolor, P. p. fusca, P. p. kotiya, P. p. delacouri, P. p. japonensis, P. p. orientalis and P. p. melas. However, because of limited sampling of African populations, this may be an underestimate of modem phylogeographic population structure. Combined phylogeographic and population diversity estimates support an origin for modem leopard lineages 470000-825000 years ago in Africa followed by their migration into and across Asia more recently (170000-300000 years ago). Recent demographic reductions likely have led to genetic impoverishment in P. p. orientalis and in the island subspecies P. p. kotiya. C1 NCI, Lab Genom Divers, Frederick, MD 21702 USA. Wildlife Conservat Soc, Hornocker Wildlife Inst, Bozeman, MT 59719 USA. Cheetah Conservat Fund, Windhoek 9000, Namibia. Conservat & Res Ctr, Front Royal, VA 22630 USA. RP O'Brien, SJ (reprint author), NCI, Lab Genom Divers, Frederick, MD 21702 USA. RI Johnson, Warren/D-4149-2016 OI Johnson, Warren/0000-0002-5954-186X NR 65 TC 81 Z9 94 U1 10 U2 67 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0962-1083 J9 MOL ECOL JI Mol. Ecol. PD NOV PY 2001 VL 10 IS 11 BP 2617 EP 2633 DI 10.1046/j.0962-1083.2001.01350.x PG 17 WC Biochemistry & Molecular Biology; Ecology; Evolutionary Biology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology; Evolutionary Biology GA 497YT UT WOS:000172483600004 PM 11883877 ER PT J AU Zhang, Y Dufau, ML AF Zhang, Y Dufau, ML TI EAR2 and EAR3/COUP-TFI regulate transcription of the rat LH receptor SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID LUTEINIZING-HORMONE RECEPTOR; NUCLEAR ORPHAN RECEPTORS; COUP-TF; ESTROGEN-RECEPTOR; RESPONSE ELEMENT; GRANULOSA-CELLS; GENE PROMOTER; FLANKING SEQUENCES; THYROID-HORMONE; FACTOR-I AB Our previous studies demonstrated regulation of the human LH receptor (hLHR) promoter by nuclear orphan receptors EAR2, EAR3/COUP-TFI (repression), and TR4 (activation) through a direct-repeat motif (hDR). The current studies investigated the differential binding of orphan receptors to rat (rLHR) and hLHR promoters, and their modulation of rLHR gene transcription in rat granulosa cells. The rLHR DR with one nucleotide difference from hDR at its core sequence mediated inhibition of the rLHR transcription, to which EAR2 and EAR3/COUP-TFI but not TR4 bound. The A/C mismatch was responsible for the lack of TR4 binding and function, but had no effect on EAR2 and EAR3/COUP-TFI. EAR2 and EAR3/COUP-TF bound to the rLHR DR with lower affinity than to the hDR, and exhibited lesser inhibitory capacity. This difference resulted from the lack of a guanine in the rDR, which is present 3' next to the hDR core. These studies have identified sequence-specific requirements for the binding of EAR2, EAR3/COUP-TFI, and TR4 to the DRs that explain their differential regulation of rat and human LHR genes. In addition, hCG treatment significantly reduced the inhibition of rLHR gene in granulosa cells and also decreased EAR2 and EAR3/COUP-TFI protein levels. These results indicate that hormonally regulated expression of EAR2 and EAR3/COUP-TFI contributes to gonadotropin-induced derepression of LHR promoter-activity in granulosa cells. C1 NICHHD, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. RP Dufau, ML (reprint author), Bldg 49,Room 6A-36,49 Covent Dr,MSC 4510, Bethesda, MD 20892 USA. NR 35 TC 21 Z9 24 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD NOV PY 2001 VL 15 IS 11 BP 1891 EP 1905 DI 10.1210/me.15.11.1891 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 486MH UT WOS:000171821200005 PM 11682620 ER PT J AU Niimi, T Keck-Waggoner, CL Popescu, NC Zhou, YH Levitt, RC Kimura, S AF Niimi, T Keck-Waggoner, CL Popescu, NC Zhou, YH Levitt, RC Kimura, S TI UGRP1, a uteroglobin/clara cell secretory protein-related protein, is a novel lung-enriched downstream target gene for the T/EBP/NKX2.1 homeodomain transcription factor SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID ENHANCER-BINDING PROTEIN; TISSUE-SPECIFIC EXPRESSION; THYROID PEROXIDASE GENE; FACTOR-I; PROMOTER; MOUSE; MORPHOGENESIS; FAMILY; TTF-1; ASTHMA AB A novel gene that is down-regulated in lungs of T/ebp/Nkx2.1-null mouse embryos has been identified using a suppressive-subtractive hybridization method. The gene product is a secreted protein, forms a homodimer, and exhibits an amino acid sequence similar to that seen in the uteroglobin/Clara cell secretory protein family of proteins. This gene, designated Ugrp1 (uteroglobin-related protein 1), consists of three exons and two introns and produces three transcripts by alternative splicing. The Ugrp1 gene was localized by fluorescence in situ hybridization to mouse chromosome 18 at region 18C-D; this region is homologous with human 5q31-34, where one of the asthma susceptibility genes has been assigned. UGRP1 mRNA is predominantly expressed in the lung, with low levels of expression in the thyroid. Expression in the lung is detectable as early as embryonic day 12.5 and increases markedly by embryonic day 16.5. In T/ebp/Nkx2.1-null embryo lungs, UGRP1 expression was significantly reduced as assessed by RTPCR analysis. Cotransfection assays using a T/EBP/NKX2.1 expression construct with Ugrp1 promoter-luciferase reporter constructs confirmed that T/EBP/NKX2.1 regulates Ugrp1 gene activity at the transcriptional level. Thus, Ugrp1 is a downstream target gene for the T/EBP/NKX2.1 homeodomain transcription factor. Changes in UGRP1 mRNA levels in lungs from antigen-sensitized mice suggest the possible involvement of UGRP1 in inflammation. C1 NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. Genaera Corp, Plymouth Meeting, PA 19462 USA. RP Kimura, S (reprint author), Aichi Med Univ, ERATO, Japan Sci & Technol Corp, Sekiguchi Biomatrix Signaling Project, Aichi 4801195, Japan. NR 56 TC 54 Z9 63 U1 0 U2 3 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD NOV PY 2001 VL 15 IS 11 BP 2021 EP 2036 DI 10.1210/me.15.11.2021 PG 16 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 486MH UT WOS:000171821200015 PM 11682631 ER PT J AU Falik-Zaccai, TC Anikster, Y Rivera, CE Horne, MK Schliamser, L Phornphutkul, C Attias, D Hyman, T White, JG Gahl, WA AF Falik-Zaccai, TC Anikster, Y Rivera, CE Horne, MK Schliamser, L Phornphutkul, C Attias, D Hyman, T White, JG Gahl, WA TI A new genetic isolate of gray platelet syndrome (GPS): Clinical, cellular, and hematologic characteristics SO MOLECULAR GENETICS AND METABOLISM LA English DT Article DE gray platelet syndrome; P-selectin; fibrinogen receptor; genetic isolate ID GLYCOPROTEIN-IIB-IIIA; ALPHA-GRANULE DEFICIENCY; BONE-MARROW; P-SELECTIN; MEGAKARYOCYTES; PLASMA; POOL; ALPHA(IIB)BETA(3); THROMBOCYTOPENIA; MYELOFIBROSIS AB Gray platelet syndrome (GPS) is a disorder characterized by thrombocytopenia and large platelets that lack a granules and their contents. We describe two siblings with GPS who are members of a Moslem Bedouin genetic isolate. The children, an 8-year-old girl and a 5-year-old boy, had characteristic pale blue platelets lacking a granules on electron microscopy. Platelet aggregation studies were normal. The girl underwent a bone marrow aspiration and biopsy which showed mild myelofibrosis and extensive emperipolesis, i.e., the passage of other hematopoietic cells through megakaryocytes. Both children lacked high-molecular-weight multimers of von Willebrand factor (vWF) and had reduced activity and antigens of vWf. Platelet activation was approximately normal when ADP was employed as agonist, but significantly impaired using the thrombin receptor-activating peptide (TRAP). These findings are explained in light of the mechanism of action of each agonist. In addition, we propose that the emperipolesis was cause increased P-selectin in megakaryocytes, and resulted in release of fibroblastic growth factors, explaining the myelofibrosis. The detailed description of these cases provides a basis for future differentiation of the various types of GPS, and for our current attempts to isolate the gene causing GPS in this genetic isolate. (C) 2001 Academic Press. C1 Technion Israel Inst Technol, Div Med Genet, Hosp Western Galillee Naharia, Rappaport Fac Med, Haifa, Israel. NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. NIH, Dept Lab Med, Div Hematol, WG Magnuson Clin Ctr, Bethesda, MD 20892 USA. Bnai Zion Med Ctr, Inst Hematol, Haifa, Israel. NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. Univ Minnesota, Dept Lab Med, Minneapolis, MN 55455 USA. RP Gahl, WA (reprint author), NICHHD, NIH, 10 Ctr Dr,MSC 1830,Bldg 10,Room 9S-241, Bethesda, MD 20892 USA. NR 33 TC 36 Z9 39 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 NOV PY 2001 VL 74 IS 3 BP 303 EP 313 DI 10.1006/mgme.2001.3247 PG 11 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA 514DX UT WOS:000173423900002 PM 11708859 ER PT J AU Kleta, R Anikster, Y Lucero, C Shotelersuk, V Huizing, M Bernardini, I Park, M Thoene, J Schneider, J Gahl, WA AF Kleta, R Anikster, Y Lucero, C Shotelersuk, V Huizing, M Bernardini, I Park, M Thoene, J Schneider, J Gahl, WA TI CTNS mutations in African American patients with cystinosis SO MOLECULAR GENETICS AND METABOLISM LA English DT Article DE ocular cystinosis; splicing; mutation analysis; African American ID NEPHROPATHIC CYSTINOSIS; CYSTEAMINE; GENE; INSUFFICIENCY; TRANSPORT; LYSOSOMES; CHILDREN; REMOVAL AB Cystinosis, an autosomal recessive lysosomal storage disorder, is rarely diagnosed in African Americans. The disease results from mutations in the gene CTNS; at least 55 such mutations have been reported. By far the most common is a 57,257-bp deletion of Northern European origin encompassing most of the CTNS gene. We performed mutation analysis on DNA from four African American patients with cystinosis. In one individual with classical, nephropathic cystinosis, we identified a new molecular defect, i.e., a homozygous GT-->CC substitution at the +5 position of IVS 5 of CTNS (IVS 5+5 GT-->CC). The out-of-frame splicing of exon 5 creates a null allele consistent with the patient's severe phenotype. Two patients were heterozygous and one homozygous for the common 57-kb deletion allele, reflecting the admixture of African and Northern European gene pools in North America. The two African Americans heterozygous for the 57-kb deletion were also hemizygous for a 928G-->A change, associated with ocular or nonnephropathic cystinosis. These two individuals are the only known African Americans with ocular cystinosis. We conclude that the diagnosis of cystinosis should be entertained in African Americans with symptoms of the disease, and that mutation analysis for the 57-kb deletion should be considered in this group of patients. (C) 2001 Academic Press. C1 NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. Tulane Univ, Sch Med, Hayward Genet Ctr, New Orleans, LA 70112 USA. Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA. RP Gahl, WA (reprint author), NICHHD, NIH, 10 Ctr Dr,MSC 1830,Bldg 10,Room 9S-241, Bethesda, MD 20892 USA. NR 36 TC 22 Z9 24 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 1096-7192 J9 MOL GENET METAB JI Mol. Genet. Metab. PD NOV PY 2001 VL 74 IS 3 BP 332 EP 337 DI 10.1006/mgme.2001.3218 PG 6 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA 514DX UT WOS:000173423900005 PM 11708862 ER PT J AU Gao, ZG Van Muijlwijk-Koezen, JE Chen, AS Muller, CE IJzerman, AP Jacobson, KA AF Gao, ZG Van Muijlwijk-Koezen, JE Chen, AS Muller, CE IJzerman, AP Jacobson, KA TI Allosteric modulation of A(3) adenosine receptors by a series of 3-(2-pyridinyl)isoquinoline derivatives SO MOLECULAR PHARMACOLOGY LA English DT Article ID MUSCARINIC ACETYLCHOLINE-RECEPTORS; AMILORIDE ANALOGS; LIGAND-BINDING; CELLS; A(2A); A(1); RAT; 2-AMINO-3-BENZOYLTHIOPHENES; INHIBITION; ACTIVATION AB Allosteric modulators of A(1) and A(2A) adenosine receptors have been described; however, for the A(3) adenosine receptor, neither an allosteric site nor a compound with allosteric effects has been described. In this study, the allosteric modulation of human A(3) adenosine receptors by a series of 3-(2-pyridinyl)isoquinoline derivatives was investigated by examining their effects on the dissociation of the agonist radioligand, [I-125]N-6-(4-amino-3-iodobenzyl)-5'-N-methylcarboxamidoadenosine (IAB-MECA), from the receptor. Several 3-(2-pyridinyl)isoquinoline derivatives, including VUF5455, VUF8502, VUF8504, and VUF8507, slowed the dissociation of the agonist radioligand [I-125]I-AB-MECA in a concentration-dependent manner, suggesting an allosteric interaction. These compounds had no effect on the dissociation of the radiolabeled antagonist [H-3]PSB-11 from the A(3) adenosine receptor, suggesting a selective enhancement of agonist binding. By comparison, compounds of similar structure (VUF8501, VUF8503, VUF8505), the classical adenosine receptor antagonist CGS15943 and the A(1) receptor allosteric enhancer PD81723 did not significantly influence the dissociation rate of [I-125]I-AB-MECA. The effect of agonist on forskolin-induced cAMP production was significantly enhanced by VUF5455. When the subtype-selectivity of the allosteric enhancement was tested the compounds had no effect on the dissociation of either [H-3]N-6-[(R)-phenylisopropyl]adenosine from the A(1) adenosine receptor or [H-3]CGS21680 from the A(2A) adenosine receptor. Probing of structure-activity relationships suggested that a carbonyl group is essential for allosterism but preferred only for competitive antagonism. The presence of a 7-methyl group decreased the competitive binding affinity without a major loss of the allosteric enhancing activity, suggesting that the structural requirements for allosteric enhancement might be distinct from those for competitive antagonism. C1 NIDDK, Mol Recognit Sect, Lab Bioorgan Chem, NIH, Bethesda, MD 20892 USA. Leiden Univ, Leiden Amsterdam Ctr Drug Res, Div Med Chem, Leiden, Netherlands. Univ Bonn, Inst Pharmaceut, D-5300 Bonn, Germany. RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Lab Bioorgan Chem, NIH, Bldg 8A,Rm B1A-19, Bethesda, MD 20892 USA. RI Jacobson, Kenneth/A-1530-2009; Muller, Christa/C-7748-2014 OI Jacobson, Kenneth/0000-0001-8104-1493; Muller, Christa/0000-0002-0013-6624 FU Intramural NIH HHS [Z99 DK999999, ZIA DK031117-22] NR 38 TC 49 Z9 50 U1 2 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 NOV PY 2001 VL 60 IS 5 BP 1057 EP 1063 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 489HE UT WOS:000171985300021 PM 11641434 ER PT J AU Pombrio, JM Giangreco, A Li, LQ Wempe, MF Anders, MW Sweet, DH Pritchard, JB Ballatori, N AF Pombrio, JM Giangreco, A Li, LQ Wempe, MF Anders, MW Sweet, DH Pritchard, JB Ballatori, N TI Mercapturic acids (N-acetylcysteine S-conjugates) as endogenous substrates for the renal organic anion transporter-1 SO MOLECULAR PHARMACOLOGY LA English DT Article ID RAT-KIDNEY; GLUTATHIONE CONJUGATION; EXPRESSION CLONING; MOLECULAR-CLONING; XENOPUS-LAEVIS; METABOLISM; CYSTEINE; NEPHROTOXICITY; LOCALIZATION; CONVERSION AB Mercapturic acids are N-acetyl-L-cysteine S-conjugates that are formed from a range of endogenous and exogenous chemicals. Although the kidney is a major site for elimination of mercapturic acids, the transport mechanisms involved have not been identified. The present study examined whether mercapturic acids are substrates for the renal basolateral organic anion transporter-1 (Oat1) from rat kidney. This carrier mediates uptake of organic anions from the bloodstream in exchange for intracellular a-ketoglutarate. Uptake of [H-3]p-aminohippuric acid (PAH) in Oat1-expressing Xenopus laevis oocytes was strongly inhibited by S-(2,4-dinitrophenyl)-N-acetyl-L-cysteine (DNP-NAC) and by all other mercapturic acids tested, including the endogenous mercapturic acid N-acetyl-leukotriene E-4 Inhibition by the mercapturic acids was competitive, which is consistent with the hypothesis that these compounds are substrates for Oat1. This conclusion was supported by the direct demonstration of saturable [S-35]DNP-NAC uptake in Oat1-expressing oocytes. [S-35]DNP-NAC uptake was inhibited by PAH and other mercapturic acids and was stimulated in oocytes preloaded with glutarate. The apparent Km value for DNP-NAC uptake was only 2 AM, indicating that this mercapturic acid is a high affinity substrate for Oat1. Together, these data indicate that clearance of endogenous mercapturic acids is an important function of the renal organic anion transporter. C1 Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Physiol & Pharmacol, Rochester, NY 14642 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RP Ballatori, N (reprint author), Univ Rochester, Sch Med & Dent, Dept Environm Med, Box EHSC,575 Elmwood Ave, Rochester, NY 14642 USA. RI Sweet, Douglas/H-7914-2013 OI Sweet, Douglas/0000-0002-8911-9184 FU NIDDK NIH HHS [DK48823]; NIEHS NIH HHS [ES01247, ES06484, ES07026] NR 40 TC 40 Z9 40 U1 0 U2 0 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 NOV PY 2001 VL 60 IS 5 BP 1091 EP 1099 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 489HE UT WOS:000171985300025 PM 11641438 ER PT J AU Luo, T Matsuo-Takasaki, M Sargent, TD AF Luo, T Matsuo-Takasaki, M Sargent, TD TI Distinct roles for distal-less genes Dlx3 and Dlx5 in regulating ectodermal development in Xenopus SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article DE Dlx3; Dlx5; neural crest; neural plate; ectoderm ID HOMEOBOX GENES; NEURAL PLATE; CRANIOFACIAL DEVELOPMENT; OVERLAPPING EXPRESSION; BRANCHIAL ARCHES; INDUCTION; MESODERM; EMBRYOS; DIFFERENTIATION; LAEVIS AB In vertebrates, there are six or more copies of genes related to the Drosophila pattern formation homeodomain gene Distal-less. Among this family, Dlx3 and Dlx5 share extensive sequence homology and have similar, but distinctive, expression patterns, suggesting that these two factors may have substantially redundant developmental functions. Here we show that at the earliest phases of embryogenesis in Xenopus, there are significant differences between Dlx3 and Dlx5 expression and that this correlates with different functions in the restriction of neural crest and neural plate boundaries, respectively. (C) 2001 Wiley-Liss, Inc. C1 NICHHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. RP Sargent, TD (reprint author), NICHHD, Genet Mol Lab, NIH, Bldg 6B,Rm 412,MSC 2790,6 Ctr Dr, Bethesda, MD 20892 USA. NR 44 TC 50 Z9 50 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD NOV PY 2001 VL 60 IS 3 BP 331 EP 337 DI 10.1002/mrd.1095 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA 479CV UT WOS:000171387100008 PM 11599044 ER PT J AU Scherr, M LeBon, J Castanotto, D Cunliffe, HE Meltzer, PS Ganser, A Riggs, AD Rossi, JJ AF Scherr, M LeBon, J Castanotto, D Cunliffe, HE Meltzer, PS Ganser, A Riggs, AD Rossi, JJ TI Detection of antisense and ribozyme accessible sites on native mRNAs: Application to NCOA3 mRNA SO MOLECULAR THERAPY LA English DT Article DE antisense; ribozyme; breast cancer; ovarian cancer; RNaseH; RNA structure; NCOA3 mRNA ID TRANSFERASE-DEPENDENT PCR; IN-VIVO; CELL-LINE; RNA; RECEPTOR; CLEAVAGE; VITRO; INHIBITION; SELECTION; EXTRACTS AB The efficacies of antisense oligonucleotides and ribozymes are greatly dependent on the accessibility of their mRNA targets. Target site accessibility is affected by both RNA structure and the proteins associated along the length of the RNA. To mimic the native state of mRNA for site identification, we have previously used endogenous mRNAs in cellular extracts as targets for defined sequence oligodeoxynucleotides (ODNs) designed to identify both antisense pairing and potential ribozyme cleavage sites. The rationale for this approach is that the specific pairing of an ODN with a mRNA forms a DNA:RNA hybrid that is cleaved by the endogenous RNaseH in the cell extract. To extend the usefulness of this basic approach, we report here the use of semi-random ODN libraries to identify hammerhead ribozyme cleavage sites. Thus, the most accessible sites for antisense and ribozyme base pairing are selected by this approach. A novel feature of the approach described here is the use of terminal transferase-dependent PCR (TDPCR) after reverse transcription to estimate the cleavage efficiency and to precisely determine the RNaseH and ribozyme cleavage sites on mRNAs in cell extracts following treatment with ODN or ribozyme libraries. As a model system, we have targeted the NCOA3 (also known as AIB-1) mRNA in cell extracts. The NCOA3 mRNA encodes a nuclear receptor co-activator that is amplified and overexpressed in a high proportion of breast and ovarian cancers. A highly accessible site on this mRNA was identified, and a ribozyme targeted to this site was demonstrated to effectively downregulate NCOA3 function in cells. C1 City Hope Natl Med Ctr, Beckman Res Inst, Div Mol Biol, Duarte, CA 91010 USA. City Hope Natl Med Ctr, Beckman Res Inst, Div Biol, Duarte, CA 91010 USA. Hannover Med Sch, Dept Hematol, D-30625 Hannover, Germany. NHGRI, Canc Genet Lab, NIH, Bethesda, MD 20892 USA. RP Rossi, JJ (reprint author), City Hope Natl Med Ctr, Beckman Res Inst, Div Mol Biol, Duarte, CA 91010 USA. FU NIAID NIH HHS [AI 29329] NR 26 TC 28 Z9 31 U1 0 U2 1 PU ACADEMIC PRESS INC 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 NOV PY 2001 VL 4 IS 5 BP 454 EP 460 DI 10.1006/mthe.2001.0481 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 492MT UT WOS:000172172700010 PM 11708882 ER PT J AU Porwollik, S Wong, RMY Sims, SH Schaaper, RM DeMarini, DM McClelland, M AF Porwollik, S Wong, RMY Sims, SH Schaaper, RM DeMarini, DM McClelland, M TI The Delta uvrB mutations in the Ames strains of Salmonella span 15 to 119 genes SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE microarray; Salmonella typhimurium; Ames strains; comparative genomic hybridization; Delta uvrB ID ESCHERICHIA-COLI; TESTER STRAINS; TYPHIMURIUM; CARCINOGENS; MUTAGENESIS AB The Delta uvrB mutations present in strains of Salmonella enterica Typhimurium used commonly in the Salmonella (Ames) mutagenicity assay were isolated independently for at least five different his mutants. These deletions all involved the galactose operon, biotin operon, nucleotide-excision-repair uvrB gene, and chlorate-resistance genes. Beyond this, the size of the deletions and the number and type of genes deleted have remained unknown for nearly 30 years. Here, we have used genomic hybridization to a Typhimurium microarray to characterize these five Delta uvrB deletions. The number of genes (and amount of DNA) deleted due to the Delta uvrB mutations are 15 (16 kb) each in TA97 and TA104,47 (50 kb) in TA100, 87 (96 kb) in TA1537, and 119 (125 kb) in TA98, accounting for 0.3, 0.3, 1.0, 1.9, and 2.6% of the genome, respectively. In addition, TA97 and TA104 contain an identical three-gene deletion elsewhere in their genomes, and, most remarkably, TA104 contains a 282-gene amplification, representing 7% of the genome. Missing genes include mfdA and mdaA, encoding a multi-drug translocase and a major nitroreductase, respectively, both absent in TA98; dps, encoding a DNA-binding protein absent in TA1537 and TA98; and dinG, encoding a lexA-regulated repair enzyme, absent in three Delta uvrB lineages. Genes involved in molybdenum cofactor biosynthesis and a number of ORFs of unknown functions are missing in all Delta uvrB strains investigated. Studies in Delta uvrB strains of Escherichia coli have found that the enhanced mutagenesis of some base analogues was due to the deletion of genes involved in molybdenum cofactor biosynthesis rather than to deletion of uvrB. These discoveries do not diminish the value of the data generated in the Ames strains. However, absence of genes other than uvrB may account for the enhanced mutagenicity of some compounds in Delta uvrB Ames strains. In general, microarrays will be useful for characterizing the extent and nature of deletion and amplification mutations. Published by Elsevier Science B.V. C1 Sidney Kimmel Canc Ctr, San Diego, CA 92121 USA. Sigma Genosys, The Woodlands, TX 77380 USA. NIEHS, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. US EPA, Environm Carcinogenesis Div MD68, Res Triangle Pk, NC 27711 USA. RP McClelland, M (reprint author), Sidney Kimmel Canc Ctr, 10835 Altman Row, San Diego, CA 92121 USA. RI McClelland, Michael/A-8583-2011 FU NIAID NIH HHS [AI34829, AI 43283] NR 22 TC 39 Z9 39 U1 0 U2 1 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 NOV 1 PY 2001 VL 483 IS 1-2 BP 1 EP 11 DI 10.1016/S0027-5107(01)00239-1 PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 488HR UT WOS:000171930600001 PM 11600126 ER PT J AU Germain, DP Kaneski, CR Brady, RO AF Germain, DP Kaneski, CR Brady, RO TI Mutation analysis of the acid beta-glucosidase gene in a patient with type 3 Gaucher disease and neutralizing antibody to alglucerase SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE Gaucher disease; lysosome; enzyme replacement therapy; neutralizing antibody; genotype ID HUMAN GLUCOCEREBROSIDASE GENE; ENZYME THERAPY; SEQUENCES AB The beneficial effects of macrophage-targeted glucocerebrosidase (alglucerase, Ceredas (TM)) in patients with Gaucher disease are well established. A minority of recipients develop transient non-neutralizing antibodies to the exogenous enzyme. A 7-year-old patient with type 3 Gaucher disease, whose clinical course began to deteriorate while receiving alglucerase developed a progressively increasing titer of IgG antibody, that blocked the catalytic activity of alglucerase. We investigated the acid p-glucosidase genotype in this patient. Direct sequencing of both cDNA and genomic PCR products was used to characterize the mutations underlying acid p-glucosidase deficiency. The patient was shown to be a compound heterozygote for a previously reported missense mutation (G377S), and a novel single nucleotide deletion (g5255deIT). The transcript originating from the latter allele was undetectable in RT-PCR experiments. We report the first characterization of a GBA genotype associated with the development of neutralizing antibody to alglucerase, in a patient affected with type 3 Gaucher disease. Our results may help to shed light on the mechanisms underlying this phenomenon which, in the rare instances where it occurs, hampers the efficacy of enzyme replacement therapy. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Hop Europeen Georges Pompidou, Dept Genet, F-75015 Paris, France. NINCDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD USA. RP Germain, DP (reprint author), Hop Europeen Georges Pompidou, Dept Genet, 20 Rue Leblanc, F-75015 Paris, France. OI Kaneski, Christine/0000-0003-1453-2502 NR 21 TC 22 Z9 23 U1 0 U2 1 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 NOV 1 PY 2001 VL 483 IS 1-2 BP 89 EP 94 DI 10.1016/S0027-5107(01)00232-9 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 488HR UT WOS:000171930600012 PM 11600137 ER PT J AU Bianco, P Robey, PG AF Bianco, P Robey, PG TI Stem cells in tissue engineering SO NATURE LA English DT Article ID MARROW STROMAL CELLS; GENE-THERAPY; IN-VITRO; BONE; TRANSPLANTATION; REGENERATION; EXPRESSION; REPAIR; VIVO; PROSPECTS AB The concept of producing 'spare parts' of the body for replacement of damaged or lost organs lies at the core of the varied biotechnological practices referred to generally as tissue engineering. Use of postnatal stem cells has the potential to significantly alter the perspective of tissue engineering. Successful long-term restoration of continuously self-renewing tissues such as skin, for example, depends on the use of extensively self-renewing stem cells. The identification and isolation of stem cells from a number of tissues provides appropriate targets for prospective gene therapies. C1 Univ Roma La Sapienza, Dipartimento Med Sperimentale & Patol, I-00161 Rome, Italy. Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA. RP Bianco, P (reprint author), Univ Roma La Sapienza, Dipartimento Med Sperimentale & Patol, I-00161 Rome, Italy. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 FU Telethon [E.1029] NR 42 TC 548 Z9 594 U1 11 U2 87 PU MACMILLAN PUBLISHERS LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 01 PY 2001 VL 414 IS 6859 BP 118 EP 121 DI 10.1038/35102181 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 487VC UT WOS:000171898900056 PM 11689957 ER PT J AU Moss, B Ward, BM AF Moss, B Ward, BM TI High-speed mass transit for poxviruses on microtubules SO NATURE CELL BIOLOGY LA English DT Article ID EXTRACELLULAR ENVELOPED VIRUS; ACTIN-BASED MOTILITY; VACCINIA VIRUS; PROTEIN; MEMBRANE; TRANSPORT; SPREAD; GENE AB Commuters can ride a high-speed mass-transit system from the city centre to the suburbs and then engage a private vehicle for the final leg home. Similarly, vaccinia virions travel to the cell periphery on microtubule tracks, disembark near the plasma membrane, and acquire individual actin tails for propulsion on microvilli towards adjacent cells. C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, 4 Ctr Dr,MSC 0445, Bethesda, MD 20892 USA. NR 25 TC 36 Z9 36 U1 0 U2 1 PU MACMILLAN PUBLISHERS LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1465-7392 J9 NAT CELL BIOL JI Nat. Cell Biol. PD NOV PY 2001 VL 3 IS 11 BP E245 EP E246 DI 10.1038/ncb1101-e245 PG 2 WC Cell Biology SC Cell Biology GA 490UJ UT WOS:000172070300002 PM 11715030 ER PT J AU Kastner, DL O'Shea, JJ AF Kastner, DL O'Shea, JJ TI A fever gene comes in from the cold SO NATURE GENETICS LA English DT Editorial Material ID CHROMOSOME 1Q44 AB The pyrin domain was first noted in the familial Mediterranean fever protein from which it takes its name. It belongs to a structural superfamily that includes death domains, death effector domains and caspase activation and recruitment domains. Several genes underlying autoinflammatory diseases have at least one of these four death domain-fold motifs. Mutations in CIAS1, encoding cryopyrin, a leukocyte-specific member of this growing superfamily, have now been shown to cause both familial cold autoinflammatory syndrome and Muckle-Wells syndrome. These new findings add to the growing body of evidence that the dysregulation of leukocyte apoptosis may be a common molecular pathway leading to inflammatory disease. C1 NIAMSD, Bethesda, MD 20892 USA. RP Kastner, DL (reprint author), NIAMSD, Bethesda, MD 20892 USA. NR 15 TC 46 Z9 47 U1 0 U2 2 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 NOV PY 2001 VL 29 IS 3 BP 241 EP 242 DI 10.1038/ng1101-241 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 488AC UT WOS:000171911000002 PM 11687785 ER PT J AU Dorner, T Lipsky, PE AF Dorner, T Lipsky, PE TI Smaller role for pol eta? SO NATURE IMMUNOLOGY LA English DT Letter ID HEAVY-CHAIN GENES C1 Univ Hosp Charite, Dept Med Rheumatol & Clin Immunol, D-10098 Berlin, Germany. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Dorner, T (reprint author), Univ Hosp Charite, Dept Med Rheumatol & Clin Immunol, D-10098 Berlin, Germany. NR 6 TC 6 Z9 6 U1 0 U2 0 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 NOV PY 2001 VL 2 IS 11 BP 982 EP 983 DI 10.1038/ni1101-982 PG 2 WC Immunology SC Immunology GA 490JY UT WOS:000172049800003 PM 11685213 ER PT J AU Rogozin, IB Pavlov, YI Kunkel, TA AF Rogozin, IB Pavlov, YI Kunkel, TA TI Smaller role for pol eta? Response 1 SO NATURE IMMUNOLOGY LA English DT Letter ID GENES C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. Russian Acad Sci, Siberian Branch, Inst Cytol & Genet, Novosibirsk 630090, Russia. Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. RP Kunkel, TA (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. NR 8 TC 4 Z9 4 U1 0 U2 0 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 NOV PY 2001 VL 2 IS 11 BP 983 EP 984 DI 10.1038/ni1101-983 PG 2 WC Immunology SC Immunology GA 490JY UT WOS:000172049800004 ER PT J AU Gearhart, PJ Zeng, XM AF Gearhart, PJ Zeng, XM TI Smaller role for pol eta? Response 2 SO NATURE IMMUNOLOGY LA English DT Letter C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. RP Gearhart, PJ (reprint author), NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. NR 2 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 2001 VL 2 IS 11 BP 984 EP 984 DI 10.1038/ni1101-984 PG 1 WC Immunology SC Immunology GA 490JY UT WOS:000172049800005 ER PT J AU Makrigiannakis, A Zoumakis, E Kalantaridou, S Coutifaris, C Margioris, AN Coukos, G Rice, KC Gravanis, A Chrousos, GP AF Makrigiannakis, A Zoumakis, E Kalantaridou, S Coutifaris, C Margioris, AN Coukos, G Rice, KC Gravanis, A Chrousos, GP TI Corticotropin-releasing hormone promotes blastocyst implantation and early maternal tolerance SO NATURE IMMUNOLOGY LA English DT Article ID ENDOMETRIAL STROMAL CELLS; I RECEPTOR ANTAGONIST; FAS LIGAND; HUMAN-PLACENTA; DEATH FACTOR; EXPRESSION; APOPTOSIS; TROPHOBLAST; CRH; FETAL AB The semi-allograft embryo in the blastocyst stage implants itself in the endometrium, yet no immune rejection processes are activated. Embryonic trophoblast and maternal decidua produce corticotropin-releasing hormone (CRH) and express Fas ligand (FasL), a proapoptotic cytokine. We found that antalarmin, a CRH receptor type I antagonist, decreased FasL expression and promoted apoptosis of activated T lymphocytes, an effect which was potentiated by CRH and inhibited by antalarmin. Female rats treated with antalarmin showed a marked decrease in implantation sites and live embryos and diminished endometrial FasL expression. Embryos from mothers that lacked T cells or from syngeneic matings were not rejected when the mothers were given antalarmin. These findings suggested that locally produced CRH promotes implantation and maintenance of early pregnancy primarily by killing activated T cells. C1 Univ Crete, Sch Med, Iraklion 71110, Greece. Hammersmith Hosp, Imperial Coll Sch Sci & Med, Dept Reprod Med, IVF Unit, London W12, England. Onassis Fdn, Athens, Greece. Univ Penn, Med Ctr, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA. NICHHD, Pediat & Reprod Endocrinol Branch, Bethesda, MD 20892 USA. NIDDKD, Med Chem Lab, Bethesda, MD 20892 USA. RP Makrigiannakis, A (reprint author), Univ Crete, Sch Med, Iraklion 71110, Greece. NR 54 TC 149 Z9 156 U1 1 U2 10 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 NOV PY 2001 VL 2 IS 11 BP 1018 EP 1024 DI 10.1038/ni719 PG 7 WC Immunology SC Immunology GA 490JY UT WOS:000172049800014 PM 11590404 ER PT J AU Chen, XN Scala, G Quinto, I Liu, WM Chun, TW Justement, JS Cohen, OJ vanCott, TC Iwanicki, M Lewis, MG Greenhouse, J Barry, T Venzon, D Fauci, AS AF Chen, XN Scala, G Quinto, I Liu, WM Chun, TW Justement, JS Cohen, OJ vanCott, TC Iwanicki, M Lewis, MG Greenhouse, J Barry, T Venzon, D Fauci, AS TI Protection of rhesus macaques against disease progression from pathogenic SHIV-89.6PD by vaccination with phage-displayed HIV-1 epitopes SO NATURE MEDICINE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; GP120 ENVELOPE GLYCOPROTEIN; RANDOM PEPTIDE LIBRARIES; FILAMENTOUS BACTERIOPHAGE; NEUTRALIZING ANTIBODIES; MONOCLONAL-ANTIBODY; CHIMERIC VIRUS; VIRAL LOAD; IN-VIVO; TYPE-1 AB The antigenic polymorphism of HIV-1 is a major obstacle in developing an effective vaccine. Accordingly, we screened random peptide libraries (RPLs) displayed on phage with antibodies from HIV-infected individuals and identified an array of HIV-specific epitopes that behave as antigenic mimics of conformational epitopes of gp120 and gp41 proteins. We report that the selected epitopes are shared by a collection of HIV-1 isolates of clades A-F. The phage-borne epitopes are immunogenic in rhesus macaques, where they elicit envelope-specific antibody responses. Upon intravenous challenge with 60 MID50 of pathogenic SHIV-89.6PD, all monkeys became infected; however, in contrast to the naive and mock-immunized monkeys, four of five mimotope-immunized monkeys experienced lower levels of peak viremia, followed by viral set points of undetectable or transient levels of viremia and a mild decline of CD4(+) T cells, and were protected from progression to AIDS-like illness. These results provide a new approach to the design of broadly protective HIV-1 vaccines. C1 NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. Univ Catanzaro, Sch Med, Dept Clin & Expt Med, Catanzaro, Italy. Univ Naples Federico II, Sch Med, Dept Biochem & Biomed Technol, Naples, Italy. HM Jackson Fdn, Rockville, MD USA. So Res Inst, Frederick, MD USA. NCI, Hematopathol Sect, NIH, Bethesda, MD 20892 USA. NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA. RP Scala, G (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. RI Venzon, David/B-3078-2008; SCALA, GIUSEPPE/A-3280-2009 FU Telethon [A.045] NR 44 TC 59 Z9 61 U1 0 U2 4 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 NOV PY 2001 VL 7 IS 11 BP 1225 EP 1231 DI 10.1038/nm1101-1225 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 490LV UT WOS:000172054100030 PM 11689887 ER PT J AU Grivel, JC Ito, Y Faga, G Santoro, F Shaheen, F Malnati, MS Fitzgerald, W Lusso, P Margolis, L AF Grivel, JC Ito, Y Faga, G Santoro, F Shaheen, F Malnati, MS Fitzgerald, W Lusso, P Margolis, L TI Suppression of CCR5-but not CXCR4-tropic HIV-1 in lymphoid tissue by human herpesvirus 6 SO NATURE MEDICINE LA English DT Article ID CD4(+) T-CELLS; SYNCYTIUM-INDUCING PHENOTYPE; VIRUS TYPE-1 INFECTION; BETA-CHEMOKINES; BIOLOGICAL PHENOTYPE; CORECEPTOR USAGE; PROGNOSTIC VALUE; CC-CHEMOKINES; IN-VIVO; REPLICATION AB HIV-1 infects target cells via a receptor complex formed by CD4 and a chemokine receptor, primarily CCR5 or CXCR4 (ref. 1). Commonly, HIV-1 transmission is mediated by CCR5-tropic variants, also designated slow/low, non-syncytia-inducer or macrophage-tropic, which dominate the early stages of HIV-1 infection and frequently persist during the entire course of the disease(2-9). In contrast, HIV-1 variants that use CXCR4 are typically detected at the later stages, and are associated with a rapid decline in CD4(+) T cells and progression to AIDS (refs. 2,7-11). Disease progression is also associated with the emergence of concurrent infections that may affect the course of HIV disease by unknown mechanisms. A lymphotropic agent frequently reactivated in HIV-Infected patients is human herpesvirus 6 (HHV-6), which has been proposed as a cofactor in AIDS progression(12). Here we show that in human lymphoid tissue ex vivo(13-15) HHV-6 affects HIV-1 infection in a coreceptor-dependent manner, suppressing CCR5-tropic but not CXCR4-tropic HIV-1 replication, as shown with both uncloned viral isolates and isogenic molecular chimeras. Furthermore, we demonstrate that HHV-6 increases the production of the CCR5 ligand RANTES ('regulated upon activation, normal T-cell expressed and secreted'), the most potent HIV-inhibitory CC chemokine(16), and that exogenous RANTES mimics the effects of HHV-6 on HIV-1, providing a mechanism for the selective blockade of CCR5-tropic HIV-1. Our data suggest that HHV-6 may profoundly influence the course of HIV-1 infection. C1 NICHHD, Lab Cellular & Mol Biophys, Bethesda, MD 20892 USA. DIBIT San Raffaele Sci Inst, Unit Human Virol, Milan, Italy. Univ Bologna, Dept Clin & Expt Med, Bologna, Italy. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. RP Margolis, L (reprint author), NICHHD, Lab Cellular & Mol Biophys, Bethesda, MD 20892 USA. NR 31 TC 81 Z9 83 U1 1 U2 2 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 NOV PY 2001 VL 7 IS 11 BP 1232 EP 1235 DI 10.1038/nm1101-1232 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 490LV UT WOS:000172054100031 PM 11689888 ER PT J AU Yang, F Feng, LY Zheng, F Johnson, SW Du, J Shen, LY Wu, CP Lu, B AF Yang, F Feng, LY Zheng, F Johnson, SW Du, J Shen, LY Wu, CP Lu, B TI GDNF acutely modulates excitability and A-type K+ channels in midbrain dopaminergic neurons SO NATURE NEUROSCIENCE LA English DT Article ID VENTRAL MESENCEPHALIC NEURONS; MICE LACKING GDNF; NEUROTROPHIC FACTOR; NERVOUS-SYSTEM; ELECTROPHYSIOLOGICAL PROPERTIES; SYNAPTIC TRANSMISSION; TYROSINE KINASE; CATION CURRENT; IN-VIVO; RECEPTOR AB Glial cell line-derived neurotrophic factor (GDNF) prevents lesion-induced death of midbrain dopaminergic neurons, but its function in normal brain remains uncertain. Here we show that GDNF acutely and reversibly potentiated the excitability of cultured midbrain neurons by inhibiting transient A-type K+ channels. The effects of GDNF were limited to large, tyrosine hydroxylase (TH)positive dopaminergic neurons, and were mediated by mitogen associated protein (MAP) kinase. Application of GDNF also elicited a MAP kinase-dependent enhancement of the excitability in dopaminergic neurons in midbrain slice. These results demonstrate an acute regulation of GDNF on ion channels and its underlying signaling mechanism, and reveal an unexpected role of GDNF in normal midbrain dopaminergic neurons. C1 NICHHD, Unit Synapse Dev & Plast, LCSN, NIH, Bethesda, MD 20892 USA. Oregon Hlth Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97201 USA. Chinese Acad Sci, Inst Neurosci, Shanghai 200031, Peoples R China. NCI, Lab Carcinogenesis & Tumor Promot, NIH, Bethesda, MD 20892 USA. RP Lu, B (reprint author), NICHHD, Unit Synapse Dev & Plast, LCSN, NIH, Bethesda, MD 20892 USA. RI Yang, Feng/C-9530-2011; Lu, Bai/A-4018-2012; Du, Jing/A-9023-2012 NR 50 TC 94 Z9 96 U1 0 U2 2 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 NOV PY 2001 VL 4 IS 11 BP 1071 EP 1078 DI 10.1038/nn734 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 489AY UT WOS:000171970900009 PM 11593232 ER PT J AU Geiger, B Bershadsky, A Pankov, R Yamada, KM AF Geiger, B Bershadsky, A Pankov, R Yamada, KM TI Transmembrane extracellular matrix-cytoskeleton crosstalk SO NATURE REVIEWS MOLECULAR CELL BIOLOGY LA English DT Review ID FOCAL ADHESION KINASE; FIBRONECTIN TYPE-III; ACTIN STRESS FIBERS; CELL-ADHESION; TYROSINE PHOSPHORYLATION; C-SRC; INTERFERENCE REFLECTION; CULTURED FIBROBLASTS; OSTEOCLAST FUNCTION; SUBSTRATE CONTACT AB Integrin-mediated cell adhesions provide dynamic, bidirectional links between the extracellular matrix and the cytoskeleton. Besides having central roles in cell migration and morphogenesis, focal adhesions and related structures convey information across the cell membrane, to regulate extracellular-matrix assembly, cell proliferation, differentiation, and death. This review describes integrin functions, mechanosensors, molecular switches and signal-transduction pathways activated and integrated by adhesion, with a unifying theme being the importance of local physical forces. C1 Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. Natl Inst Craniofacial & Dent Res, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. RP Geiger, B (reprint author), Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. RI Pankov, Roumen/B-3284-2014; OI Pankov, Roumen/0000-0002-3157-3659; Yamada, Kenneth/0000-0003-1512-6805 NR 118 TC 1321 Z9 1346 U1 22 U2 208 PU NATURE PUBLISHING GROUP PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1471-0072 J9 NAT REV MOL CELL BIO JI Nat. Rev. Mol. Cell Biol. PD NOV PY 2001 VL 2 IS 11 BP 793 EP 805 DI 10.1038/35099066 PG 13 WC Cell Biology SC Cell Biology GA 489RJ UT WOS:000172005200017 PM 11715046 ER PT J AU Beard, WA Wilson, SH AF Beard, WA Wilson, SH TI DNA polymerases lose their grip SO NATURE STRUCTURAL BIOLOGY LA English DT Editorial Material ID REPAIR; BETA AB Structural characterization of a variety of DNA polymerases has likened the polymerase domain to a hand that grasps DNA with functional subdomains referred to as fingers, palm and thumb. The solution structure of the African swine fever virus DNA polymerase X indicates that it does not have a hand-like architecture and suggests a mechanism by which the polymerase may compensate for the lack of a dedicated DNA binding subdomain. C1 NIH, Natl Inst Environm Hlth Sci, Lab Struct Biol, Res Triangle Pk, NC 27709 USA. RP Wilson, SH (reprint author), NIH, Natl Inst Environm Hlth Sci, Lab Struct Biol, POB 12233, Res Triangle Pk, NC 27709 USA. NR 18 TC 10 Z9 11 U1 0 U2 0 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD NOV PY 2001 VL 8 IS 11 BP 915 EP 917 DI 10.1038/nsb1101-915 PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 488AD UT WOS:000171911100004 PM 11685231 ER PT J AU Chou, JJ Li, SP Klee, CB Bax, A AF Chou, JJ Li, SP Klee, CB Bax, A TI Solution structure of Ca2+-calmodulin reveals flexible hand-like properties of its domains SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID LIQUID-CRYSTALLINE PHASE; CALMODULIN-PEPTIDE COMPLEX; CALCIUM-FREE CALMODULIN; X-RAY STRUCTURES; DIPOLAR COUPLINGS; MOLECULAR RECOGNITION; NMR-SPECTROSCOPY; MULTIDIMENSIONAL NMR; PROTEIN-STRUCTURE; RELAXATION-TIMES AB The solution structure of Ca2+-ligated calmodulin is determined from residual dipolar couplings measured in a liquid crystalline medium and from a large number of heteronuclear J couplings for defining side chains. Although the C-terminal domain solution structure is similar to the X-ray crystal structure, the EF hands of the N-terminal domain are considerably less open. The substantial differences in interhelical angles correspond to negligible changes in short interproton distances and, therefore, cannot be identified by comparison of NOEs and X-ray data. NOE analysis, however, excludes a two-state equilibrium in which the closed apo conformation is partially populated in the Ca2+-ligated state. The difference between the crystal and solution structures of Ca2+-calmodulin indicates considerable backbone plasticity within the domains of calmodulin, which is key to their ability to bind a wide range of targets. In contrast, the vast majority of side chains making up the target binding surface are locked into the same chi (1) rotameric states as in complexes with target peptide. C1 NIDDKD, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Bax, A (reprint author), NIDDKD, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. RI Chou, James/N-9840-2013 NR 50 TC 256 Z9 258 U1 0 U2 18 PU NATURE AMERICA INC PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD NOV PY 2001 VL 8 IS 11 BP 990 EP 997 DI 10.1038/nsb1101-990 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 488AD UT WOS:000171911100021 PM 11685248 ER PT J AU Mintzer, MZ Griffiths, RR Contoreggi, C Kimes, AS London, ED Ernst, M AF Mintzer, MZ Griffiths, RR Contoreggi, C Kimes, AS London, ED Ernst, M TI Effects of triazolam on brain activity during episodic memory encoding: A PET study SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE triazolam; benzodiazepines; episodic memory; encoding; positron emission tomography; regional cerebral blood flow ID POSITRON-EMISSION TOMOGRAPHY; MEDIAL TEMPORAL-LOBE; BENZODIAZEPINE RECEPTORS; SUSTAINED ATTENTION; ANTERIOR CINGULATE; INDUCED AMNESIA; FRONTAL-CORTEX; LONG-TERM; ACTIVATION; RETRIEVAL AB It is well documented that acute administration of the benzodiazepine hypnotic drug triazolam (Halcion (R)) impairs episodic memory encoding. We examined the neuroanatomical substrates of this effect in healthy adult volunteers using a double-blind, within-subject design. Following oral capsule administration (0.25 mg/70 kg triazolam or placebo), regional cerebral bloodflow (rCBF) was measured using positron emission tomography (PET) with O-15-H2O during the performance of semantic categorization, orthographic categorization, and visual fixation (resting) tasks. rCBF associated with episodic memory encoding was measured by the difference in rCBF during the orthographic categorization task relative to that during the semantic categorization task. Results in the placebo condition (n = 9) replicated those of previous nonpharmacological encoding studies (activation in the left prefrontal cortex, cerebellum, anterior cingulate cortex, temporal cortex, and occipital cortex). Relative to placebo, results in the triazolam condition (n = 6) revealed significantly impaired memory performance, and deactivation during encoding in a subset of areas shown previously to be associated with encoding (anterior cingulate cortex, cerebellum, and precuneus). Results are discussed in relation to triazolam's effects on mnemonic versus attentional processes. (C) 2001 American College of Neuropsychopharmacology. Published by Elsevier Science Inc. C1 Johns Hopkins Univ, Sch Med, Behav Biol Res Ctr, Dept Psychiat & Behav Sci, Baltimore, MD 21224 USA. Natl Inst Drug Abuse, Intramural Res Program, Baltimore, MD USA. RP Mintzer, MZ (reprint author), Johns Hopkins Univ, Sch Med, Behav Biol Res Ctr, Dept Psychiat & Behav Sci, 5510 Nathan Shock Dr, Baltimore, MD 21224 USA. FU NIDA NIH HHS [DA-11936, DA-03889] NR 73 TC 19 Z9 19 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD NOV PY 2001 VL 25 IS 5 BP 744 EP 756 DI 10.1016/S0893-133X(01)00280-9 PG 13 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 488TR UT WOS:000171952200015 PM 11682258 ER PT J AU Mendelson, WB Basile, AS AF Mendelson, WB Basile, AS TI The hypnotic actions of the fatty acid amide, oleamide SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE oleamide; fatty acids; sleep; hypnotics ID CANNABINOID RECEPTOR; BRAIN LIPIDS; INDUCE SLEEP; PHOSPHORYLATION; MODULATION; ANTAGONIST; BINDING AB Oleamide is an endogenous fatty acid amide which can be synthesized de novo in the mammalian nervous system, and has been detected in human plasma. It accumulates in the CSF of rats after six hours of sleep deprivation and induces sleep in naive rats and mice. Inhibition of the primary catabolic enzyme of oleamide (fatty acid amide hydrolase) by trifluoromethyl-octadecenone reduces sleep latency and increases total sleep time when given centrally to rats and peripherally to mice. While the mechanism of action of oleamide is unclear, it has been demonstrated to increase the amplitude of currents grated by 5-HT2a, 5HT2c and GABAa receptors. Moreover, the action of oleamide most relevant to sleep induction involves, in part, cannabinergic pathways, as evidenced by the ability of the cannabinoid antagonist SR 141716 to inhibit the hypnotic actions of OA. Nonetheless, enhancement of cannabinergic function may not be the only mechanism by which OA alters sleep, as it can act synergistically with subthreshold doses of triazolam (0.125 mug) to reduce sleep latency. These findings raise the possibility that OA may be representative of a group of compounds which might be developed into clinically-used hypnotics, and are discussed in the context of fatty acid derivatives as modulators of neuronal function. (C) 2001 American College of Neuropsychopharmacology. Published by Elsevier Science Inc. C1 Univ Chicago, Dept Psychiat, Sleep Res Lab, Chicago, IL 60637 USA. NIDDK, Bioorgan Chem Lab, Neurosci Grp, NIH, Bethesda, MD 20892 USA. RP Mendelson, WB (reprint author), Univ Chicago, Dept Psychiat, Sleep Res Lab, 5841 S Maryland Ave,MC 3077, Chicago, IL 60637 USA. FU NHLBI NIH HHS [K07 HL03640]; NIA NIH HHS [2PO1 AG 11412-03] NR 27 TC 26 Z9 28 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD NOV PY 2001 VL 25 SU 5 BP S36 EP S39 DI 10.1016/S0893-133X(01)00341-4 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 490RZ UT WOS:000172066000007 PM 11682271 ER PT J AU Vasan, RS Larson, MG Leip, EP Evans, JC O'Donnell, CJ Kannel, WB Levy, D AF Vasan, RS Larson, MG Leip, EP Evans, JC O'Donnell, CJ Kannel, WB Levy, D TI Impact of high-normal blood pressure on the risk of cardiovascular disease. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CORONARY HEART-DISEASE; ISOLATED SYSTOLIC HYPERTENSION; REGRESSION DILUTION; MEN; MORTALITY; WOMEN; RECOMMENDATIONS; METAANALYSIS; POPULATION; PREVENTION AB Background: Information is limited regarding the risk of cardiovascular disease in persons with high-normal blood pressure (systolic pressure of 130 to 139 mm Hg, diastolic pressure of 85 to 89 mm Hg, or both). Methods: We investigated the association between blood-pressure category at base line and the incidence of cardiovascular disease on follow-up among 6859 participants in the Framingham Heart Study who were initially free of hypertension and cardiovascular disease. Results: A stepwise increase in cardiovascular event rates was noted in persons with higher base-line blood-pressure categories. The 10-year cumulative incidence of cardiovascular disease in subjects 35 to 64 years of age who had high-normal blood pressure was 4 percent (95 percent confidence interval, 2 to 5 percent) for women and 8 percent (95 percent confidence interval, 6 to 10 percent) for men; in older subjects (those 65 to 90 years old), the incidence was 18 percent (95 percent confidence interval, 12 to 23 percent) for women and 25 percent (95 percent confidence interval, 17 to 34 percent) for men. As compared with optimal blood pressure, high-normal blood pressure was associated with a risk-factor-adjusted hazard ratio for cardiovascular disease of 2.5 (95 percent confidence interval, 1.6 to 4.1) in women and 1.6 (95 percent confidence interval, 1.1 to 2.2) in men. Conclusions: High-normal blood pressure is associated with an increased risk of cardiovascular disease. Our findings emphasize the need to determine whether lowering high-normal blood pressure can reduce the risk of cardiovascular disease. (N Engl J Med 2001;345:1291-7.) Copyright (C) 2001 Massachusetts Medical Society. C1 Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA. Boston Univ, Sch Med, Cardiol Sect, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Epidemiol & Prevent Med, Boston, MA 02118 USA. Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. NHLBI, Bethesda, MD 20892 USA. RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, 5 Thurber St, Framingham, MA 01702 USA. OI Ramachandran, Vasan/0000-0001-7357-5970 FU NHLBI NIH HHS [K24 HL 04334-01A1, N01-HC-38038] NR 34 TC 950 Z9 1024 U1 3 U2 51 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 1 PY 2001 VL 345 IS 18 BP 1291 EP 1297 DI 10.1056/NEJMoa003417 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 487UX UT WOS:000171896300001 PM 11794147 ER PT J AU Gautier, JF Del Parigi, A Chen, KW Salbe, AD Bandy, D Pratley, RE Ravussin, E Reiman, EM Tataranni, PA AF Gautier, JF Del Parigi, A Chen, KW Salbe, AD Bandy, D Pratley, RE Ravussin, E Reiman, EM Tataranni, PA TI Effect of satiation on brain activity in obese and lean women SO OBESITY RESEARCH LA English DT Article DE brain; functional imaging; positron emission tomography; magnetic resonance imaging; satiation ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; EXPOSURE; AMYGDALA; SATIETY; HUMANS; FOOD AB Objective: To investigate the response of the brains of women to the ingestion of a meal. Research Methods and Procedures: We used measures of regional cerebral blood flow (rCBF), a marker of neuronal activity, by positron emission tomography to describe the functional anatomy of satiation, i.e., the response to a liquid meal in the context of extreme hunger (36-hour fast) in 10 lean (BMI less than or equal to 25 kg/m(2); 32 +/- 10 years old, 61 +/- 7 kg; mean +/- SD) and 12 obese (BMI greater than or equal to 35 kg/m(2); 30 +/- 7 years old, 110 +/- 14 kg) women. Results: In lean and obese women, satiation produced significant increases in rCBF in the vicinity of the prefrontal cortex (p < 0.005). Satiation also produced significant decreases in rCBF in several regions including the thalamus, insular cortex, parahippocampal gyrus, temporal cortex, and cerebellum (in lean and obese women), and hypothalamus, cingulate, nucleus accumbens, and amygdala (in obese women only; all p < 0.005). Compared with lean women, obese women had significantly greater increases in rCBF in the ventral prefrontal cortex and had significantly greater decreases in the paralimbic areas and in areas of the frontal and temporal cortex. Discussion: This study indicates that satiation elicits differential brain responses in obese and lean women. It also lends additional support to the hypothesis that the paralimbic areas participate in a central orexigenic network modulated by the prefrontal cortex through feedback loops. C1 NIDDKD, Clin Diabet & Nutr Sect, NIH, Phoenix, AZ 85016 USA. Hop St Louis, Dept Endocrinol, Paris, France. Good Samaritan Reg Med Ctr, Positron Emiss Tomog Ctr, Phoenix, AZ USA. Pennington Biomed Res Ctr, Baton Rouge, LA USA. Univ Arizona, Dept Psychiat, Tucson, AZ USA. RP Tataranni, PA (reprint author), NIDDKD, Clin Diabet & Nutr Sect, NIH, 4212 N 16Th St, Phoenix, AZ 85016 USA. RI Chen, kewei/P-6304-2015 OI Chen, kewei/0000-0001-8497-3069 NR 21 TC 129 Z9 130 U1 0 U2 4 PU NORTH AMER ASSOC STUDY OBESITY PI ROCHESTER PA C/O DR MICHAEL JENSEN, MAYO MEDICAL CENTER, MAYO CLIN 200 FIRST ST, SW, ROCHESTER, MN 55905 USA SN 1071-7323 J9 OBES RES JI Obes. Res. PD NOV PY 2001 VL 9 IS 11 BP 676 EP 684 DI 10.1038/oby.2001.92 PG 9 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 493ZQ UT WOS:000172253700004 PM 11707534 ER PT J AU Iwao, S Iwao, N Muller, DC Elahi, D Shimokata, H Andres, R AF Iwao, S Iwao, N Muller, DC Elahi, D Shimokata, H Andres, R TI Does waist circumference add to the predictive power of the body mass index for coronary risk? SO OBESITY RESEARCH LA English DT Article DE body mass index; waist circumference; coronary risk factor ID DENSITY-LIPOPROTEIN CHOLESTEROL; ABDOMINAL SAGITTAL DIAMETER; FAT DISTRIBUTION; CARDIOVASCULAR RISK; GLUCOSE-TOLERANCE; COMPUTED-TOMOGRAPHY; BLOOD-PRESSURE; POSTMENOPAUSAL WOMEN; PLASMA-INSULIN; SERUM-LIPIDS AB Objectives: To examine the power of the combined measurements of body mass index (BMI) and waist circumference (WC) for the prediction of abnormality in coronary heart disease risk factors and to determine whether the additional measurement of WC is predictive in older men and women. Research Methods and Procedures. 1190 men and 751 women of the Baltimore Longitudinal Study of Aging were dichotomized into younger (< 65 years) and older (65+ years) age groups. Coronary risk factors in the realms of glucose/insulin metabolism, blood pressure, and plasma lipids were assessed. The relationship of BMI and WC, singly and combined, to 10 risk factors for coronary heart disease was examined. Results: In younger and older men and women, BMI and WC are highly correlated (0.84 to 0.88). BMI and WC are also significantly correlated to all 10 coronary risk factors in younger men and women and to 8 of the 10 in the older men and women. Both partial correlation and logistic regression analyses revealed a modest but significant improvement in the prediction of coronary risk in younger men and women by WC after controlling for the level of BMI. There was no improvement in the older subjects. Discussion: WC adds only modestly to the prediction of coronary risk in younger subjects once BMI is known, and adds nothing to the production of risk in older subjects. C1 NIA, NIH, Baltimore, MD 21224 USA. Massachusetts Gen Hosp, Geriatr Res Lab, Boston, MA 02114 USA. Natl Inst Longev Sci, Longitudinal Study Aging, Nagoya, Aichi, Japan. RP Andres, R (reprint author), NIA, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 51 TC 62 Z9 65 U1 0 U2 1 PU NORTH AMER ASSOC STUDY OBESITY PI ROCHESTER PA C/O DR MICHAEL JENSEN, MAYO MEDICAL CENTER, MAYO CLIN 200 FIRST ST, SW, ROCHESTER, MN 55905 USA SN 1071-7323 J9 OBES RES JI Obes. Res. PD NOV PY 2001 VL 9 IS 11 BP 685 EP 695 DI 10.1038/oby.2001.93 PG 11 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 493ZQ UT WOS:000172253700005 PM 11707535 ER PT J AU Yancey, MK Zhang, J Schwarz, J Dietrich, CS Klebanoff, M AF Yancey, MK Zhang, J Schwarz, J Dietrich, CS Klebanoff, M TI Labor epidural analgesia and intrapartum maternal hyperthermia SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID CESAREAN DELIVERY; RANDOMIZED TRIAL; FEVER; TEMPERATURE; RISK AB OBJECTIVE: To determine if women receiving continuous epidural analgesia are more likely to develop intrapartum. fever and related neonatal effects. METHODS: We conducted a retrospective cohort analysis of nulliparous women with term gestations in spontaneous labor delivered during a 12-month period immediately before the availability of on-demand labor epidural analgesia (Before group) and a similar group of nulliparas delivered after labor epidural analgesia was available on request (After group). RESULTS: The frequency of epidural increased from 1% before the availability of on-request epidural analgesia to 83% after epidural analgesia was available on request. A maximal temperature of at least 100.4F was detected in three of 498 (0.6%) women in the Before group, and in 63 of 572 women (11.0%) in the After group (relative risk [RR] = 18.3, 95% confidence interval [0] 5.8, 57.8, P < .01). Logistic regression analysis demonstrated that on-request labor epidural analgesia was associated with an intrapartum. temperature of at least 99.5F (RR = 3.0, 95% CI 2.3, 3.6, P < .001) and intrapartum. temperature of at least 100.4F (RR = 20.2, 95% CI 7.0, 86.0, P < .001). There were statistically significant increases in the proportion of newborns who had complete blood counts (24% versus 13.5%, RR = 1.5, 95% CI 1.3, 1.8, P < .01) and blood cultures (30.7% versus 8.6%, RR = 1.7, 95% CI 1.2, 2.4, P < .05) in the After period compared with the Before group; however, there was no statistically significant difference in the proportion of infants who received antibiotic therapy for presumed sepsis between the After and Before periods (5.8% versus 4.6%, RR = 1.15, 95% CI 0.8, 1.6, P = .38). No infants in either group had culture-proven sepsis. CONCLUSION: The use of labor epidural analgesia is associated with a clinically significant increase in the incidence of intrapartum fever. (Obstet Gynecol 2001;98:763-70. (C) 2001 by the American College of Obstetricians and Gynecologists). C1 Tripler Army Med Ctr, Dept Obstet & Gynecol, MCHK OB, Honolulu, HI 96859 USA. NICHHD, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. RP Yancey, MK (reprint author), Tripler Army Med Ctr, Dept Obstet & Gynecol, MCHK OB, 1 Jarrett White Rd, Honolulu, HI 96859 USA. FU NICHD NIH HHS [YI-HD-8290] NR 17 TC 35 Z9 36 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD NOV PY 2001 VL 98 IS 5 BP 763 EP 770 DI 10.1016/S0029-7844(01)01537-X PN 1 PG 8 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 488TT UT WOS:000171952400010 PM 11704166 ER PT J AU Rowland, JH Varrucchio, CG Trimble, EL Gore-Langton, RE AF Rowland, JH Varrucchio, CG Trimble, EL Gore-Langton, RE TI Health-related quality of life in cancer prevention clinical trials SO ONCOLOGY-NEW YORK LA English DT Article ID SURGICAL-ADJUVANT-BREAST; BOWEL-PROJECT P-1; OF-LIFE; PROSTATE-CANCER; CHEMOPREVENTION; TAMOXIFEN C1 NCI, Bethesda, MD 20892 USA. RP Rowland, JH (reprint author), NCI, Bethesda, MD 20892 USA. NR 9 TC 2 Z9 2 U1 0 U2 0 PU P R R INC PI MELVILLE PA 48 SOUTH SERVICE RD, MELVILLE, NY 11747 USA SN 0890-9091 J9 ONCOLOGY-NY JI Oncology-NY PD NOV PY 2001 VL 15 IS 11 BP 1455 EP + PG 3 WC Oncology SC Oncology GA 525LF UT WOS:000174071000013 PM 11758873 ER PT J AU Brennan, MT Sankar, V Baccaglini, L Pillemer, SR Kingman, A Nunez, O Young, NS Atkinson, JC AF Brennan, MT Sankar, V Baccaglini, L Pillemer, SR Kingman, A Nunez, O Young, NS Atkinson, JC TI Oral manifestations in patients with aplastic anemia SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Article; Proceedings Paper CT Annual Meeting of the Academy-of-Oral-Medicine CY APR 12, 2000 CL LAS VEGAS, NEVADA SP Acad Oral Med ID GINGIVAL AB Objective. The aim of the present study was to characterize the prevalence and risks of oral complications in aplastic anemia (AA). Study design. Approximately 79 patients with AA (age, 37 +/- 17 years) and 66 control patients with schizophrenia (age, 33 +/- 12 years) were examined. Records were reviewed for demographic, clinical, and radiographic information. Prior medical therapy, laboratory values, disease duration, and medical treatment response were noted for patients with AA. Odds ratios (OR) and 95% Cl were calculated for oral manifestations in cases and in control subjects. Univariate analysis identified important variables for logistic regression. Results. Patients with AA presented more frequently with oral petechiae (OR = 49; 95% Cl, 2.9-825), gingival hyperplasia (OR = 27; 95% Cl, 1.6-463.5), spontaneous gingival bleeding (OR = 27; 95% Cl, 1.6-463.5), and herpetic lesions (OR = 27; 95% Ct, 1.6-463.5). Prior cyclosporine use was associated with gingival hyperplasia (P = .0001). No other predictors for oral manifestations or treatment outcomes were found. Conclusions. Oral soft tissue changes and infections were more common in patients with AA. Prior cyclosporine use was predictive of the presence of gingival hyperplasia. C1 NIDCR, Sjogrens Syndrome Clin, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD USA. NIDCR, Biostat Core, Div Intramural Res, NIH, Bethesda, MD USA. NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. Univ Maryland, Dept Oral Med & Diagnost Sci, Baltimore, MD 21201 USA. RP Brennan, MT (reprint author), Carolinas Med Ctr, Dept Oral Med, 1000 Blythe Blvd,MEB-409, Charlotte, NC 28232 USA. NR 15 TC 13 Z9 15 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD NOV PY 2001 VL 92 IS 5 BP 503 EP 508 DI 10.1067/moe.2001.116506 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 493FJ UT WOS:000172211100010 PM 11709685 ER PT J AU Begley, D Mohiddin, S Fananapazir, L AF Begley, D Mohiddin, S Fananapazir, L TI Dual chamber pacemaker therapy for mid-cavity obstructive hypertrophic cardiomyopathy SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY LA English DT Article DE pacing; hypertrophic cardiomyopathy; mid-cavity obstruction ID OUTFLOW TRACT OBSTRUCTION; MONOMORPHIC VENTRICULAR-TACHYCARDIA; MITRAL-VALVE REPLACEMENT; APICAL ANEURYSM; DOUBLE-BLIND; IMPROVEMENT; MANAGEMENT; CROSSOVER; MYECTOMY; MYOTOMY AB Intracavitary LV obstruction is an important determinant of clinical outcome in hypertrophic cardiomyopathy (HCM). In a minority of patients the obstruction is at the level of the papillary muscles. Mid-cavity obstructive HCM may be associated with a distal LV aneurysm and a worse prognosis. It is often not amenable to standard cardiac surgery for LV out-flow obstruction. The long-term effects (mean follow-up 4.8 +/- 2.9 years) of dual chamber (DDD) pacemaker therapy in 14 patients with mid-cavity obstructive HCM (mean age 34 +/- 16 years, range 15-65 years) were studied. Patients were evaluated by cardiac catheterization at baseline and 6 months to 1 year after receiving DDD pacemakers off all drug therapy. Symptoms were improved in all patients and NYHA functional class reduced from 2.8 +/- 0.1 to 1.9 +/- 0.4 (P < 0.0005), Intracavitary LV pressure gradients was reduced significantly (43 +/- 36 vs 84 +/- 31 mmHg at baseline, P < 0.0005). There was a significant associated reduction in apical LV systolic pressure (152 +/- 37 vs 188 +/- 34 mmHg, P < 0.001). In addition, there was a trend towards increased exercise tolerance (445 +/- 123 vs 396 +/- 165). Cardiac output and LV filling pressures were unchanged. In conclusion, chronic DDD pacing results in significant symptomatic and hemodynamic improvement in this uncommon but important subset of patients with obstructive HCM in whom the role of cardiac surgery is less well defined compared with the more typical outflow tract location of LV obstruction. C1 NHLBI, Inherited Cardiac Dis Sect, NIH, Bethesda, MD 20892 USA. RP Fananapazir, L (reprint author), NHLBI, Inherited Cardiac Dis Sect, NIH, Bldg 10,Rm 7B-14, Bethesda, MD 20892 USA. NR 43 TC 9 Z9 10 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 USA SN 0147-8389 J9 PACE JI PACE-Pacing Clin. Electrophysiol. PD NOV PY 2001 VL 24 IS 11 BP 1639 EP 1644 DI 10.1046/j.1460-9592.2001.01639.x PG 6 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical SC Cardiovascular System & Cardiology; Engineering GA 493JV UT WOS:000172220200009 PM 11816633 ER PT J AU Duncan, R Alvarez, R Jaffe, CL Wiese, M Klutch, M Shakarian, A Dwyer, D Nakhasi, HL AF Duncan, R Alvarez, R Jaffe, CL Wiese, M Klutch, M Shakarian, A Dwyer, D Nakhasi, HL TI Early response gene expression during differentiation of cultured Leishmania donovani SO PARASITOLOGY RESEARCH LA English DT Article ID DEVELOPMENTALLY-REGULATED GENE; HEAT-SHOCK PROTEINS; MAP KINASE KINASE; GLUCOSE-TRANSPORTER; CLONING; AMASTIGOTES; IDENTIFICATION; PROMASTIGOTES; CHAGASI; LIPOPHOSPHOGLYCAN AB The promastigote form of the unicellular parasite, Leishmania donovani, must differentiate into the amastigote form to establish an infection in a mammalian host. Identification of genes whose expression changes during differentiation could help reveal mechanisms of Leishmania gene regulation and identify targets for controlling the diseases caused by this human pathogen. Two genomic clones were isolated, P9 that is more highly expressed in promastigotes than in axenic amastigotes and A14 that is preferentially expressed in axenic amastigotes. Analysis of the DNA sequences revealed open reading frames that would encode 55.5 kDa and 100 kDa proteins, respectively, with no homology to known proteins. The mRNA level for these genes during 24 h time courses of parasite differentiation in culture was compared to two genes known to be differentially expressed, c-lpk2 and mkk. Changes in RNA level occurred within 2 h for each gene and continued in advance of morphological changes. The expression levels of these four genes in axenic amastigotes correlated with results from animal-derived parasites. C1 US FDA, Ctr Biol Evaluat & Res, Lab Bacterial Parasit & Unconvent Agents, Bethesda, MD 20892 USA. US FDA, Lab DNA Viruses, Ctr Biol Evaluat & Res, Bethesda, MD USA. Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Parasitol, IL-91010 Jerusalem, Israel. Max Planck Inst Biol, D-7400 Tubingen, Germany. NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. RP Duncan, R (reprint author), US FDA, Ctr Biol Evaluat & Res, Lab Bacterial Parasit & Unconvent Agents, Bldg 29,Rm 425,HFM 310,8800 Rockville Pk, Bethesda, MD 20892 USA. RI Duncan, Robert/I-8168-2015 OI Duncan, Robert/0000-0001-8409-2501 NR 43 TC 19 Z9 19 U1 0 U2 2 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0932-0113 J9 PARASITOL RES JI Parasitol. Res. PD NOV PY 2001 VL 87 IS 11 BP 897 EP 906 PG 10 WC Parasitology SC Parasitology GA 495VU UT WOS:000172361700002 PM 11728012 ER PT J AU Bradenberg, HK Graham, BS AF Bradenberg, HK Graham, BS TI Hospitalization costs of respiratory syncytial virus infection SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Letter DE respiratory syncytial virus; hospitalization costs C1 Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA. NIH, Vaccine Res Ctr, Bethesda, MD USA. RP Bradenberg, HK (reprint author), Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 2001 VL 20 IS 11 BP 1100 EP 1101 PG 2 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA 492UU UT WOS:000172186600024 ER PT J AU Gafni, RI Weise, M Robrecht, DT Meyers, JL Barnes, KM De-Levi, S Baron, J AF Gafni, RI Weise, M Robrecht, DT Meyers, JL Barnes, KM De-Levi, S Baron, J TI Catch-up growth is associated with delayed senescence of the growth plate in rabbits SO PEDIATRIC RESEARCH LA English DT Article; Proceedings Paper CT Joint Meeting of the Society-Pediatric-Research/Pediatric-Academic-Societies/American-Academy -Pediatrics CY MAY 12-16, 2000 CL BOSTON, MASSACHUSETTS SP Pediat Acad Soc, Soc Pediat Res, Amer Acad Pediat ID BONE-GROWTH; REPLICATIVE SENESCENCE; HORMONE; DEXAMETHASONE; SUPPRESSION; MECHANISMS; RATS; AGES AB In mammals, release from growth-inhibiting conditions results in catch-up growth. To explain this phenomenon, we proposed the following model: 1) The normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of replications that growth plate chondrocytes have undergone. 2) Conditions that suppress growth plate chondrocyte proliferation therefore slow senescence. 3) After transient growth inhibition, growth plates are thus less senescent and hence show a greater growth rate than expected for acre, resulting in catch-up growth. To test this model, we administered dexamethasone to growing rabbits to suppress linear growth. After stopping dexamethasone, catch-Lip growth occurred. In distal femoral growth plates of untreated controls, we observed a senescent decline in the growth rate and in the heights of the proliferative zone, hypertrophic zone, and total growth plate. During the period of catch-up growth, in the animals previously treated with dexamethasone, the senescent decline in all these variables was delayed. Prior treatment with dexamethasone also delayed epiphyseal fusion, These findings support our model that linear catch-up growth is caused, at least in part, by a delay in growth plate senescence. C1 NICHHD, Unit Growth & Dev, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Gafni, RI (reprint author), NICHHD, Unit Growth & Dev, Dev Endocrinol Branch, NIH, Bldg 10,Room 10N262,10 Ctr Dr MSC 1862, Bethesda, MD 20892 USA. NR 27 TC 66 Z9 68 U1 2 U2 6 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 NOV PY 2001 VL 50 IS 5 BP 618 EP 623 DI 10.1203/00006450-200111000-00014 PG 6 WC Pediatrics SC Pediatrics GA 484TY UT WOS:000171706700015 PM 11641457 ER PT J AU Pio, R Martinez, A Cuttitta, F AF Pio, R Martinez, A Cuttitta, F TI Cancer and diabetes: two pathological conditions in which adrenomedullin may be involved SO PEPTIDES LA English DT Article; Proceedings Paper CT 2nd International Conference on Adrenomedullin and PAMP CY NOV, 2000 CL MIYAZAKI, JAPAN DE adrenomedullin; binding protein; cancer; diabetes; embryogenesis; factor H; growth; insulin secretion ID COMPLEMENT FACTOR-H; PROTEIN FACTOR-H; ANGIOGENIC FACTOR ADRENOMEDULLIN; ADRENOCORTICAL CARCINOMA-CELLS; NITRIC-OXIDE SYNTHASE; GENE-RELATED PEPTIDE; SMOOTH-MUSCLE CELLS; INDUCIBLE FACTOR-I; SWISS 3T3 CELLS; PLASMA ADRENOMEDULLIN AB Adrenomedullin (AM) is a regulatory peptide involved in several physiological processes. Among them, AM has been implicated in the regulation of growth, both with mitogenic and antiproliferative activities on normal cells. AM is widely expressed during embryogenesis and may have a significant role in the proliferation and differentiation processes associated with development. AM is also expressed by cancer cell lines and tumors and has been implicated in the growth of malignant cells. Some additional activities associated with AM (antiapoptotic capabilities, angiogenic potential, and upregulation in hypoxic conditions), together with its wide distribution in cancer, suggest that AM may be an important factor in carcinogenesis. Besides its implication in growth, embryogenesis and tumor biology, AM is also involved in pancreatic regulation and diabetes. AM regulates insulin secretion and is overexpressed in the plasma of diabetic patients. Several findings indicate that AM may participate in the pathogenesis and/or clinical complications of this disease. (C) 2001 Elsevier Science Inc. All rights reserved. C1 NCI, Dept Cell & Canc Biol, NIH, Bethesda, MD 20892 USA. Univ Navarra, Sch Med, Dept Biochem, Pamplona 31080, Spain. Univ Navarra, Sch Med, Dept Histol & Pathol, Pamplona 31080, Spain. RP Martinez, A (reprint author), NCI, Dept Cell & Canc Biol, NIH, Bethesda, MD 20892 USA. 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 112 TC 10 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 0196-9781 J9 PEPTIDES JI Peptides PD NOV PY 2001 VL 22 IS 11 BP 1719 EP 1729 DI 10.1016/S0196-9781(01)00530-7 PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA 506YN UT WOS:000172999500004 PM 11754957 ER PT J AU Lan, Q Chow, WH Lissowska, J Hein, DW Buetow, K Engel, LS Ji, BT Zatonski, W Rothman, N AF Lan, Q Chow, WH Lissowska, J Hein, DW Buetow, K Engel, LS Ji, BT Zatonski, W Rothman, N TI Glutathione S-transferase genotypes and stomach cancer in a population-based case-control study in Warsaw, Poland SO PHARMACOGENETICS LA English DT Article ID GENETIC-POLYMORPHISM; HUMAN ERYTHROCYTES; GSTT1 GENOTYPES; ETHYLENE-OXIDE; METHYL-BROMIDE; COLON-CANCER; RISK-FACTORS; LUNG-CANCER; HUMAN BLOOD; SUSCEPTIBILITY AB Glutathione S-transferases are important in the detoxification of a wide range of human carcinogens. Previous studies have shown inconsistent associations between the GSTT1 and GSTM1 null genotypes and stomach cancer risk. We investigated the relationship between these and related genotypes and stomach cancer risk in a population-based case-control study in Warsaw, Poland, where stomach cancer incidence and mortality rates are among the highest in Europe. DNA from blood samples was available for 304 stomach cancer patients and 427 control subjects. We observed a 1.48-fold increased risk for stomach cancer (95% confidence interval 0.97-2.25) in patients with the GSTT1 null genotype but no evidence of increased risk associated with the GSTM1, GSTM3 or GSTP1 genotypes. Furthermore, the stomach cancer risk associated with the GSTT1 null genotype varied by age at diagnosis, with odds ratios of 3.85, 1.91, 1.78 and 0.59 for those diagnosed at ages less than 50, 50-59, 60-69 and 70 years or older, respectively (P trend = 0.01). This was due to a shift in the GSTT1 genotype distribution across age groups among stomach cancer patients only. These results suggest that the GSTT1 null genotype may be associated with increased risk of stomach cancer. Pharmacogenetics 11:655-661 (C) 2001 Lippincott Williams & Wilkins. C1 NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Ctr Canc, Div Canc Epidemiol & Prevent, Warsaw, Poland. M Sklodowska Curie Inst Oncol, Warsaw, Poland. Univ Louisville, Sch Med, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA. RP Lan, Q (reprint author), NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, MSC 7240,6120 Execut Blvd,EPS 8109, Bethesda, MD 20892 USA. RI Hein, David/A-9707-2008; OI Lissowska, Jolanta/0000-0003-2695-5799 FU NCI NIH HHS [CA-34627, R01 CA034627, R01 CA034627-16] NR 35 TC 48 Z9 50 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD NOV PY 2001 VL 11 IS 8 BP 655 EP 661 DI 10.1097/00008571-200111000-00003 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA 493TY UT WOS:000172240600003 PM 11692073 ER PT J AU McGriff, NJ Csako, G Kabbani, M Diep, L Chrousos, GP Pucino, F AF McGriff, NJ Csako, G Kabbani, M Diep, L Chrousos, GP Pucino, F TI Treatment options for a patient experiencing pruritic rash associated with transdermal testosterone: A review of the literature SO PHARMACOTHERAPY LA English DT Article ID PROSTATE-SPECIFIC ANTIGEN; ALLERGIC CONTACT-DERMATITIS; CLINICAL RESEARCH-CENTER; ANDROGEN REPLACEMENT THERAPY; HYPOGONADAL MEN; HEALTHY-MEN; PHARMACOKINETICS; 7-ALPHA-METHYL-19-NORTESTOSTERONE; PHARMACODYNAMICS; IMPLANTS AB A 22-year-old man with hypogonadotropic hypogonadism was receiving monthly intramuscular injections of testosterone replacement therapy The patient refused to self-administer the injections because of discomfort, so the therapy was switched to testosterone patches. He experienced a pruritic, macular, erythematous rash underneath the reservoir area of two different transdermal formulations, which did not improve after pretreatment with topical corticosteroids. Eventually, he tolerated application of a testosterone gel and his serum testosterone levels returned to normal after 1 month of therapy. Commercially available and investigational testosterone products and therapeutic monitoring guidelines for androgen replacement are reviewed. C1 NIH, Warren G Magnuson Clin Ctr, Dept Pharm, Bethesda, MD 20892 USA. NIH, Warren G Magnuson Clin Ctr, Dept Lab Med, Bethesda, MD 20892 USA. NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. USN, Natl Med Ctr, Bethesda, MD 20084 USA. RP McGriff, NJ (reprint author), Univ Sci Philadelphia, Dept Pharm Practice & Adm, 600 S 43rd St,Box 8, Philadelphia, PA 19104 USA. NR 62 TC 7 Z9 7 U1 0 U2 1 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD NOV PY 2001 VL 21 IS 11 BP 1425 EP 1435 DI 10.1592/phco.21.17.1425.34428 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 490AR UT WOS:000172027000016 PM 11714217 ER PT J AU Pandeya, SN Sriram, D Yogeeswari, P Stables, JP AF Pandeya, SN Sriram, D Yogeeswari, P Stables, JP TI Anticonvulsant and neurotoxicity evaluation of 5-(un)-substituted isatinimino derivatives SO PHARMAZIE LA English DT Article ID ANTIEPILEPTIC DRUG DEVELOPMENT; MANNICH-BASES; SCHIFF; SEMICARBAZONES; ANTIBACTERIAL; ANTIFUNGAL AB Various Schiff bases were prepared by reacting 5-(un)-substituted isatin with some heterocyclic compounds, viz., N-[4-(4'-chloropherlyl-thiazol-2-yl] semicarbazide, 3-amino-2-methylmercaptoquinazolin-4-one, 3-(4'-pylidyl)-4-amino-5-mercapto-4(H)-1,2,4-triazole and 4-(4'-chlorophenyl)-6-(4"-methylphenyl)-2-aminopyrimidine. The compounds were evaluated for anticonvulsant and neurotoxic properties. The compound 3-(3',4'-dihydro-2'-methylmercapto-4'-oxoquinazolin-3'-yl) iminoisatin (3) emerged as the most active analogue showing anti-MES and anti-PTZ activities better than valproic acid. All the compounds showed lower neurotoxicity than phenytoin and carbamazepine. C1 Banaras Hindu Univ, Inst Technol, Dept Pharmaceut, Varanasi 221005, Uttar Pradesh, India. Birla Inst Technol & Sci, Pharm Grp, Pilani, Rajasthan, India. NIH, Preclin Pharmacol Sect, Epilepsy Branch, Bethesda, MD 20892 USA. RP Pandeya, SN (reprint author), Banaras Hindu Univ, Inst Technol, Dept Pharmaceut, Varanasi 221005, Uttar Pradesh, India. NR 14 TC 10 Z9 12 U1 0 U2 1 PU GOVI-VERLAG GMBH PI ESCHBORN PA PHARMAZEUTISCHER VERLAG GINNHEIMER STRASSE 26, D-65760 ESCHBORN, GERMANY SN 0031-7144 J9 PHARMAZIE JI Pharmazie PD NOV PY 2001 VL 56 IS 11 BP 875 EP 876 PG 2 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA 494NG UT WOS:000172288300010 PM 11817174 ER PT J AU Allen, JP Reinert, DF Volk, RJ AF Allen, JP Reinert, DF Volk, RJ TI The alcohol use disorders identification test: An aid to recognition of alcohol problems in primary care patients SO PREVENTIVE MEDICINE LA English DT Article DE alcohol screening; Alcohol Use Disorders Identification Test AUDIT; brief intervention in primary care ID SCREENING INSTRUMENTS; TEST AUDIT; EMERGENCY ROOM; PROBLEM DRINKING; CONSUMPTION QUESTIONS; BRIEF INTERVENTIONS; CUT POINTS; PERFORMANCE; VALIDITY; CAGE AB Background. Misuse of alcohol is associated with a range of medical problems. Fortunately, a simple pencil-and-paper measure, the Alcohol Use Disorders Identification Test, can effectively and efficiently screen for early-stage alcohol abuse as well as provide the physician information that can assist in brief intervention. Objective. The objective of this article is to briefly summarize research published on the Alcohol Use Disorders Identification Test and suggest its potential role in brief intervention in primary care settings. Methods. Scientific literature on the Alcohol Use Disorders Identification Test though 2000 was reviewed and synthesized to address issues relevant to use of the test in primary health care settings. Results. The Alcohol Use Disorders Identification Test is quite sensitive and specific and compares favorably with alternative self-report screens for alcohol problems. (C) 2001 American Health Foundation and Academic Press. C1 NIAAA, Rockville, MD 20892 USA. Concept Seminary Coll, Conception, MO USA. Baylor Coll Med, Houston, TX 77030 USA. RP Allen, JP (reprint author), NIAAA, Willco Bldg,Suite 505,6000 Execut Blvd,MSC 7003, Bethesda, MD 20892 USA. OI Reinert, Duane/0000-0002-5292-4382; Volk, Robert/0000-0001-8811-5854 FU NIAAA NIH HHS [N01AA81015] NR 39 TC 42 Z9 43 U1 1 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-7435 J9 PREV MED JI Prev. Med. PD NOV PY 2001 VL 33 IS 5 BP 428 EP 433 DI 10.1006/pmed.2001.0910 PG 6 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 490XG UT WOS:000172078500012 PM 11676584 ER PT J AU de Smet, MD Chan, CC AF de Smet, MD Chan, CC TI Regulation of ocular inflammation - what experimental and human studies have taught us SO PROGRESS IN RETINAL AND EYE RESEARCH LA English DT Review ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; ENDOTOXIN-INDUCED UVEITIS; RETINAL-S-ANTIGEN; KOYANAGI-HARADA-DISEASE; MYELIN BASIC-PROTEIN; TUMOR-NECROSIS-FACTOR; HEAT-SHOCK-PROTEIN; CELLULAR IMMUNE-RESPONSES; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; INDUCED GRANULOMATOUS ENDOPHTHALMITIS AB Study of models of ocular autoimmunity and of autoimmune uveitis in humans has lead to a shift in the perceived nature of immune privilege from one based on anatomical isolation oft lie eye to a more dynamic, active process of immune tolerance. Using a variety of available models, the basis for this dynamic process of immune regulation is reviewed. The protective role of humoral immunity, the co-stimulatory function of B cells in EAU as well as the influence of cytokines within the inflammatory cascade are outlined. Modulation of the immune response and in particular the possible role of macrophages is explored. Within the current paradyme, a major effector cell is the CD4+ lymphocyte. Its maturation into a Th1 or Th2 phenotype process appears dependent on a number of exogenous factors, which while genetically determined can be manipulated prior to disease onset, Activation of CD4+ cells is dependent on presentation of immunoreactive peptide fragments, These fragments are well characterized in the Lewis rat for S-Ag and interphotoreceptor retinoid binding protein (IRBP). Mapping of the immunoreactivity to S-Ag has been recently completed in uveitis patients. An overlap with certain determinants identified in experimental models has been observed, in at least 2 disease entities. However, the response profile is not Fixed in time and is subject to determinant spread. Future studies will be aimed at identifying with more detail immunologic triggers of inflammation in patients. and at better defining the interplay between effector and regulatory pathways both in the eye and in the systemic circulation. Published by Elsevier Science Ltd. C1 Univ Amsterdam, Dept Ophthalmol, Amsterdam, Netherlands. NEI, Immunopathol Lab, Bethesda, MD 20892 USA. RP de Smet, MD (reprint author), Univ Amsterdam, Dept Ophthalmol, Kruislaan 403, Amsterdam, Netherlands. EM m.d.desmet@amc.uva.nl OI de Smet, Marc/0000-0002-9217-5603 NR 373 TC 61 Z9 62 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1350-9462 J9 PROG RETIN EYE RES JI Prog. Retin. Eye Res. PD NOV PY 2001 VL 20 IS 6 BP 761 EP 797 DI 10.1016/S1350-9462(01)00011-8 PG 37 WC Ophthalmology SC Ophthalmology GA 485WH UT WOS:000171786100003 PM 11587917 ER PT J AU Oriji, GK Schanz, N AF Oriji, GK Schanz, N TI Nitric oxide in CsA-induced hypertension: role of beta-adrenoceptor antagonist and thromboxane A(2) SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID A-INDUCED HYPERTENSION; PERFUSED RAT KIDNEYS; HIGH-SODIUM DIET; CYCLOSPORINE-A; NEPHROTOXICITY; PROPRANOLOL; INHIBITION; TERTATOLOL AB Cyclosporine A (CsA) is an immunosuppressive agent, which also causes hypertension. The effect of CsA on vascular responses was determined in Sprague-Dawley rats and rat aortic rings. Male rats weighing 250-300 g were given either CsA (25 mg/kg/day) in olive oil or vehicle by intraperitoneal (ip) injection for 7 days. CsA administration produced a 42% increase (P < 0.001) in mean arterial pressure (MAP) which reached a plateau after 3 days. The level of both nitrate/nitrite (NO2/NO3), metabolites of nitric oxide (NO), decreased by 50% (P < 0.001), but the level of thromboxane A(2).(TBXA(2)) increased by 75% (P < 0.001), in the urine. When 10(-9) M of CsA was added acutely to intact aortic rings from untreated rats, NO2/NO3 production decreased by 83% (P < 0.011), but TBXA(2). production increased by 86% (P < 0.001). The effects of CsA were reversed both in vivo and in vitro by pretreatment with propranolol (15 mg/kg/day ip), beta-adrenoceptor antagonist. There were no changes in MAP and tension in rats treated with prop alone. In addition, in aorta of rats that were treated with CsA ip for 7 days, CsA significantly activated protein kinase C (PKC) translocation. This suggests that PKC mediate, in part, CsA-induced hypertension. In summary, CsA inhibits endothelial NO formation, activate PKC, and increase TBXA(2) production, with resulting increase in MAP, and this changes can be overcome by pretreatment with propranolol. (C) 2001 Harcourt Publishers Ltd. C1 William Paterson Univ, Coll Sci & Hlth, Dept Biol, Lab Hypertens Res, Wayne, NJ 07470 USA. NHLBI, Hypertens Endocrine Branch, NIH, Bethesda, MD 20892 USA. RP Oriji, GK (reprint author), William Paterson Univ, Coll Sci & Hlth, Dept Biol, Lab Hypertens Res, Wayne, NJ 07470 USA. NR 20 TC 10 Z9 10 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 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD NOV-DEC PY 2001 VL 65 IS 5-6 BP 259 EP 263 DI 10.1054/plef.2001.0323 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 534HE UT WOS:000174578400005 PM 11993718 ER PT J AU Neumeister, A Willeit, M Praschak-Rieder, N Asenbaum, S Stastny, J Hilger, E Pirker, W Konstantinidis, A Kasper, S AF Neumeister, A Willeit, M Praschak-Rieder, N Asenbaum, S Stastny, J Hilger, E Pirker, W Konstantinidis, A Kasper, S TI Dopamine transporter availability in symptomatic depressed patients with seasonal affective disorder and healthy controls SO PSYCHOLOGICAL MEDICINE LA English DT Article; Proceedings Paper CT Annual Meeting of the Society-for-Light-Treatment-and-Biological-Rhythms CY MAY 08, 1998 CL AMELIA ISLAND, FLORIDA SP Soc Light Treatment & Biol Rhythms ID I-123 BETA-CIT; EMISSION COMPUTED-TOMOGRAPHY; RAPID TRYPTOPHAN DEPLETION; H-3 PAROXETINE BINDING; SEROTONIN UPTAKE SITES; HUMAN-BRAIN; LIGHT THERAPY; META-CHLOROPHENYLPIPERAZINE; BEHAVIORAL-RESPONSES; MAJOR DEPRESSION AB Background. During recent years hypotheses about the pathophysiology of seasonal affective disorder/winter type (SAD) have focused monoaminergic mechanisms. There is substantial evidence that serotonergic systems play an important role. The potential role of catecholaminergic pathways has not been fully explored. Methods. Eleven drug-free, symptomatic depressed patients with SAD and 11 healthy age- and gender-matched healthy controls were invited to participate in a I-123 beta -CIT single photon emission computed tomography (SPECT) study to assess striatal density of dopamine transporters (DATs). The cerebellum was used as reference region. Ratios were calculated between mean counts in left and right striatum and cerebellum. These ratios minus 1 represent specific/non-displaceable binding and are assumed to be directly related to DAT availability at the time of binding equilibrium. Results. Displaceable I-123 beta -CIT binding in the area corresponding to the left striatum was significantly reduced in SAD patients compared to healthy controls (10(.)49 +/-0(.)91 v. 11(.)95 +/-1(.)54, respectively; 2-tailed P = 0(.)017, Mann-Whitney U test). Conclusions. These data suggest reductions in the availability of striatal DAT binding sites in untreated symptomatic depressed SAD patients. It remains unclear whether these reductions represent a primary defect or an attempt to overcome a state of possible lowered dopamine availability in the synaptic cleft during a depressive episode of SAD. However, these findings provide evidence that brain dopaminergic systems may be involved in the pathophysiology of SAD. C1 Univ Vienna, Dept Neurol, Vienna, Austria. Univ Vienna, Dept Gen Psychiat, Vienna, Austria. RP Neumeister, A (reprint author), NIMH, Mood & Anxiety Disorders Program, 9000 Rockville Pike,Bldg 1-B3-10, Bethesda, MD 20892 USA. NR 39 TC 60 Z9 60 U1 2 U2 3 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD NOV PY 2001 VL 31 IS 8 BP 1467 EP 1473 PG 7 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 494HL UT WOS:000172276000013 PM 11722161 ER PT J AU Epstein, SA Gonzales, JJ Weinfurt, K Boekeloo, B Yuan, N Chase, G AF Epstein, SA Gonzales, JJ Weinfurt, K Boekeloo, B Yuan, N Chase, G TI Are psychiatrists' characteristics related to how they care for depression in the medically ill? Results from a national case-vignette survey SO PSYCHOSOMATICS LA English DT Article ID PRACTICE PATTERNS; PHARMACOTHERAPY; QUALITY AB The authors' goal was to examine the relationship between psychiatrists' characteristics and their decisions regarding depression care. A national sampling of 278 psychiatrists answered diagnosis and treatment questions for one of four case vignettes with depression and various degrees of medical comorbidity They also responded to a questionnaire assessing practice and demographic characteristics. Tendency to diagnose major depression was significantly associated with being board certified, being in practice for less time, having a greater percentage of patients with managed care, and having a greater percentage of patients on psychotropic medications. Tendency to recommend an antidepressant was significantly associated with the psychiatrist being male, being less satisfied with practice, and having a greater percentage of patients on psychotropic medications. These findings remained significant even after controlling for case characteristics. Diagnostic and prescribing tendencies of psychiatrists appear to be associated with specific physician characteristics and not simply case characteristics. These findings have implications for further studies of predictors of quality of care. C1 Georgetown Univ, Med Ctr, Dept Psychiat, Washington, DC 20007 USA. NIMH, Bethesda, MD 20892 USA. Duke Univ, Ctr Med, Durham, NC USA. Univ Maryland, College Pk, MD USA. Bowling Green State Univ, Bowling Green, OH USA. Henry Ford Hlth Sci Ctr, Detroit, MI USA. RP Epstein, SA (reprint author), Georgetown Univ, Med Ctr, Dept Psychiat, 3800 Reservoir Rd NW, Washington, DC 20007 USA. NR 23 TC 22 Z9 22 U1 0 U2 0 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 2001 VL 42 IS 6 BP 482 EP 489 DI 10.1176/appi.psy.42.6.482 PG 8 WC Psychiatry; Psychology SC Psychiatry; Psychology GA 513HD UT WOS:000173371400005 PM 11815683 ER PT J AU Kirschstein, RL Ruffin, J AF Kirschstein, RL Ruffin, J TI A call to action SO PUBLIC HEALTH REPORTS LA English DT Editorial Material C1 NIH, Natl Ctr Minor Hlth & Hlth Dispar, Bethesda, MD 20892 USA. RP Kirschstein, RL (reprint author), NIH, Natl Ctr Minor Hlth & Hlth Dispar, 1 Ctr Dr,MS-CO148,Bldg 1,Rm 126, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPERINTENDENT DOCUMENTS,, WASHINGTON, DC 20402-9325 USA SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD NOV-DEC PY 2001 VL 116 IS 6 BP 515 EP 516 DI 10.1093/phr/116.6.515 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 586VR UT WOS:000177607300003 PM 12196609 ER PT J AU Taylor, KL Turner, RO Davis, JL Johnson, L Schwartz, MD Kerner, J Leak, C AF Taylor, KL Turner, RO Davis, JL Johnson, L Schwartz, MD Kerner, J Leak, C TI Improving knowledge of the prostate cancer screening dilemma among African American men: An academic-community partnership in Washington, DC SO PUBLIC HEALTH REPORTS LA English DT Article ID DIGITAL RECTAL EXAMINATION; DECISION; ANTIGEN; MAMMOGRAPHY; BELIEFS; TESTS; TRIAL AB Objective. Studies have shown that African American men are at greater risk than other men for prostate cancer in terms of both incidence and mortality. At the same time, the utility of screening asymptomatic men for prostate cancer remains controversial. The combination of high incidence and high mortality with the uncertain benefits of screening poses a difficult problem for African American men. This study was part of an ongoing project that sought to develop and evaluate health education materials designed to help African American men make an informed decision about prostate cancer screening. The project represented a collaboration between the Most Worshipful Prince Hall Grand Lodge of the District of Columbia and the Lombardi Cancer Center of Georgetown University. Methods. The authors conducted eight focus groups with 44 members of the Prince Hall Masons. The focus groups covered men's understanding of prostate cancer screening and their preferences for methods of health education. Results. Participants demonstrated a high level of awareness of the availability of prostate cancer screening, a low awareness of the screening controversy, and a desire for detailed epidemiologic information and information about the benefits and limitations of screening. The preferred forms of educational materials were video and print-based materials, which the research team has recently developed. Conclusions. These findings demonstrate the feasibility of developing an academic-community collaboration with the goal of improving a health-related problem in the African American community. A randomized trial is underway to evaluate the impact of the video and print education materials. C1 Georgetown Univ, Div Canc Control, Med Ctr, Canc Control Program,Lombardi Canc Ctr, Washington, DC 20007 USA. Partners Community Hlth, PLLC, S Riding, VA USA. NCI, Div Canc Control & Populat Sci, Washington, DC USA. RP Taylor, KL (reprint author), Georgetown Univ, Div Canc Control, Med Ctr, Canc Control Program,Lombardi Canc Ctr, 2233 Wisconsin Ave NW,Ste 317, Washington, DC 20007 USA. NR 46 TC 28 Z9 28 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPERINTENDENT DOCUMENTS,, WASHINGTON, DC 20402-9325 USA SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD NOV-DEC PY 2001 VL 116 IS 6 BP 590 EP 598 DI 10.1016/S0033-3549(04)50092-4 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 586VR UT WOS:000177607300013 PM 12196619 ER PT J AU Harris, RK Becker, ED De Menezes, SMC Goodfellow, R Granger, P AF Harris, RK Becker, ED De Menezes, SMC Goodfellow, R Granger, P TI NMR nomenclature. Nuclear spin properties and conventions for chemical shifts - (IUPAC recommendations 2001) SO PURE AND APPLIED CHEMISTRY LA English DT Article ID SOLID-STATE NMR; MAGNETIC-RESONANCE SPECTROSCOPY; FOURIER-TRANSFORM NMR; ORGANOMETALLIC COMPOUNDS; TEMPERATURE-DEPENDENCE; QUADRUPOLE MOMENTS; C-13; PROTON; STANDARDS; ION AB A unified scale is recommended for reporting the NMR chemical shifts of till nuclei relative to the (1)H resonance of tetramethylsilane (TMS). The unified scale is designed to provide a precise ratio, Xi, of the resonance frequency of a given nuclide to that of the primary reference, the (1)H resonance of TMS in dilute solution (volume fraction, phi < 1%) in chloroform. Referencing procedures are discussed, including matters of practical application of the unified scale. Special attention is paid to recommended reference samples, and values of Xi for secondary references on the unified scale are listed, many of which are the results of new measurements. Some earlier recommendations relating to the reporting of chemical shifts are endorsed. The chemical shift, delta, is redefined to avoid previous ambiguities but to leave practical usage unchanged. Relations between the unified scale and recently published recommendations for referencing in aqueous solutions (for specific use in biochemical work) are discussed, as well as the special effects of working in the solid state with magic-angle spinning. In all, nine new recommendations relating to chemical shifts are made. Standardized nuclear spin data are also presented in tabular form for the stable (and some unstable) isotopes of all elements with nonzero quantum numbers. The information given includes quantum numbers, isotopic abundances, magnetic moments, magnetogyric ratios and receptivities, together with quadrupole moments and line-width factors where appropriate. C1 Univ Durham, Dept Chem, Durham DH1 3LE, England. NIH, Bethesda, MD 20892 USA. Ilha Fundao, QUIMICA, CENPES, PETROBRAS, BR-21949900 Rio De Janeiro, RJ, Brazil. Univ Bristol, Sch Chem, Bristol BS8 1TS, Avon, England. Univ Strasbourg 1, Inst Chim, F-67008 Strasbourg, France. RP Harris, RK (reprint author), Univ Durham, Dept Chem, South Rd, Durham DH1 3LE, England. NR 75 TC 544 Z9 548 U1 5 U2 64 PU INT UNION PURE APPLIED CHEMISTRY PI RES TRIANGLE PK PA 104 TW ALEXANDER DR, PO BOX 13757, RES TRIANGLE PK, NC 27709-3757 USA SN 0033-4545 J9 PURE APPL CHEM JI Pure Appl. Chem. PD NOV PY 2001 VL 73 IS 11 BP 1795 EP 1818 DI 10.1351/pac200173111795 PG 24 WC Chemistry, Multidisciplinary SC Chemistry GA 524FY UT WOS:000174003500010 ER PT J AU Costes, S Sachs, R Hlatky, L Vannais, D Waldren, C Fouladi, B AF Costes, S Sachs, R Hlatky, L Vannais, D Waldren, C Fouladi, B TI Large-mutation spectra induced at hemizygous loci by low-LET radiation: Evidence for intrachromosomal proximity effects SO RADIATION RESEARCH LA English DT Article ID CHINESE-HAMSTER CELLS; RAY-INDUCED MUTATIONS; DOUBLE-STRAND BREAKS; HUMAN HPRT GENE; IONIZING-RADIATION; CHROMOSOME-ABERRATIONS; ANCHOR SYNTHESIS; MAMMALIAN-CELLS; LARGE DELETIONS; DOSE-RESPONSE AB A mathematical model is used to analyze mutant spectra for large mutations induced by low-LET radiation. The model equations are based mainly on two-break misrejoining that leads to deletions or translocations. It is assumed, as a working hypothesis, that the initial damage induced by low-LET radiation is located randomly in the genome. Specifically, we analyzed data for two hemizygous loci: CD59(-) mutants, mainly very large-scale deletions (>3 Mbp), in human-hamster hybrid cells, and data from the literature on those HPRT-mutants which involve at least deletion of the whole gene, and often of additional flanking markers (similar to 50-kbp to similar to4.4-Mbp deletions). For five data sets, we estimated f, the probability that two given breaks on the same chromosome will misrejoin to make a deletion, as a function of the separation between the breaks. We found that f is larger for nearby breaks than for breaks that are more widely separated; i.e., there is a "proximity effect". For acute irradiation, the values off determined from the data are consistent with the corresponding break misrejoining parameters found previously in quantitative modeling of chromosome aberrations. The value off was somewhat smaller for protracted irradiation than for acute irradiation at a given total dose; i.e., the mutation data show a decrease that was smaller than expected for dose protraction by fractionation or low dose rate. (C) 2001 by Radiation Research Society. C1 Univ Calif Berkeley, Dept Math, Berkeley, CA 94720 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Colorado State Univ, Radiol Hlth Sci MRB, Ft Collins, CO 80523 USA. RP Costes, S (reprint author), NCI, Bldg 538, Frederick, MD 21702 USA. RI Costes, Sylvain/D-2522-2013 OI Costes, Sylvain/0000-0002-8542-2389 FU NCI NIH HHS [CA 36447, CA 86823, 5T32 CA 09236]; NIGMS NIH HHS [GM 57245] NR 47 TC 11 Z9 11 U1 0 U2 0 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 NOV PY 2001 VL 156 IS 5 BP 545 EP 557 DI 10.1667/0033-7587(2001)156[0545:LMSIAH]2.0.CO;2 PN 1 PG 13 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA 489NZ UT WOS:000171999000012 PM 11604068 ER PT J AU Amundson, SA Bittner, M Meltzer, P Trent, J Fornace, AJ AF Amundson, SA Bittner, M Meltzer, P Trent, J Fornace, AJ TI Induction of gene expression as a monitor of exposure to ionizing radiation SO RADIATION RESEARCH LA English DT Article ID ANTICANCER DRUG SCREEN; TUMOR-CELL LINES; MOLECULAR PHARMACOLOGY; GENOTOXIC STRESS; CDNA MICROARRAY; DIVERSE PANEL; HUMAN CANCER; MECHANISM; AGENTS; DNA AB The complex molecular responses to genotoxic stress are mediated by a variety of regulatory pathways. The transcription factor TP53 plays a central role in the cellular response to DNA-damaging agents such as ionizing radiation, but other pathways also play important roles. In addition, differences in radiation quality, such as the exposure to high-LET radiation that occurs during space travel, may influence the pattern of responses. The premise is developed that stress gene responses can be employed as molecular markers for radiation exposure using a combination of informatics and functional genomics approaches. Published studies from our laboratory have already demonstrated such transcriptional responses with doses of gamma rays as low as 2 cGy, and in peripheral blood lymphocytes (PBLs) irradiated ex vivo with doses as low as 20 cGy. We have also found several genes elevated in vivo 24 h after whole-body irradiation of mice with 20 cGy. Such studies should provide insight into the molecular responses to physiologically relevant doses, which cannot necessarily be extrapolated from high-dose studies. In addition, ongoing experiments are identifying large numbers of potential biomarkers using microarray hybridization and various irradiation protocols including expression at different times after exposure to low- and high-LET radiation. Computation-intensive informatics analysis methods are also being developed for management of the complex gene expression profiles resulting from these experiments. With further development of these approaches, it may be feasible to monitor changes in gene expression after low-dose radiation exposure and other physiological stresses that may be encountered during manned space flight, such as the planned mission to Mars. (C) 2001 by Radiation Research Society. C1 NCI, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NHGRI, Bethesda, MD 20892 USA. RP Amundson, SA (reprint author), NCI, Div Basic Sci, NIH, 37 Convent Dr,Bldg 37,Rm 5C09, Bethesda, MD 20892 USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 33 TC 106 Z9 117 U1 2 U2 10 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 NOV PY 2001 VL 156 IS 5 BP 657 EP 661 DI 10.1667/0033-7587(2001)156[0657:IOGEAA]2.0.CO;2 PN 2 PG 5 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA 489PB UT WOS:000171999200016 PM 11604088 ER PT J AU De Angelis, G Caldora, M Santaquilani, M Scipione, R Verdecchia, A AF De Angelis, G Caldora, M Santaquilani, M Scipione, R Verdecchia, A TI Health risks from radiation exposure for civilian aviation flight personnel: A study of Italian airline crew members SO RADIATION RESEARCH LA English DT Article ID CANCER INCIDENCE; CABIN ATTENDANTS; PILOTS; MORTALITY; METAANALYSIS; COHORT; FIELDS AB A study of the effects of exposures of civilian aviation flight personnel to atmospheric ionizing radiation (including high-energy neutrons) is being performed. The results of previous studies and of the criteria required for a more satisfactory outcome in future studies are presented, along with a description of the protocol for the Italian national study. A description of the cohort is given in terms of its size, composition and member eligibility. The various ways of determining the exposure and the health status of past and current aircrew members are discussed, and follow-up procedures are described. An overview of the data management and processing philosophy adopted in the Italian study is given with regard to flight routes, radiation dose evaluation along the flight paths, and construction of exposure matrices. Other studies of potential interest are also discussed. The study is still in progress, so the results are preliminary. (C) 2001 by Radiation Research Society. C1 Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy. NASA, Langley Res Ctr, Hampton, VA 23665 USA. NCI, DCCPS, NIH, Bethesda, MD 20892 USA. RP De Angelis, G (reprint author), Ist Super Sanita, Epidemiol & Biostat Lab, Viale Regina Elena 299,LEB Bldg 19, I-00161 Rome, Italy. RI Santaquilani, Mariano/K-4433-2016 OI Santaquilani, Mariano/0000-0002-9123-654X NR 54 TC 7 Z9 8 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 NOV PY 2001 VL 156 IS 5 BP 689 EP 694 PN 2 PG 6 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA 489PB UT WOS:000171999200022 PM 11604094 ER PT J AU Avila, NA Bechtle, J Dwyer, AJ Ferrans, VJ Moss, J AF Avila, NA Bechtle, J Dwyer, AJ Ferrans, VJ Moss, J TI Lymphangioleiomyomatosis: CT of diurnal variation of lymphangioleiomyomas SO RADIOLOGY LA English DT Article DE lung, diseases; lymphangiomyomatosis; lymphatic system, diseases; lymphatic system, flow dynamics; retroperitoneal space, diseases ID PULMONARY LYMPHANGIOMYOMATOSIS; ANGIOMYOLIPOMAS AB PURPOSE: To evaluate the imaging and clinical features of lymphangioleiomyomas and to describe the phenomenon of diurnal variation in the size of lymphangioleiomyomas in patients with lymphangioleiomyomatosis. MATERIALS AND METHODS: One hundred twenty-eight patients with lymphangioleiomyomatosis underwent chest and abdominopelvic computed tomography (CT). Thirteen patients underwent CT in the morning and afternoon of the same day to assess diurnal variation in lymphangioleiomyoma size. RESULTS: Twenty-seven of 128 patients (21%) had 54 lymphangioleiomyomas. The vast majority (96%) of these masses contained material of low attenuation at CT. Associated CT findings included enlarged abdominal lymph nodes, pleural effusions, ascites, and dilatation of the thoracic duct. The prevalence of lymphangioleiomyomas was 15% in patients who had mild pulmonary disease, 19% in patients who had moderate disease, and 26% in patients who had severe disease. Diurnal variation in size of masses was demonstrated in 12 of 13 patients. Seven of the 27 patients who had masses underwent biopsy; all seven were confirmed to have lymphangioleiomyomas. The most common symptoms associated with lymphangioleiomyomas were bloating, abdominal pain, and edema of the lower extremities. The majority of the patients reported worsening of symptoms as the day progressed. CONCLUSION: Lymphangioleiomyomas are common in patients with lymphangioleiomyomatosis. Diurnal variation in size may explain worsening of symptoms during the day. C1 NIH, Dept Diagnost Radiol, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Pathol Sect, NIH, Bethesda, MD 20892 USA. RP Avila, NA (reprint author), NIH, Dept Diagnost Radiol, Warren Grant Magnuson Clin Ctr, Bldg 10,Rm 1C-660,10 Ctr Dr MSC 1182, Bethesda, MD 20892 USA. NR 20 TC 29 Z9 37 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 NOV PY 2001 VL 221 IS 2 BP 415 EP 421 DI 10.1148/radiol.2212001448 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 489ZU UT WOS:000172023800020 PM 11687685 ER PT J AU Hull, SC Prasad, K AF Hull, SC Prasad, K TI Reading between the lines: Direct-to-consumer advertising of genetic testing in the USA SO REPRODUCTIVE HEALTH MATTERS LA English DT Article DE breast cancer; genetic testing; risk assessment; advertising; USA ID 20-YEAR FOLLOW-UP; BREAST-CANCER; OVARIAN-CANCER; BRCA1 MUTATIONS; FAMILY HISTORY; RISK; POPULATION; CARCINOMA; PROGNOSIS; CARRIERS AB This article critiques on advertisement in a theatre playbill by a bio-technology company for its commercial test for the BRCA1 and BRCA2 genetic mutation, which may indicate a higher risk for breast and ovarian cancer. The advertisement targets a vulnerable audience attending a play about one woman's isolated and painful death from ovarian cancer. It promotes a product with incomplete and at times incorrect information, and it misguides women by suggesting that they contact the company directly about this test, rather than encouraging them to talk to their health core providers about genetic testing and their personal risk of breast cancer. In on era in which more genetic tests will be integrated into clinical practice, we con expect on increase in direct-to-consumer marketing for such tests. This advertisement is on example of what we need to be on guard against. C1 NHGRI, Bioeth Sect, Med Genet Branch, NIH, Bethesda, MD 20892 USA. RP Hull, SC (reprint author), NHGRI, Bioeth Sect, Med Genet Branch, NIH, Bethesda, MD 20892 USA. NR 23 TC 20 Z9 20 U1 1 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0968-8080 J9 REPROD HEALTH MATTER JI Reprod. Health Matters PD NOV PY 2001 VL 9 IS 18 BP 44 EP 48 DI 10.1016/S0968-8080(01)90089-8 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 498GZ UT WOS:000172502600007 PM 11765398 ER PT J AU Delclos, KB Bucci, TJ Lomax, LG Latendresse, JR Warbritton, A Weis, CC Newbold, RR AF Delclos, KB Bucci, TJ Lomax, LG Latendresse, JR Warbritton, A Weis, CC Newbold, RR TI Effects of dietary genistein exposure during development on male and female CD (Sprague-Dawley) rats SO REPRODUCTIVE TOXICOLOGY LA English DT Article DE genistein; isoflavones; soy; endocrine disruptors; reproductive toxicity ID REPRODUCTIVE ORGAN DEVELOPMENT; PREMENOPAUSAL JAPANESE WOMEN; SUPPRESSES MAMMARY-CANCER; ESTROGEN-RECEPTORS ALPHA; IN-VIVO; SOY ISOFLAVONES; BISPHENOL-A; POSTMENOPAUSAL WOMEN; NEONATAL EXPOSURE; PHYTO-ESTROGENS AB Genistein is a naturally occurring isoflavone that interacts with estrogen receptors and multiple other molecular targets. Human exposure to genistein is predominantly through consumption of soy products, including soy-based infant formula and dietary supplements. A dose range-finding study was conducted as a prelude to a multigeneration bioassay to assess potential toxicities associated with genistein consumption. Genistein was administered in a soy- and alfalfa-free diet at 0, 5, 25, 100, 250, 625, or t250 ppm to pregnant dams starting on Gestation day 7 and continuing throughout pregnancy. Dietary exposure of the dams continued through lactation, and pups were maintained on the same dosed feed as their mother after weaning until sacrifice at Postnatal day 50. Body weight and feed consumption of the treated dams prior to parturition showed a decreasing trend with a significant reduction at the highest dose. Litter birth weight was depressed in the t250 ppm dose group, and pups of both sexes in that dose group had significantly decreased body weights relative to controls at the time of sacrifice. The most pronounced organ weight effects in the pups were decreased ventral prostate weight in males at the 1250 ppm dose and a trend toward higher pituitary gland to body weight ratios in both sexes. Histopathologic examination of female pups revealed ductal/alveolar hyperplasia of the mammary glands at 250 to 1250 ppm. Ductal/alveolar hyperplasia and hypertrophy also occurred in males, with significant effects seen at 25 ppm and above. Abnormal cellular maturation in the vagina was observed at 625 and 1250 ppm, and abnormal ovarian antral follicles were observed at 1250 ppm. In males, aberrant or delayed spermatogenesis in the seminiferous tubules relative to controls wag observed at 1250 ppm, There was a deficit of sperm in the epididymis at 625 and 1250 ppm relative to controls, although testicular spermatid head counts and epididymal spermatozoa counts did not show significant differences from controls at these doses. Both sexes showed an increase in the incidence and/or severity of renal tubal mineralization at doses of 250 ppm and above. Dietary genistein thus produced effects in multiple estrogen-sensitive tissues in males and females that are generally consistent with its estrogenic activity. These effects occurred within exposure ranges achievable in humans. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA. Pathol Associates Int, Jefferson, AR 72079 USA. NIEHS, Environm Toxicol Program, Toxicol Lab, Dev Endocrinol Sect, Res Triangle Pk, NC 27709 USA. RP Delclos, KB (reprint author), Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA. EM bdelclos@nctr.fda.gov RI Latendresse, John/A-9215-2009 FU PHS HHS [224-93-0001] NR 91 TC 127 Z9 139 U1 1 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PD NOV-DEC PY 2001 VL 15 IS 6 BP 647 EP 663 DI 10.1016/S0890-6238(01)00177-0 PG 17 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA 501GF UT WOS:000172676400006 PM 11738518 ER PT J AU Miller, FW Rider, LG Chung, YL Cooper, R Danko, K Farewell, V Lundberg, I Morrison, C Oakley, L Oakley, I Pilkington, C Vencovsky, J Vincent, K Scott, DL Isenberg, DA AF Miller, FW Rider, LG Chung, YL Cooper, R Danko, K Farewell, V Lundberg, I Morrison, C Oakley, L Oakley, I Pilkington, C Vencovsky, J Vincent, K Scott, DL Isenberg, DA CA Int Myositis Outcome Assessment Co TI Proposed preliminary core set measures for disease outcome assessment in adult and juvenile idiopathic inflammatory myopathies SO RHEUMATOLOGY LA English DT Article DE idiopathic inflammatory myopathies; outcome measures ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INTRAVENOUS GAMMA-GLOBULIN; HEALTH ASSESSMENT QUESTIONNAIRE; RHEUMATOLOGY DAMAGE INDEX; INCLUSION-BODY MYOSITIS; MUSCLE TESTING MMT; POLYMYOSITIS-DERMATOMYOSITIS; REFRACTORY POLYMYOSITIS; CONTROLLED TRIAL; THERAPY AB In order to develop a preliminary core set of disease outcome measures for use in clinical trials of idiopathic inflammatory myopathies (IIM), we evaluated those measures used in previous trials, assessed the validation of published instruments and discussed these at an international consensus conference. The initial proposals were further refined by a multidisciplinary group of adult and paediatric specialists experienced in IIM using the Delphi method. The proposed preliminary core set of disease activity measures consists of five domains: physician and patient parent global assessments of disease activity; muscle strength: physical function, serum activity of muscle enzymes; and an assessment tool to capture extra-skeletal muscle disease activity. The group recommended further development of a core set of disease damage measures for assessment of persistent changes in anatomy, pathology and function of at least 6 months' duration. The group recommended that patient-reported outcomes should include generic health-related quality of life assessments using the Medical Outcomes Study 36-item Short Form (SF-36) health survey in adult IIM patients and a validated quality of life instrument for paediatric patients. We propose the core set of outcome measures as a minimum group of assessments to include in all IIM therapeutic studies. The use of this core set should assist in standardizing outcome measurement and in optimizing therapeutic trials in myositis. C1 US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA. Hammersmith Hosp, MRI Unit, London W12 0HS, England. Hope Hosp, Ctr Rheumat Dis, Salford M6 8HD, Lancs, England. Univ Debrecen, Dept Internal Med, Debrecen, Hungary. UCL, London WC1E 6BT, England. Karolinska Inst, Dept Med, Rheumatol Unit, S-17176 Stockholm, Sweden. Kings Coll Hosp Dulwich, Dept Rheumatol, London SE22 8PT, England. Dermatomyositis & Polymyositis Support Grp, Southampton SO19 9HR, Hants, England. Middlesex Hosp, Ctr Rheumatol, London W1P 9PL, England. Inst Rheumatol, Prague 12850 2, Czech Republic. Weston Educ Ctr, Dept Acad Rheumatol GKT, London SE5 9PJ, England. Kings Coll Hosp Dulwich, London W1P 9PG, England. UCL Hosp, Ctr Rheumatol, London W1P 9PC, England. RP Miller, FW (reprint author), NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH, 9 Mem Dr,Room 1W101,MSC 0958, Bethesda, MD 20892 USA. RI Song, Yeong Wook/J-2765-2012; OI Farewell, Vernon/0000-0001-6704-5295; Isenberg, David/0000-0001-9514-2455; Rider, Lisa/0000-0002-6912-2458; Miller, Frederick/0000-0003-2831-9593 NR 57 TC 135 Z9 138 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1462-0324 EI 1462-0332 J9 RHEUMATOLOGY JI RHEUMATOLOGY PD NOV PY 2001 VL 40 IS 11 BP 1262 EP 1273 DI 10.1093/rheumatology/40.11.1262 PG 12 WC Rheumatology SC Rheumatology GA 496CQ UT WOS:000172378500009 PM 11709610 ER PT J AU Artlett, CM Miller, FW Rider, LG AF Artlett, CM Miller, FW Rider, LG CA Childhood Myositis Heterogeneity C TI Persistent maternally derived peripheral microchimerism is associated with the juvenile idiopathic inflammatory myopathies SO RHEUMATOLOGY LA English DT Article DE microchimerism; maternal-fetal exchange; dermatomyositis; polymyositis; graft versus host reaction; inflammatory myopathy ID SYSTEMIC-SCLEROSIS; CELLS; DERMATOMYOSITIS; ORIGIN; IDENTIFICATION; POLYMYOSITIS; ANTIGENS; DISEASE; LIFE AB Objective. Fetal cells have been demonstrated in the active lesions of adult women with systemic sclerosis. Because the juvenile idiopathic inflammatory myopathies (JIIM) share clinical and histopathological features with systemic sclerosis and graft-vs-host disease, we explored the possibility that maternal cells persist and play a role in the pathogenesis of JIIM. Methods. DNA samples extracted from peripheral blood of 28 JIIM patients (14 females. 14 males) and 23 healthy controls were assessed for microchimerism by the HLA Cw polymerase chain reaction method. HLA Cw alleles from eight mothers and three healthy siblings of JIIM patients were also examined. Results. A microchimeric allele was identified in 19 of 26 JIIM patients whose data were able to be interpreted, compared with two of 21 healthy controls (P<0.001). Subjects with microchimerism ranged in age from 4 to 28 yr. In eight cases in which maternal peripheral blood was available. the additional Cw allele present in the patients was confirmed to be identical to a maternal allele. Three healthy siblings of JIIM patients did not have evidence of a microchimeric Cw allele. Conclusion. Maternal cells can persist in the peripheral blood of their children up to three decades after birth, and are found in a higher proportion in JIIM patients compared with controls. These findings, with other data, suggest that maternal cells may be involved in the immunopathogenesis of JIIM. C1 Thomas Jefferson Univ, Div Rheumatol, Philadelphia, PA 19107 USA. US FDA, Ctr Biol Evaluat & Res, Div Monoclonal Antibodies, Bethesda, MD USA. NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. RP Artlett, CM (reprint author), Thomas Jefferson Univ, Div Rheumatol, 233 S 10th St, Philadelphia, PA 19107 USA. OI Rider, Lisa/0000-0002-6912-2458; Miller, Frederick/0000-0003-2831-9593 NR 22 TC 28 Z9 28 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1462-0324 J9 RHEUMATOLOGY JI RHEUMATOLOGY PD NOV PY 2001 VL 40 IS 11 BP 1279 EP 1284 DI 10.1093/rheumatology/40.11.1279 PG 6 WC Rheumatology SC Rheumatology GA 496CQ UT WOS:000172378500011 PM 11709612 ER PT J AU Hebert, JL Khugyani, F Athar, M Kopelovich, L Epstein, EH Aszterbaum, M AF Hebert, JL Khugyani, F Athar, M Kopelovich, L Epstein, EH Aszterbaum, M TI Chemoprevention of basal cell carcinomas in the ptc1(+/-) mouse - Green and black tea SO SKIN PHARMACOLOGY AND APPLIED SKIN PHYSIOLOGY LA English DT Article DE basal cell carcinoma; mouse model; skin cancer; ptc1; ultraviolet radiation; cancer; chemoprevention ID ULTRAVIOLET-B LIGHT; HAIRLESS MICE; SKH-1 MICE; SKIN-CANCER; POLYPHENOLS; PREVENTION; PROTECTION; GROWTH; PHOTOCARCINOGENESIS; CARCINOGENESIS AB Skin cancers are a rising menace as their incidence increases, attributed in part to increasing ultraviolet radiation exposure. This increasing problem has stimulated efforts to devise useful preventive approaches. The uncertain efficacy of exhortations to avoid sun exposure and to use protective clothing and sunscreens to reduce damage when exposed argue for the development of an oral chemopreventive agent. Bickers and others have studied the effects and mechanisms of tea and of its putative active components on inhibition of skin cancer in experimental models. To continue this work, we have studied the effects of oral green tea and black tea on a new model of ultraviolet-induced skin carcinogenesis - the development of basal cell carcinomas in ptc1(+/-) mice. To our surprise, we have found that tea preparations which others have used to prevent squamous cell carcinoma formation in mice fail to inhibit basal cell carcinogenesis in our model, suggesting that prevention of this cancer may require special, tumor-specific approaches. Copyright (C) 2001 S. Karger AG, Basel. C1 Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA. Columbia Univ, Dept Dermatol, New York, NY 10027 USA. NCI, Div Canc Prevent, Bethesda, MD 20892 USA. RP Aszterbaum, M (reprint author), San Francisco Gen Hosp, Room 269,Bldg 100,1001 Potrero Ave, San Francisco, CA 94110 USA. FU NCI NIH HHS [CA 81888] NR 23 TC 11 Z9 11 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1422-2868 J9 SKIN PHARMACOL APPL JI Skin Pharmacol. Appl. Skin Physiol. PD NOV-DEC PY 2001 VL 14 IS 6 BP 358 EP 362 DI 10.1159/000056369 PG 5 WC Dermatology; Pharmacology & Pharmacy SC Dermatology; Pharmacology & Pharmacy GA 483DY UT WOS:000171619500003 PM 11598435 ER PT J AU Warach, S AF Warach, S TI Tissue viability thresholds in acute stroke - The 4-factor model SO STROKE LA English DT Editorial Material C1 NINCDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. RP Warach, S (reprint author), NINCDS, Stroke Branch, NIH, 36 Convent Dr,MSC 4129,Room 4A03, Bethesda, MD 20892 USA. NR 11 TC 44 Z9 45 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 2001 VL 32 IS 11 BP 2460 EP 2461 PG 2 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 490PG UT WOS:000172059800002 PM 11692000 ER PT J AU Rost, NS Wolf, PA Kase, CS Kelly-Hayes, M Silbershatz, H Massaro, JM D'Agostino, RB Franzblau, C Wilson, PWF AF Rost, NS Wolf, PA Kase, CS Kelly-Hayes, M Silbershatz, H Massaro, JM D'Agostino, RB Franzblau, C Wilson, PWF TI Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack - The Framingham Study SO STROKE LA English DT Article DE atherosclerosis; C-reactive protein; inflammation; ischemic stroke; risk factors; TIA ID CORONARY HEART-DISEASE; ACUTE MYOCARDIAL-INFARCTION; CARDIOVASCULAR-DISEASE; UNSTABLE ANGINA; ARTERY DISEASE; SUDDEN-DEATH; INFLAMMATION; SERUM; MECHANISMS; PECTORIS AB Background-The role of C-reactive protein (CRP) as a novel plasma marker of atherothrombotic disease is currently under investigation. Previous studies have mostly related CRP to coronary heart disease, were often restricted to a case-control design, and failed to include pertinent risk factors to evaluate the joint and net effect of CRP on the outcome. We related plasma CRP levels to incidence of first ischemic stroke or transient ischemic attack (TIA) in the Framingham Study original cohort. Methods-There were 591 men and 871 women free of stroke/TIA during their 1980 to 1982 clinic examinations, when their mean age was 69.7 years. CRP levels were measured by using an enzyme immunoassay on previously frozen serum samples. Analyses were based on sex-specific CRP quartiles. Risk ratios (RRs) were derived, and series of trend analyses were performed. Results-During 12 to 14 years of follow-up, 196 ischemic strokes and TIAs occurred. Independent of age, men in the highest CRP quartile had 2 times the risk of ischemic stroke/TIA (RR=2.0, P=0.027), and women had almost 3 times the risk (RR = 2.7, P = 0.0003) compared with those in the lowest quartile. Assessment of the trend in risk across quartiles showed unadjusted risk increase for men (RR=1.347, P=0.0025) and women (RR=1.441, P=0.0001). After adjustment for smoking, total/HDL cholesterol, systolic blood pressure, and diabetes, the increase in risk across CRP quartiles remained statistically significant for both men (P=0.0365) and women (P=0.0084). Conclusions-Independent of other cardiovascular risk factors, elevated plasma CRP levels significantly predict the risk of future ischemic stroke and TIA in the elderly. C1 Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Math & Stat, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Epidemiol & Biostat, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. RP Wolf, PA (reprint author), Boston Univ, Sch Med, Dept Neurol, 715 Alban7 St,B-608, Boston, MA 02118 USA. FU NHLBI NIH HHS [N01-HC-38038]; NINDS NIH HHS [5-RO1-NS-17950-19] NR 38 TC 453 Z9 491 U1 3 U2 17 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 2001 VL 32 IS 11 BP 2575 EP 2579 DI 10.1161/hs1101.098151 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 490PG UT WOS:000172059800022 PM 11692019 ER PT J AU Mima, T Toma, K Koshy, B Hallett, M AF Mima, T Toma, K Koshy, B Hallett, M TI Coherence between cortical and muscular activities after subcortical stroke SO STROKE LA English DT Article DE electroencephalogram; electromyogram; motor cortex ID POSITRON-EMISSION-TOMOGRAPHY; HEMIPLEGIC CEREBRAL-PALSY; MOTOR CORTEX; ISOMETRIC CONTRACTION; MAGNETIC STIMULATION; HAND MUSCLE; REORGANIZATION; RECOVERY; PLASTICITY; PATHWAYS AB Background and Purpose-Functional connection between the motor cortex and muscle can be measured by electroencephalogram-electromyogram (EEG-EMG) coherence. To evaluate the functional connection to muscle between contralateral and ipsilateral motor cortices after pyramidal tract lesions, we investigated 6 patients with chronic subcortical stroke. Methods-High-resolution EEG and EMG of the hand, forearm, and biceps muscles were recorded during 3 tonic contraction tasks: (1) elbow flexion, (2) wrist extension, and (3) power grip. To evaluate the cortical control of EMG, EEG-EMG coherence was computed. Results-EEG-EMG coherence was localized over the contralateral sensorimotor area in all circumstances, and there was no significant coherence at the ipsilateral side. EEG-EMG coherence was significantly smaller on the affected side for the hand and forearm muscles but not for the biceps muscle. Conclusions-All direct functional connections to muscle after recovered subcortical stroke come from the contralateral. motor cortex. The different effects of the lesion on the proximal and distal muscles appear to be associated with the strength of the corticospinal pathway. C1 NINCDS, Med Neurol Branch, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA. RP Hallett, M (reprint author), NINCDS, Med Neurol Branch, Human Motor Control Sect, NIH, Bldg 10,Room 5N226,10 Ctr Dr,MSC1428, Bethesda, MD 20892 USA. OI Mima, Tatsuya/0000-0001-7787-4855 NR 27 TC 58 Z9 62 U1 3 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 NOV PY 2001 VL 32 IS 11 BP 2597 EP 2601 DI 10.1161/hs1101.098764 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 490PG UT WOS:000172059800027 PM 11692023 ER PT J AU Furuya, K Takeda, H Azhar, S McCarron, RM Chen, Y Ruetzler, CA Wolcott, KM DeGraba, TJ Rothlein, R Hugli, TE del Zoppo, GJ Hallenbeck, JM AF Furuya, K Takeda, H Azhar, S McCarron, RM Chen, Y Ruetzler, CA Wolcott, KM DeGraba, TJ Rothlein, R Hugli, TE del Zoppo, GJ Hallenbeck, JM TI Examination of several potential mechanisms for the negative outcome in a clinical stroke trial of enlimomab, a murine anti-human intercellular adhesion molecule-1 antibody - A bedside-to-bench study SO STROKE LA English DT Article DE antibodies; cell adhesion molecules; cerebral ischemia; clinical trials; leukocytes; rats ID CEREBRAL-ARTERY OCCLUSION; ISCHEMIC CELL-DAMAGE; MONOCLONAL-ANTIBODY; ANTI-ICAM-1 ANTIBODY; REPERFUSION INJURY; WISTAR RAT; ICAM-1; BLOOD; EXPRESSION; ACTIVATION AB Background and Purpose-Enlimomab, a murine monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-stroke trial. We did a beds ide-to-bench study in standardized rat stroke models to explore mechanisms for these untoward results. Methods-After focal brain ischemia in Wistar rats and spontaneously hypertensive rats (SHR), we administered murine anti-rat ICAM-1 antibody (1A29), subclass-matched murine immunoglobulin (IgG1), or vehicle intravenously. To examine whether rat anti-mouse antibodies were generated against the mouse protein and whether these were deleterious, we sensitized Wistar rats with 1A29 or vehicle 7 days before surgery. Infarct volume, tissue myeloperoxidase activity, neutrophil CD11b expression, and microvascular E-selectin, P-selectin, and ICAM-1 expression were examined 48 hours after surgery. Complement activation was serially assessed for 2 hours after a single injection of either 1A29 or vehicle. Results- 1A29 treatment did not significantly reduce infarct size in either strain. 1A29 sensitization augmented infarct size and generated rat anti-mouse antibodies. Although 1A29 inhibited neutrophil trafficking shown by reduction in brain myeloperoxidase activity, circulating neutrophils were activated and displayed CD11b upregulation. Complement was activated in 1A29-sensitized Wistar rats and 1A29-treated SHR. E-selectin (SHR), endothelial P-selectin (Wistar and SHR), and ICAM-1 (SHR) were upregulated in animals treated with 1A29. Conclusions-Administration to rats of a murine antibody preparation against ICAM-1, 1A29, elicits the production of host antibodies against the protein, activation of circulating neutrophils, complement activation, and sustained microvascular activation. These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute ischemic stroke. C1 NINCDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. Natl Med Res Ctr, Resuscitat Med Dept, Silver Spring, MD USA. Uniformed Serv Univ Hlth Sci, Biomed Instrumentat Ctr, Flow Cytometry Facil, Bethesda, MD 20814 USA. Boehringer Ingelheim Pharmaceut Inc, Dept Immunol, Ridgefield, CT 06877 USA. Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA. Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA. RP Hallenbeck, JM (reprint author), NINCDS, Stroke Branch, NIH, 36 Convent Dr,MSC 4128,Bldg 36,Rm 4A03, Bethesda, MD 20892 USA. NR 43 TC 105 Z9 112 U1 2 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 2001 VL 32 IS 11 BP 2665 EP 2674 DI 10.1161/hs3211.098535 PG 10 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 490PG UT WOS:000172059800036 PM 11692032 ER PT J AU Kaplan, N Morris, R AF Kaplan, N Morris, R TI Prospects for association-based fine mapping of a susceptibility gene for a complex disease SO THEORETICAL POPULATION BIOLOGY LA English DT Article DE fine mapping; linkage disequilibrium; association test; TDT; coalescent process ID LINKAGE-DISEQUILIBRIUM; TRANSMISSION/DISEQUILIBRIUM TEST; FOUNDER POPULATIONS; SAMPLE-SIZE; SCALE; RECOMBINATION; TRANSMISSION; HAPLOTYPES; ALLELE; MODELS AB The potential of association studies for fine-mapping loci with common disease susceptibility alleles for complex genetic diseases in outbred populations is unclear. For a battery of tightly linked anonymous genetic markers spanning a candidate region centered around a disease locus, simulation methods based on a coalescent process with mutation, recombination, and genetic drift were used to study the spatial distribution of markers with large noncentrality parameters in a case-control study design. Simulations with a disease allele at intermediate frequency, presumably representing an old mutation, tend to exhibit the largest noncentrality parameter values at markers near the disease locus. In contrast, simulations with a disease allele at low frequency, presumably representing a young mutation, often exhibit the largest noncentrality parameter values at markers scattered over the candidate region. In the former case, sample sizes or marker densities sufficient to detect association are likely to lead to useful localization, whereas, in the latter case, localization of the disease locus within the candidate region is much less likely, regardless of the sample size or density of the map. The simulations suggest that for a single marker analysis, the simple strategy of choosing the marker with smallest associated P value to begin a laboratory search for the disease locus performs adequately for a common disease allele. (C) 2001 Elsevier Science. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. RP Kaplan, N (reprint author), NIEHS, Biostat Branch, POB 12233, Res Triangle Pk, NC 27709 USA. NR 45 TC 12 Z9 12 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 0040-5809 J9 THEOR POPUL BIOL JI Theor. Popul. Biol. PD NOV PY 2001 VL 60 IS 3 BP 181 EP 191 DI 10.1006/tpbi.2001.1537 PG 11 WC Ecology; Evolutionary Biology; Genetics & Heredity SC Environmental Sciences & Ecology; Evolutionary Biology; Genetics & Heredity GA 530TT UT WOS:000174375600006 PM 11855952 ER PT J AU Kaplan, NL Martin, ER AF Kaplan, NL Martin, ER TI Power calculations for a general class of tests of linkage and association that use nuclear families with affected and unaffected sibs SO THEORETICAL POPULATION BIOLOGY LA English DT Article DE linkage disequilibrium; association; TDT; nuclear families ID DISEQUILIBRIUM AB Family-based tests of association are now often used when trying to fine-map a disease susceptibility locus. Recently, several tests of linkage and association have been proposed that use nuclear families with multiple affected and unaffected sibs rather than just case-parent triads. In this paper we propose a test that generalizes these previous tests. Formulae are derived to calculate the power of the test for a randomly mating population. These power calculations are used to determine conditions under which it is advantageous to include unaffected sibs in the analysis. (C) 2001 Elsevier Science. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Dept Med, Ctr Human Genet, Durham, NC 27708 USA. RP Kaplan, NL (reprint author), NIEHS, Biostat Branch, POB 12233, Res Triangle Pk, NC 27709 USA. FU NIMH NIH HHS [MH59528]; NINDS NIH HHS [NS39764-02] NR 11 TC 10 Z9 11 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 0040-5809 J9 THEOR POPUL BIOL JI Theor. Popul. Biol. PD NOV PY 2001 VL 60 IS 3 BP 193 EP 201 DI 10.1006/tpbi.2001.1541 PG 9 WC Ecology; Evolutionary Biology; Genetics & Heredity SC Environmental Sciences & Ecology; Evolutionary Biology; Genetics & Heredity GA 530TT UT WOS:000174375600007 PM 11855953 ER PT J AU Jindo, T Wine, RN Li, LH Chapin, RE AF Jindo, T Wine, RN Li, LH Chapin, RE TI Protein kinase activity is central to rat germ cell apoptosis induced by methoxyacetic acid SO TOXICOLOGIC PATHOLOGY LA English DT Article DE apoptosis; EGME; MAA; protein kinase inhibitors; 2D PAGE; seminiferous tubule culture; rats ID LIGHT-CHAIN PHOSPHORYLATION; SPERMATOCYTE APOPTOSIS; POLYACRYLAMIDE GELS; ALKOXYACETIC ACIDS; DNA FRAGMENTATION; GLYCOL ETHERS; IN-VITRO; INDUCTION; RESISTANCE; TOXICITY AB Methoxyacetic acid (MAA) is a major metabolite of ethylene glycol monomethyl ether (EGME). Previous investigations of the testicular lesion induced by EGME have found that dividing meiotic cells are the most sensitive, although several stages of spermatocytes are also vulnerable. Preliminary data from this lab suggested the involvement of protein kinase activity in the development of this lesion, a hypothesis explored in the present studies. We used cultured seminiferous tubules (STs) from juvenile rats (25-day-old), exposed in vitro to MAA and several inhibitors of protein kinases. Nineteen h following a 5-h exposure to 5 mM MAA (the plasma level in vivo after a toxic dose of EGME), apoptotic spermatocytes were seen in early- and late-stage STs. Cell death was prevented by cotreatment with broad-spectrum inhibitors of protein kinases such as H-7, H-8, K-252a, W-7, and genistein. In corroboration, immunocytochemistry with antibodies to various kinases (PKCmu, zeta, and gamma, AKAP220, CaMKII, MLCK, and Src) showed increased staining around dying spermatocytes following EGME treatment in vivo. 2D-PAGE, autoradiography, and nanospray mass spectrometry was used to separate and identify proteins whose phosphorylation status was most greatly changed following exposure to MAA. One protein was identified by sequence analysis as being glucose-regulated protein 94 (grp94). Western blotting and immunocytochemistry confirmed this finding. The data we present implicate kinase activities in the pathogenesis of this lesion and suggest the involvement of Sertoli cells. C1 NIEHS, Reprod Toxicol Grp, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA. Daiichi Pharmaceut, Drug Safety Res Lab, Tokyo, Japan. Off Environm Hlth Hazard Assessment, Sacramento, CA 95812 USA. Dupont Merck Pharmaceut Co, Stine Haskell Res Ctr, Newark, DE 19711 USA. RP Wine, RN (reprint author), NIEHS, Reprod Toxicol Grp, Natl Toxicol Program, 111 TW Alexander Dr,Bldg 101,Mail Drop E1-06, Res Triangle Pk, NC 27709 USA. OI Chapin, Robert/0000-0002-5997-1261 NR 40 TC 22 Z9 22 U1 1 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD NOV 1 PY 2001 VL 29 IS 6 BP 607 EP 616 DI 10.1080/019262301753385933 PG 10 WC Pathology; Toxicology SC Pathology; Toxicology GA 558DW UT WOS:000175951900003 PM 11794376 ER PT J AU Gold, LS Manley, NB Slone, TH Ward, JM AF Gold, LS Manley, NB Slone, TH Ward, JM TI Compendium of chemical carcinogens by target organ: Results of chronic bioassays in rats, mice, hamsters, dogs, and monkeys SO TOXICOLOGIC PATHOLOGY LA English DT Review DE human carcinogen; tumor site; animal cancer test; Carcinogenic Potency Database; species comparisons; mutagenicity; monkeys ID POTENCY DATABASE; PROGRAM; RISK AB Acompendium of carcinogenesis bioassay results organized by target organ is presented for 738 chemicals that are carcinogenic in chronic-exposure, long-term bioassays in at least 1 species. This compendium is based primarily on experiments in rats or mice; results in hamsters, monkeys, and dogs are also reported. The compendium can be used to identify chemicals that induce tumors at particular sites and to determine whether target sites are the same for chemicals positive in more than 1 species. The source of information is the Carcinogenic Potency Database (CPDB), which includes results of 6073 experiments on 1458 chemicals (positive or negative for carcinogenicity) that have been reported in Technical Reports of the National Cancer Institute/National Toxicology Program or in papers in the general published literature. The published CPDB includes detailed analyses of each test and citations. The CPDB is publicly available in several formats (http://potency.berkeley.edu). Chemical carcinogens are reported for 35 different target organs in rats or mice. Target organs in humans are also summarized for 82 agents that have been evaluated as human carcinogens at a particular target site by the International Agency for Research on Cancer (IARC). Comparisons are provided of target organs for mutagens versus nonmutagens and rats versus mice. C1 Ernest Orlando Lawrence Berkeley Natl Lab, Div Life Sci, Berkeley, CA 94720 USA. Univ Calif Berkeley, Div Biochem & Mol Biol, Berkeley, CA 94720 USA. NCI, Ctr Canc Res, Vet & Tumor Pathol Sect, Frederick, MD 21702 USA. RP Gold, LS (reprint author), Ernest Orlando Lawrence Berkeley Natl Lab, Div Life Sci, Mail Stop 946, Berkeley, CA 94720 USA. FU NIEHS NIH HHS [ESO1896] NR 17 TC 74 Z9 74 U1 3 U2 5 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD NOV 1 PY 2001 VL 29 IS 6 BP 639 EP 652 DI 10.1080/019262301753385979 PG 14 WC Pathology; Toxicology SC Pathology; Toxicology GA 558DW UT WOS:000175951900007 PM 11794380 ER PT J AU Haines, DC Chattopadhyay, S Ward, JM AF Haines, DC Chattopadhyay, S Ward, JM TI Pathology of aging B6;129 mice SO TOXICOLOGIC PATHOLOGY LA English DT Article DE lymphoma; genetically engineered mice; lung tumors; liver tumors; glomerulonephritis; otitis media; hyalinosis ID WILD-TYPE MICE; OTITIS-MEDIA; P53-DEFICIENT MICE; B-CELL; LEUKEMIA; LACKING; WEIGHT AB Fifty male and 49 female B6;129 mice (wild-type, +/+) were maintained until 2 years of age to study their age-related pathology. By 104-105 weeks, 14/50 (28%) of the males and 30/49 (61%) of the females were still alive. The most common contributing cause of morbidity or mortality was lymphoma. Lymphoma was observed in 21/50 (42%) of the males and 33/49 (67%) of the females with the most common sites being mesenteric lymph nodes, gut associated lymphoid tissue (Peyer's patches), and spleen. The lymphoma most often appeared to arise in the mesenteric node. Immunohistochemistry revealed CD45R expression as well as infiltration by many CD3+ cells. IgH gene rearrangements were found in typical mesenteric node lymphomas indicating B-cell origin. They bore similarities to the human T-cell rich, B-cell lymphomas. Other tumors included hepatocellular adenoma or carcinoma (male 12%, females 10%), lung alveolar Type II cell adenoma or carcinoma (male 32%, female 20%), thyroid follicular adenoma or carcinoma (male 2%, female 8%), ovarian tumors (17%), and endometrial tumors (6%). Nonneoplastic lesions included amyloid-like material in the nasal septum (male and female 100%), otitis media (male 84%, female 79%), epididymal epithelial karyomegaly (88%), melanosis (high incidences in various tissues including brain, parathyroid, and spleen), membranoproliferative glomerulonephritis (male 52%, female 71%), hyalinosis with extracellular crystals in several tissues (respiratory tract, gall bladder, stomach), islet cell hyperplasia (male 45%, female 29%) and esophageal dilation (male 10%, female 6%). The B6; 129 mouse is a mouse with aging lesions similar to those in other mouse strains but with a characteristic common lymphoma. C1 NCI, Ctr Canc Res, Vet & Tumor Pathol Sect, Frederick, MD 21702 USA. SAIC Frederick, Pathol Histotechnol Lab, Vet Pathol Sect, Frederick, MD USA. NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA. RP Ward, JM (reprint author), NCI, Ctr Canc Res, Vet & Tumor Pathol Sect, Fairview 201,POB B, Frederick, MD 21702 USA. FU NCI NIH HHS [N01-CO-56000] NR 39 TC 81 Z9 84 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD NOV 1 PY 2001 VL 29 IS 6 BP 653 EP 661 DI 10.1080/019262301753385988 PG 9 WC Pathology; Toxicology SC Pathology; Toxicology GA 558DW UT WOS:000175951900008 PM 11794381 ER PT J AU Mahler, JF AF Mahler, JF TI Mutant models of prolonged life span SO TOXICOLOGIC PATHOLOGY LA English DT Article ID OXIDATIVE STRESS; SACCHAROMYCES-CEREVISIAE; CAENORHABDITIS-ELEGANS; REPLICATIVE SENESCENCE; CALORIE RESTRICTION; MECHANISMS; EXTENSION; LONGEVITY; MUTATION; PROTEIN AB Aging is an important biological process that affects all creatures. For humans, age-related diseases and the question of why we age and die also have tremendous social and philosophical impact. We can therefore expect that models to study mechanisms of the aging process will always attract much interest. Until recently, the mutant model approach to study molecular mechanisms of aging has been limited to lower animals such as yeast, worms, and flies. However, given the current power of genetic technology in mammals, we can expect that phenotypes of prolonged life span will increasingly be seen in mice and subject to evaluation by pathologists. A brief review of current models is presented. C1 NIEHS, Lab Expt Pathol, Res Triangle Pk, NC 27709 USA. RP Mahler, JF (reprint author), NIEHS, Lab Expt Pathol, POB 12233, Res Triangle Pk, NC 27709 USA. NR 31 TC 1 Z9 2 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD NOV 1 PY 2001 VL 29 IS 6 BP 673 EP 676 DI 10.1080/019262301753386013 PG 4 WC Pathology; Toxicology SC Pathology; Toxicology GA 558DW UT WOS:000175951900011 PM 11794384 ER PT J AU Gottschling, BC Maronpot, RR Hailey, JR Peddada, S Moomaw, CR Klaunig, JE Nyska, A AF Gottschling, BC Maronpot, RR Hailey, JR Peddada, S Moomaw, CR Klaunig, JE Nyska, A TI The role of oxidative stress in indium phosphide-induced lung carcinogenesis in rats SO TOXICOLOGICAL SCIENCES LA English DT Article DE indium phosphide; oxidative stress; inflammation; lung carcinogenesis; immunohistochemistry ID MESSENGER-RNA EXPRESSION; NITRIC-OXIDE SYNTHASE; SIGNAL-TRANSDUCTION; INDUCED APOPTOSIS; IN-VITRO; TOXICITY; CANCER; TRANSFERASES; MECHANISMS; PATHOLOGY AB Indium phosphide (IP), widely used in the microelectronics industry, was tested for potential carcinogenicity. Sixty male and 60 female Fischer 344 rats were exposed by aerosol for 6 h/day, 5 days/week, for 21 weeks (0.1 or 0.3 mg/m(3); stop exposure groups) or 105 weeks (0 or 0.03 mg/m(3) groups) with interim groups (10 animals/group/sex) evaluated at 3 months. After 3-month exposure, severe pulmonary inflammation with numerous infiltrating macrophages and alveolar proteinosis appeared. After 2 years, dose-dependent high incidences of alveolar[bronchiolar adenomas and carcinomas occurred in both sexes; four cases of squamous cell carcinomas appeared in males (0.3 mg/m(3)), and a variety of nonneoplastic lung lesions, including simple and atypical hyperplasia, chronic active inflammation, and squamous cyst, occurred in both sexes. To investigate whether inflammation-related oxidative stress functioned in the pathogenesis of IP-related pulmonary lesions, we stained lungs of control and high-dose animals immunohistochemically for four markers indicative of oxidative stress: inducible nitric oxide synthase (i-NOS), cyclooxygenase-2 (COX-2), glutathione-S-transferase Pi (GST-Pi), and 8-hydroxydeoxyguanosine (8-OHdG). Paraffin-embedded samples from the 3-month and 2-year control and treated females were used. i-NOS and COX-2 were highly, expressed in inflammatory foci after 3 months; at 2 years, all four markers were expressed in nonneoplastic and neoplastic lesions. Most i-NOS staining, mainly in macrophages, occurred in chronic inflammatory and atypical hyperplastic lesions. GST-Pi and 8-OHdG expression occurred in cells of carcinoma epithelium, atypical hyperplasia, and squamous cysts. These findings suggest that IP inhalation causes pulmonary inflammation associated with oxidative stress, resulting in progression to atypical hyperplasia and neoplasia. C1 Indiana Univ, Sch Med, Dept Pharmacol & Toxicol, Div Toxicol, Indianapolis, IN 46202 USA. NIEHS, Lab Expt Pathol, Res Triangle Pk, NC 27709 USA. RP Nyska, A (reprint author), Indiana Univ, Sch Med, Dept Pharmacol & Toxicol, Div Toxicol, 635 Barnhill Dr,MS 1021, Indianapolis, IN 46202 USA. RI Peddada, Shyamal/D-1278-2012 NR 39 TC 53 Z9 57 U1 0 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1096-6080 J9 TOXICOL SCI JI Toxicol. Sci. PD NOV PY 2001 VL 64 IS 1 BP 28 EP 40 PG 13 WC Toxicology SC Toxicology GA 486ZL UT WOS:000171849200007 PM 11606799 ER PT J AU Rios, M Hue-Roye, K Storry, JR Lee, T Miller, JL Reid, ME AF Rios, M Hue-Roye, K Storry, JR Lee, T Miller, JL Reid, ME TI Molecular basis of the Dombrock null phenotype SO TRANSFUSION LA English DT Article ID BLOOD; GLYCOPROTEIN; IDENTIFICATION; GY(A); HY AB BACKGROUND: The Dombrock blood group system consists of two antithetical antigens, Do(a) and Do(b), and three high-incidence antigens, Gregory (Gy(a)), Holley (Hy), and Joseph (Jo(a)). The null phenotype of the Dombrock blood group system (Do(null)) was identified when it was found that Gy(a-) RBCs also lack Do(a), Do(b), Hy, and Jo(a). STUDY DESIGN AND METHODS: DNA from three Gy(a-) persons was analyzed. PCR products for each of the three DO exons and their flanking intronic regions were sequenced in both directions. The cDNA from two of the people was subjected to PCR using primers in exon 1 and exon 3, and the products were sequenced. RESULTS: The Do(null) phenotype is associated with a single nucleotide, mutation in the acceptor splice site of DO (lVS1-2a >g), which results in outsplicing of exon 2. CONCLUSION: Outsplicing of exon 2 is predicted to cause a -1 frameshift and a premature stop codon. Any product of such a transcript would lack the glycosyl-phosphatidylinositol-anchor motif, and RBCs would be devoid of the Do glycoprotein. C1 New York Blood Ctr, Immunochem Lab, New York, NY 10021 USA. NIDDKD, NIH, Bethesda, MD 20892 USA. RP Rios, M (reprint author), New York Blood Ctr, Immunochem Lab, 310 E 67th St, New York, NY 10021 USA. FU NHLBI NIH HHS [HL54459] NR 12 TC 17 Z9 18 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 NOV PY 2001 VL 41 IS 11 BP 1405 EP 1407 DI 10.1046/j.1537-2995.2001.41111405.x PG 3 WC Hematology SC Hematology GA 497AE UT WOS:000172429900016 PM 11724986 ER PT J AU Shi, PA Pomper, GJ Metzger, ME Donahue, RE Leitman, SF Dunbar, CE AF Shi, PA Pomper, GJ Metzger, ME Donahue, RE Leitman, SF Dunbar, CE TI Assessment of rapid remobilization intervals with G-CSF and SCF in murine and rhesus macaque models SO TRANSFUSION LA English DT Article ID STEM-CELL FACTOR; COLONY-STIMULATING FACTOR; HEMATOPOIETIC PROGENITOR CELLS; BONE-MARROW TRANSPLANTATION; BREAST-CANCER PATIENTS; HIGH-DOSE CHEMOTHERAPY; NON-HODGKINS-LYMPHOMA; PERIPHERAL-BLOOD; MULTIPLE-MYELOMA; HEALTHY DONORS AB BACKGROUND: Defining the optimum regimen and time for repeat peripheral blood progenitor cell mobilization would have important clinical applications. STUDY DESIGN AND METHODS: Remobilization with SCF and G-CSF at 2 weeks after an initial mobilization in mice and at 2 or 4 weeks after an initial mobilization in nonhuman primates was examined. In mice, competitive repopulation assays were used to measure long-term progenitor cell-repopulating activity. In monkeys, mobilization of hematopoietic progenitor CFUs was used as a surrogate marker for progenitor cell-repopulating ability. RESULTS: Efficacy of progenitor cell remobilization differed in the two animal species. In mice, peripheral blood progenitor cell-repopulating ability with repeat mobilization at 2 weeks was 70 percent of that with the initial mobilization. In monkeys, there was no significant difference in peripheral blood progenitor cell mobilization between the initial and the repeat mobilizations at 2 weeks. In mobilizations separated by 4 weeks, however, peripheral blood progenitor cell mobilization was higher than that with initial mobilizations. CONCLUSION: In animal models, mobilization of peripheral blood progenitor cells with remobilization after a 2-week interval is similar to or moderately decreased from that with the initial mobilization. Progenitor cell collection at this time point may be useful in certain clinical circumstances. A 4-week interval between remobilizations may be preferable, Clinical trials in humans would be useful to clarify these issues. C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD USA. RP Shi, PA (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,Rm 7C103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 42 TC 9 Z9 10 U1 0 U2 1 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 USA SN 0041-1132 J9 TRANSFUSION JI Transfusion PD NOV PY 2001 VL 41 IS 11 BP 1438 EP 1444 DI 10.1046/j.1537-2995.2001.41111438.x PG 7 WC Hematology SC Hematology GA 497AE UT WOS:000172429900022 PM 11724992 ER PT J AU Veenstra, GJC Wolffe, AP AF Veenstra, GJC Wolffe, AP TI Gene-selective developmental roles of general transcription factors SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Review ID TATA-BINDING PROTEIN; RNA-POLYMERASE-II; TBP-LIKE FACTOR; CELL-CYCLE PROGRESSION; DNA-BINDING; C-ELEGANS; IN-VIVO; DROSOPHILA; ACTIVATION; COMPLEX AB Innumerable transcription factors integrate cellular and intercellular sign a Is to generate a profile of expressed genes that is characteristic of the biochemical and cellular properties of the cell. This profile of expressed genes changes dynamically along with the developmental stage and differentiation state of the cell. The biochemical machinery upon which transcription factors integrate their signals is referred to as the general transcription machinery. However this machinery is not of universal composition, and variants of the general transcription factors play specific roles in embryonic development, reflecting the constraints and requirements of developmental gene regulation. C1 NICHHD, Mol Genet Lab, Bethesda, MD 20892 USA. Sangamo Biosci, Richmond, CA USA. RP Veenstra, GJC (reprint author), NICHHD, Mol Genet Lab, Bethesda, MD 20892 USA. RI Veenstra, Gert Jan C./D-4963-2012 OI Veenstra, Gert Jan C./0000-0002-7787-4940 NR 49 TC 46 Z9 48 U1 0 U2 1 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD NOV PY 2001 VL 26 IS 11 BP 665 EP 671 DI 10.1016/S0968-0004(01)01970-3 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 494DR UT WOS:000172266900007 PM 11701325 ER PT J AU Strausberg, RL Greenhut, SF Grouse, LH Schaefer, CF Buetow, KH AF Strausberg, RL Greenhut, SF Grouse, LH Schaefer, CF Buetow, KH TI In silico analysis of cancer through the cancer genome anatomy project SO TRENDS IN CELL BIOLOGY LA English DT Review ID GENE-EXPRESSION; DATABASE; DISCOVERY; ANTIGENS AB The Cancer Genome Anatomy Project (CGAP) was designed and implemented to provide public datasets, material resources and informatics tools to serve as a platform to support the elucidation of the molecular signatures of cancer. This overview of CGAP describes the status of this effort to develop resources based on gene expression, polymorphism identification and chromosome aberrations, and we describe a variety of analytical tools designed to facilitate in silico analysis of these datasets. C1 NCI, Bethesda, MD 20892 USA. RP Strausberg, RL (reprint author), NCI, Bethesda, MD 20892 USA. NR 19 TC 36 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0962-8924 J9 TRENDS CELL BIOL JI Trends Cell Biol. PD NOV PY 2001 VL 11 IS 11 BP S66 EP S71 DI 10.1016/S0962-8924(01)82370-9 PG 6 WC Cell Biology SC Cell Biology GA 486WD UT WOS:000171839200028 PM 11684445 ER PT J AU Stojilkovic, SS AF Stojilkovic, SS TI A novel view of the function of pituitary folliculo-stellate cell network SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID ANTERIOR-PITUITARY; INTERCELLULAR COMMUNICATION; TRANSIENTS; INVITRO; SLICES AB Folliculo-stellate (FS) cells are a non-endocrine population of cells abundant in the anterior pituitary lobe of many species. These cells are structurally interconnected in an extensive and complex tridimensional configuration, but their properties and functions have not been completely characterized. The expression of gap-junction channels in FS cells supports the hypothesis that they also operate as a network of functionally interconnected cells. Further evidence comes from a recent study with rat pituitary slices that demonstrated the presence of spontaneous, voltage- and inositol 1,4,5-trisphosphate-induced intercellular calcium signals that were abolished by gap junction channel blockers. The study also revealed an unexpected feature of FS cells-their excitability. Thus, although agranular, these cells share the common 'neuronal language' with granular (endocrine) cell types that might provide an efficient mechanism for the synchronization of intrapituitary electrical and calcium signaling. C1 NICHHD, Sect Cellular Signaling, ERRB, NIH, Bethesda, MD 20892 USA. RP Stojilkovic, SS (reprint author), NICHHD, Sect Cellular Signaling, ERRB, NIH, Bldg 49 Room 6A-36, Bethesda, MD 20892 USA. NR 15 TC 20 Z9 20 U1 0 U2 1 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD NOV PY 2001 VL 12 IS 9 BP 378 EP 380 DI 10.1016/S1043-2760(01)00476-3 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 487EJ UT WOS:000171860400002 PM 11595527 ER PT J AU Mitsiades, N Poulaki, V Mitsiades, CS Koutras, DA Chrousos, GR AF Mitsiades, N Poulaki, V Mitsiades, CS Koutras, DA Chrousos, GR TI Apoptosis induced FasL and TRAIL/Apo2L in the pathogenesis of thyroid diseases SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID TRAIL-INDUCED APOPTOSIS; INDUCED-PROXIMITY MODEL; MEDIATED APOPTOSIS; FOLLICULAR CELLS; AUTOIMMUNE-THYROIDITIS; HASHIMOTOS-THYROIDITIS; LIGAND EXPRESSION; GRAVES-DISEASE; DEATH RECEPTORS; IMMUNE EVASION AB FasL and TRAIL/Apo2L participate in cell-mediated cytotoxicity by inducing apoptosis in susceptible cells via respective cell surface receptors. Normal and neoplastic thyroid tissues are resistant-to FasL-induced apoptosis but are sensitized by Th-1-type cytokines. In Hashimoto's thyroiditis, both FasL and its receptor, Fas, are strongly upregulated and their interaction leads to the suicidal/fratricidal death of thyrocytes. In Graves' disease, FasL expression in thyroid follicular cells is induced by thionamides and kills infiltrating lymphocytes. In this condition, Th-2-type cytokines upregulate the anti-apoptotic molecules FLIP and Bcl-x(L) and protect thyrocytes from apoptosis. FasL is expressed by neoplastic thyrocytes and induces apoptosis of infiltrating lymphocytes. TRAIL/Apo2L kills thyroid carcinoma cells but spares normal thyrocytes,thus providing a potential therapy for thyroid cancer. C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA USA. Univ Athens, Sch Med, GR-11527 Athens, Greece. NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Mitsiades, N (reprint author), Dana Farber Canc Inst, Dept Adult Oncol, Mayer Bldg,Room M557,44 Binney St, Boston, MA 02115 USA. NR 60 TC 42 Z9 43 U1 0 U2 0 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD NOV PY 2001 VL 12 IS 9 BP 384 EP 390 DI 10.1016/S1043-2760(01)00441-6 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 487EJ UT WOS:000171860400014 PM 11595539 ER PT J AU Shillingford, JM Hennighausen, L AF Shillingford, JM Hennighausen, L TI Experimental mouse genetics - answering fundamental questions about mammary gland biology SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID GROWTH-FACTOR RECEPTOR; PROGESTERONE-RECEPTOR; MICE LACKING; DUCTAL MORPHOGENESIS; C/EBP-BETA; FUNCTIONAL-DIFFERENTIATION; TARGETED DISRUPTION; EPITHELIAL-CELLS; TYROSINE KINASE; MILK-EJECTION AB Contemporary gene-targeting techniques now make it possible to alter specific genes in the genome. As a result, a plethora of mouse models have been generated that allow researchers to dissect cell-signaling pathways involved in mammary gland development and in breast cancer. But what have we learned so far? What do these models teach us? This review presents a global picture of how the analyses and comparison of individual knockout mouse models provide important insights into basic mammary gland biology. Particular emphasis is placed upon what is currently known about the signaling pathways involved in the establishment of the mammary ductal tree, and its subsequent proliferation at pregnancy and lactation. In addition to these well-established pathways, we address recent data that describe the role of lesser-known genes in the development of the mammary epithelium. C1 NIH, Lab Genet & Physiol, Bethesda, MD 20817 USA. RP Shillingford, JM (reprint author), NIH, Lab Genet & Physiol, 9000 Rockville Pike, Bethesda, MD 20817 USA. EM jonshi@helix.nih.gov NR 60 TC 20 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD NOV PY 2001 VL 12 IS 9 BP 402 EP 408 DI 10.1016/S1043-2760(01)00471-4 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 487EJ UT WOS:000171860400017 PM 11595542 ER PT J AU Fitzgerald, JR Musser, JM AF Fitzgerald, JR Musser, JM TI Evolutionary genomics of pathogenic bacteria SO TRENDS IN MICROBIOLOGY LA English DT Review ID HELICOBACTER-PYLORI; MYCOBACTERIUM-TUBERCULOSIS; STAPHYLOCOCCUS-AUREUS; CHLAMYDIA-PNEUMONIAE; GENETIC DIVERSITY; ESCHERICHIA-COLI; SEQUENCE; TRACHOMATIS; STRAIN AB Complete genome sequences are now available for multiple strains of several bacterial pathogens and comparative analysis of these sequences is providing important insights into the evolution of bacterial virulence. Recently, DNA microarray analysis of many strains of several pathogenic species has contributed to our understanding of bacterial diversity, evolution and pathogenesis. Comparative genomics has shown that pathogens such as Escherichia coli, Helicobacter pylori and Staphylococcus aureus contain extensive variation in gene content whereas Mycobacterium tuberculosis nucleotide divergence is very limited. Overall, these approaches are proving to be a powerful means of exploring bacterial diversity, and are providing an important framework for the analysis of the evolution of pathogenesis and the development of novel antimicrobial agents. C1 NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, NIH, Hamilton, MT 59840 USA. RP Fitzgerald, JR (reprint author), NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, NIH, 903 S 4th St, Hamilton, MT 59840 USA. NR 40 TC 84 Z9 91 U1 1 U2 6 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0966-842X J9 TRENDS MICROBIOL JI Trends Microbiol. PD NOV PY 2001 VL 9 IS 11 BP 547 EP 553 DI 10.1016/S0966-842X(01)02228-4 PG 7 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA 492DN UT WOS:000172153300015 PM 11825715 ER PT J AU Taylor, JG Choi, EH Foster, CB Chanock, SJ AF Taylor, JG Choi, EH Foster, CB Chanock, SJ TI Using genetic variation to study human disease SO TRENDS IN MOLECULAR MEDICINE LA English DT Review ID SINGLE-NUCLEOTIDE POLYMORPHISMS; HUMAN-GENOME; LINKAGE DISEQUILIBRIUM; POPULATION STRATIFICATION; SEQUENCE VARIATION; PROMOTER REGION; SUSCEPTIBILITY; ASSOCIATION; VARIANTS; BINDING AB The generation of a draft sequence of the human genome has spawned a unique opportunity to investigate the role of genetic variation in human diseases. The difference between any two human genomes has been estimated to be less than 0.1% overall, but still, this means that there are at least several million nucleotide differences per individual. The study of single nucleotide polymorphisms (SNPs), the most common type of variant, is likely to contribute substantially to deciphering genetic determinants of common and rare diseases. The effort to identify SNPs has been accelerated by three developments: the availability of sequence data from the genome project, improved informatic tools for searching the former and high-throughput genotype platforms. With these new tools in hand, dissecting the genetics of disease will rapidly move forward, although a number of formidable challenges will have to be met to see its promise realized in clinical medicine. C1 NCI, Sect Genomic Variat, Pediat Oncol Branch, Ctr Adv Technol, Gaithersburg, MD 20877 USA. RP Chanock, SJ (reprint author), NCI, Sect Genomic Variat, Pediat Oncol Branch, Ctr Adv Technol, 8717 Grovemont Circle, Gaithersburg, MD 20877 USA. EM sc83a@nih.gov OI Taylor, James/0000-0002-4421-1809 NR 33 TC 80 Z9 91 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1471-4914 J9 TRENDS MOL MED JI Trends Mol. Med PD NOV PY 2001 VL 7 IS 11 BP 507 EP 512 DI 10.1016/S1471-4914(01)02183-9 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 490AH UT WOS:000172025600023 PM 11689336 ER PT J AU Prolla, TA Mattson, MP AF Prolla, TA Mattson, MP TI Molecular mechanisms of brain aging and neurodegenerative disorders: lessons from dietary restriction SO TRENDS IN NEUROSCIENCES LA English DT Review ID CORTICAL SYNAPTIC TERMINALS; AMYLOID BETA-PEPTIDE; EXTENDED LIFE-SPAN; ALZHEIMERS-DISEASE; CALORIC RESTRICTION; OXIDATIVE STRESS; HIPPOCAMPAL-NEURONS; PARKINSONS-DISEASE; FOOD RESTRICTION; DENTATE GYRUS AB The application of modern molecular and cell biology technologies to studies of the neurobiology of aging provides a window on the molecular substrates of successful brain aging and neurodegenerative disorders. Aging is associated with increased oxidative stress, disturbances in energy metabolism and inflammation-like processes. Dietary restriction (DR) can extends lifespan and might increase the resistance of the nervous system to age-related neurodegenerative disorders. The neuroprotective effect of DR involves a preconditioning response in which the production of neurotrophic factors and protein chaperones is increased resulting in protection against oxyradical production, stabilization of cellular calcium homeostasis, and inhibition of apoptosis. DR might also enhance neurogenesis, synaptic plasticity and self-repair mechanisms. C1 Univ Wisconsin, Dept Genet, Madison, WI 53706 USA. Univ Wisconsin, Dept Med Genet, Madison, WI 53706 USA. NIA, Neurosci Lab, Gerontol Res Ctr, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. RP Prolla, TA (reprint author), Univ Wisconsin, Dept Genet, 445 Henry Mall, Madison, WI 53706 USA. RI Mattson, Mark/F-6038-2012 NR 78 TC 91 Z9 92 U1 0 U2 5 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD NOV PY 2001 VL 24 IS 11 SU S BP S21 EP S31 DI 10.1016/S0166-2236(00)01957-3 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 492AX UT WOS:000172144400005 PM 11881742 ER PT J AU Aultman, KS Beaty, BJ Walker, ED AF Aultman, KS Beaty, BJ Walker, ED TI Genetically manipulated vectors of human disease: a practical overview SO TRENDS IN PARASITOLOGY LA English DT Editorial Material ID YELLOW-FEVER MOSQUITO; AEDES-AEGYPTI; SYMBIOTIC BACTERIA; TRANSFORMATION; POPULATIONS; RESISTANCE; PROSPECTS; WOLBACHIA; FLIES AB Achievements in genetic engineering of vector insects have raised hopes for their use as public health tools. To evaluate the potential value of genetically manipulated (GM) vectors, the authors propose that a series of important preliminary studies must be conducted. Practical next steps in developing these studies are also discussed. C1 NIAID, Parasitol & Int Programs Branch, Bethesda, MD 20892 USA. Colorado State Univ, Dept Microbiol, Arhropod Borne & Infect Dis, Ft Collins, CO 80523 USA. Michigan State Univ, Dept Entomol, E Lansing, MI 48824 USA. RP Aultman, KS (reprint author), NIAID, Parasitol & Int Programs Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 27 TC 24 Z9 24 U1 1 U2 3 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 NOV PY 2001 VL 17 IS 11 BP 507 EP 509 DI 10.1016/S1471-4922(01)02094-3 PG 3 WC Parasitology SC Parasitology GA 487VT UT WOS:000171900300001 PM 11872381 ER PT J AU Smith, JD Gamain, B Baruch, DI Kyes, S AF Smith, JD Gamain, B Baruch, DI Kyes, S TI Decoding the language of var genes and Plasmodium falciparum sequestration SO TRENDS IN PARASITOLOGY LA English DT Review ID ERYTHROCYTE-MEMBRANE PROTEIN-1; CHONDROITIN SULFATE-A; INTERCELLULAR-ADHESION MOLECULE-1; HISTIDINE-RICH PROTEIN; INFECTED ERYTHROCYTES; BINDING DOMAINS; ANTIGENIC VARIATION; GEOGRAPHIC REGIONS; P-FALCIPARUM; RED-CELLS AB Sequestration and rosetting are key determinants of Plasmodium falciparum pathogenesis. They are mediated by a large family of variant proteins called P. falciparum erythrocyte membrane protein 1 (PfEMP1). PfEMP1 proteins are multispecific binding receptors that are transported to parasite-induced, 'knob-like' binding structures at the erythrocyte surface. To evade immunity and extend infections, parasites clonally vary their expressed PfEMP1. Thus, PfEMP1 are functionally selected for binding while immune selection acts to diversity the family. Here,we describe a new way to analyse PfEMP1 sequence that provides insight into domain function and protein architecture with potential implications for malaria disease. C1 Colorado State Univ, Dept Pathol, Ft Collins, CO 80523 USA. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. John Radcliffe Hosp, Mol Parasitol Grp, Inst Mol Med, Nuffield Dept Med, Oxford OX3 9DU, England. RP Smith, JD (reprint author), Colorado State Univ, Dept Pathol, Ft Collins, CO 80523 USA. NR 58 TC 69 Z9 70 U1 0 U2 4 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 NOV PY 2001 VL 17 IS 11 BP 538 EP 545 DI 10.1016/S1471-4922(01)02079-7 PG 8 WC Parasitology SC Parasitology GA 487VT UT WOS:000171900300008 PM 11872399 ER PT J AU Bridge, H Cumming, BG Parker, AJ AF Bridge, H Cumming, BG Parker, AJ TI Modeling V1 neuronal responses to orientation disparity SO VISUAL NEUROSCIENCE LA English DT Article DE orientation disparity; energy model; cortical area V1 ID CATS VISUAL-CORTEX; STRIATE CORTEX; COMPLEX CELLS; BINOCULAR ORGANIZATION; DEPTH DISCRIMINATION; RECEPTIVE-FIELDS; PERCEPTION; SELECTIVITY; STEREOPSIS AB The contribution of interocular orientation differences to depth perception, at either the neuronal or the psychophysical level, is unclear. To understand the responses of binocular neurons to orientation disparity, we extended the energy model of Ohzawa et al. (1990) to incorporate binocular differences in receptive-field orientation. The responses of the model to grating stimuli with interocular orientation differences were examined, along with the responses to random dot stereograms (RDS) depicting slanted surfaces. The responses to combinations of stimulus orientations in the two eyes were left-right separable, which means there was no consistent response to the binocular orientation difference. All existing neuronal data concerning orientation disparity can be well described by this type of model (even a version with no disparity selectivity). The disparity sensitive model is nonetheless sensitive to changes in RDS slant, although it requires narrow orientation bandwidth to produce substantial modulation. The disparity-insensitive model shows no selectivity to slant in this stimulus. Several modifications to the model were attempted to improve its selectivity for orientation disparity and/or slant. A model built by summing several disparity-sensitive models showed left-right inseparable responses, responding maximally to a consistent orientation difference. Despite this property, the selectivity for slant in RDS stimuli was no better than the simple disparity-selective model. The range of models evaluated here demonstrate that interocular orientation differences are neither necessary nor sufficient for signaling slant. In contrast, within the framework of the energy model, positional disparity sensitivity appears to be both necessary and sufficient. C1 Univ Oxford, Physiol Lab, Oxford OX1 3PT, England. NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA. RP Bridge, H (reprint author), Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England. RI Parker, Andrew/I-7867-2013 OI Parker, Andrew/0000-0001-5800-0407 NR 29 TC 6 Z9 6 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0952-5238 J9 VISUAL NEUROSCI JI Visual Neurosci. PD NOV-DEC PY 2001 VL 18 IS 6 BP 879 EP 891 DI 10.1017/S0952523801186049 PG 13 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA 548RM UT WOS:000175403200004 PM 12020078 ER PT J AU Veenstra, GJC Wolffe, AP AF Veenstra, GJC Wolffe, AP TI Constitutive genomic methylation during embryonic development of Xenopus SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE DNA methylation; Xenopus; demethylation; embryo; mid-blastula transitions; CpG ID DNA METHYLATION; HISTONE DEACETYLASE; DROSOPHILA-MELANOGASTER; MIDBLASTULA TRANSITION; CYTOSINE METHYLATION; PATERNAL GENOME; MOUSE EMBRYO; COMPLEX; TRANSCRIPTION; DEMETHYLATION AB Methylation of CpG dinucleotides is a predominant modification of genomic DNA in many species, especially in vertebrates. This modification, generally associated with transcriptional repression, is rapidly and globally lost during mammalian pre-implantation development. This loss of methylation is gradually reversed during subsequent stages of development. Here we show that the amphibian Xenopus laevis maintains high levels of DNA methylation during early embryonic development. The methylation status of specific loci is independent of the temporal expression profile. The observations have profound implications for the regulation of early embryonic gene regulation and genome function. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NICHHD, Mol Embryol Lab, Bethesda, MD 20892 USA. RP Veenstra, GJC (reprint author), NIH, Genet Mol Lab, Bldg 6B,Rm 420, Bethesda, MD 20892 USA. RI Veenstra, Gert Jan C./D-4963-2012 OI Veenstra, Gert Jan C./0000-0002-7787-4940 NR 33 TC 19 Z9 19 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD OCT 31 PY 2001 VL 1521 IS 1-3 BP 39 EP 44 DI 10.1016/S0167-4781(01)00280-9 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 491DB UT WOS:000172091800005 PM 11690634 ER PT J AU Peters, JM Park, Y Gonzalez, FJ Pariza, MW AF Peters, JM Park, Y Gonzalez, FJ Pariza, MW TI Influence of conjugated linoleic acid on body composition and target gene expression in peroxisome proliferator-activated receptor alpha-null mice SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS LA English DT Article DE body composition; gene expression; conjugated linoleic acid; peroxisome proliferator-activated receptor alpha ID STEAROYL-COA DESATURASE; PPAR-ALPHA; FATTY-ACIDS; TRANS-10,CIS-12 ISOMER; LIPOPROTEIN METABOLISM; ADIPOSE-TISSUE; MOUSE; RAT; ATHEROSCLEROSIS; EICOSANOIDS AB The mechanisms underlying the beneficial effects of conjugated linoleic acid (CLA) are unknown, but one hypothesis is that they are mediated by the nuclear receptor, peroxisome proliferator-activated receptor (PPAR alpha). In this work, the effect of dietary CLA on body weight gain, body composition, serum lipids and tissue specific PPAR target gene expression was examined in PPAR alpha -null mice. Male wild-type or PPAR alpha -null mice were fed either a control diet or one containing 0.5% CLA for a period of 4 weeks. Weight gain in wild-type and PPAR alpha -null mice fed CLA was similar, and significantly less than controls. Whole body fat content was lower in wild-type and PPAR alpha -null mice while whole body protein content was increased in both genotypes fed CLA compared to controls. Serum triglycerides were lowered in both genotypes as a result of dietary CLA. While CLA feeding resulted in specific activation of PPAR alpha in liver, alterations in Ever, adipose and muscle mRNAs were also found that were independent of PPAR alpha genotype including those encoding uncoupling proteins (UCPs), mitochondrial fatty acid oxidizing enzymes, and fatty acid transporter. These results demonstrate that despite specific activation of PPAR alpha -dependent gene expression, the influence of CLA on body composition appears to be independent of PPAR alpha. Further, CLA causes increased levels of mRNAs encoding lipid metabolizing and mitochondrial uncoupling proteins that likely contribute to the mechanisms underlying reduced fat/increased lean body mass resulting from consumption of dietary CLA. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Penn State Univ, Dept Vet Sci, Fenske Lab 226, University Pk, PA 16802 USA. Penn State Univ, Ctr Mol Toxicol, Fenske Lab 226, University Pk, PA 16802 USA. Univ Wisconsin, Inst Food Res, Dept Food Microbiol & Toxicol, Madison, WI 53706 USA. NCI, Lab Metab, Bethesda, MD 20892 USA. RP Peters, JM (reprint author), Penn State Univ, Dept Vet Sci, Fenske Lab 226, University Pk, PA 16802 USA. RI Park, Yeonhwa/B-9064-2008; Peters, Jeffrey/D-8847-2011 OI Park, Yeonhwa/0000-0001-9727-0899; NR 48 TC 107 Z9 111 U1 0 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1388-1981 J9 BBA-MOL CELL BIOL L JI Biochim. Biophys. Acta Mol. Cell Biol. Lipids PD OCT 31 PY 2001 VL 1533 IS 3 BP 233 EP 242 DI 10.1016/S1388-1981(01)00155-X PG 10 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 494DJ UT WOS:000172266200006 PM 11731333 ER PT J AU Loftus, SK Larson, DM Watkins-Chow, D Church, DM Pavan, WJ AF Loftus, SK Larson, DM Watkins-Chow, D Church, DM Pavan, WJ TI Generation of RCAS vectors useful for functional genomic analyses SO DNA RESEARCH LA English DT Article DE RCAS; tv-a; retrovirus; recombination; Gateway; gene expression ID ROUS-SARCOMA VIRUS; SITE-SPECIFIC RECOMBINATION; RETROVIRAL VECTORS; AVIAN-SARCOMA; GENE-TRANSFER; DNA-SYNTHESIS; CELL-LINE; SYSTEM; MICE; INTEGRATION AB Avian leukosis type A virus-derived retroviral vectors have been used to introduce genes into cells expressing the corresponding avian receptor tv-a. This includes the use of Replication-Competent Avian sarcoma-leukosis virus (ASLV) long terminal repeat (LTR) with Splice acceptor (RCAS) vectors in the analysis of avian development, human and murine cell cultures, murine cell lineage studies and cancer biology. Previously, cloning of genes into this virus was difficult due to the large size of the vector and sparse cloning sites. To overcome some of the disadvantages of traditional cloning using the RCASBP-Y vector, we have modified the RCASBP-Y to incorporate "Gateway" site-specific recombination cloning of genes into the construct, either with or without HA epitope tags. We have found the repetitive "att" sequences, which are the targets for site-specific recombination, do not impair the production of infectious viral particles or the expression of the gene of interest. This is the first instance of site-specific recombination being used to generate retroviral gene constructs. These viral constructs will allow for the efficient transfer and expression of cDNAs needed for functional genomic analyses. C1 NHGRI, Mouse Embryol Sect, Genet Dis Res Inst, NIH, Bethesda, MD 20892 USA. NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA. RP Loftus, SK (reprint author), NHGRI, Mouse Embryol Sect, Genet Dis Res Inst, NIH, Bldg 49,Room 4A67,49 Convent Dr,MSC4472, Bethesda, MD 20892 USA. NR 23 TC 38 Z9 39 U1 0 U2 3 PU UNIVERSAL ACADEMY PRESS INC PI TOKYO PA ORDER DEPT., C P O BOX 235, TOKYO, 100-8691, JAPAN SN 1340-2838 J9 DNA RES JI DNA Res. PD OCT 31 PY 2001 VL 8 IS 5 BP 221 EP 226 DI 10.1093/dnares/8.5.221 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 497KL UT WOS:000172454400004 PM 11759842 ER PT J AU Fiorenza, MT Mukhopadhyay, M Westphal, H AF Fiorenza, MT Mukhopadhyay, M Westphal, H TI Expression screening for Lhx3 downstream genes identifies Thg-1pit as a novel mouse gene involved in pituitary development SO GENE LA English DT Article DE THG-1; TSC-22/DIP/bun; leucine zipper; TSC-box ID BETA-STIMULATED CLONE-22; SLEEP-INDUCING PEPTIDE; LEUCINE-ZIPPER; HOMEOBOX GENES; TSC-22; ORGANOGENESIS; HOMOLOG; TRANSCRIPTION; REGULATOR; PROTEINS AB Thg-1pit, a novel mouse gene, was detected in a screen for genes that are differentially expressed in the developing pituitary of wild-type and Lhx3 null mutant embryos. The predicted translation product of the Thg-1pit gene contains a C-terminal TSC-box adjacent to a leucine zipper motif. These features are characteristic for the TSC-22/DIP/bun family of proteins. The onset of prominent Thg-1pit expression coincides with Lhx3 activation at early stages of pituitary development. Expression is further enhanced as cells begin to differentiate within the developing pituitary gland. No expression is observed in the pituitary rudiment of mutants that lack Lhx3 function. A possible role is thus suggested for Lhx3 activities in the regulation of Thg-1pit function during early steps of pituitary organogenesis. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. RP Westphal, H (reprint author), NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. OI Fiorenza, Maria Teresa/0000-0002-5079-4019 NR 27 TC 10 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 31 PY 2001 VL 278 IS 1-2 BP 125 EP 130 DI 10.1016/S0378-1119(01)00715-6 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 498WR UT WOS:000172537000012 PM 11707329 ER PT J AU Fu, SD Stevenson, H Strovel, JW Haga, SB Stamberg, J Do, K Berg, PE AF Fu, SD Stevenson, H Strovel, JW Haga, SB Stamberg, J Do, K Berg, PE TI Distinct functions of two isoforms of a homeobox gene, BP1 and DLX7, in the regulation of the beta-globin gene SO GENE LA English DT Article DE hemoglobin; homeodomain; distal-less; mapping ID DROSOPHILA KRUPPEL PROTEIN; HOMEODOMAIN PROTEINS; LIMB DEVELOPMENT; TRANSCRIPTION; EXPRESSION; MUTATION; BINDING; DOMAINS; HOX AB Homeotic proteins are transcription factors that regulate the expression of multiple genes involved in development and differentiation. We previously isolated a cDNA encoding such a protein from the human leukemia cell line K562, termed Beta Protein 1 (BP1), which is involved in negative regulation of the human beta -globin gene. Sequence comparison revealed that BP1 is a member of the distal-less (DLX) family of homeobox genes and that it shares its homeodomain and 3' sequences with another DLX cDNA, DLX7. BP1 and DLX7 exhibit unique 5' regions, diverging at nucleotide 565 of BP1. We mapped this new distal-less family member BP1 to chromosome 17q21-22 by FISH and PCR, which is the same locus to which DLX7 has been mapped. These results strongly suggest that BP1 and DLX7 are isoforms (derived from the same gene). Since our previous data demonstrated that BP1 and DLX7 are frequently co-expressed, we determined whether DLX7 is also involved in the negative regulation of the beta -globin gene. Mobility shift assays demonstrated that both BP1 and DLX7 proteins, synthesized in vitro, bind to the same BP1 binding site. However, using transient assays, we showed that although BP1 represses activity of a reporter gene through either of two silencer DNA sequences upstream of the beta -globin gene, DLX7 did not show repressor activity against the beta -globin promoter. Further characterization of these apparent isoforms is of significance since they are jointly expressed in acute myeloid leukemia and in many leukemia cell lines. (C) 2001 Elsevier Science B.V. All rights reserved. C1 George Washington Univ, Med Ctr, Dept Biochem & Mol Biol, Washington, DC 20037 USA. Univ Maryland, Sch Med, Dept Pediat, Div Genet, Baltimore, MD 21201 USA. NIH, Off Biotechnol Act, Bethesda, MD 20892 USA. RP Berg, PE (reprint author), George Washington Univ, Med Ctr, Dept Biochem & Mol Biol, Ross Bldg,Room 533,2300 Eye St NW, Washington, DC 20037 USA. FU NIDDK NIH HHS [R01 DK53533] NR 30 TC 27 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 31 PY 2001 VL 278 IS 1-2 BP 131 EP 139 DI 10.1016/S0378-1119(01)00716-8 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 498WR UT WOS:000172537000013 PM 11707330 ER PT J AU Jo, D Lyu, MS Cho, EG Park, D Kozak, CA Kim, MG AF Jo, D Lyu, MS Cho, EG Park, D Kozak, CA Kim, MG TI Identification and genetic mapping of the mouse Fkbp9 gene encoding a new member of FK506-binding protein family SO MOLECULES AND CELLS LA English DT Article DE FKBP; genetic mapping ID RAPAMYCIN-BINDING-PROTEIN; THYMIC STROMAL CELLS; MOLECULAR-CLONING; RECEPTOR; SEQUENCE AB We have isolated a gene from a cDNA library generated from the thymus of a mouse with severe combined immune deficiency, termed FKBP9, that encodes a protein related to FK506-binding protein 6 (65 kDa, FKBP65). FKBP9 contains four peptidyl-prolyl cis-trans isomerase (PPIase) signature and two EF-hand domains which is identical to FKBP6/65 in overall structural organization. However, the two proteins share only 66% amino acid identity. FKBP9 is expressed at high levels in mouse heart, muscle, lung, and kidney. While FKBP6 was previously mapped to chromosome 11, the Fkbp9 gene was mapped to mouse chromosome 6 by analysis of a multilocus cross. These results identify a new member of the mouse FKBP protein family located on a separate chromosome. C1 NIAID, Cellular & Mol Immunol Lab, NIH, Bethesda, MD 20892 USA. Kwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea. NIH, Mol Microbiol Lab, Bethesda, MD 20892 USA. Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea. RP Kim, MG (reprint author), NIAID, Cellular & Mol Immunol Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 17 TC 5 Z9 6 U1 0 U2 0 PU SPRINGER-VERLAG SINGAPORE PTE LTD PI SINGAPORE PA #04-01 CENCON I, 1 TANNERY RD, SINGAPORE 347719, SINGAPORE SN 1016-8478 J9 MOL CELLS JI Mol. Cells PD OCT 31 PY 2001 VL 12 IS 2 BP 272 EP 275 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 488GC UT WOS:000171927000021 PM 11710534 ER PT J AU Ogata, H Sato, H Takatsuka, J De Luca, LM AF Ogata, H Sato, H Takatsuka, J De Luca, LM TI Human breast cancer MDA-MB-231 cells fail to express the neurofibromin protein, lack its type I mRNA isoform and show accumulation of P-MAPK and activated Ras SO CANCER LETTERS LA English DT Article DE neurofibromin; activated ras; phosphorylated MAPK; breast cancer cells ID HUMAN-TUMORS; NF1 GENE; MUTATIONS; VIVO; LINE; ONCOGENE; GAP AB Neurofibromin is a tumor suppressor protein, which is similar in function to the GTPase activating protein (GAP), p120GAP, in that it accelerates inactivation of Ras. Mutations in the NF1 gene cause neurofibromatosis type 1, NF1, an autosomal dominant disease with a diverse spectrum of clinical manifestations, including neurofibromas. Ras activation (GTP binding) is induced by the GTP exchange factor Sos and its inactivation is regulated through the GAPs (p120GAP and neurofibromin). Strikingly, neurofibromin was nearly absent in MB-231 human breast cancer cells and present in the remaining four cell lines studied, with higher levels in BT-474 and MB-453 than in MCF-7 and BT-20 cells, as tested with polyclonal antibodies to both the N-terminal as well as the C-terminal peptides. Coordinated with the near absence of neurofibromin, these cells also presented with much greater levels of P-MAPK and activated Ras. Further, RT-PCR analysis demonstrated the absence of expression of NFI mRNA type I isoform only in the MB-231 cell lines. This result documents for the first time an altered NFI expression at the protein and mRNA levels in MDA-MB-231 breast cancer cells. Published by Elsevier Science Ireland Ltd. C1 NIH, Cellular Carcinogenesis & Tumor Promot Lab, Bethesda, MD 20892 USA. RP De Luca, LM (reprint author), NIH, Cellular Carcinogenesis & Tumor Promot Lab, Bldg 37,Room 3A-17,37 Convent Dr, Bethesda, MD 20892 USA. NR 25 TC 32 Z9 32 U1 0 U2 0 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 OCT 30 PY 2001 VL 172 IS 2 BP 159 EP 164 DI 10.1016/S0304-3835(01)00648-6 PG 6 WC Oncology SC Oncology GA 478LK UT WOS:000171347500009 PM 11566491 ER PT J AU Phillips, TM AF Phillips, TM TI Multi-analyte analysis of biological fluids with a recycling immunoaffinity column array SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Article DE immunoaffinity; antibody array; laser-induced fluorescence; on-line detection ID ANTIBODY IMMOBILIZATION; IMMUNOASSAY; CHROMATOGRAPHY; CYTOKINES; FUTURE AB A system for isolating and measuring up to 30 analytes in a single biological sample is described. The system is based on recycling a pre-labeled sample through an array of capillary immunoaffinity columns, each packed with,lass beads, coated with a different antibody, thus enabling each column to isolate and extract a single analyte. Detection of the bound analytes is achieved by laser-induced fluorescence (LIF), using a laboratory-built scanning detector coupled to a fiber-optic spectrometer. The array can be regenerated up to 200 times, provided a suitable temperature is maintained. The individual immunoaffinity columns are able to bind between 2.9 and 3.6 ng of analyte, depending upon the individual column, with lower limits of detection (LOD) in the order of 1.6-2.8 pg/ml. The inter- and intra-assay coefficients of variation (CV) for all 30 columns in the array were less than 6.03 +/- 0.33 at analyte concentrations of 100 pg/ml. Comparison to standard enzyme-immunoassays demonstrated r(2) values in the range of 0.9151-0.9855 when analyzed by least-squares linear regression. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NIH, Ultramicro Analyt Immunochem Resource, Div Bioeng & Phys Sci, Off Res Serv, Bethesda, MD 20892 USA. RP Phillips, TM (reprint author), NIH, Ultramicro Analyt Immunochem Resource, Div Bioeng & Phys Sci, Off Res Serv, Bldg 13-3E42,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 22 TC 30 Z9 31 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-022X J9 J BIOCHEM BIOPH METH JI J. Biochem. Biophys. Methods PD OCT 30 PY 2001 VL 49 IS 1-3 BP 253 EP 262 DI 10.1016/S0165-022X(01)00202-0 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 497RF UT WOS:000172468700015 PM 11694283 ER PT J AU Hoover, DR Blackwelder, WC AF Hoover, DR Blackwelder, WC TI Allocation of subjects to test null relative risks smaller than one SO STATISTICS IN MEDICINE LA English DT Article ID INTERVAL ESTIMATION; CONTROLLED TRIAL; CLINICAL-TRIALS; SAMPLE-SIZE; VACCINE; PROPORTIONS; PERTUSSIS; FORMULAS; TABLES; POWER AB Allocating a proportion k' = 1/(1 + rootr(o)) of subjects to an intervention is a practical approach to approximately maximize power for testing whether an intervention reduces relative risk of disease below a null ratio r(o) < 1. Furthermore, allocating k(s)', a convenient fraction close to k', to intervention performs nearly as well; for example, allocating k(s)'=3/5 for 0.5r(o)>0.33,2/3 for 0.33 greater than or equal tor(o)>0.17 and 3/4 for 0.17 greater than or equal to r(o) greater than or equal to 0.10. Both k' and k(s)' are easily calculated and invariant to alterations in disease rate estimates under null and alternative hypotheses, when ro remains constant. In examples that we studied, allocating k' (or k(s)') subjects to intervention achieved close to the minimum possible sample size, given test size and power (equivalently, maximum power, given test size and sample size), for likelihood score tests. Compared to equal allocation, k' and k(s)' reduced sample sizes by amounts ranging from similar to 5.5 per cent for r(o) = 0.50 to similar to 24 per cent for r(o) = 0.10. These sample size savings may be particularly important for large studies of prophylactic interventions such as vaccines. While k' was derived from variance minimization for an arcsine transformation, we do not recommend the arcsine test, since its true size exceeded the nominal value. In contrast, the true size for the uncorrected score test was less than the nominal size. A skewness correction made the size of the score test very close to the nominal level and slightly increased power. We recommend using the score test, or the skewness-corrected score test, for planing studies designed to show a ratio of proportions is less than a prespecified null ratio r(o) < 1. Copyright (C) 2001 John Wiley & Sons, Ltd. C1 Rutgers State Univ, Dept Stat, Piscataway, NJ 08854 USA. NIAID, Bethesda, MD 20892 USA. RP Hoover, DR (reprint author), Rutgers State Univ, Dept Stat, 473 Hill Ctr,110 Frelinghuysen Rd, Piscataway, NJ 08854 USA. FU NIMH NIH HHS [MH43450] NR 24 TC 3 Z9 3 U1 1 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0277-6715 J9 STAT MED JI Stat. Med. PD OCT 30 PY 2001 VL 20 IS 20 BP 3071 EP 3082 DI 10.1002/sim.946.abs PG 12 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA 482EY UT WOS:000171563800006 PM 11590633 ER PT J AU Weins, A Schwarz, K Faul, C Barisoni, L Linke, WA Mundel, P AF Weins, A Schwarz, K Faul, C Barisoni, L Linke, WA Mundel, P TI Differentiation- and stress-dependent nuclear cytoplasmic redistribution of myopodin, a novel actin-bundling protein SO JOURNAL OF CELL BIOLOGY LA English DT Article DE actin-binding protein; muscle differentiation; nuclear-cytoplasmic translocation; synaptopodin gene family; Z-disc ID FOCAL SEGMENTAL GLOMERULOSCLEROSIS; BINDING PROTEIN; SKELETAL-MUSCLE; CARDIAC-MUSCLE; ALPHA-ACTININ; HEAT-SHOCK; CELLS; NEBULIN; SIGNALS; TRANSLOCATION AB W e report the cloning and functional characterization of myopodin, the second member of the synaptopodin gene family. Myopodin shows no significant homology to any known protein except synaptopodin. Northern blot analysis resulted in a 3.6-kb transcript for mouse skeletal and heart muscle. Western blots showed an 80-kD signal for skeletal and a 95-kD signal for heart muscle. Myopodin contains one PPXY motif and multiple PXXP motifs. Myopodin colocalizes with alpha -actinin and is found at the Z-disc as shown by immunogold electron microscopy. In myoblasts, myopodin shows preferential nuclear localization. During myotube differentiation, myopodin binds to stress fibers in a punctuated pattern before incorporation into the Z-disc. Myopodin can directly bind to actin and contains a novel actin binding site in the center of the protein. Myopodin has actin-bundling activity as shown by formation of latrunculin-A-sensitive cytosolic actin bundles and nuclear actin loops in transfected cells expressing green fluorescent protein-myopodin. Under stress conditions, myopodin accumulates in the nucleus and is depleted from the cytoplasm. Nuclear export of myopodin is sensitive to leptomycin B, despite the absence of a classical nuclear export sequence. We propose a dual role for myopodin as a structural protein also participating in signaling pathways between the Z-disc and the nucleus. C1 Yeshiva Univ Albert Einstein Coll Med, Div Nephrol, Dept Med, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Anat & Cell Biol, Bronx, NY 10461 USA. Univ Heidelberg, Dept Physiol, D-69120 Heidelberg, Germany. NIDDK, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21287 USA. RP Mundel, P (reprint author), Yeshiva Univ Albert Einstein Coll Med, Div Nephrol, Dept Med, 1300 Morris Pk Ave, Bronx, NY 10461 USA. RI Faul, Christian/D-1549-2011; Linke, Wolfgang/E-8662-2012 FU NIDDK NIH HHS [R01 DK057683, DK57683-01] NR 48 TC 82 Z9 85 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT 29 PY 2001 VL 155 IS 3 BP 393 EP 403 DI 10.1083/jcb.200012039 PG 11 WC Cell Biology SC Cell Biology GA 487YB UT WOS:000171905900007 PM 11673475 ER PT J AU Forster, HP Emanuel, E Grady, C AF Forster, HP Emanuel, E Grady, C TI The 2000 revision of the Declaration of Helsinki: a step forward or more confusion? SO LANCET LA English DT Article ID DEVELOPING-COUNTRIES; TRIALS; TRANSMISSION; ETHICS AB At a time when there was great attention and intense public controversy surrounding clinical (especially multinational) research, the 52nd general assembly of the World Medical Association (WMA) adopted the 5th revision of the Declaration of Helsinki (in October, 2000)-available at www.wma.net. These revisions are the most substantial adaptations since those adopted by the 29th WMA assembly In October, 1975. The commitment to revision of the declaration acknowledged that deficiencies and disagreements in interpretation needed to be corrected and that ethical standards evolve. Nevertheless, this revision process resulted in a controversial version of the declaration. Reports on the revisions have focused mainly on clinical trials that use placebos;(1,2) but because of the role of the Declaration of Helsinki in the ethics of research, a more thorough examination is needed. Here, we analyse the process of revision and the major changes made to the declaration. C1 NIH, Dept Clin Bioeth, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Grady, C (reprint author), NIH, Dept Clin Bioeth, Warren G Magnuson Clin Ctr, Bldg 10,Room 1C118, Bethesda, MD 20892 USA. NR 31 TC 47 Z9 49 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 OCT 27 PY 2001 VL 358 IS 9291 BP 1449 EP 1453 DI 10.1016/S0140-6736(01)06534-5 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 488MK UT WOS:000171940100037 PM 11705513 ER PT J AU Malozowski, S AF Malozowski, S TI Role of hormones in puberty SO LANCET LA English DT Letter C1 NIDDKD, Div Diabet Endocrinol & Metab Dis, Bethesda, MD 20892 USA. RP Malozowski, S (reprint author), NIDDKD, Div Diabet Endocrinol & Metab Dis, 6707 Democracy Blvd, Bethesda, MD 20892 USA. NR 4 TC 0 Z9 0 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 OCT 27 PY 2001 VL 358 IS 9291 BP 1459 EP 1459 DI 10.1016/S0140-6736(01)06506-0 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 488MK UT WOS:000171940100050 PM 11705528 ER PT J AU Hoffmann, SC Stanley, EM Cox, ED Craighead, N DiMercurio, BS Koziol, DE Harlan, DM Kirk, AD Blair, PJ AF Hoffmann, SC Stanley, EM Cox, ED Craighead, N DiMercurio, BS Koziol, DE Harlan, DM Kirk, AD Blair, PJ TI Association of cytokine polymorphic inheritance and in vitro cytokine production in anti-CD3/CD28-stimulated peripheral blood lymphocytes SO TRANSPLANTATION LA English DT Article ID NECROSIS-FACTOR-ALPHA; JUVENILE CHRONIC ARTHRITIS; CD4(+) T-CELLS; TNF-ALPHA; RENAL-TRANSPLANTATION; MONONUCLEAR-CELLS; PROMOTER POLYMORPHISM; INDUCED APOPTOSIS; GENE PROMOTER; IL-2 GENE AB Background. Genetic variations in cytokine genes are thought to regulate cytokine protein production. However, studies using T cell mitogens have not always demonstrated a significant relationship between cytokine polymorphisms and in vitro protein production. Furthermore, the functional consequence of a polymorphism at position -330 in the IL-2 gene has not been described. We associated in vitro protein production with cytokine gene polymorphic genotypes after costimulation of cultured peripheral blood lymphocytes. Methods. PBL were isolated from forty healthy volunteers. Cytokine protein production was assessed by enzyme-linked immunosorbent assay. Polymorphisms in interleukin- (IL) 2, IL-6, IL-10, tumor necrosis factor (TNF-alpha), tumor growth factor (TGF-beta), and interferon (IFN-gamma) were determined by polymerase chain reaction (PCR). Results. Statistical difference between protein production and cytokine polymorphic variants in the IL-10, IFN-gamma, and TNF-alpha genes was not evident after 48-hour stimulation with concanavalin-A. In contrast, after anti-CD3/CD28 stimulation significant differences (P <0.05) were found among high and low producers for IL-2, IL-6, and among high, intermediate, and low producers for IFN-gamma, and IL-10. Augmented levels of IL-2 in individuals that were homozygous for the polymorphic IL-2 allele were due to an early and sustained enhancement of IL-2 production. No association was found among TNF-alpha and TGF-beta genotypes and protein production. Conclusion. Polymorphisms in IL-2, IL-6, IL-10, and IFN-gamma genes are associated with their protein production after anti-CD3/CD28 stimulation. The profound effect of the IL-2 gene polymorphism in homozygous individuals may serve as a marker for those that could mount the most vigorous allo- or autoimmune responses, or perhaps become tolerant more easily. C1 Natl Naval Med Res Inst, NIDDK, Navy Transplantat & Autoimmun Branch, Bethesda, MD 20889 USA. Walter Reed Army Med Ctr, Dept Surg, Washington, DC 20307 USA. NIH, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Dept Med, Bethesda, MD 20889 USA. RP Blair, PJ (reprint author), Natl Naval Med Res Inst, NIDDK, Navy Transplantat & Autoimmun Branch, Bldg 46,Rm 2421,8901 Wisconsin Ave, Bethesda, MD 20889 USA. RI Kirk, Allan/B-6905-2012 NR 49 TC 250 Z9 266 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 27 PY 2001 VL 72 IS 8 BP 1444 EP 1450 DI 10.1097/00007890-200110270-00019 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 488QV UT WOS:000171947900019 PM 11685118 ER PT J AU Massicot-Fisher, J Noel, P Madsen, JC AF Massicot-Fisher, J Noel, P Madsen, JC TI Recommendations of the National Heart, Lung and Blood Institute Heart and Lung Tolerance Working Group SO TRANSPLANTATION LA English DT Article ID BONE-MARROW INFUSION; MINIATURE SWINE; TRANSPLANTATION C1 NHLBI, Div Heart & Vasc Dis, NIH, Bethesda, MD 20892 USA. NHLBI, Div Lung Dis, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp,Transplantat Biol Res Ctr, Dept Surg,Div Cardiac Surg, Boston, MA USA. RP Massicot-Fisher, J (reprint author), NHLBI, Div Heart & Vasc Dis, NIH, 6701 Rockledge Dr,MSC 7940, Bethesda, MD 20892 USA. NR 9 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 27 PY 2001 VL 72 IS 8 BP 1467 EP 1470 DI 10.1097/00007890-200110270-00028 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 488QV UT WOS:000171947900028 PM 11685126 ER PT J AU Hodge, DR Xiao, WH Clausen, PA Heidecker, G Szyf, M Farrar, WL AF Hodge, DR Xiao, WH Clausen, PA Heidecker, G Szyf, M Farrar, WL TI Interleukin-6 regulation of the human DNA methyltransferase (HDNMT) gene in human erythroleukemia cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROSTATE-CANCER; BINDING PROTEIN; METHYLATED DNA; EXPRESSION; PROMOTER; IL-6; 5-METHYLCYTOSINE; DIFFERENTIATION; INDUCTION; TISSUES AB Methylation of mammalian DNA by the DNA methyltransferase enzyme (dnmt-1) at CpG dinucleotide sequences has been recognized as an important epigenetic control mechanism in regulating the expression of cellular genes (Yen, R. W., Vertino, P. M., Nelkin, B. D., Yu, J. J., el-Deiry, W., Cumaraswamy, A., Lennon, G. G., Trask, B. J., Celano, P., and Baylin, S. B. (1992) Nucleic Acids Res. 20, 2287-2291; Ramehandani, S., Bigey, P., and Szyf, M. (1998) Biol. Chem. 379, 535-5401). Here we show that interleukin (IL)-6 regulates the methyltransferase promoter and resulting enzyme activity, which requires transcriptional activation by the Fli-1 transcription factor (Spyropoulos, D. D., Pharr, P. N., Lavenburg, K. R., Jackers, P., Papas, T. S., Ogawa, M., and Watson, D. K. (1998) Mol. Cell. Biol. 15, 5643-5652). The data suggest that inflammatory cytokines such as IL-6 may exert many epigenetic changes in cells via the regulation of the methyltransferase gene. Furthermore, IL-6 regulation of transcription factors like Fli-1, which can help to direct cells along opposing differentiation pathways, may in fact be reflected in part by their ability to regulate the methylation of cellular genes. C1 NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick,NIH, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Cytokine Mol Mechanisms Sect, NIH, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, NIH, Frederick, MD 21702 USA. Invitrogen Corp, Gaithersburg, MD 20852 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Leukocyte Biol, NIH, Frederick, MD 21702 USA. McGill Univ, Dept Pharmacol, Montreal, PQ H3G 1Y6, Canada. RP Hodge, DR (reprint author), NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick,NIH, Frederick, MD 21702 USA. RI Xiao, Weihua/N-2775-2013 OI Xiao, Weihua/0000-0001-9102-6326 FU NCI NIH HHS [N01-CO-56000] NR 33 TC 105 Z9 115 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 39508 EP 39511 DI 10.1074/jbc.C100343200 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200003 PM 11551897 ER PT J AU Pummill, PE Kempner, ES DeAngelis, PL AF Pummill, PE Kempner, ES DeAngelis, PL TI Functional molecular mass of a vertebrate hyaluronan synthase as determined by radiation inactivation analysis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STREPTOCOCCUS-PYOGENES; LEUCONOSTOC-MESENTEROIDES; CHITIN OLIGOSACCHARIDES; SYNTHESIZE HYALURONAN; PASTEURELLA-MULTOCIDA; TARGET ANALYSIS; DG42 GENE; IN-VITRO; XENOPUS; PROTEIN AB Hyaluronan (RA), a linear polysaccharide composed of N-acetylglucosamine-glucuronic acid repeats, is found in the extracellular matrix of vertebrate tissues as well as the capsule of several pathogenic bacteria. The HA synthases (HASs) are dual-action glycosyltransferases that catalyze the addition of two different sugars from UDP-linked precursors to the growing HA chain. The prototypical vertebrate hyaluronan synthase, x1-HAS1 (or DG42) from Xenopus laevis, is a 588-residue membrane protein. Recently, the streptococcal enzyme was found to function as a monomer of protein with similar to 16 lipid molecules. The vertebrate enzymes are larger than the streptococcal enzymes; based on the vertebrate HAS deduced amino acid sequence, two additional membrane-associated regions at the carboxyl terminus are predicted. We have utilized radiation inactivation to measure the target size of yeast-derived recombinant x1HAS1. The target size of HAS activity was confirmed using two internal standards. First, samples were spiked with glucose-6-phosphate dehydrogenase, an enzyme of known molecular weight. Second, parallel samples of native x1HAS1 and a x1HAS1-green fluorescent protein fusion (833 residues) were compared; substantial confidence was gained by using this novel internal standard. Our test also corroborated the basic tenets of radiation inactivation theory. We found that the vertebrate HAS protein functions catalytically as a monomer. C1 Univ Oklahoma, Hlth Sci Ctr, Dept Biochem & Mol Biol, Oklahoma City, OK 73104 USA. NIAMSD, Phys Biol Lab, NIH, Bethesda, MD 20892 USA. RP DeAngelis, PL (reprint author), Univ Oklahoma, Hlth Sci Ctr, Dept Biochem & Mol Biol, 940 Stanton L Young Blvd, Oklahoma City, OK 73104 USA. FU NIGMS NIH HHS [GM 56497] NR 37 TC 22 Z9 23 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 39832 EP 39835 DI 10.1074/jbc.M105489200 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200044 PM 11517224 ER PT J AU Venkatesan, S Petrovic, A Locati, M Kim, YO Weissman, D Murphy, PM AF Venkatesan, S Petrovic, A Locati, M Kim, YO Weissman, D Murphy, PM TI A membrane-proximal basic domain and cysteine cluster in the C-terminal tail of CCR5 constitute a bipartite motif critical for cell surface expression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-COUPLED RECEPTORS; IMMUNODEFICIENCY-VIRUS TYPE-1; CYCLOPHILIN HOMOLOG NINAA; HIV-1 CORECEPTOR ACTIVITY; MACROPHAGE-TROPIC HIV-1; ACETYL-D-GALACTOSAMINE; CHEMOKINE RECEPTOR; ENDOPLASMIC-RETICULUM; O-GLYCOSYLATION; GOLGI-COMPLEX AB We examined the structural requirements for cell surface expression, signaling, and human immunodeficiency virus co-receptor activity for the chemokine receptor, CCR5. Serial C-terminal truncation of CCR5 resulted in progressive loss of cell surface expression; mutants truncated at the 317th position and shorter were not detected at the cell surface. Alanine substitution of basic residues in the membrane-proximal domain (residues 314-322) in the context of a full-length C-tail resulted in severe reduction in surface expression. C-terminal truncation that excised the three cysteines in this domain reduced surface expression, but further truncation of upstream basic residue(s) abolished surface expression. Substituting the carboxyl-terminal domain of CXCR4 for that of CCR5 failed to rectify the trafficking defect of the tailless CCR5. In contrast, tailless CXCR4 or a CXCR4 chimera that exchanged the native cytoplasmic domain for that of wild type CCR5 was expressed at the cell surface. Deletion mutants that expressed at the cell surface responded to chemokine stimulation and mediated human immunodeficiency virus entry. Substitution of all serine and threonine residues in the C-terminal tail of CCR5 abolished chemokine-mediated receptor phosphorylation but preserved downstream signaling (Ca2+ flux), while substitutions of tyrosine residues in the C-tail affected neither phenotype. CCR5 mutants that failed to traffic to the plasma membrane did not exhibit obvious changes in metabolic turnover and were retained in the Golgi or pre-Golgi compartments(s). Thus, the basic domain (-KHIAKRF-) and the cysteine cluster (-CKCC-) in the C-terminal tail of CCR5 function cooperatively for optimal surface expression. C1 NIAID, LMM, NIH, Bethesda, MD 20892 USA. NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. Univ Penn, Div Infect Dis, Philadelphia, PA 19104 USA. RP Venkatesan, S (reprint author), NIAID, LMM, NIH, Bldg 10,Rm 6A05, Bethesda, MD 20892 USA. RI Locati, Massimo/H-8404-2015 OI Locati, Massimo/0000-0003-3077-590X NR 84 TC 47 Z9 47 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 40133 EP 40145 DI 10.1074/jbc.M105722200 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200085 PM 11514564 ER PT J AU Zhao, XH Varnai, P Tuymetova, G Balla, A Toth, ZE Oker-Blom, C Roder, J Jeromin, A Balla, T AF Zhao, XH Varnai, P Tuymetova, G Balla, A Toth, ZE Oker-Blom, C Roder, J Jeromin, A Balla, T TI Interaction of neuronal calcium sensor-1 (NCS-1) with phosphatidylinositol 4-kinase beta stimulates lipid kinase activity and affects membrane trafficking in COS-7 cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHOSPHOINOSITIDE KINASES; FREQUENIN; METABOLISM; PROTEIN; PHOSPHORYLATION; PTDINS(4,5)P-2; SECRETION; HOMOLOG; STT4P; GOLGI AB Phosphatidylinositol 4-kinases (PI4K) catalyze the first step in the synthesis of phosphatidylinositol 4,5-bisphosphate, an important lipid regulator of several cellular functions. Here we show that the Ca2+-binding protein, neuronal calcium sensor-1 (NCS-1), can physically associate with the type III P14K beta with functional consequences affecting the kinase. Recombinant P14K beta, but not its glutathione S-transferase-fused form, showed enhanced PI kinase activity when incubated with recombinant NCS-1, but only if the latter was myristoylated. Similarly, in vitro translated NCS-1, but not its myristoylation-defective mutant, was found associated with recombinant- or in vitro translated PI4K beta in PI4K beta -immunoprecipitates. When expressed in COS-7 cells, PI4K beta and NCS-1 formed a complex that could be immunoprecipitated with antibodies against either proteins, and PI 4-kinase activity was present in anti-NCS-1 immunoprecipitates. Expressed NCS-1-YFP showed colocalization with endogenous PI4K beta primarily in the Golgi, but it was also present in the walls of numerous large perinuclear vesicles. Co-expression of a catalytically inactive PI4K beta inhibited the development of this vesicular phenotype. Transfection of PI4K beta and NCS-1 had no effect on basal PIP synthesis in permeabilized COS-7 cells, but it increased the wortmannin-sensitive [P-32]phosphate incorporation into phosphatidylinositol 4-phosphate during Ca2+-induced phospholipase C activation. These results together indicate that NCS-1 is able to interact with PI4K beta also in mammalian cells and may play a role in the regulation of this enzyme in specific cellular compartments affecting vesicular trafficking. C1 NICHHD, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. Univ Jyvaskyla, Dept Biol & Environm Sci, FIN-40351 Jyvaskyla, Finland. Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada. RP Balla, T (reprint author), NICHHD, Endocrinol & Reprod Res Branch, NIH, Bldg 49,Rm 6A35,49 Convent Dr, Bethesda, MD 20892 USA. RI Roder, John/G-6468-2013; OI Balla, Tamas/0000-0002-9077-3335; Balla, Andras/0000-0002-6450-2793 NR 32 TC 106 Z9 113 U1 0 U2 11 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 40183 EP 40189 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200090 PM 11526106 ER PT J AU Yang, DM Pan, Z Takeshima, H Wu, CH Nagaraj, RY Ma, JJ Cheng, HP AF Yang, DM Pan, Z Takeshima, H Wu, CH Nagaraj, RY Ma, JJ Cheng, HP TI RyR3 amplifies RyR1-mediated Ca2+-induced Ca2+ release in neonatal mammalian skeletal muscle SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHANNEL RYANODINE RECEPTOR; SARCOPLASMIC-RETICULUM; MOLECULAR-CLONING; CONTRACTION; EXPRESSION; TYPE-3; CDNA; ISOFORMS; MYOTUBES; MYOCYTES AB The neonatal mammalian skeletal muscle contains both type 1 and type 3 ryanodine receptors (RyR1 and RyR3) located in the sarcoplasmic reticulum membrane. An allosteric interaction between RyR1 and dihydropyridine receptors located in the plasma membrane mediates voltage-induced Ca2+ release (VICR) from the sarcoplasmic reticulum. RyR3, which disappears in adult muscle, is not involved in VICR, and the role of the transiently expressed RyR3 remains elusive. Here we demonstrate that RyR1 participates in both VICR an Ca2+-induced Ca2+ release (CICR) and that RyR3 amplifies RyR1-mediated CICR in neonatal skeletal muscle. Confocal measurements of intracellular Ca2+ in primary cultured mouse skeletal myotubes reveal active sites of Ca2+ release caused by peripheral coupling between dihydropyridine receptors and RyR1. In myotubes lacking RyR3, the peripheral VICR component is unaffected, and RyR1s alone are able to support inward CICR propagation in most cells at an average speed of similar to 190 mum/s. With the co-presence of RyR1 and RyR3 in wild-type cells, unmitigated radial CICR propagates at 2,440 mum/s. Because neonatal skeletal muscle lacks a well developed transverse tubule system, the RyM reinforcement of CICR seems to ensure a robust, uniform, and synchronous activation of Ca2+ release throughout the cell body. Such functional interplay between RyR1 and RyR3 can serve important roles in Ca2+ signaling of cell differentiation and muscle contraction. C1 NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Case Western Reserve Univ, Dept Physiol & Biophys, Cleveland, OH 44106 USA. Peking Univ, Coll Life Sci, Natl Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China. Kurume Univ, Inst Life Sci, Div Cell Biol, Fukuoka 8390861, Japan. RP Ma, JJ (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, 675 Hoes Lane, Piscataway, NJ 08854 USA. FU NCI NIH HHS [R01-CA95739]; NIA NIH HHS [R01-AG15556] NR 37 TC 35 Z9 38 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 40210 EP 40214 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200093 PM 11500519 ER PT J AU Huang, CS Li, JX Ding, M Leonard, SS Wang, LY Castranova, V Vallyathan, V Shi, XL AF Huang, CS Li, JX Ding, M Leonard, SS Wang, LY Castranova, V Vallyathan, V Shi, XL TI UV induces phosphorylation of protein kinase B (Akt) at Ser-473 and Thr-308 in mouse epidermal Cl 41 cells through hydrogen peroxide SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PLECKSTRIN HOMOLOGY DOMAIN; SERINE-THREONINE KINASE; GROWTH-FACTOR RECEPTOR; SIGNAL-TRANSDUCTION; PHOSPHATIDYLINOSITOL 3-KINASE; TRANSGENIC MICE; P38 KINASE; ACTIVATION; PATHWAY; GENE AB The exposure of mammalian cells to UV irradiation leads to the activation of transcription factors and protein kinases, which are believed to be responsible for the carcinogenic effects of excessive sun exposure. The present study investigated the effect of UV exposure on reactive oxygen species (ROS) generation and protein kinase B (Akt) phosphorylation in epidermal cells and determined if a relationship exists between these UV responses. Exposure of mouse epidermal JB6 Cl 41 cells to UV radiation led to specific phosphorylation of Akt at Ser-473 and Thr-308 in a time-dependent manner. This phosphorylation was confirmed by the observation that overexpression of Akt mutant, Akt-T308/S473A, attenuated phosphorylation of Akt at Ser-473 and Thr-308. UV radiation also generated ROS as measured by electron spin resonance (ESR) in JB6 Cl 41 cells. The generation of ROS by UV radiation was measured further by H2O2 and O . (-)(2) fluorescence staining assays. The mechanism of ROS generation involved reduction of molecular oxygen to O . (-)(2) which generated H2O2 through dismutation. H2O2 produced . OH via a metal-independent pathway. The scavenging of UV-generated H2O2 by N-acety-L-cyteine (NAC, a general antioxidant) or catalase (a specific H2O2 inhibitor) inhibited Akt phosphorylation at Ser-473 and Thr-308, whereas the pretreatment of cells with sodium formate (an (OH)-O-. radical scavenger) or superoxide dismutase (an O . (-)(2) radical scavenger) did not show any inhibitory effects. Furthermore, treatment of cells with H2O2 increased UV-induced phosphorylation of Akt at Ser-473 and Thr-308. These results demonstrate that UV radiation generates a whole spectrum of ROS including O . (-)(2), (OH)-O-., and H2O2 and induces phosphorylation of Akt at Ser-473. Among the various ROS, H2O2 seems most potent in mediating UV-induced phosphorylation of Akt at Ser-473 and Thr-308. It is possible that Akt may play a role in the carcinogenesis effects by UV radiation. C1 NYU, Sch Med, Nelson Inst Environm Med, New York, NY 10016 USA. NYU, Sch Med, Kaplan Comprehens Canc Ctr, New York, NY 10016 USA. NIOSH, Hlth Effects Lab Div, NIH, Morgantown, WV 26505 USA. RP Huang, CS (reprint author), NYU, Sch Med, Nelson Inst Environm Med, 550 1St Ave, New York, NY 10016 USA. RI Shi, Xianglin/B-8588-2012; OI Huang, Chuanshu/0000-0003-4133-5096 NR 51 TC 73 Z9 75 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 40234 EP 40240 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200096 PM 11507090 ER PT J AU Xiao, B Shi, GB Gao, JH Blaszczyk, J Liu, Q Ji, XH Yan, HG AF Xiao, B Shi, GB Gao, JH Blaszczyk, J Liu, Q Ji, XH Yan, HG TI Unusual conformational changes in 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase as revealed by X-ray crystallography and NMR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID N-15 RESONANCE ASSIGNMENTS; ESCHERICHIA-COLI; PROTEIN; BINDING; REFINEMENT; PROGRAM; COMPLEX; H-1 AB The crystal structure of Escherichia coli 6-hydroxy-methyl-7,8-dihydropterin pyrophosphokinase (HPPK) in complex with MgADP has been determined at 1.5-Angstrom resolution with a crystallographic R factor of 0.191. The solution structure of HPPK in complex with Mg2+ and beta,gamma -methyleneadenosine 5'-triphosphate (MgAMPPCP) has been determined using a simulated annealing pro. tocol with 3,523 experimental NMR restraints. The root mean square deviation of the ensemble of 20 refined conformers that represent the solution structure from the mean coordinate set derived from them is 0.74 +/- 0.26 A for all backbone atoms and 0.49 +/- 0.22 Angstrom when residues Pro(14), Pro(44)-Gln(50), and Arg(84)-Pro(91) are excluded. Binding of MgADP causes significant changes in the conformation and dynamical property of three loops of HPPK that are involved in catalysis. A dramatic, unusual conformational change is that loop 3 moves away from the active center significantly with some residues moving by > 17 Angstrom. The binding of MgADP also stabilizes loop 1 and loop 3 but makes loop 2 more mobile. Very similar conformational and dynamical changes are observed in the NAM solution structure of HPPK(.)MgAMPPCP. The conformational and dynamical changes may play important roles in both substrate binding and product release in the catalytic cycle. C1 NCI, Macromol Crystallog Lab, NIH, Frederick, MD 21702 USA. Michigan State Univ, Dept Biochem, E Lansing, MI 48824 USA. RP Ji, XH (reprint author), NCI, Macromol Crystallog Lab, NIH, Frederick, MD 21702 USA. RI Ji, Xinhua/C-9664-2012 OI Ji, Xinhua/0000-0001-6942-1514 FU NIGMS NIH HHS [GM 51901] NR 24 TC 34 Z9 36 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 26 PY 2001 VL 276 IS 43 BP 40274 EP 40281 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 485XR UT WOS:000171789200102 PM 11546767 ER PT J AU Zhang, L Xing, GQ Barker, JL Chang, Y Maric, D Ma, W Li, BS Rubinow, DR AF Zhang, L Xing, GQ Barker, JL Chang, Y Maric, D Ma, W Li, BS Rubinow, DR TI alpha-lipoic acid protects rat cortical neurons against cell death induced by amyloid and hydrogen peroxide through the Akt signalling pathway SO NEUROSCIENCE LETTERS LA English DT Article DE lipoic acid; cell death; Alzheimer's disease; antioxidants; apoptosis; neuron ID PHOSPHATIDYLINOSITOL 3-KINASE; OXIDATIVE STRESS; IN-VITRO; APOPTOSIS; PEPTIDE; NEUROPROTECTION; ANTIOXIDANTS; HOMEOSTASIS AB Substantial evidence suggests that the accumulation of beta -amyloid (A beta)-derived peptides contributes to the aetiology of Alzheimer's disease (AD) by stimulating formation of free radicals. Thus, the antioxidant alpha -lipoate, which is able to cross the blood-brain barrier, would seem an ideal substance in the treatment of AD. We have investigated the potential effectiveness of alpha -lipoic acid (LA) against cytotoxicity induced by A beta peptide (31-35) (30 muM) and hydrogen peroxide (H2O2) (100 muM) with the cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) reduction and fluorescence dye propidium iodide assays in primary neurons of rat cerebral cortex. We found that treatment with LA protected cortical neurons against cytotoxicity induced by A beta or H2O2. In addition, LA-induced increase in the level of Akt in the neurons was observed by Western blot. The LA-induced neuroprotection and Akt increase were attenuated by pretreatment with the phosphatidylinositol 3-kinase inhibitor, LY294002 (50 muM). Our data suggest that the neuroprotective effects of the antioxidant LA are partly mediated through activation of the PKB/Akt signaling pathway. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved. C1 NIMH, Behav Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NIMH, Biol Psychiat Branch, NIH, Bethesda, MD 20892 USA. NINCDS, Neurophysiol Lab, NIH, Bethesda, MD 20892 USA. USN, Ctr Biomol Sci & Engn, Res Lab, Washington, DC 20375 USA. NINCDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Zhang, L (reprint author), NIMH, Behav Endocrinol Branch, NIH, Bldg 10,Room 3N238, Bethesda, MD 20892 USA. NR 17 TC 82 Z9 97 U1 0 U2 7 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 OCT 26 PY 2001 VL 312 IS 3 BP 125 EP 128 DI 10.1016/S0304-3940(01)02205-4 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 490NX UT WOS:000172058900001 PM 11602326 ER PT J AU Fetsch, PA Abati, A AF Fetsch, PA Abati, A TI Immunocytochemistry in effusion cytology - A contemporary review SO CANCER CYTOPATHOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the International Academy of Pathology CY OCT 19, 2000 CL NAGOYA, JAPAN SP Internal Acad Pathol DE immunocytochemistry; effusion; adenocarcinoma (ACA); malignant mesothelioma (MM); cytospin; cell block; ThinPrep ID DIFFERENTIATING EPITHELIAL MESOTHELIOMA; LOGISTIC-REGRESSION ANALYSIS; MALIGNANT MESOTHELIOMA; E-CADHERIN; SEROUS EFFUSIONS; N-CADHERIN; IMMUNOHISTOCHEMICAL DIAGNOSIS; METASTATIC ADENOCARCINOMA; PLEURAL MESOTHELIOMAS; LUNG ADENOCARCINOMAS AB BACKGROUND. Cytology plays a pivotal role in the diagnosis of pleural effusions. In many cases, immunocytochemistry (ICC) is required to elucidate the etiology of the atypical cells. Effusions are samples that present unique problems for ICC. To date there is no standardization of ICC methods for effusions and cytology in general. METHODS. The authors review the most commonly used cytologic preparations, fixatives, and antibodies used in effusion ICC. RESULTS. Through the utilization of cell block preparations and a panel of antibodies appropriate for the differential diagnosis in question, ICC conditions utilized in surgical pathology can be most closely replicated. CONCLUSIONS. ICC may provide reliable insights into various diagnostic dilemmas in effusion cytology, provided that laboratory standardization practices are followed. (C) 2001 American Cancer Society. C1 NCI, Cytopathol Sect, NIH, Bethesda, MD 20892 USA. RP Abati, A (reprint author), NCI, Cytopathol Sect, NIH, Bldg 10,Room 2A19, Bethesda, MD 20892 USA. NR 81 TC 75 Z9 90 U1 0 U2 10 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0008-543X J9 CANCER CYTOPATHOL JI Cancer Cytopathol. PD OCT 25 PY 2001 VL 93 IS 5 BP 293 EP 308 DI 10.1002/cncr.9044 PG 16 WC Oncology; Pathology SC Oncology; Pathology GA 483MC UT WOS:000171638000001 PM 11668464 ER PT J AU Graziano, G Lee, B AF Graziano, G Lee, B TI Hydration of aromatic hydrocarbons SO JOURNAL OF PHYSICAL CHEMISTRY B LA English DT Article ID SCALED-PARTICLE THEORY; THERMODYNAMIC FUNCTIONS; TEMPERATURE-DEPENDENCE; SOLVENT REORGANIZATION; HYDROPHOBIC HYDRATION; MOLECULAR-DYNAMICS; AQUEOUS-SOLUTIONS; ENTHALPY-ENTROPY; CAVITY FORMATION; HYDROGEN-BONDS AB The transfer of benzene and toluene from gas phase into water is a spontaneous process at room temperature under Ben-Naim's standard conditions. This strongly contrasts with the behavior of aliphatic hydrocarbons, for which the Gibbs energy of transfer is large and positive. To understand this difference in behavior between the aromatics and aliphatics, we analyze the hydration of benzene and toluene in a large temperature range using available experimental and computer simulation data. We introduce a small but important modification in the definition of the solvent reorganization enthalpy in order to handle slightly polar solutes such as the aromatic hydrocarbons, which form weak hydrogen-bonds with water. The analysis shows that, for aromatic hydrocarbons, the van der Waals interaction energy overwhelms the Gibbs energy cost for cavity creation at room temperature, thus rendering the hydration process spontaneous. The formation of the weak hydrogen-bonds between the aromatic ring and water appears to be largely compensating and not to contribute significantly to the hydration Gibbs energy. C1 NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Sannio, Fac Sci, I-82100 Benevento, Italy. RP Lee, B (reprint author), NCI, Mol Biol Lab, NIH, Bldg 37,Room 4B15,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA. OI Graziano, Giuseppe/0000-0001-6935-8172 NR 56 TC 57 Z9 58 U1 0 U2 8 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1089-5647 J9 J PHYS CHEM B JI J. Phys. Chem. B PD OCT 25 PY 2001 VL 105 IS 42 BP 10367 EP 10372 DI 10.1021/jp011382d PG 6 WC Chemistry, Physical SC Chemistry GA 486EH UT WOS:000171805100031 ER PT J AU Yamashita, H Nevalainen, MT Xu, J LeBaron, MJ Wagner, KU Erwin, RA Harmon, JM Hennighausen, L Kirken, RA Rui, H AF Yamashita, H Nevalainen, MT Xu, J LeBaron, MJ Wagner, KU Erwin, RA Harmon, JM Hennighausen, L Kirken, RA Rui, H TI Role of serine phosphorylation of Stat5a in prolactin-stimulated beta-casein gene expression SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE prolactin; Stat5 transcriptional regulation; glucocorticoid receptors; mouse mammary glands; beta-casein promoter ID TRANSCRIPTIONALLY ACTIVE STAT1; DNA-BINDING; GLUCOCORTICOID-RECEPTOR; SIGNAL-TRANSDUCTION; MAMMARY-GLAND; ACTIVATION; CELLS; KINASE; GAMMA; INTERLEUKIN-2 AB Milk production remains suppressed in mammals during late pregnancy despite high levels of lactogenic polypeptide hormones. At parturition, associated with a precipitous fall in circulating progesterone, rising glucocorticoid levels synergize with prolactin to initiate copious milk production, This synergy is mediated at least in part through the coordinated activation of glucocorticoid receptors and transcription factor Stat5, particularly Stat5a. Here we show that two proline-juxtaposed serine residues within the transactivation domain of Stat5a are phosphorylated in the mammary gland during late gestation and lactation, and that these phosphorylation sites inhibit the transcriptional activity of Stat5a in the absence of glucocorticoid receptor costimulation. Specifically, transfection assays revealed that phosphorylation of residues S725 and S779 of Stat5a cooperatively suppressed prolactin-stimulated transcription from the beta -casein promoter in both COS-7 kidney and MCF-7 mammary cells. This suppression was associated with shortened duration and reduced amplitude of nuclear DNA binding activity of wild type Stat5a relative to that of the serine phosphorylation-defective Stat5 mutant. However, costimulation of glucocorticoid receptors completely reversed the suppressive effect of Stat5a serine phosphorylation on P-casein gene transcription. We propose that serine phosphorylation within the transactivation domain may limit the activity of Stat5a in the absence of proper coactivation by glucocorticoid receptors. C1 Uniformed Serv Univ Hlth Sci, Dept Pathol, US Mil Canc Inst, Bethesda, MD 20814 USA. Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA. Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE USA. NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD USA. Univ Texas, Hlth Sci Ctr, Dept Integrat Biol & Pharmacol, Houston, TX USA. RP Rui, H (reprint author), Uniformed Serv Univ Hlth Sci, Dept Pathol, US Mil Canc Inst, Bethesda, MD 20814 USA. EM hrui@usuhs.mil RI Wagner, Kay-Uwe/B-6044-2009 FU NCI NIH HHS [R01 CA83813]; NIDDK NIH HHS [R01 DK52013] NR 36 TC 53 Z9 54 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD OCT 25 PY 2001 VL 183 IS 1-2 BP 151 EP 163 DI 10.1016/S0303-7207(01)00546-9 PG 13 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 490WX UT WOS:000172077600018 PM 11604235 ER PT J AU Berke, JD Sgambato, V Zhu, PP Lavoie, B Vincent, M Krause, M Hyman, SE AF Berke, JD Sgambato, V Zhu, PP Lavoie, B Vincent, M Krause, M Hyman, SE TI Dopamine and glutamate induce distinct striatal splice forms of ania-6, an RNA polymerase II-associated cyclin SO NEURON LA English DT Article ID PRE-MESSENGER-RNA; DEPENDENT PROTEIN-KINASE; C-TERMINAL DOMAIN; ALZHEIMERS-DISEASE; REGULATORY SUBUNIT; IN-VIVO; TRANSCRIPTION; EXPRESSION; PHOSPHORYLATION; RECEPTOR AB Control of neuronal gene expression by drugs or neurotransmitters is a critical step in long-term neural plasticity. Here, we show that a gene induced in the striatum by cocaine or direct dopamine stimulation, ania-6, is a member of a novel family of cyclins with homology to cyclins K/T/H/C. Further, different types of neurotransmitter stimulation cause selective induction of distinct ania-6 isoforms, through alternative splicing. The longer Ania-6 protein colocalizes with nuclear speckles and is associated with key elements of the RNA elongation/processing complex, including the hyperphosphorylated form of RNA polymerase II, the splicing factor SC-35, and the p110 PITSLRE cyclin-dependent kinase. Distinct types of neuronal stimulation may therefore differentially modulate nuclear RNA processing, through altered transcription and splicing of ania-6. C1 NINCDS, Mol Plast Sect, Bethesda, MD 20892 USA. NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA. NIMH, Bethesda, MD 20892 USA. Harvard Univ, Neurosci Program, Boston, MA 02115 USA. Univ Laval, CREFSIP, Quebec City, PQ G1K 7P4, Canada. Univ Laval, Dept Med, Quebec City, PQ G1K 7P4, Canada. RP Hyman, SE (reprint author), NINCDS, Mol Plast Sect, Bethesda, MD 20892 USA. NR 61 TC 66 Z9 74 U1 1 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTES AVE,, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD OCT 25 PY 2001 VL 32 IS 2 BP 277 EP 287 DI 10.1016/S0896-6273(01)00465-2 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 487UG UT WOS:000171893700012 PM 11683997 ER PT J AU Miller, FG AF Miller, FG TI Is the placebo powerless? SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. RP Miller, FG (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 1 TC 9 Z9 9 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 25 PY 2001 VL 345 IS 17 BP 1277 EP 1277 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 485RU UT WOS:000171773100013 PM 11680454 ER PT J AU Robinson, GW Wagner, KU Hennighausen, L AF Robinson, GW Wagner, KU Hennighausen, L TI Functional mammary gland development and oncogene-induced tumor formation are not affected by the absence of the retinoblastoma gene SO ONCOGENE LA English DT Article DE mammary gland; tumor suppressor gene; oncogenes; pocket proteins; breast cancer ID G(1) CONTROL; EXPRESSION; MICE; DIFFERENTIATION; EPITHELIUM; PROTEIN; IMMORTALIZATION; TGF-BETA-1; MUTATION; PROSTATE AB results in impaired mammary gland development and neoplasia. We investigated the consequences of the absence of pRb in mammary epithelial cells during normal development and in mice that express an oncogene in the mammary epithelium. Since pRb-deficiency results in embryonic lethality, we transplanted pRb-null mammary anlagen into wild hosts. pRb-deficient mammary epithelia were capable of functional differentiation in term animals and they regenerated a differentiated gland even after multiple pregnancies. In serial transplantations no significant differences were found in outgrowth of pRb-deficient and wild type epithelia indicating that the absence of pRb does not lead to transformation. Likewise the effect of a TGF beta1 transgene was not altered in the absence of pRb. The susceptibility of mammary epithelium to form tumors was assessed in three different models. No differences in tumor incidence were found between wild type and Rb +/- WAP-int3, MMTV-PyMT transgenic and Brcal(-/-) epithelia. These results demonstrate that the absence of pRb does not affect normal mammary gland development and tumorigenesis in three different mouse models investigated and suggest that loss of more than one member of the pRb pathway is required to induce mammary tumors. C1 NIDDKD, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA. RP Robinson, GW (reprint author), NIDDK, LGP, NIH, 8 Ctr Dr,Bldg 8,Rm 101, Bethesda, MD 20892 USA. RI Wagner, Kay-Uwe/B-6044-2009; Robinson, Gertraud/I-2136-2012 NR 30 TC 28 Z9 28 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 25 PY 2001 VL 20 IS 48 BP 7115 EP 7119 DI 10.1038/sj.onc.1204888 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 485DY UT WOS:000171739300016 PM 11704837 ER PT J AU Teng, MN Whitehead, SS Collins, PL AF Teng, MN Whitehead, SS Collins, PL TI Contribution of the respiratory syncytial virus G glycoprotein and its secreted and membrane-bound forms to virus replication in vitro and in vivo SO VIROLOGY LA English DT Article ID TRANSCRIPTION ELONGATION-FACTOR; ALTERED GROWTH-CHARACTERISTICS; FUSION GLYCOPROTEIN; CYTOPLASMIC TAILS; M2-2 PROTEIN; SUBGROUP-B; SH GENE; ATTACHMENT; RSV; CELLS AB The surface glycoproteins of viruses can play important roles in viral attachment, entry, and morphogenesis. Here, we investigated the role of the attachment G glycoprotein of human respiratory syncytial virus (RSV) in viral infection. RSV G is produced both as a complete, transmembrane form and as an N-terminally truncated form that is secreted. Using reverse genetics, we created mutant recombinant RSVs (rRSV) that do not express G (DeltaG) or express either the secreted or the membrane-bound form of G only (sG and mG, respectively). In Vero cells, the DeltaG virus formed plaques and grew as efficiently as wild-type rRSV and mG. In contrast, DeltaG replicated less efficiently and did not form distinct plaques in HEp-2 cells. This defect was primarily at the level of the initiation of Infection, with only a minor additional effect at the level of packaging. Replication of DeltaG in the respiratory tract of mice was very highly restricted, indicating that G is important in vivo. Although the G protein expressed by the sG virus was confirmed to be secreted, this virus grew at least as efficiently as wild-type in HEp-2 cells and was only moderately attenuated in vivo. Thus, the G protein was important for efficient replication in HEp-2 cells and in vivo, but this function could be supplied in large part by the secreted form and thus does not require the cytoplasmic and transmembrane domains. Amino acids 184-198 have been identified as the major heparin-binding domain of the G protein and were implicated in mediating binding to cells [S. A, Feldman at al., 1999, J. Virol. 73, 6610-6617]. Heparin-like glycosaminoglycans also appeared to be important for infection in vitro by direct clinical isolates of RSV. Deletion of amino acids 187-197 from rRSV did not reduce its sensitivity to neutralization in vitro by incubation with soluble heparin, did not reduce Its efficiency of growth in vitro, and resulted in only a modest reduction in vivo. Thus, the putative heparin-binding domain is not the sole determinant of heparin sensitivity and Is not a critical functional domain. C1 Natl Inst Allergy & Infect Dis, Infect Dis Lab, Bethesda, MD 20892 USA. RP Collins, PL (reprint author), Natl Inst Allergy & Infect Dis, Infect Dis Lab, 7 Ctr Dr,MSC 0720, Bethesda, MD 20892 USA. RI Teng, Michael/I-5006-2012 OI Teng, Michael/0000-0002-0722-3659 FU NIAID NIH HHS [AI-0087] NR 40 TC 135 Z9 139 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD OCT 25 PY 2001 VL 289 IS 2 BP 283 EP 296 DI 10.1006/viro.2001.1138 PG 14 WC Virology SC Virology GA 493UX UT WOS:000172242800014 PM 11689051 ER PT J AU Korte, T Epand, RF Epand, RM Blumenthal, R AF Korte, T Epand, RF Epand, RM Blumenthal, R TI Role of the Glu residues of the influenza hemagglutinin fusion peptide in the pH dependence of fusion activity SO VIROLOGY LA English DT Article ID MEDIATED MEMBRANE-FUSION; VIRUS HEMAGGLUTININ; CONFORMATIONAL CHANGE; VIRAL MEMBRANE; COILED COILS; ACTIVATION; MECHANISM; COMPLEXES; SUBUNIT; BINDING AB To elucidate the role of the fusion peptide in Influenza hemagglutinin (HA)-mediated fusion, we compared pH-dependent conformational changes and fusion mediated by wild-type and a mutant HA in which Glu residues at positions 11 and 15 of the fusion peptide are substituted for valine. The pH dependence of conformational changes and kinetics of fusion with erythrocytes was the same for both forms of HA The time for commitment and the temperature dependence of HA-mediated fusion were also the same. However, striking differences were observed between wild-type and mutant fusion peptides in their interactions with lipid membranes at neutral and acidic pH. Since elimination of the negatively charged residues allows the exposed fusion peptide to penetrate the bilayer at pH values closer to neutral, but does not affect conformational changes and fusion activity in intact HA, we conclude that conformational changes are tightly coupled to fusion peptide insertion in the overall HA-mediated fusion cascade. (C) 2001 Academic Press. C1 NCI, NIH, Ctr Canc Res, Lab Expt & Computat Biol, Frederick, MD 21702 USA. McMaster Univ, Dept Biochem, Hamilton, ON L8N 3Z5, Canada. RP Blumenthal, R (reprint author), NCI, NIH, Ctr Canc Res, Lab Expt & Computat Biol, POB B,Bldg 469,Rm 216A,Miller Dr, Frederick, MD 21702 USA. NR 34 TC 24 Z9 24 U1 0 U2 5 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD OCT 25 PY 2001 VL 289 IS 2 BP 353 EP 361 DI 10.1006/viro.2001.1108 PG 9 WC Virology SC Virology GA 493UX UT WOS:000172242800020 PM 11689057 ER PT J AU Nakamura, K Kimura, S Yamazaki, M Kawaguchi, A Inoue, K Sakai, T AF Nakamura, K Kimura, S Yamazaki, M Kawaguchi, A Inoue, K Sakai, T TI Immunohistochemical analyses of thyroid-specific enhancer-binding protein in the fetal and adult rat hypothalami and pituitary glands SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE T/EBP; NKX2.1; development; hypothalamus; pituitary gland; rat; immunohistochemistry ID TRANSCRIPTION FACTOR-I; TISSUE-SPECIFIC EXPRESSION; THYROTROPIN RECEPTOR GENE; THYROGLOBULIN PROMOTER; PEROXIDASE GENE; RATHKES-POUCH; B GENE; LUNG; CELL; TTF-1 AB Thyroid-specific enhancer-binding protein (T/EBP), also known as NKX2.1 or TTF-1, regulates the expression of thyroid- and lung-specific genes. The t/ebp/Nkx2.1-null mutant mouse was stillborn but lacked the thyroid gland, pituitary gland, ventral region of the forebrain and normal lungs. These data demonstrated that T/EBP/NKX2.1 plays an important role not only in tissue-specific gene expressions in adults but also in genesis of these organs during development. Although the expression of t/ebp/Nkv2.1 in the brain has been reported, its function in the brain remains unknown. The present study was designed to determine the localization of T/EBP/NKX2.1 in the hypothalamus and pituitary gland of fetal and adult rats by immunohistochemistry as the first step toward understanding the function of T/EBP/NKX2.1 in the rat brain. In the fetal rat hypothalamus, T/EBP/NKX2.1 was localized widely in the ventral hypothalamic areas. In the adult rat brain, T/EBP/NKX2.1 was localized in the ventromedial hypothalamic nucleus, medial tuberal nucleus, arcuate nucleus and mammillary body. No T/EBP/NXX2.1 immunoreactivity was observed in the anterior or intermediate lobe of the pituitary gland in either fetal or adult rats. On the other hand, immunoreactive T/EBP/NKX2.1 was found in the posterior lobe of the pituitary gland. This paper presents results of detailed analyses of the distributions of T/EBP/NKX2.1 protein in the fetal and adult rat hypothalami and pituitary glands, and these results should provide important information for understanding the function of T/EBP/NKX2.1 in the brain. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Saitama Univ, Fac Sci, Dept Regulat Biol, Urawa, Saitama 3388570, Japan. NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. RP Sakai, T (reprint author), Saitama Univ, Fac Sci, Dept Regulat Biol, 255 Shimo Ohkubo, Urawa, Saitama 3388570, Japan. NR 33 TC 28 Z9 28 U1 0 U2 1 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 OCT 24 PY 2001 VL 130 IS 2 BP 159 EP 166 DI 10.1016/S0165-3806(01)00226-7 PG 8 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 499LV UT WOS:000172573400001 ER PT J AU Gardin, JM Weissman, NJ Leung, C Panza, JA Fernicola, D Davis, KD Constantine, GD Reid, CL AF Gardin, JM Weissman, NJ Leung, C Panza, JA Fernicola, D Davis, KD Constantine, GD Reid, CL TI Clinical and echocardiographic follow-up of patients previously treated with dexfenfluramine or phentermine/fenfluramine SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID AORTIC REGURGITATION; FENFLURAMINE; PHENTERMINE; PREVALENCE; ABNORMALITIES AB Context Use of anorexigen therapy is associated with valvular abnormalities, although there is limited information on long-term changes in valvular regurgitation following discontinuation of these agents. Objective To evaluate changes in valvular regurgitation, valve morphology, and clinical parameters 1 year after an initial echocardiogram in patients previously treated with dexfenfluramine or phentermine/fenfluramine and in untreated controls. Design and Setting A reader-blinded, multicenter, echocardiographic and clinical 1-year follow-up study at 25 outpatient clinical sites. Patients A total of 1142 obese patients (1466 participated in the initial study) who had follow-up echocardiogram; all but 4 had a follow-up medical history and physical examination. Follow-up time from discontinuation of drug to follow-up echocardiogram for 371 dexfenfluramine patients was 17.5 months (range, 13-26 months) and for 340 phentermine/fenfluramine patients was 18.7 months (range, 13-26 months) after discontinuation of drug therapy. Main Outcome Measure Change in grade of valvular regurgitation and valve morphology and mobility. Results Echocardiographic changes in aortic regurgitation were observed in 8 controls (7 [1.7%] had decreases; 1 [0.2%]had an increase); 29 dexfenfluramine patients (23 [6.4%] had decreases; 6 [1.7%] had increases; P<.001 vs controls); and 15 phentermine/fenfluramine patients (4.5% all decreases; P=.03 vs controls). No statistically significant differences were observed when treated patients were compared with controls for changes in medical history, physical findings, mitral regurgitation, aortic or mitral leaflet mobility or thickness, pulmonary artery systolic pressure, ejection fraction, valve surgery, or cardiovascular events. Conclusion Progression of valvular abnormalities is unlikely in patients 1 year after an initial echocardiogram and 13 to 26 months after discontinuation of dexfenfluramine and phentermine/fenfluramine. C1 Univ Calif Irvine, Dept Med, Irvine, CA 92717 USA. Washington Hosp Ctr, Inst Cardiovasc Res, Washington, DC 20010 USA. NHLBI, Cardiol Branch, Bethesda, MD 20892 USA. Wyeth Ayerst Res, Philadelphia, PA USA. RP Gardin, JM (reprint author), St Johns Hosp, Div Cardiol, 22201 Moross Rd,BP 2,Suite 470, Detroit, MI 48236 USA. NR 12 TC 22 Z9 22 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 OCT 24 PY 2001 VL 286 IS 16 BP 2011 EP 2014 DI 10.1001/jama.286.16.2011 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 485JD UT WOS:000171750500025 PM 11667938 ER PT J AU Dianova, II Bohr, VA Dianov, GL AF Dianova, II Bohr, VA Dianov, GL TI Interaction of human AP endonuclease 1 with flap endonuclease 1 and proliferating cell nuclear antigen involved in long-patch base excision repair SO BIOCHEMISTRY LA English DT Article ID DNA-POLYMERASE-BETA; PURIFIED HUMAN PROTEINS; HUMAN APURINIC ENDONUCLEASE; LIGASE-I; MAMMALIAN-CELLS; BINDING; PATHWAY; RECONSTITUTION; GLYCOSYLASE; REPLICATION AB To understand the mechanism involved in the coordination of the sequential repair reactions that lead to long-patch BER, we have investigated interactions between proteins involved in this pathway. We find that human AP endonuclease I (APE1) physically interacts with flap endonuclease I (FEN1) and with proliferating cell nuclear antigen. An oligonucleotide substrate containing a reduced abasic site, which was pre-incised with APE1, was employed to reconstitute the excision step of long-patch BER with purified human DNA polymerase beta and FEN1. We demonstrate that addition of APE1 to the excision reaction mixture slightly (1.5-2-fold) stimulates the removal of the displaced flap by FEN1. These results suggest the possibility that long-patch BER is coordinated and directed by protein-protein interactions. C1 MRC, Radiat & Genome Stabil Unit, Harwell OX11 0RD, Berks, England. NIA, Mol Gerontol Lab, NIH, Bethesda, MD 20892 USA. RP Dianov, GL (reprint author), MRC, Radiat & Genome Stabil Unit, Harwell OX11 0RD, Berks, England. NR 48 TC 110 Z9 115 U1 1 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 23 PY 2001 VL 40 IS 42 BP 12639 EP 12644 DI 10.1021/bi011117i PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 486CP UT WOS:000171801100020 PM 11601988 ER PT J AU Selengut, JD AF Selengut, JD TI MDP-1 is a new and distinct member of the haloacid dehalogenase family of aspartate-dependent phosphohydrolases SO BIOCHEMISTRY LA English DT Article ID P-TYPE ATPASE; NUCLEOTIDE-BINDING DOMAIN; CRYSTAL-STRUCTURE; SARCOPLASMIC-RETICULUM; L-2-HALOACID DEHALOGENASE; FUNCTIONAL CONSEQUENCES; BACTERIAL CHEMOTAXIS; PHOSPHATASE-ACTIVITY; ANGSTROM RESOLUTION; RESPONSE REGULATOR AB MDP-1 is a eukaryotic magnesium-dependent acid phosphatase with little sequence homology to previously characterized phosphatases. The presence of a conserved motif (Asp-X-Asp-X-Thr) in the N terminus of MDP-1 suggested a relationship to the haloacid dehalogenase (HAD) superfamily, which contains a number of magnesium-dependent acid phosphatases. These phosphatases utilize an aspartate nucleophile and contain a number of conserved active-site residues and hydrophobic patches, which can be plausibly aligned with conserved residues in MDP-1. Seven site-specific point mutants of MDP-I were produced by modifying the catalytic aspartate, serine, and lysine residues to asparagine or glutamate, alanine, and arginine, respectively. The activity of these mutants confirms the assignment of MDP-I as a member of the HAD superfamily. Detailed comparison of the sequence of the 15 MDP-I sequences from various organisms with other HAD superfamily sequences suggests that MDP-I is not closely related to any particular member of the superfamily. The crystal structures of several HAD family enzymes identify a domain proximal to the active site responsible for important interactions with low molecular weight substrates. The absence of this domain or any other that might perform the same function in MDP-1 suggests an "open" active site capable of interactions with large substrates such as proteins. This suggestion was experimentally confirmed by demonstration that MDP-I is competent to catalyze the dephosphorylation of tyrosine-phosphorylated proteins. C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Selengut, JD (reprint author), NHLBI, Biochem Lab, NIH, 50 South Dr,Bldg 50-2347, Bethesda, MD 20892 USA. NR 26 TC 56 Z9 59 U1 0 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 23 PY 2001 VL 40 IS 42 BP 12704 EP 12711 DI 10.1021/bi011405e PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 486CP UT WOS:000171801100027 PM 11601995 ER PT J AU Wolf, YI Rogozin, IB Grishin, NV Tatusov, RL Koonin, EV AF Wolf, Yuri I. Rogozin, Igor B. Grishin, Nick V. Tatusov, Roman L. Koonin, Eugene V. TI Genome trees constructed using five different approaches suggest new major bacterial clades SO BMC EVOLUTIONARY BIOLOGY LA English DT Article AB Background: The availability of multiple complete genome sequences from diverse taxa prompts the development of new phylogenetic approaches, which attempt to incorporate information derived from comparative analysis of complete gene sets or large subsets thereof. Such attempts are particularly relevant because of the major role of horizontal gene transfer and lineage-specific gene loss, at least in the evolution of prokaryotes. Results: Five largely independent approaches were employed to construct trees for completely sequenced bacterial and archaeal genomes: i) presence-absence of genomes in clusters of orthologous genes; ii) conservation of local gene order (gene pairs) among prokaryotic genomes; iii) parameters of identity distribution for probable orthologs; iv) analysis of concatenated alignments of ribosomal proteins; v) comparison of trees constructed for multiple protein families. All constructed trees support the separation of the two primary prokaryotic domains, bacteria and archaea, as well as some terminal bifurcations within the bacterial and archaeal domains. Beyond these obvious groupings, the trees made with different methods appeared to differ substantially in terms of the relative contributions of phylogenetic relationships and similarities in gene repertoires caused by similar life styles and horizontal gene transfer to the tree topology. The trees based on presence-absence of genomes in orthologous clusters and the trees based on conserved gene pairs appear to be strongly affected by gene loss and horizontal gene transfer. The trees based on identity distributions for orthologs and particularly the tree made of concatenated ribosomal protein sequences seemed to carry a stronger phylogenetic signal. The latter tree supported three potential high-level bacterial clades,: i) Chlamydia-Spirochetes, ii) Thermotogales-Aquificales (bacterial hyperthermophiles), and ii) Actinomycetes-Deinococcales-Cyanobacteria. The latter group also appeared to join the low-GC Gram-positive bacteria at a deeper tree node. These new groupings of bacteria were supported by the analysis of alternative topologies in the concatenated ribosomal protein tree using the Kishino-Hasegawa test and by a census of the topologies of 132 individual groups of orthologous proteins. Additionally, the results of this analysis put into question the sister-group relationship between the two major archaeal groups, Euryarchaeota and Crenarchaeota, and suggest instead that Euryarchaeota might be a paraphyletic group with respect to Crenarchaeota. Conclusions: We conclude that, the extensive horizontal gene flow and lineage-specific gene loss notwithstanding, extension of phylogenetic analysis to the genome scale has the potential of uncovering deep evolutionary relationships between prokaryotic lineages. C1 [Wolf, Yuri I.; Rogozin, Igor B.; Tatusov, Roman L.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. [Grishin, Nick V.] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA. [Grishin, Nick V.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA. RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. EM wolf@ncbi.nlm.nih.gov; rogozin@ncbi.nim.nih.gov; grishin@chop.swmed.edu; tatusov@ncbi.nlm.nih.gov; koonin@ncbi.nlm.nih.gov NR 51 TC 218 Z9 235 U1 0 U2 10 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1471-2148 J9 BMC EVOL BIOL JI BMC Evol. Biol. PD OCT 23 PY 2001 VL 1 AR 8 DI 10.1186/1471-2148-1-8 PG 22 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA V13CH UT WOS:000207644400001 PM 11734060 ER PT J AU Deak, LR Flockhart, DA Tanus-Santos, JE Desai, M Abernethy, DR Freedman, JE AF Deak, LR Flockhart, DA Tanus-Santos, JE Desai, M Abernethy, DR Freedman, JE TI The T-(786)-> C polymorphism in the promoter region of endothelial nitric oxide synthase is associated with decreased platelet-derived nitric oxide and enhanced aggregation SO CIRCULATION LA English DT Meeting Abstract C1 Georgetown Univ, Washington, DC USA. NIA, NIH, Baltimore, MD 21224 USA. RI Tanus-Santos, Jose/A-4451-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 54 BP 12 EP 12 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000054 ER PT J AU Chen, ZG Lovanna, JL Moucadel, V Eggerman, TL Patterson, AP AF Chen, ZG Lovanna, JL Moucadel, V Eggerman, TL Patterson, AP TI Cdx1, an important factor in small intestinal development, upregulates apoB mRNA editing SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD USA. INSERM 315, Lab Res Physiol & Pathol Digest, Marseille, France. Ctr Biol Evaluat & Res, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 67 BP 15 EP 15 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000067 ER PT J AU Gollob, M Green, M Tang, A Gollob, T Hassan, A Bachinski, LL Fananapazir, L Roberts, R AF Gollob, M Green, M Tang, A Gollob, T Hassan, A Bachinski, LL Fananapazir, L Roberts, R TI Clinical and genetic heterogeneity in familial Wolff-Parkinson-White syndrome SO CIRCULATION LA English DT Meeting Abstract C1 Baylor Coll Med, Houston, TX 77030 USA. Univ Ottawa, Ottawa, ON K1N 6N5, Canada. Univ Ottawa, Inst Heart, Ottawa, ON, Canada. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 95 BP 21 EP 21 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000095 ER PT J AU Hagemann, D Pepe, S Xiao, RP AF Hagemann, D Pepe, S Xiao, RP TI Electrical pacing selectively increases phospholamban phosphorylation at Thr(7) independent of phosphorylation of Ser(16) in perfused rat hearts SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIA, Baltimore, MD USA. Baker Med Res Inst, Melbourne, Vic, Australia. NR 0 TC 0 Z9 0 U1 2 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 278 BP 58 EP 58 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000278 ER PT J AU Chakir, K Zhang, SJ Zhu, WZ Ziman, B Xian, Y Kobilka, B Xiao, RP AF Chakir, K Zhang, SJ Zhu, WZ Ziman, B Xian, Y Kobilka, B Xiao, RP TI Role of the third intracellular loop and C-terminal domains in beta 2-AR spontaneous activation SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIA, Lab CV Sci, Baltimore, MD USA. Stanford Univ, Med Ctr, Palo Alto, CA 94304 USA. NR 0 TC 0 Z9 0 U1 2 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 293 BP 61 EP 61 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000293 ER PT J AU Spiecker, M Darius, H Hankeln, T Soufi, M Friedl, H Schaefer, JR Schmidt, ER Zeldin, DC Liao, JK AF Spiecker, M Darius, H Hankeln, T Soufi, M Friedl, H Schaefer, JR Schmidt, ER Zeldin, DC Liao, JK TI Expression of vascular antiinflammatory eicosanoids producing cytochrome P450 2J2 (CYP2J2) is reduced by promoter single nucleotide polymorphism SO CIRCULATION LA English DT Meeting Abstract C1 Ruhr Univ Bochum, St Josef Hosp, D-4630 Bochum, Germany. Univ Mainz, D-6500 Mainz, Germany. Univ Marburg, Marburg, Germany. NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 1 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 314 BP 65 EP 65 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000313 ER PT J AU Campia, U Bryant, MB Cardillo, C Panza, JA AF Campia, U Bryant, MB Cardillo, C Panza, JA TI Acute systemic hyperinsulinemia impairs flow-mediated dilation of the brachial artery in hypercholesterolemic patients SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 394 BP 81 EP 82 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000391 ER PT J AU Landmesser, UE McCann, L Holland, S Price, R Mitch, W Harrison, DG AF Landmesser, UE McCann, L Holland, S Price, R Mitch, W Harrison, DG TI Mechanisms underlying uncoupling of the endothelial nitric oxide synthase in hypertension SO CIRCULATION LA English DT Meeting Abstract C1 Emory Univ, Sch Med, Atlanta, GA USA. NIH, Bethesda, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 474 BP 98 EP 98 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000471 ER PT J AU Cross, HR Murphy, E Zheng, MZ Wang, YB Steenbergen, C AF Cross, HR Murphy, E Zheng, MZ Wang, YB Steenbergen, C TI Effect of attenuation of p38 alpha or p38 beta MAP kinase activity on myocardial contractility and ischemic injury SO CIRCULATION LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Durham, NC USA. NIEHS, Res Triangle Pk, NC 27709 USA. Univ Maryland, Baltimore, MD 21201 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 487 BP 101 EP 101 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000484 ER PT J AU Zhu, JH Katz, RJ Quyyumi, AA Rott, D Zalles-Ganley, A Ogunmakinwa, J Wasserman, AG Epstein, SE AF Zhu, JH Katz, RJ Quyyumi, AA Rott, D Zalles-Ganley, A Ogunmakinwa, J Wasserman, AG Epstein, SE TI Association of serum antibodies to heat-shock protein 65 with coronary calcification levels SO CIRCULATION LA English DT Meeting Abstract C1 Washington Hosp Ctr, Washington, DC 20010 USA. George Washington Univ, Washington, DC USA. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 571 BP 119 EP 119 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000568 ER PT J AU Leclercq, C Faris, O Halperin, H McVeigh, E Kass, DA AF Leclercq, C Faris, O Halperin, H McVeigh, E Kass, DA TI Regional disparity of calcium handling and stress protein expression in failing hearts with dyssynchronous contraction SO CIRCULATION LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 614 BP 128 EP 128 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000610 ER PT J AU Zhu, WZ Hagemann, D Chakir, K Xiao, RP AF Zhu, WZ Hagemann, D Chakir, K Xiao, RP TI beta 1-adrenergic receptor induced cardiac apoptosis is mediated by Ca2+/calmodulin-dependent kinase II rather than PKA SO CIRCULATION LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 1 Z9 1 U1 2 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 687 BP 143 EP 143 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000683 ER PT J AU Jo, SH Hagemann, D Xiao, RP AF Jo, SH Hagemann, D Xiao, RP TI beta 2-adrenergic Gi signaling negates the concurrent Gs-mediated cardiac phospholamban phosphorylation by activation of phosphoinositide 3 kinase SO CIRCULATION LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 2 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 694 BP 144 EP 144 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000690 ER PT J AU Neufeld, EB Sabol, S Remaley, AT Ito, T Demosky, SJ Stonik, J Santamarina-Fojo, S Brewer, HB AF Neufeld, EB Sabol, S Remaley, AT Ito, T Demosky, SJ Stonik, J Santamarina-Fojo, S Brewer, HB TI Cellular localization and trafficking of human ABCG1 SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Mol Dis Branch, Bethesda, MD 20892 USA. NIH, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 708 BP 147 EP 147 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000704 ER PT J AU Remaley, AT Thomas, F Stonik, J Demosky, SJ Neufeld, EB Bocharov, AV Vishnyakova, TG Patterson, AP Eggerman, T Santamarina-Fojo, S Brewer, HB AF Remaley, AT Thomas, F Stonik, J Demosky, SJ Neufeld, EB Bocharov, AV Vishnyakova, TG Patterson, AP Eggerman, T Santamarina-Fojo, S Brewer, HB TI ABCA1 transporter dependent and independent lipid efflux to synthetic peptide acceptors SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD USA. NIH, Mol Dis Branch, Bethesda, MD USA. US FDA, Bethesda, MD 20014 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 709 BP 147 EP 147 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000705 ER PT J AU Baranova, I Vishnyakova, T Bocharov, A Chen, ZG Remaley, AT Stonik, J Eggerman, TL Patterson, AP AF Baranova, I Vishnyakova, T Bocharov, A Chen, ZG Remaley, AT Stonik, J Eggerman, TL Patterson, AP TI Lipopolysaccharide (LPS) down regulates both scavenger receptor B1 (SRB1) and ATP binding cassette A1 (ABCA1) in raw cells SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD USA. US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 711 BP 148 EP 148 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000707 ER PT J AU Joyce, C Vaisman, BL Amar, MJ Lambert, G Fruchart-Najib, J Neufeld, EB Remaley, AT Shamburek, RD Brewer, HB Santamarina-Fojo, S AF Joyce, C Vaisman, BL Amar, MJ Lambert, G Fruchart-Najib, J Neufeld, EB Remaley, AT Shamburek, RD Brewer, HB Santamarina-Fojo, S TI Human ABCA1 transgenic mice: Hepatic and macrophage expression of ABCA1 increases plasma HDL concentrations and enhances biliary cholesterol excretion SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Mol Dis Branch, Bethesda, MD USA. NIH, NHLBI, Bethesda, MD USA. Inst Pasteur, F-59019 Lille, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 715 BP 148 EP 149 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000711 ER PT J AU Yang, XP Freeman, L Knapper, C Remaley, AT Brewer, HB Santamarina-Fojo, S AF Yang, XP Freeman, L Knapper, C Remaley, AT Brewer, HB Santamarina-Fojo, S TI The e-box motif mediates repression of human ABCA1 gene expression SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Mol Dis Branch, Bethesda, MD USA. NIH, NHLBI, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 714 BP 148 EP 148 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000710 ER PT J AU Benjamin, EJ Larson, MG Kupka, MJ Mitchell, GF Keaney, JF Vasan, RS Lehman, B Fan, SX Osypiuk, E Vita, JA AF Benjamin, EJ Larson, MG Kupka, MJ Mitchell, GF Keaney, JF Vasan, RS Lehman, B Fan, SX Osypiuk, E Vita, JA TI Cross-sectional correlates of brachial artery endothelial function in the community. The NHLBI's Framingham Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Boston Univ, Sch Med, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. CV Engn Inc, Holliston, MA USA. Boston Univ, Med Ctr, Boston, MA USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 730 BP 152 EP 152 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000726 ER PT J AU Yacono, BC Voltchikhina, SA Cheng, L Lakatta, EG Talan, MI AF Yacono, BC Voltchikhina, SA Cheng, L Lakatta, EG Talan, MI TI The evolution of ejection fraction decline post myocardial infarction (MI) without cardiac dilatation: A murine model of heart failure (HF) with impaired preload reserve. SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIA, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 792 BP 164 EP 165 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000788 ER PT J AU Halcox, JPJ Nour, KRA Zalos, G Mincemoyer, R Schenke, WH Quyyumi, AA AF Halcox, JPJ Nour, KRA Zalos, G Mincemoyer, R Schenke, WH Quyyumi, AA TI Type-B endothelin receptor activation contributes to vasodilator tone in the human coronary microcirculation SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD USA. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 838 BP 174 EP 174 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000833 ER PT J AU Bui, MN Hathaway, L Arai, A O'Flahavan, S Rettmann, D Aletras, A Cannon, RO AF Bui, MN Hathaway, L Arai, A O'Flahavan, S Rettmann, D Aletras, A Cannon, RO TI Hormone replacement therapy improves carotid artery compliance SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. RI Rettmann, Dan/G-5265-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 886 BP 183 EP 183 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000881 ER PT J AU Neuss, M Fleck, E Chesley, AT Monticone, R Lundberg, MS Crow, M AF Neuss, M Fleck, E Chesley, AT Monticone, R Lundberg, MS Crow, M TI The muscle-specific regulator of apoptosis, ARC, prevents oxidant stress-mediated cell death by preserving mitochondrial function SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIA, Baltimore, MD USA. German Heart Inst, Berlin, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 901 BP 188 EP 188 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000896 ER PT J AU Wang, TJ Levy, D Leip, EP Benjamin, EJ Sutherland, P Wilson, PWF Vasan, RS AF Wang, TJ Levy, D Leip, EP Benjamin, EJ Sutherland, P Wilson, PWF Vasan, RS TI Determinants of natriuretic peptide levels in a healthy population and derivation of reference limits SO CIRCULATION LA English DT Meeting Abstract C1 Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. Massachusetts Gen Hosp, Boston, MA USA. Boston Univ, Sch Med, Boston, MA 02118 USA. Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 906 BP 189 EP 189 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000900 ER PT J AU Xu, XH Verheule, S Song, LS Chen, LY Yan, GF Engle, SK Chang, HP Olgin, J Shou, W AF Xu, XH Verheule, S Song, LS Chen, LY Yan, GF Engle, SK Chang, HP Olgin, J Shou, W TI Cardiac overexpression of FKBP12 leads to cardiac arrhythmia and sudden death SO CIRCULATION LA English DT Meeting Abstract C1 Herman B Wells Ctr Pediat Res, Indianapolis, IN USA. Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA. NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 912 BP 190 EP 190 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000906 ER PT J AU Wang, SQ Cheng, HP AF Wang, SQ Cheng, HP TI Local refractoriness and quantal nature of calcium sparks in cardiac myocytes SO CIRCULATION LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 922 BP 192 EP 192 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000916 ER PT J AU Song, LS Gula, A Muth, JN Wang, SQ Xiao, RP Josephson, I Lakatta, EG Schwartz, A Chang, HP AF Song, LS Gula, A Muth, JN Wang, SQ Xiao, RP Josephson, I Lakatta, EG Schwartz, A Chang, HP TI Coupling between overexpressed L-type calcium channels and ryanodine receptors in transgenic mouse cardiac myocytes SO CIRCULATION LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD 21224 USA. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Univ Cincinnati, Inst Mol Pharmacol & Biophys, Cincinnati, OH 45221 USA. NR 0 TC 0 Z9 0 U1 2 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 926 BP 194 EP 194 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000920 ER PT J AU Vinogradova, TM Bogdanov, KY Lakatta, EG AF Vinogradova, TM Bogdanov, KY Lakatta, EG TI Recruitment and synchronization of localized pre action potential ryanodine receptor Ca2+ release underlies beta-adrenergic acceleration of the cardiac pacemaker SO CIRCULATION LA English DT Meeting Abstract C1 NIA, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 930 BP 194 EP 195 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000924 ER PT J AU Yang, HT Tweedie, D Wang, S Gula, A Vinogradova, T Bogdanov, K Allen, PD Stern, MD Lakatta, EG Boheler, KR AF Yang, HT Tweedie, D Wang, S Gula, A Vinogradova, T Bogdanov, K Allen, PD Stern, MD Lakatta, EG Boheler, KR TI Cardiac ryanodine receptor2 (RyR2) regulates the spontaneous rate of contraction of cardiomyocytes differentiated from embryonic stem cells SO CIRCULATION LA English DT Meeting Abstract C1 Shanghai Inst Biol Sci, Shanghai, Peoples R China. NIA, NIH, Baltimore, MD USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 2 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 929 BP 194 EP 194 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895000923 ER PT J AU Yang, BC Bradbury, JA Graves, J Min, JY Xiao, YF Murphy, E Zeldin, DC AF Yang, BC Bradbury, JA Graves, J Min, JY Xiao, YF Murphy, E Zeldin, DC TI CYP2J2 transgenic mice show improved cardiac function following global ischemia and enhanced acute preconditioning SO CIRCULATION LA English DT Meeting Abstract C1 Harvard Univ, Boston, MA 02115 USA. NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1035 BP 215 EP 215 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001027 ER PT J AU Tosaka, T Katchman, AN Knollmann, BC Woosley, RL Casimiro, M Vary, J Pfeifer, K Ebert, SN AF Tosaka, T Katchman, AN Knollmann, BC Woosley, RL Casimiro, M Vary, J Pfeifer, K Ebert, SN TI Increased incidence of drug-induced ventricular arrhythmias in isolated perfused mouse hearts harboring targeted "Knock-In" point mutations in the Kcnq1 (Kvlqt1) gene SO CIRCULATION LA English DT Meeting Abstract C1 Georgetown Univ, Arlington, VA USA. Georgetown Univ, Washington, DC USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1068 BP 222 EP 222 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001060 ER PT J AU McMahon, TJ Gow, AJ Huang, YCT Pawloski, JR Stamler, JS AF McMahon, TJ Gow, AJ Huang, YCT Pawloski, JR Stamler, JS TI Modulation of hypoxic pulmonary vasoconstriction by erythrocytic nitric oxide SO CIRCULATION LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Durham, NC USA. NIEHS, Res Triangle Pk, NC 27709 USA. Howard Hughes Med Inst, Durham, NC USA. RI Gow, Andrew/N-8566-2013; McMahon, Timothy/K-3986-2012 OI Gow, Andrew/0000-0003-0876-5158; McMahon, Timothy/0000-0002-3404-3223 NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1193 BP 248 EP 248 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001183 ER PT J AU Balaban, RS French, SA Bose, S AF Balaban, RS French, SA Bose, S TI Sarcoplasmic-reticulum (SR) and mitochondria communication: Evidence for a balanced effect of Ca2+ on SR ATP-hydrolysis and mitochondrial ATP-production SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1220 BP 254 EP 254 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001209 ER PT J AU Tenaglia, A Mendelsohn, FO Anderson, RD Rocha-Singh, K Hillegass, WB Crowley, JJ Guzman, R Saucedo, JF Moon, T Whitehouse, MJ Lederman, RJ Annex, BH AF Tenaglia, A Mendelsohn, FO Anderson, RD Rocha-Singh, K Hillegass, WB Crowley, JJ Guzman, R Saucedo, JF Moon, T Whitehouse, MJ Lederman, RJ Annex, BH TI Diabetics respond to fibroblast growth factor-2. Findings in the therapeutic angiogenesis with FGF-2 for intermittent claudication (TRAFFIC) trial. SO CIRCULATION LA English DT Meeting Abstract C1 Tulane Univ, Med Ctr, New Orleans, LA USA. Cardiol PC, Birmingham, AL USA. Heart Specialists Sarasota, Sarasota, FL USA. Prairie CV Consultants, Springfield, IL USA. Heart Grp, Evansville, IN USA. Univ Coll Hosp Galway, Galway, Ireland. Vanderbilt Univ, Med Ctr, Nashville, TN USA. Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Chiron Corp, Emeryville, CA 94608 USA. NIH, Bethesda, MD 20892 USA. Duke Univ, Med Ctr, Durham, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1259 BP 262 EP 262 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001248 ER PT J AU Pagliaro, P Mancardi, D Rastaldo, R Penna, C Feelisch, M Wink, DA Kass, DA Paolocci, N AF Pagliaro, P Mancardi, D Rastaldo, R Penna, C Feelisch, M Wink, DA Kass, DA Paolocci, N TI Nitroxyl anion is a preconditioning agent in isolated rat heart SO CIRCULATION LA English DT Meeting Abstract C1 Univ Turin, Orbassano, Italy. Louisiana State Univ, Shreveport, LA 71105 USA. NCI, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RI Pagliaro, Pasquale/E-5239-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1265 BP 263 EP 264 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001254 ER PT J AU Nong, ZX Amar, MJ Gonzalez, H Vaisman, BL Paigen, B Bensadoun, A Neufeld, EB Brewer, HB Santamarina-Fojo, S AF Nong, ZX Amar, MJ Gonzalez, H Vaisman, BL Paigen, B Bensadoun, A Neufeld, EB Brewer, HB Santamarina-Fojo, S TI Hepatic lipase expression in macrophages modulates aortic atherosclerosis in apoE-KO mice: Bone marrow transplantation in apoE-KO and apoE-KO x HL-KO mice SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Mol Dis Branch, Bethesda, MD USA. Jackson Lab, Bar Harbor, ME 04609 USA. Cornell Univ, Ithaca, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1290 BP 268 EP 269 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001279 ER PT J AU Lambert, G Amar, MJ Shamburek, RD Cain, WJ Santamarina-Fojo, S Brewer, HB AF Lambert, G Amar, MJ Shamburek, RD Cain, WJ Santamarina-Fojo, S Brewer, HB TI Sites of catabolism of apoA-I and apoA-II using Tyramine Cellobiose in control mice and mice with genetic dyslipoproteinemias SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Mol Dis Branch, Bethesda, MD 20892 USA. Univ Delaware, Newark, DE USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1293 BP 269 EP 269 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001282 ER PT J AU Anversa, P Kajstura, J Chimenti, S Limana, F Jakoniuk, I Quaini, F Nadal-Ginard, B Bodine, DM Orlic, D AF Anversa, P Kajstura, J Chimenti, S Limana, F Jakoniuk, I Quaini, F Nadal-Ginard, B Bodine, DM Orlic, D TI Cytokine-mediated mobilization of bone marrow cells repairs the infarcted heart improving function and decreasing mortality SO CIRCULATION LA English DT Meeting Abstract C1 New York Med Coll, Valhalla, NY 10595 USA. NIH, NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1302 BP 271 EP 271 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001291 ER PT J AU Winitsky, SO Gopal, TV Hassanzadeh, S Epstein, ND AF Winitsky, SO Gopal, TV Hassanzadeh, S Epstein, ND TI The development of autonomously beating cardiac-like cells from adult murine skeletal muscle SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1301 BP 271 EP 271 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001290 ER PT J AU Halcox, JPJ McDermott, D Lessie, MD Epstein, ND Murphy, P Quyyumi, AA AF Halcox, JPJ McDermott, D Lessie, MD Epstein, ND Murphy, P Quyyumi, AA TI A CCR5 chemokine receptor promoter polymorphism is associated with increased prevalence and severity of coronary atherosclerosis SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD 20892 USA. NIH, NIAID, Host Def Lab, Bethesda, MD 20892 USA. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1359 BP 283 EP 283 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001348 ER PT J AU Worgall, TS Zapata, F Magana, MM Oelkers, PM Osborne, TF Davis-Hayman, S Nash, TE Deckelbaum, RJ AF Worgall, TS Zapata, F Magana, MM Oelkers, PM Osborne, TF Davis-Hayman, S Nash, TE Deckelbaum, RJ TI Sterol and fatty acid regulatory pathways in a Giardia lamblia derived promoter: Evidence for SREBP as an ancient transcription factor SO CIRCULATION LA English DT Meeting Abstract C1 Columbia Univ, New York, NY USA. Univ Calif Irvine, Irvine, CA USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1402 BP 291 EP 291 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001391 ER PT J AU Macgowan, GA Shroff, SG Du, CW Koretsky, AP AF Macgowan, GA Shroff, SG Du, CW Koretsky, AP TI Dysfunction in transgenic perfused mouse hearts expressing mutant troponin I lacking protein kinase C phosphorylation sites is dependent on decreased perfusate calcium. SO CIRCULATION LA English DT Meeting Abstract C1 Univ Pittsburgh, Pittsburgh, PA USA. Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1514 BP 314 EP 314 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001502 ER PT J AU Boehm, M True, AL San, H Akyuerek, LM Tashiro, J Crook, MF Nabel, GJ Nabel, EG AF Boehm, M True, AL San, H Akyuerek, LM Tashiro, J Crook, MF Nabel, GJ Nabel, EG TI Deletion of the p27Kip1 and p21Cip1 loci accelerates cellular proliferation and impairs arterial wound repair SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1553 BP 322 EP 323 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001541 ER PT J AU Yoshimoto, T Boehm, M Nallamshetty, S Nabel, GJ Nabel, EG AF Yoshimoto, T Boehm, M Nallamshetty, S Nabel, GJ Nabel, EG TI Protein arginine methyltransferase 2 (PRMT2) regulates G(1)/S transition of the cell cycle through the inhibition of pRB phosphorylation SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD 20892 USA. NIH, NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1552 BP 322 EP 322 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001540 ER PT J AU O'Donnell, CJ Larson, MG Kupka, MJ Jaffer, FA Clouse, ME Levy, D Manning, WJ AF O'Donnell, CJ Larson, MG Kupka, MJ Jaffer, FA Clouse, ME Levy, D Manning, WJ TI Subclinical aortic atherosclerosis detected by MRI is associated with aortic and coronary calcification and carotid intimal medial thickness in the Framingham Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1788 BP 375 EP 375 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001773 ER PT J AU Balady, GJ Larson, MG Vasan, RS O'Donnell, CJ Levy, D AF Balady, GJ Larson, MG Vasan, RS O'Donnell, CJ Levy, D TI Does treadmill exercise testing predict coronary disease risk in asymptomatic persons after accounting for Framingham risk score? SO CIRCULATION LA English DT Meeting Abstract C1 Boston Univ, Med Ctr, Boston, MA USA. Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1794 BP 376 EP 377 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001779 ER PT J AU Wassmuth, R Wasserman, B Sorger, JM Taylor, JL Arai, AE AF Wassmuth, R Wasserman, B Sorger, JM Taylor, JL Arai, AE TI Magnetic resonance gadolinium enhancement of atheroma in LDL-receptor deficient rabbits SO CIRCULATION LA English DT Meeting Abstract C1 Franz Volhard Clin, Berlin, Germany. Johns Hopkins Univ, Baltimore, MD USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 1792 BP 376 EP 376 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001777 ER PT J AU Herzog, CA Ma, JZ Collins, AJ AF Herzog, CA Ma, JZ Collins, AJ TI Repeat coronary revascularization rates after angioplasty, stenting, bypass surgery and competing death risk in dialysis patients SO CIRCULATION LA English DT Meeting Abstract C1 NIDDK, CV Special Study Ctr, US Renal Data Syst, Minneapolis Med Res Fdn,NIH, Minneapolis, MN USA. NIDDK, Minneapolis Med Res Fdn, NIH, Minneapolis, MN USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2016 BP 424 EP 424 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895001998 ER PT J AU Greenspon, AJ Hart, R Dawson, D Silver, M Greer, S Schron, E Goldman, L Hellkamp, A Lee, KL Lamas, G AF Greenspon, AJ Hart, R Dawson, D Silver, M Greer, S Schron, E Goldman, L Hellkamp, A Lee, KL Lamas, G TI Predictors of stroke in patients paced for sick sinus syndrome SO CIRCULATION LA English DT Meeting Abstract C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Gaston Mem Hosp, Gastonia, NC USA. Baptist Med Ctr, Little Rock, AR USA. NHLBI, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Duke Univ, Durham, NC 27706 USA. Duke Clin Res Inst, Durham, NC USA. Mt Sinai Med Ctr, Miami, FL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2021 BP 425 EP 425 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002003 ER PT J AU Paolocci, N Feelisch, M Saavedra, WF Hare, JM Wink, DA Kass, DA AF Paolocci, N Feelisch, M Saavedra, WF Hare, JM Wink, DA Kass, DA TI The positive inotropic action of nitroxyl in vivo is mediated by calcitonin gene-related peptide SO CIRCULATION LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Louisiana State Univ, Shreveport, LA 71105 USA. Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2062 BP 435 EP 435 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002044 ER PT J AU Liao, DP Duan, YK Lin, HM Sharrett, RA Chambless, LE Boerwinkle, E Heiss, G AF Liao, DP Duan, YK Lin, HM Sharrett, RA Chambless, LE Boerwinkle, E Heiss, G TI Genetic polymorphisms of two Renin-Angiotensin System components and arterial stiffness and cardiovascular disease SO CIRCULATION LA English DT Meeting Abstract C1 Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Hershey, PA 17033 USA. NHLBI, Bethesda, MD 20892 USA. Univ N Carolina, Chapel Hill, NC USA. Univ Texas, Texas Med Ctr, Houston, TX 77025 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2125 BP 448 EP 448 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002107 ER PT J AU Vernalis, MN Ocuin, E Remaley, AT Scally, JP Walizer, E Sampson, M Arthur, C Runner, J Northrup, G Taylor, AJ AF Vernalis, MN Ocuin, E Remaley, AT Scally, JP Walizer, E Sampson, M Arthur, C Runner, J Northrup, G Taylor, AJ TI Do lifestyle changes negate the adverse effect of ultra-low fat diets on HDL cholesterol and apoprotein A-I? The Ornish diet and lifestyle modification program SO CIRCULATION LA English DT Meeting Abstract C1 Walter Reed Army Med Ctr, Washington, DC 20307 USA. NIH, NHLBI, Bethesda, MD USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2218 BP 468 EP 468 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002200 ER PT J AU Talbot, LA Metter, EJ Fleg, JL AF Talbot, LA Metter, EJ Fleg, JL TI Have national physical activity recommendations favorably impacted leisure-time physical activity patterns in healthy men and women? A cross sectional examination of four decades SO CIRCULATION LA English DT Meeting Abstract C1 Johns Hopkins Univ, Baltimore, MD USA. NIH, NIA, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2236 BP 472 EP 472 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002218 ER PT J AU Talbot, LA Morrell, CH Fleg, JL Metter, J AF Talbot, LA Morrell, CH Fleg, JL Metter, J TI Contributions of leisure time physical activity and its rate of change to all cause mortality in healthy men and women SO CIRCULATION LA English DT Meeting Abstract C1 Johns Hopkins Univ, Baltimore, MD USA. Loyola Coll, Baltimore, MD 21210 USA. NIH, NIA, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2237 BP 472 EP 472 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002219 ER PT J AU Hougaku, H Fleg, JL Lakatta, EG Kemper, MK Earley, CJ Metter, EJ AF Hougaku, H Fleg, JL Lakatta, EG Kemper, MK Earley, CJ Metter, EJ TI Light to moderate alcohol intake alters age-associated arterial stiffness SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIA, LCI, Baltimore, MD USA. NIH, NIA, LCS, Baltimore, MD USA. Dept Neurol, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2378 BP 502 EP 502 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002360 ER PT J AU Yataco, AR Sung, JD Fleisher, LA Bacher, AC Turner, KL Deregis, JR Stewart, KJ Fleg, JL AF Yataco, AR Sung, JD Fleisher, LA Bacher, AC Turner, KL Deregis, JR Stewart, KJ Fleg, JL TI Habitual physical activity but not peak aerobic capacity predicts heart rate variability in older adults SO CIRCULATION LA English DT Meeting Abstract C1 Int Res Ctr, Towson, MD USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. NIH, NIA, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2382 BP 503 EP 503 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002364 ER PT J AU Walsh, CR Larson, MG Kupka, MJ Manning, WJ Clouse, ME O'Donnell, CJ AF Walsh, CR Larson, MG Kupka, MJ Manning, WJ Clouse, ME O'Donnell, CJ TI Prevalence of aortic valve calcium detected by electron beam computed tomography and association with calcium deposits in the coronary arteries and aorta SO CIRCULATION LA English DT Meeting Abstract C1 Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 2 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 OCT 23 PY 2001 VL 104 IS 17 SU S MA 2541 BP 537 EP 537 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002522 ER PT J AU Russo, GT Friso, S Jacques, PF Rogers, GT Cucinotta, D Wilson, PW Schaefer, EJ Ordovas, JM Rosenberg, IH Selhub, J AF Russo, GT Friso, S Jacques, PF Rogers, GT Cucinotta, D Wilson, PW Schaefer, EJ Ordovas, JM Rosenberg, IH Selhub, J TI Role of the C677T mutation in the methylenetetrahydrofolate reductase gene and its interactions with common and emerging determinants of homocysteinemia in the Framingham Offspring Study SO CIRCULATION LA English DT Meeting Abstract C1 Univ Messina, I-98100 Messina, Italy. Tufts Univ, JM USDA HNRC, Vitamin Metab Lab, Boston, MA 02111 USA. Tufts Univ, JM USDA HNRC, Boston, MA 02111 USA. Tufts Univ, Boston, MA 02111 USA. Tufts Univ, JM USDA HNRC, Lipid Metab Lab, Boston, MA 02111 USA. NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. RI cucinotta, domenico/F-4832-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2717 BP 574 EP 574 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002695 ER PT J AU Yamada, H Jones, M Shiota, T Qin, JX Greenberg, NL Kim, YJ Watanabe, J Cardon, LA Abe, Y Tsujino, H Kanda, R Thomas, JD AF Yamada, H Jones, M Shiota, T Qin, JX Greenberg, NL Kim, YJ Watanabe, J Cardon, LA Abe, Y Tsujino, H Kanda, R Thomas, JD TI Assessment of nonuniformity of the transmural myocaridal velocity profile by angle corrected tissue Doppler imaging: Characterization of normal, transmurally infarcted and nontransmurally infarcted myocardium SO CIRCULATION LA English DT Meeting Abstract C1 Cleveland Clin Fdn, Cleveland, OH 44195 USA. NHLBI, Bethesda, MD 20892 USA. Toshiba Med Syst Res & Dev Ctr, Tochigi, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 2968 BP 628 EP + PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002944 ER PT J AU Christian, TF Rettmann, D Liao, S Balaban, RS Arai, AE AF Christian, TF Rettmann, D Liao, S Balaban, RS Arai, AE TI Double-bolus method for quantitation of myocardial perfusion by first-pass cardiac MRI SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3022 BP 639 EP 639 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002998 ER PT J AU Rekhraj, S Kwong, RY Davis, JE Graninger, G Balaban, RS Arai, AE AF Rekhraj, S Kwong, RY Davis, JE Graninger, G Balaban, RS Arai, AE TI Accuracy of multislice perfusion dipyridamole sress MRI SO CIRCULATION 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 LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3023 BP 639 EP 639 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895002999 ER PT J AU Sierra-Galan, LM Agyeman, KO Fananapazir, L Arai, AE AF Sierra-Galan, LM Agyeman, KO Fananapazir, L Arai, AE TI Myocardial function is abnormal in hypertrophic cardiomyopathy in MRI gadolinium hyperenhanced and 'MRI normal' myocardium SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3025 BP 640 EP 640 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003001 ER PT J AU El-Sedfy, GM Rusk, RA Jones, M Sachdev, V Sahn, DJ AF El-Sedfy, GM Rusk, RA Jones, M Sachdev, V Sahn, DJ TI Real time 3D echo for computing mitral valve regurgitation severity from the difference in LV and RV stroke volumes in a chronic animal model SO CIRCULATION LA English DT Meeting Abstract C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3082 BP 652 EP 652 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003058 ER PT J AU Flaker, G Greenspon, A Tardiff, B Schron, E Goldman, L Hellkamp, A Lee, KL Lamas, GA AF Flaker, G Greenspon, A Tardiff, B Schron, E Goldman, L Hellkamp, A Lee, KL Lamas, GA TI Cause of death in elderly patients with pacemakers for sick sinus syndrome SO CIRCULATION LA English DT Meeting Abstract C1 Univ Missouri, Columbia, MO 65211 USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Duke Univ, Durham, NC 27706 USA. NHLBI, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Duke Clin Res Inst, Durham, NC USA. Mt Sinai Med Ctr, Miami, FL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3104 BP 657 EP 657 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003079 ER PT J AU Lindenfeld, J Ghali, JK Krause-Steinrauf, H Thaneemit-Chen, S Rosenberg, YD Lowes, BD Larsen, RL Yancy, C Young, JB Adams, KF Peberdy, MA Kahn, SS AF Lindenfeld, J Ghali, JK Krause-Steinrauf, H Thaneemit-Chen, S Rosenberg, YD Lowes, BD Larsen, RL Yancy, C Young, JB Adams, KF Peberdy, MA Kahn, SS TI Plasma norepinephrine predicts prognosis in women with advanced heart failure in the beta-blocker evaluation of survival trial (BEST) SO CIRCULATION LA English DT Meeting Abstract C1 Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Cardiac Ctr Louisiana, Shreveport, LA USA. NHLBI, Menlo Pk, CA USA. VA Palo Alto Cooperat Study Program, Coordinating Ctr, Menlo Pk, CA USA. BEST Invest, Denver, CO USA. NHLBI, Bethesda, MD 20892 USA. Duke Univ, Med Ctr, Durham, NC USA. Univ Texas, SW Med Ctr, Austin, TX 78712 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. N Carolina Cent Univ, Durham, NC USA. Virginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USA. Cedars Sinai Med Ctr, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3112 BP 659 EP 659 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003087 ER PT J AU Lipshultz, SE Easley, KA Orav, EJ Kaplan, S Starc, TJ Bricker, JT Lai, WW Moodie, DS Sopko, G Schluchter, MD Colan, SD AF Lipshultz, SE Easley, KA Orav, EJ Kaplan, S Starc, TJ Bricker, JT Lai, WW Moodie, DS Sopko, G Schluchter, MD Colan, SD TI Cardiovascular status of infants and children of HIV-infected women: The prospective (PCHIV)-C-2-H-2 study SO CIRCULATION LA English DT Meeting Abstract C1 Univ Rochester, Rochester, NY USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Columbia Univ, Presbyterian Hosp, New York, NY USA. Baylor Coll Med, Houston, TX 77030 USA. Mt Sinai Sch Med, New York, NY USA. NHLBI, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Childrens Hosp, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3198 BP 678 EP 678 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003173 ER PT J AU Campia, U Bryant, MB Cardillo, C Panza, JA AF Campia, U Bryant, MB Cardillo, C Panza, JA TI Role of endothelin in the impaired endothelial vasodilator function of patients with essential hypertension SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3266 BP 692 EP 692 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003239 ER PT J AU Dilsizian, V Shirani, J Lee, YHC Kiesewetter, D Jagoda, EM Loredo, ML Eckelman, WC AF Dilsizian, V Shirani, J Lee, YHC Kiesewetter, D Jagoda, EM Loredo, ML Eckelman, WC TI Specific binding of [F-18]fluorobenzyl-lisinopril to angiotensin converting enzyme in human heart tissue of ischemic cardiomyopathy SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Albert Einstein Coll Med, Bronx, NY 10467 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3276 BP 694 EP 694 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003249 ER PT J AU Cook, JR Steinberg, JS Vidaillet, H Zimmerman, P Epstein, AE Dalquist, J AF Cook, JR Steinberg, JS Vidaillet, H Zimmerman, P Epstein, AE Dalquist, J CA Affirm Investigators TI Gender differences in the characteristics and prior treatment of atrial fibrillation: Preliminary data from the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study SO CIRCULATION LA English DT Meeting Abstract C1 Baystate Med Ctr, Springfield, MA USA. St Lukes Roosevelt Hosp, New York, NY 10025 USA. Marshfield Clin Fdn Med Res & Educ, Marshfield, WI USA. Heart Grp, Evansville, IN USA. Univ Alabama, Birmingham, AL USA. Axio Res Corp, Seattle, WA USA. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3298 BP 699 EP 699 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003271 ER PT J AU Herzog, CA Ma, JZ Collins, AJ AF Herzog, CA Ma, JZ Collins, AJ TI Long term survival of dialysis patients in the US after coronary angioplasty, coronary artery stenting, and coronary artery bypass surgery SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NIDDK, Minneapolis Med Res Fdn, US Renal Data Syst,CV Special Study Ctr, Minneapolis, MN USA. NIH, NIDDK, Minneapolis Med Res Fdn, Minneapolis, MN USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3319 BP 703 EP 704 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003292 ER PT J AU Herzog, CA Ma, JZ Collins, AJ AF Herzog, CA Ma, JZ Collins, AJ TI Long term outcome of renal transplant recipients in the US after coronary artery bypass surgery, coronary angioplasty, and coronary stenting SO CIRCULATION LA English DT Meeting Abstract C1 NIDDKD, CV Special Study Ctr, US Renal Data Syst, Minneapolis Med Res Fdn,NIH, Minneapolis, MN USA. NIDDKD, Minneapolis Med Res Fdn, NIH, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3321 BP 704 EP 704 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003294 ER PT J AU Kwong, RY Rekhraj, S Aletras, AH Arai, AE AF Kwong, RY Rekhraj, S Aletras, AH Arai, AE TI Receiver operator curve analysis defines abnormal thresholds for quantitative systolic wall thickening by MRI SO CIRCULATION LA English DT Meeting Abstract C1 NIH, NHLBI, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3408 BP 722 EP 722 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003380 ER PT J AU Yang, H Pu, M Daugherty, DW Popovic, Z Cardon, LA Zetts, AD Jones, M AF Yang, H Pu, M Daugherty, DW Popovic, Z Cardon, LA Zetts, AD Jones, M TI The pulmonary venous flow determinants of left atrial pressure under different loading conditions in a chronic animal model with mitral regurgitation SO CIRCULATION LA English DT Meeting Abstract C1 Cleveland Clin Fdn, Cleveland, OH 44195 USA. NIH, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3465 BP 734 EP 734 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003436 ER PT J AU Domanski, M Krause-Steinrauf, H Deedwania, P Ghali, J Gilbert, EM Katz, RJ Lindenfeld, J Lowes, B Martin, W McGrew, F Bristow, M AF Domanski, M Krause-Steinrauf, H Deedwania, P Ghali, J Gilbert, EM Katz, RJ Lindenfeld, J Lowes, B Martin, W McGrew, F Bristow, M TI The effect of buicindolol in diabetic and non-diabetic patients with advanced heart failure SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. VA Palo Alto Cooperat Study Program Coordinating, Bethesda, MD 20892 USA. VA Med Ctr, Fresno, CA USA. Cardiac Ctr Louisiana, Shreveport, LA USA. Univ Utah, Salt Lake City, UT 84112 USA. George Washington Univ, Washington, DC USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. VA Med Ctr, St Louis, MO USA. Baptist Mem Hosp, Memphis, TN 38146 USA. RI bristow, michael/G-7850-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3552 BP 754 EP 754 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003523 ER PT J AU Bristow, MR Krause-Steinrauf, H Abraham, WT Chang-Seng, L Hattler, B Kruger, S Llindenfeld, JA Lowes, BD Olson, L Thaneemit-Chen, S Zelis, R AF Bristow, MR Krause-Steinrauf, H Abraham, WT Chang-Seng, L Hattler, B Kruger, S Llindenfeld, JA Lowes, BD Olson, L Thaneemit-Chen, S Zelis, R TI Sympatholytic effect of bucindolol adversely affected survival, and was disproportionately observed in the class IV subgroup of BEST SO CIRCULATION LA English DT Meeting Abstract C1 Univ Colorado, Hlth Sci Ctr, Denver, CO USA. NHLBI, Palo Alto, CA USA. VA Palo Alto Cooperat Study Program Coordinating, Palo Alto, CA USA. Univ Kentucky, Lexington, KY 40506 USA. Univ Rochester, Rochester, NY 14627 USA. VA Med Ctr, Denver, CO USA. NB Heart Inst, Omaha, NE USA. VA CSPCC, Palo Alto, CA USA. Penn State Univ, Hershey, PA USA. RI bristow, michael/G-7850-2011 NR 0 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3554 BP 755 EP 755 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003525 ER PT J AU Herzog, CA Ma, JZ Collins, AJ AF Herzog, CA Ma, JZ Collins, AJ TI Long-term survival of dialysis patients in the US after cardiac valve replacement: ACC/AHA guidelines on prosthetic valve selection should be changed SO CIRCULATION LA English DT Meeting Abstract C1 NIDDK, Minneapolis Med Res Fdn, US Renal Data Syst,CV Special Study Ctr, NIH, Minneapolis, MN USA. NIDDK, Minneapolis Med Res Fdn, NIH, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3576 BP 760 EP 760 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003547 ER PT J AU Kraitchman, DL Sampath, S Derbyshire, JA Bluemke, DA Gerber, BL Prince, JL Osman, NF AF Kraitchman, DL Sampath, S Derbyshire, JA Bluemke, DA Gerber, BL Prince, JL Osman, NF TI Quantitative ischemia detection during cardiac MR stress testing SO CIRCULATION LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Johns Hopkins Univ, Dept Elect Engn, Baltimore, MD USA. NIH, Bethesda, MD 20892 USA. Johns Hopkins Med Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. RI Prince, Jerry/A-3281-2010; Gerber, Bernhard/H-5838-2011 OI Prince, Jerry/0000-0002-6553-0876; NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3623 BP 769 EP 769 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003593 ER PT J AU Kwong, RY Rekhraj, S Schussheim, AE Davis, JE Balaban, RS Arai, AE AF Kwong, RY Rekhraj, S Schussheim, AE Davis, JE Balaban, RS Arai, AE TI Urgent assessment of emergency room chest pain patients with non-diagnostic electrocardiogram with adenosine stress MRI SO CIRCULATION LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3624 BP 769 EP 769 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003594 ER PT J AU Rekhraj, S Kwong, RY Balaban, RS Arai, AE AF Rekhraj, S Kwong, RY Balaban, RS Arai, AE TI Rest MRI perfusion defect underestimates size of myocardial infarction. SO CIRCULATION 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 LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3629 BP 770 EP 770 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003599 ER PT J AU Lewis, CE McCreath, HE West, DE Loria, C Kiefe, CI Hulley, SB AF Lewis, CE McCreath, HE West, DE Loria, C Kiefe, CI Hulley, SB TI The obesity epidemic rolls on: 15 years in CARDIA SO CIRCULATION LA English DT Meeting Abstract C1 Univ Alabama, Birmingham, AL USA. NHLBI, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3699 BP 787 EP 787 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003669 ER PT J AU O'Donnell, CJ Cupples, LA Kiel, DP Hannan, M Wilson, PWF AF O'Donnell, CJ Cupples, LA Kiel, DP Hannan, M Wilson, PWF TI Do subclinical arterial calcific deposits predict coronary heart disease risk beyond risk factor profiles? SO CIRCULATION LA English DT Meeting Abstract C1 Framingham Heart Dis Epidemiol Study, NHLBI, Framingham, MA USA. Boston Univ, Sch Publ Hlth, Boston, MA USA. Hebrew Rehabil Ctr Aged, Boston, MA USA. Boston Univ, Sch Med, Boston, MA 02118 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3732 BP 794 EP 795 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003702 ER PT J AU Eisenstein, EL Yusuf, S Bourassa, MG Egan, DA Williford, WO Horney, A Mark, D AF Eisenstein, EL Yusuf, S Bourassa, MG Egan, DA Williford, WO Horney, A Mark, D TI What is the economic value of digoxin therapy in congestive heart failure patients? Results from the DIG trial SO CIRCULATION LA English DT Meeting Abstract C1 Duke Clin Res Inst, Durham, NC USA. McMaster Univ, Hamilton, ON, Canada. Inst Cardiol Montreal, Montreal, PQ, Canada. NHLBI, Bethesda, MD 20892 USA. Dept Vet Affairs, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3744 BP 798 EP 798 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003714 ER PT J AU Murabito, JM Evans, JC Nieto, K Levy, D Wilson, PW AF Murabito, JM Evans, JC Nieto, K Levy, D Wilson, PW TI Prognostic significance of peripheral arterial disease in the oldest old: The Framingham Study SO CIRCULATION LA English DT Meeting Abstract C1 Boston Univ, Sch Med, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3787 BP 806 EP 807 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003757 ER PT J AU Chen, W Srinivasan, SR Ellsworth, DL Boerwinkle, E Berenson, GS AF Chen, W Srinivasan, SR Ellsworth, DL Boerwinkle, E Berenson, GS TI Hepatic lipase gone polymorphism (C-514T) influences serial changes in HDL cholesterol and triglycerides from childhood to young adulthood: The Bogalusa heart study SO CIRCULATION LA English DT Meeting Abstract C1 Tulane Univ, Hlth Sci Ctr, New Orleans, LA USA. NHLBI, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Houston, TX USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3788 BP 807 EP 807 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003758 ER PT J AU Liu, K Colangelo, L Daviglus, M Loria, C Jacobs, DR Hulley, S AF Liu, K Colangelo, L Daviglus, M Loria, C Jacobs, DR Hulley, S TI Relevance of obesity and lifestyle factors in determining black-white difference in blood pressure: The CARDIA study. SO CIRCULATION LA English DT Meeting Abstract C1 Northwestern Univ, Sch Med, Chicago, IL USA. NHLBI, Bethesda, MD 20892 USA. Univ Minnesota, Minneapolis, MN USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3799 BP 809 EP 809 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003769 ER PT J AU Lloyd-Jones, DM Evans, JC Levy, D AF Lloyd-Jones, DM Evans, JC Levy, D TI Predictors of initiation of antihypertensive therapy in the community SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. RI Lloyd-Jones, Donald/C-5899-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3809 BP 811 EP 811 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003779 ER PT J AU Obarzanek, E Proschan, MA Moore, TJ Sacks, FM Svetkey, LP Appel, LJ Vollmer, WM Most-Windhauser, MM Cutler, JA AF Obarzanek, E Proschan, MA Moore, TJ Sacks, FM Svetkey, LP Appel, LJ Vollmer, WM Most-Windhauser, MM Cutler, JA TI Variability in blood pressure response to salt intake SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Bethesda, MD 20892 USA. Boston Univ, Boston, MA 02215 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Duke Hypertens Ctr, Durham, NC USA. Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA. Kaiser Permanente Ctr Hlth Res, Portland, OR USA. Pennington Biomed Res Ctr, Baton Rouge, LA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3810 BP 811 EP 812 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003780 ER PT J AU Walsh, CR Larson, MG Leip, E Levy, D AF Walsh, CR Larson, MG Leip, E Levy, D TI Serum potassium is not associated with risk of cardiovascular disease: The Framingham Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3807 BP 811 EP 811 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003777 ER PT J AU Merz, CNNB Olson, MB Matthews, KA Sharaf, BL Pepine, CJ Reis, SE Pohost, GM Reichek, N Rogers, WJ Kelsey, SF Sopkp, G AF Merz, CNNB Olson, MB Matthews, KA Sharaf, BL Pepine, CJ Reis, SE Pohost, GM Reichek, N Rogers, WJ Kelsey, SF Sopkp, G TI Higher physical activity level does not improve the preditive accuracy of angina for CAD in women: The NHLBI-sponsored WISE SO CIRCULATION LA English DT Meeting Abstract C1 Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. Brown Univ, Providence, RI 02912 USA. Univ Florida, Gainesville, FL 32611 USA. Univ Alabama, Birmingham, AL USA. Allegheny Gen Hosp, Pittsburgh, PA 15212 USA. NHLBI, Bethesda, MD 20892 USA. RI Reis, Steven/J-3957-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3838 BP 819 EP 819 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003808 ER PT J AU Ferrucci, L Furberg, CD Penninx, BW Di Bari, M Williamson, JD Guralnik, JM Chen, JG Applegate, WB Pahor, M AF Ferrucci, L Furberg, CD Penninx, BW Di Bari, M Williamson, JD Guralnik, JM Chen, JG Applegate, WB Pahor, M TI Global cardiovascular risk and treatment of systolic hypertension in older patients SO CIRCULATION LA English DT Meeting Abstract C1 Lab Clin Epidemiol, Florence, Italy. Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA. Wake Forest Univ, Sticht Ctr Aging, Winston Salem, NC USA. NIH, Bethesda, MD 20892 USA. RI DI BARI, MAURO/J-1524-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3848 BP 823 EP 823 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003818 ER PT J AU Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV AF Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV TI Combined QRS area and ST depression criteria for prediction of all-cause and cardiovascular mortality: The Strong Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Cornell Univ, Weill Med Coll, New York, NY USA. NHLBI, Bethesda, MD 20892 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Univ Arizona, Med Ctr, Tucson, AZ USA. MedStar Res Inst, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3859 BP 825 EP 826 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003829 ER PT J AU Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV AF Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV TI The combination of echocardiographic and electrocardiographic criteria improve prediction of mortality: The Strong Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Cornell Univ, Weill Med Coll, New York, NY USA. NHLBI, Bethesda, MD 20892 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Univ Arizona, Med Ctr, Tucson, AZ USA. MedStar Res Inst, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3858 BP 825 EP 825 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003828 ER PT J AU Onder, G Penninx, B Balkrishnan, R Williamson, J Di Bari, M Fried, L Guralnik, J Pahor, M AF Onder, G Penninx, B Balkrishnan, R Williamson, J Di Bari, M Fried, L Guralnik, J Pahor, M TI ACE inhibitors use and decline in muscle strength and walking speed in older women SO CIRCULATION LA English DT Meeting Abstract C1 Wake Forest Univ, Sticht Ctr Aging, Winston Salem, NC 27109 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. NIA, NIH, Bethesda, MD 20892 USA. RI DI BARI, MAURO/J-1524-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3857 BP 825 EP 825 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003827 ER PT J AU Schaefer, EJ Audelin, MC McNamara, JR D'Agostino, R Wilson, PW AF Schaefer, EJ Audelin, MC McNamara, JR D'Agostino, R Wilson, PW CA NHLBI TI Remnant-like particles and carotid atherosclerosis: Results from the Framingham Offspring Study SO CIRCULATION LA English DT Meeting Abstract C1 Tufts Univ, New England Med Ctr, Boston, MA 02111 USA. Boston Univ, Boston, MA 02215 USA. NHLBI, Framingham Heart Dis Epidemiol Study, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3861 BP 826 EP 826 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003831 ER PT J AU Chen, W Srinivasan, SR Ellsworth, DL Boerwinkle, E Berenson, GS AF Chen, W Srinivasan, SR Ellsworth, DL Boerwinkle, E Berenson, GS TI Endothelial nitric oxide synthase polymorphism (G894T) and insulin resistance have an interaction effect on serial changes in blood pressure levels from childhood to young adulthood: The Bogalusa heart study SO CIRCULATION LA English DT Meeting Abstract C1 Tulane Hlth Sci Ctr, New Orleans, LA USA. NHLBI, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Houston, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3868 BP 827 EP 828 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003838 ER PT J AU Vasan, RS Larson, MG Levy, D Corey, D O'Donnell, CJ Benjamin, EJ AF Vasan, RS Larson, MG Levy, D Corey, D O'Donnell, CJ Benjamin, EJ TI Heritability and genetic linkage for aortic root and left atrial size: The Framingham Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Boston Univ, Sch Med, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3875 BP 829 EP 829 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003845 ER PT J AU Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV AF Okin, PM Roman, MJ Fabsitz, RR Lee, ET Galloway, JM Howard, BV TI Electrocardiographic prediction of mortality in diabetics: The Strong Heart Study SO CIRCULATION LA English DT Meeting Abstract C1 Cornell Univ, Weill Med Coll, New York, NY USA. NHLBI, Bethesda, MD 20892 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Univ Arizona, Med Ctr, Tucson, AZ USA. MedStar Res Inst, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 SU S MA 3892 BP 832 EP 832 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 487UW UT WOS:000171895003862 ER PT J AU Carney, RM Blumenthal, JA Stein, PK Watkins, L Catellier, D Berkman, LF Czajkowski, SM O'Connor, C Stone, PH Freedland, KE AF Carney, RM Blumenthal, JA Stein, PK Watkins, L Catellier, D Berkman, LF Czajkowski, SM O'Connor, C Stone, PH Freedland, KE TI Depression, heart rate variability, and acute myocardial infarction SO CIRCULATION LA English DT Article DE depression; myocardial infarction; heart rate variability ID CORONARY-ARTERY DISEASE; SYMPATHETIC NERVOUS-SYSTEM; ARRHYTHMIA; POWER; NOREPINEPHRINE; MORTALITY; SURVIVAL; PLASMA AB Background-Clinical depression is associated with an increased risk for mortality in patients with a recent myocardial infarction (MI). Reduced heart rate variability (HRV) has been suggested as a possible explanation for this association. The purpose of this study was to determine if depression is associated with reduced HRV in patients with a recent MI. Methods and Results-Three hundred eighty acute MI patients with depression and 424 acute MI patients without depression were recruited. All underwent 24-hour ambulatory electrocardiographic monitoring after hospital discharge. In univariate analyses, 4 indices of HRV were significantly lower in patients with depression than in patients without depression. Variables associated with HRV were then compared between patients with and without depression, and potential confounds were identified. These variables (age, sex, diabetes, and present cigarette smoking) were entered into an analysis of covariance model, followed by depression status. In the final model, all but one HRV index (high-frequency power) remained significantly lower in patients with depression than in patients without depression. Conclusions-We conclude that greater autonomic dysfunction, as reflected by decreased HRV, is a plausible mechanism linking depression to increased cardiac mortality in post-MI patients. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA. Duke Univ, Dept Psychiat, Durham, NC 27706 USA. Duke Univ, Dept Med, Durham, NC 27706 USA. Univ N Carolina, Dept Biostat, Raleigh, NC USA. Harvard Univ, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Dept Med, Boston, MA 02115 USA. NHLBI, Bethesda, MD 20892 USA. RP Carney, RM (reprint author), Behav Med Ctr, 4625 Lindell Blvd,Suite 420, St Louis, MO 63108 USA. FU NHLBI NIH HHS [N01-HC-55148, 1UO-1HL58946, N01-HC-55140, N01-HC-55142, N01-HC-55146] NR 34 TC 403 Z9 426 U1 6 U2 25 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 23 PY 2001 VL 104 IS 17 BP 2024 EP 2028 DI 10.1161/hc4201.097834 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 486QQ UT WOS:000171828800009 PM 11673340 ER PT J AU Launer, LJ White, LR Petrovitch, H Ross, GW Curb, JD AF Launer, LJ White, LR Petrovitch, H Ross, GW Curb, JD TI Cholesterol and neuropathologic markers of AD - A population-based autopsy study SO NEUROLOGY LA English DT Article ID AMYLOID-BETA-PEPTIDE; DENSITY-LIPOPROTEIN CHOLESTEROL; APOLIPOPROTEIN-E GENOTYPE; JAPANESE-AMERICAN MEN; ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; BLOOD-PRESSURE; APOE GENOTYPE; HUMAN BRAIN; DEMENTIA AB Objective: To examine the association of plasma cholesterol (total and high-density [HDL] and low-density lipoprotein) levels with neuritic plaques (NP) and neurofibrillary tangles (NFT) in a population-based autopsy series of 218 Japanese American men followed as a part of the Honolulu-Asia Aging Study. Methods: Cholesterol levels were measured in late life (average age at death 84.6 years) in all subjects (n = 218) and in midlife (20 years before late life) in a subsample (n = 89); for the analyses, levels were categorized into quintiles, with the lowest quintile serving as the reference. Tissue from four areas of neocortex and two areas of hippocampus was prepared with Bielschowsky silver-stained sections and evaluated by one of three neuropathologists who were blinded to clinical information. Diffuse and neuritic plaques and NFT were counted in field areas standardized to 1 mm(2). Fields were selected from areas with the highest numbers of lesions, and the field with the highest count was taken to represent the brain area. Results: After adjusting for age at death, education, APOE allele, dementia, neuropathologic infarction, and blood pressure, a strong linear association was found for increasing late-life HDL cholesterol (HDL-C) levels and an increasing number of neocortical NP (5th versus 1st quintile: count ratio [95% CI] 2.30 [1.05 to 5.06]) and hippocampal (2.63 [1.25 to 5.50]) and neocortical (4.20 [1.73 to 10.16]) NFT. Trends were similar for the midlife HDL-C levels. Conclusions: The constituents of HDL-C may play a role in the formation of AD pathology, and these processes are reflected in peripheral measures. C1 NIA, EDBP, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA. Pacific Hlth Res Inst, Honolulu, HI USA. Dept Vet Adm Honolulu, Honolulu, HI USA. Kuakini Med Ctr, Honolulu Heart Program, Honolulu, HI 96817 USA. Univ Hawaii, John A Burns Sch Med, Dept Med, Honolulu, HI 96822 USA. RP Launer, LJ (reprint author), NIA, EDBP, Lab Epidemiol Demog & Biometry, NIH, Gateway Bldg 3C-309,7201 Wisconsin Ave, Bethesda, MD 20892 USA. FU NHLBI NIH HHS [N01-HC-05102]; NIA NIH HHS [N01-AG-4-2149] NR 39 TC 101 Z9 110 U1 2 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD OCT 23 PY 2001 VL 57 IS 8 BP 1447 EP 1452 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 484GH UT WOS:000171681500018 PM 11673587 ER PT J AU Piatigorsky, J Norman, B Dishaw, LJ Kos, L Horwitz, J Steinbach, PJ Kozmik, Z AF Piatigorsky, J Norman, B Dishaw, LJ Kos, L Horwitz, J Steinbach, PJ Kozmik, Z TI J3-crystallin of the jellyfish lens: Similarity to saposins SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GLUTATHIONE-S-TRANSFERASE; LYSOSOMAL STORAGE DISORDERS; ACTIVATOR PROTEINS; ALDEHYDE DEHYDROGENASE; DETOXIFICATION ENZYMES; CUBOMEDUSAN JELLYFISH; NEUROTROPHIC FACTOR; SECONDARY STRUCTURE; ALPHA-CRYSTALLIN; SCHWANN-CELLS AB J3-crystallin, one of the three major eye-lens proteins of the cubomedusan jellyfish (Tripedalia cystophora), shows similarity to vertebrate saposins, which are multifunctional proteins that bridge lysosomal hydrolases to lipids and activate enzyme activity. Sequence alignment of deduced J3-crystallin indicates two saposin-like motifs arranged in tandem, each containing six cysteines characteristic of this protein family. The J3-crystallin cDNA encodes a putative precursor analogous to vertebrate prosaposins. The J3-crystallin gene has seven exons, with exons 2-4 encoding the protein. Exon 3 encodes a circularly permutated saposin motif, called a swaposin, found in plant aspartic proteases. J3-crystallin RNA was found in the cubomedusan lens, statocyst, in bands radiating from the pigmented region of the ocellus, in the tentacle tip by in situ hybridization, and in the embryo and larva by reverse transcription-PCR. Our data suggest a crystallin role for the multifunctional saposin protein family in the jellyfish lens. This finding extends the gene sharing evolutionary strategy for lens crystallins to the cnidarians and indicates that the putative primordial saposin/swaposin J3-crystallin reflects both the chaperone and enzyme connections of the vertebrate crystallins. C1 NEI, Mol & Dev Biol Lab, Bethesda, MD 20892 USA. NIH, Ctr Mol Modeling, Ctr Informat Technol, Bethesda, MD 20892 USA. Florida Int Univ, Miami, FL 33199 USA. Univ Calif Los Angeles, Sch Med, Jules Stein Eye Inst, Los Angeles, CA 90095 USA. RP Piatigorsky, J (reprint author), NEI, Mol & Dev Biol Lab, 6 Ctr Dr,Bldg 6-Room 2-1, Bethesda, MD 20892 USA. RI Kozmik, Zbynek/G-3581-2014; Kozmik, Zbynek/I-8807-2014; Dishaw, Larry/A-9930-2010 OI Dishaw, Larry/0000-0002-2705-4573 NR 60 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 OCT 23 PY 2001 VL 98 IS 22 BP 12362 EP 12367 DI 10.1073/pnas.231310698 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 486EU UT WOS:000171806100016 PM 11675486 ER PT J AU Gegonne, A Weissman, JD Singer, DS AF Gegonne, A Weissman, JD Singer, DS TI TAF(II)55 binding to TAF(II)250 inhibits its acetyltransferase activity SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GENERAL TRANSCRIPTION FACTORS; RNA-POLYMERASE-II; TFIID SUBUNITS; DNA-DAMAGE; PROTEIN; DROSOPHILA; ACTIVATORS; CHROMATIN; RECEPTOR; PROMOTER AB The general transcription factor, TFIID, consists of the TATA-binding protein (TBP) associated with a series of TBP-associated factors (TAFs) that together participate in the assembly of the transcription preinitiation complex. One of the TAFs, TAF(II)250, has acetyltransferase (AT) activity that is necessary for transcription of MHC class I genes: inhibition of the AT activity represses transcription. To identify potential cellular factors that might regulate the AT activity of TAF(II)250, a yeast two-hybrid library was screened with a TAF(II)250 segment (amino acids 848-1279) that spanned part of its AT domain and it's the domain that binds to the protein, RAP74. The TFIID component, TAF(II)55, was isolated and found to interact predominantly with the RAP74-binding domain. TAF(II)55 binding to TAF(II)250 inhibits its AT activity. Importantly, the addition of recombinant TAF(II)55 to in vitro transcription assays inhibits TAF(II)250-dependent MHC class I transcription. Thus, TAF(II)55 is capable of regulating TAF(II)250 function by modulating its AT activity. C1 NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. RP Singer, DS (reprint author), NCI, Expt Immunol Branch, Bldg 10,Room 4B-36, Bethesda, MD 20892 USA. NR 23 TC 28 Z9 29 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 OCT 23 PY 2001 VL 98 IS 22 BP 12432 EP 12437 DI 10.1073/pnas.211444798 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 486EU UT WOS:000171806100028 PM 11592977 ER PT J AU Kanovsky, M Raffo, A Drew, L Rosal, R Do, T Friedman, FK Rubinstein, P Visser, J Robinson, R Brandt-Rauf, PW Michl, J Fine, RL Pincus, MR AF Kanovsky, M Raffo, A Drew, L Rosal, R Do, T Friedman, FK Rubinstein, P Visser, J Robinson, R Brandt-Rauf, PW Michl, J Fine, RL Pincus, MR TI Peptides from the amino terminal mdm-2-binding domain of p53, designed from conformational analysis, are selectively cytotoxic to transformed cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CHEMOTHERAPEUTIC-AGENTS; CANCER-CELLS; MDM2; APOPTOSIS; PROTEINS; GROWTH AB We have synthesized three peptides from the mdm-2 binding domain of human p53, residues 12-26 (PPLSQETFSDLWKLL), residues 12-20, and 17-26. To enable transport of the peptides across the cell membrane and at the same time to maximize the active mdm-2 binding a-helical conformation for these peptides, each was attached at its carboxyl terminus to the penetratin sequence, KKWKMRRNQFWVKVQRG, that contains many positively charged residues that stabilize an a-helix when present on its carboxyl terminal end. All three peptides were cytotoxic to human cancer cells in culture, whereas a control, unrelated peptide attached to the same penetratin sequence had no effect on these cell lines. The same three cytotoxic peptides had no effect on the growth of normal cells, including human cord blood-derived stem cells. These peptides were as effective in causing cell death in p53-null cancer cells as in those having mutant or normal p53. Peptide-induced cell death is not accompanied by expression of apoptosis-associated proteins such as Bax and waf(p21). Based on these findings, we conclude that the antiproliferative effects of these p53-derived peptides are not completely dependent on p53 activity and may prove useful as general anticancer agents. C1 Suny Downstate Med Ctr, Dept Pathol, Brooklyn, NY 11203 USA. Suny Downstate Med Ctr, Dept Anat & Cell Biol, Brooklyn, NY 11203 USA. Suny Downstate Med Ctr, Dept Microbiol & Immunol, Brooklyn, NY 11203 USA. Harbor Vet Affairs Med Ctr, Dept Pathol & Lab Med, Brooklyn, NY 11209 USA. Columbia Univ Coll Phys & Surg, Div Med Oncol, Expt Therapeut Program, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Div Environm Sci, New York, NY 10032 USA. NIH, Lab Metab, Bethesda, MD 20892 USA. New York Blood Ctr, New York, NY 10021 USA. RP Kanovsky, M (reprint author), Suny Downstate Med Ctr, Dept Pathol, 450 Clarkson Ave, Brooklyn, NY 11203 USA. RI Friedman, Fred/D-4208-2016 FU NCI NIH HHS [R01 CA 42500, R01 CA 82528, R01 CA042500]; NIOSH CDC HHS [R01 OH004192, R01 OH04192] NR 22 TC 72 Z9 79 U1 1 U2 7 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 23 PY 2001 VL 98 IS 22 BP 12438 EP 12443 DI 10.1073/pnas.211280698 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 486EU UT WOS:000171806100029 PM 11606716 ER PT J AU Li, BS Sun, MK Zhang, L Takahashi, S Ma, W Vinade, L Kulkarni, AB Brady, RO Pant, HC AF Li, BS Sun, MK Zhang, L Takahashi, S Ma, W Vinade, L Kulkarni, AB Brady, RO Pant, HC TI Regulation of NMDA receptors by cyclin-dependent kinase-5 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID D-ASPARTATE RECEPTOR; LONG-TERM POTENTIATION; PROTEIN-KINASE; TYROSINE PHOSPHORYLATION; GLUTAMATE RECEPTORS; RAT-BRAIN; SUBUNIT; CDK5; NEURONS; CHANNEL AB Members of the N-methyl-D-aspartate (NMDA) class of glutamate receptors (NMDARs) are critical for development, synaptic transmission, learning and memory; they are targets of pathological disorders in the central nervous system. NMDARs are phosphorylated by both serine/threonine and tyrosine kinases. Here, we demonstrate that cyclin dependent kinase-5 (Cdk5) associates with and phosphorylates NR2A subunits at Ser-1232 in vitro and in intact cells. Moreover, we show that roscovitine, a selective Cdk5 inhibitor, blocks both long-term potentiation induction and NMDA-evoked currents in rat CA1 hippocampal neurons. These results suggest that Cdk5 plays a key role in synaptic transmission and plasticity through its up-regulation of NMDARs. C1 NINCDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. NINCDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. NINCDS, Neurobiol Lab, NIH, Bethesda, MD 20892 USA. NIMH, Behav Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Funct Genom Unit, NIH, Bethesda, MD 20892 USA. USN, Res Lab, Ctr Biomol Sci & Engn, Washington, DC 20375 USA. NINCDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Pant, HC (reprint author), NINCDS, Neurochem Lab, NIH, Bldg 36,Rm 4D24,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 52 TC 174 Z9 186 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 OCT 23 PY 2001 VL 98 IS 22 BP 12742 EP 12747 DI 10.1073/pnas.211428098 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 486EU UT WOS:000171806100081 PM 11675505 ER PT J AU Seshadri, S Wolf, PA Beiser, A Vasan, RS Wilson, PWF Kase, CS Kelly-Hayes, M Kannel, WB D'Agostino, RB AF Seshadri, S Wolf, PA Beiser, A Vasan, RS Wilson, PWF Kase, CS Kelly-Hayes, M Kannel, WB D'Agostino, RB TI Elevated midlife blood pressure increases stroke risk in elderly persons - The framingham study SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CARDIOVASCULAR-DISEASE; REGRESSION DILUTION; HEART-DISEASE; HYPERTENSION; MORTALITY; PROFILE; COHORT; TRENDS AB Background: Stroke risk predictions are traditionally based on current blood pressure (13P). The potential impact of a subject's past BP experience (antecedent BP) is unknown. We assessed the incremental impact of antecedent BP on the risk of ischemic stroke. Methods: A total of 5197 stroke-free subjects (2330 men) in the community-based Framingham Study cohort were enrolled from September 29, 1948, to April 25, 1953, and followed up to December 31, 1998. We determined the 10-year risk of completed initial ischemic stroke for 60-, 70-, and 80-year-old subjects as a function of their current BP (at baseline), recent antecedent BP (average of readings at biennial examinations 1-9 years before baseline), and remote antecedent BP (average at biennial examinations 10-19 years earlier), with adjustment for smoking and diabetes mellitus. Models incorporating antecedent BP were also adjusted for baseline BP. The effect of each BP component (systolic 13P, diastolic BP, and pulse pressure) was assessed separately. Results: Four hundred ninety-one ischemic strokes (209 in men) were observed in eligible subjects. The antecedent BP influenced the 10-year stroke risk at the age of 60 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.68 [95% confidence interval, 1.25-2.25]; and men, 1.92 [95% confidence interval, 1.39-2.66]) and at the age of 70 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.66 [95% confidence interval, 1.28-2.14]; and men, 1.30 [95% confidence interval, 0.97-1.75]). This effect was evident for recent and remote antecedent BP, consistent in hypertensive and nonhypertensive subjects, and demonstrable for all BP components. Conclusions: Antecedent BP contributes to the future risk of ischemic stroke. Optimal prevention of late-life stroke will likely require control of midlife BP. C1 Boston Univ, Sch Med, Dept Neurol, Neurol Epidemiol & Genet Div, Boston, MA 02118 USA. NHLBI, Framingham Study, Framingham, MA USA. Boston Univ, Sch Med, Dept Epidemiol & Prevent Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Boston, MA USA. Boston Univ, Dept Math, Boston, MA 02215 USA. RP Wolf, PA (reprint author), Boston Univ, Sch Med, Dept Neurol, Neurol Epidemiol & Genet Div, 715 Albany St,Room B-608, Boston, MA 02118 USA. OI Ramachandran, Vasan/0000-0001-7357-5970 FU NHLBI NIH HHS [HC 38038]; NINDS NIH HHS [NS 17950] NR 33 TC 46 Z9 47 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD OCT 22 PY 2001 VL 161 IS 19 BP 2343 EP 2350 DI 10.1001/archinte.161.19.2343 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 483RL UT WOS:000171649600008 PM 11606150 ER PT J AU Adelt, S Plettenburg, O Dallmann, G Ritter, FP Shears, SB Altenbach, HJ Vogel, G AF Adelt, S Plettenburg, O Dallmann, G Ritter, FP Shears, SB Altenbach, HJ Vogel, G TI Regiospecific phosphohydrolases from Dictyostelium as tools for the chemoenzymatic synthesis of the enantiomers D-myo-inositol 1,2,4-trisphosphate and D-myo-inositol 2,3,6-trisphosphate: Non-physiological, potential analogues of biologically active D-myo-inositol 1,3,4-trisphosphate SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID 1,2,4,5-TETRAKISPHOSPHATE AB A new de novo synthesis of the enantiomeric pair D-myo-inositol 1,2,4-trisphosphate and D-myo-inositol 2,3,6-trisphosphate is described. Starting from enantiopure dibromocyclohexenediol, several C-2 Symmetrical building blocks were synthesized which gave access to D-myo-inositol 1,2,4,5-tetrakisphosphate and D-Myo-inositol 1,2,3,6-tetrakisphosphate. Exploiting the high regiospecificity of two partially purified phosphohydrolases from Dictyostelium, a 5-phosphatase and a phytase, the inositol tetrakisphosphates were converted enzymatically to the target compounds. Their potential to modulate the activity of Ins(3,4,5,6)P-4 I-kinase was investigated and compared with the effects Of D-myo-inositol 1,3,4-trisphosphate. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 Berg Univ Gesamthsch Wuppertal, Inst Organ Chem & Biochem, D-42097 Wuppertal, Germany. NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. RP Vogel, G (reprint author), Berg Univ Gesamthsch Wuppertal, Inst Organ Chem & Biochem, Gaussstr 20, D-42097 Wuppertal, Germany. NR 11 TC 18 Z9 18 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD OCT 22 PY 2001 VL 11 IS 20 BP 2705 EP 2708 DI 10.1016/S0960-894X(01)00536-4 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA 481CX UT WOS:000171503300010 PM 11591506 ER PT J AU Radmacher, MD Simon, R Desper, R Taetle, R Schaffer, AA Nelson, MA AF Radmacher, MD Simon, R Desper, R Taetle, R Schaffer, AA Nelson, MA TI Graph models of oncogenesis with an application to melanoma SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Article ID NONRANDOM CHROMOSOME-ABNORMALITIES; COMPARATIVE GENOMIC HYBRIDIZATION; CUTANEOUS MALIGNANT-MELANOMA; OVARIAN ADENOCARCINOMA; TREE MODELS; CANCER; 11Q23 AB We describe several analytical techniques for use in developing genetic models of oncogenesis including: methods for the selection of important genetic events, construction of graph models (including distance-based trees, branching trees, contingency trees and directed acyclic graph models) from these events and methods for interpretation of the resulting models. The models can be used to make predictions about: which genetic events tend to occur early, which events tend to occur together and the likely order of events. Unlike simple path models of oncogenesis, our models allow dependencies to exist between specific genetic changes and allow for multiple, divergent paths in tumor progression. A variety of genetic events can be used with the graph models including chromosome breaks, losses or gains of large DNA regions, small mutations and changes in methylation. As an application of the techniques, we use a recently published cytogenetic analysis of 206 melanoma cases [Nelson et al. (2000), Cancer Genet. Cytogenet. 122, 101-109] to derive graph models for chromosome breaks in melanoma. Among our predictions are: (1) breaks in 6q1 and 1q1 are early events, with 6q1 preferentially occurring first and increasing the probability of a break in 1q1 and (2) breaks in the two sets {1p1, 1p2, 9q1}, and {1q1, 7p2, 9p2} tend to occur together. This study illustrates that the application of graph models to genetic data from tumor sets provide new information on the interrelationships among genetic changes during tumor progression. (C), 2001 Academic Press. C1 NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA. NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA. Univ Arizona, Arizona Canc Ctr, Dept Med, Tucson, AZ USA. Univ Arizona, Arizona Canc Ctr, Dept Pathol, Tucson, AZ USA. RP Radmacher, MD (reprint author), NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA. RI Schaffer, Alejandro/F-2902-2012 FU NCI NIH HHS [CA70145] NR 30 TC 24 Z9 24 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-5193 J9 J THEOR BIOL JI J. Theor. Biol. PD OCT 21 PY 2001 VL 212 IS 4 BP 535 EP 548 DI 10.1006/jtbi.2001.2395 PG 14 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA 487GL UT WOS:000171865300005 PM 11597184 ER PT J AU Eshleman, SH Mracna, M Guay, LA Deseyve, M Cunningham, S Mirochnick, M Musoke, P Fleming, T Fowler, MG Mofenson, LM Mmiro, F Jackson, JB AF Eshleman, SH Mracna, M Guay, LA Deseyve, M Cunningham, S Mirochnick, M Musoke, P Fleming, T Fowler, MG Mofenson, LM Mmiro, F Jackson, JB TI Selection and fading of resistance mutations in women and infants receiving nevirapine to prevent HIV-1 vertical transmission (HIVNET 012) SO AIDS LA English DT Article DE clinical trial; drug resistance; genotype; HIV-1; infant; nevirapine; pregnancy; prophylaxis; Uganda; vertical transmission ID HUMAN-IMMUNODEFICIENCY-VIRUS; PHARMACOKINETICS; ADULTS AB Objective: To examine the emergence and fading of NVP resistance (NVPR) mutations in HIV-1-infected Ugandan women and infants who received single dose NVP to prevent HIV-1 vertical transmission. Design: We examined NVPR in women and infants who received NVP in the HIVNET 012 clinical trial, including 41 out of 48 women with infected infants, 70 random ly-selected women with uninfected infants, and 33 out of 49 infected infants. Methods: Plasma HIV-1 was analyzed using the Applied Biosystems ViroSeq HIV-1 Genotyping System. Results: NVPR mutations were detected in 21 out of 111 (19%) women tested 6-8 weeks after delivery. The rate of NVPR was similar among women whose infants were or were not HIV-1 infected. K103N was the most common mutation detected. NVPR mutations faded from detection within 12-24 months in all 11 evaluable women. High baseline viral load and low baseline CD4 cell count were associated with development of NVPR. NVPR mutations were detected in 11 out of 24 (46%) evaluable infants who were infected by 6-8 weeks of age. The most common NVPR mutation detected in infants was Y181C. Those mutations faded from detection by 12 months of age in all seven evaluable infants. Of nine evaluable infants with late HIV-1 infection, only one had evidence of NVPR. Conclusions: NVPR was detected more frequently in infants than women following NVP prophylaxis, and different patterns of NVPR mutations were detected in women versus infants. NVPR was detected infrequently in infants with late HIV-1 infection. NVP-resistant HIV-1 faded from detection in women and infants overtime. (C) 2001 Lippincott Williams & Wilkins. C1 Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21205 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA. Makerere Univ, Dept Paediat, Kampala, Uganda. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. NIAID, Div AIDS, NIH, Rockville, MD 20852 USA. NICHHD, Pediat Adolescent & Maternal AIDS Branch, NIH, Rockville, MD USA. Makerere Univ, Dept Obstet & Gynaecol, Kampala, Uganda. RP Eshleman, SH (reprint author), Johns Hopkins Med Inst, Dept Pathol, Ross Bldg 646,720 Rutland Ave, Baltimore, MD 21205 USA. OI Mofenson, Lynne/0000-0002-2818-9808 FU NIAID NIH HHS [N01-AI-35173, N01-AI-45200, N0I-AI-35173-417, U01-AI-46745, U01-AI-48054]; PHS HHS [R29 34348] NR 10 TC 286 Z9 294 U1 1 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD OCT 19 PY 2001 VL 15 IS 15 BP 1951 EP 1957 DI 10.1097/00002030-200110190-00006 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 485TJ UT WOS:000171779700006 PM 11600822 ER PT J AU Rajini, B Shridas, P Sundari, CS Muralidhar, D Chandani, S Thomas, F Sharma, Y AF Rajini, B Shridas, P Sundari, CS Muralidhar, D Chandani, S Thomas, F Sharma, Y TI Calcium binding properties of gamma-crystallin - Calcium ion binds at the Greek key beta gamma-crystallin fold SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SPORE COAT PROTEIN; DYE STAINS-ALL; X-RAY-ANALYSIS; EYE LENS; PRECURSOR STRUCTURE; NONLENS MEMBER; SUPERFAMILY; VERTEBRATE; CALMODULIN; EVOLUTION AB The beta- and gamma -crystalline are closely related lens proteins that are members of the beta gamma -crystallin superfamily, which also include many non-lens members. Although beta -crystallin is known to be a calcium-binding protein, this property has not been reported in gamma -crystallin. We have studied the calcium binding properties of gamma -crystallin, and we show that it binds 4 mol eq of calcium with a dissociation constant of 90 muM. It also binds the calcium-mimic spectral probes, terbium and Stains-all. Calcium binding does not significantly influence protein secondary and tertiary structures. We present evidence that the Greek key crystallin fold is the site for calcium ion binding in gamma -crystallin. Peptides corresponding to Greek key motif of gamma -crystallin (42 residues) and their mutants were synthesized and studied for calcium binding. These peptides adopt beta -sheet conformation and form aggregates producing beta -sandwich. Our results with peptides show that, in Greek key motif, the amino acid adjacent to the conserved aromatic corner in the "a" strand and three amino acids of the "d" strand participate in calcium binding. We suggest that the beta gamma superfamily represents a novel class of calcium-binding proteins with the Greek key beta gamma -crystallin fold as potential calcium-binding sites. These results are of significance in understanding the mechanism of calcium homeostasis in the lens. C1 Ctr Cellular & Mol Biol, Hyderabad 500007, Andhra Pradesh, India. NHLBI, NIH, Bethesda, MD 20892 USA. RP Sharma, Y (reprint author), Ctr Cellular & Mol Biol, Uppal Rd, Hyderabad 500007, Andhra Pradesh, India. NR 44 TC 68 Z9 70 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 38464 EP 38471 DI 10.1074/jbc.M102164200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200020 PM 11502736 ER PT J AU Longley, MJ Nguyen, D Kunkel, TA Copeland, WC AF Longley, MJ Nguyen, D Kunkel, TA Copeland, WC TI The fidelity of human DNA polymerase gamma with and without exonucleolytic proofreading and the p55 accessory subunit SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN MITOCHONDRIAL GENOME; TRANSFER-RNA SYNTHETASES; BASE EXCISION-REPAIR; OXIDATIVE DAMAGE; SACCHAROMYCES-CEREVISIAE; 3'->5' EXONUCLEASE; HUMAN-CELLS; SUBSTRATE-SPECIFICITY; INSERTION FIDELITY; DROSOPHILA EMBRYOS AB Mutations in human mitochondrial DNA influence aging, induce severe neuromuscular pathologies, cause maternally inherited metabolic diseases, and suppress apoptosis. Since the genetic stability of mitochondrial DNA depends on the accuracy of DNA polymerase gamma (pol gamma), we investigated the fidelity of DNA synthesis by human pol gamma. Comparison of the wild-type 140-kDa catalytic subunit to its exonuclease-deficient derivative indicates poly has high base substitution fidelity that results from high nucleotide selectivity and exonucleolytic proofreading. pol gamma is also relatively accurate for single-base additions and deletions in non-iterated and short repetitive sequences. However, when copying homopolymeric sequences longer than four nucleotides, poly has low frameshift fidelity and also generates base substitutions inferred to result from a primer dislocation mechanism. The ability of pol gamma both to make and to proofread dislocation intermediates is the first such evidence for a family A polymerase. Including the p55 accessory subunit, which confers processivity to the pol gamma catalytic subunit, decreases frameshift and base substitution fidelity. Kinetic analyses indicate that p55 promotes extension of mismatched termini to lower the fidelity. These data suggest that homopolymeric runs in mitochondrial DNA may be particularly prone to frameshift mutation in vivo due to replication errors by pol gamma. C1 NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Copeland, WC (reprint author), NIEHS, Mol Genet Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 77 TC 147 Z9 147 U1 0 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 38555 EP 38562 DI 10.1074/jbc.M105230200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200032 PM 11504725 ER PT J AU Opavsky, R Haviernik, P Jurkovicova, D Garin, MT Copeland, NG Gilbert, DJ Jenkins, NA Bies, J Garfield, S Pastorekova, S Oue, A Wolff, L AF Opavsky, R Haviernik, P Jurkovicova, D Garin, MT Copeland, NG Gilbert, DJ Jenkins, NA Bies, J Garfield, S Pastorekova, S Oue, A Wolff, L TI Molecular characterization of the mouse Tem1/endosialin gene regulated by cell density in vitro and expressed in normal tissues in vivo SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MURINE LEUKEMIA-VIRUS; ENDOTHELIAL-CELLS; CYTOPLASMIC DOMAIN; THROMBOMODULIN; ANGIOGENESIS; PROTEIN; THROMBIN; SURFACE; CANCER; IDENTIFICATION AB Human tumor endothelial marker 1/endosialin (TEM1/ endosialin) was recently identified as a novel tumor endothelial cell surface marker potentially involved in angiogenesis, although no specific function for this novel gene has been assigned so far. It was reported to be expressed in tumor endothelium but not in normal endothelium with the exception of perhaps the corpus luteum. Here we describe the cDNA and genomic sequences for the mouse Tem1/endosialin homolog, the identification and characterization of its promoter region, and an extensive characterization of its expression pattern in murine and human tissues and murine cell lines in vitro. The single copy gene that was mapped to chromosome 19 is intronless and encodes a 92-kDa protein that has 77.5% overall homology to the human protein. The remarkable findings are 1) this gene is ubiquitously expressed in normal human and mouse somatic tissues and during development, and 2) its expression at the mRNA level is density-dependent and up-regulated in serum-starved cells. In vitro, its expression is limited to cells of embryonic, endothelial, and preadipocyte origin, suggesting that the wide distribution of its expression in vivo is due to the presence of vascular endothelial cells in all the tissues. The ubiquitous expression in vivo is in contrast to previously reported expression limited to corpus luteum and highly angiogenic tissues such as tumors and wound tissue. C1 NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA. NCI, Mouse Canc Genet Program, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Slovak Acad Sci, Mol Virol Lab, Canc Res Inst, Bratislava 83392, Slovakia. NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. Slovak Acad Sci, Inst Virol, Bratislava 84245, Slovakia. NCI, Basic Res Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NIMH, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Wolff, L (reprint author), NCI, Cellular Oncol Lab, NIH, Bldg 37,Rm 2D11,37 Convent Dr, Bethesda, MD 20892 USA. NR 39 TC 41 Z9 47 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 38795 EP 38807 DI 10.1074/jbc.M105241200 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200063 PM 11489895 ER PT J AU Yamashita, Y Kajigaya, S Yoshida, K Ueno, S Ota, J Ohmine, K Ueda, M Miyazato, A Ohya, K Kitamura, T Ozawa, K Mano, H AF Yamashita, Y Kajigaya, S Yoshida, K Ueno, S Ota, J Ohmine, K Ueda, M Miyazato, A Ohya, K Kitamura, T Ozawa, K Mano, H TI Sak serine-threonine kinase acts as an effector of Tec tyrosine kinase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-SERINE/THREONINE KINASE; MOLECULAR-CLONING; DROSOPHILA; GENE; IDENTIFICATION; EXPRESSION; DEGRADATION; ENCODES; GROWTH; INVIVO AB The murine sak gene encodes a putative serine-threonine kinase which is homologous to the members of the Plk/Polo family. Although Sak protein is presumed to be involved in cell growth mechanism, efforts have failed to demonstrate its kinase activity. Little has been, therefore, elucidated how Sak is regulated and how Sak contributes to cell proliferation. Tee is a cytoplasmic protein-tyrosine kinase (PTK) which becomes activated by the stimulation of cytokine receptors, lymphocyte surface antigens, heterotrimeric G protein-linked receptors, and integrins. To clarify the in vivo function of Tee, we have tried to isolate the second messengers of Tee by using the yeast two-hybrid screening. One of such Tec-binding proteins turned out to be Sak. In human kidney 293 cells, Sak became tyrosine-phosphorylated by Tee, and the serine-threonine kinase activity of Sak was detected only under the presence of Tee, suggesting Sak to be an effector molecule of Tee. In addition, Tee activity efficiently protects Sak from the "PEST" sequence-dependent proteolysis. Internal deletion of the PEST sequences led to the stabilization of Sak proteins, and expression of these mutants acted suppressive to cell growth. Our data collectively supports a novel role of Sak acting in the PTK-mediated signaling pathway. C1 Jichi Med Sch, Div Funct Genom, Minami Kawachi, Tochigi 3290498, Japan. Jichi Med Sch, Div Cardiol, Minami Kawachi, Tochigi 3290498, Japan. Jichi Med Sch, Div Hematol, Minami Kawachi, Tochigi 3290498, Japan. NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. Univ Tokyo, Inst Med Sci, Dept Hematopoiet Factors, Tokyo 1088639, Japan. RP Mano, H (reprint author), Jichi Med Sch, Div Funct Genom, 3311-1 Yakushiji, Minami Kawachi, Tochigi 3290498, Japan. NR 27 TC 30 Z9 32 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39012 EP 39020 DI 10.1074/jbc.M106249200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200090 PM 11489907 ER PT J AU Hoover, DM Chertov, O Lubkowski, J AF Hoover, DM Chertov, O Lubkowski, J TI The structure of human beta-defensin-1 - New insights into structural properties of beta-defensins SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ANTIMICROBIAL PEPTIDES; DIFFRACTION DATA; PROTEINS; REPLACEMENT; ANTIBIOTICS; REFINEMENT; MECHANISMS; PROGRAM; PACKAGE AB Defensins are a class of small cationic peptides found in higher organisms that serve as both antimicrobial and cell signaling molecules. The exact mechanism of the antimicrobial activity of defensins is not known, but two models have been postulated, one involving pore formation and the other involving nonspecific electrostatic interaction with the bacterial membrane. Here we report the high resolution structures of human beta -defensin-1 (hBD1) in two crystallographic space groups. The structure of a single molecule is very similar to that of human beta -defensin-2 (hBD2), confirming the presence of an N-terminal alpha -helix. However, while the packing of hBD1 is conserved across both space groups, there is no evidence for any larger quaternary structure similar to octameric hBD2. Furthermore, the topology of hBD1 dimers that are formed between monomers in the asymmetric unit is distinct from both hBD2 and other mammalian alpha -defensins. The structures of hBD1 and hBD2 provide a first step toward understanding the structural basis of antimicrobial and chemotactic properties of human beta -defensins. C1 NCI, Macromol Crystallog Lab, NIH, Ft Detrick, MD 21702 USA. NCI, Intramural Res Support Program, LMI, SAIC Frederick,NIH, Ft Detrick, MD 21702 USA. RP Lubkowski, J (reprint author), NCI, Macromol Crystallog Lab, NIH, POB B, Ft Detrick, MD 21701 USA. FU NCI NIH HHS [N01-CO-56000] NR 35 TC 130 Z9 136 U1 1 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39021 EP 39026 DI 10.1074/jbc.M103830200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200091 PM 11486002 ER PT J AU Akiyama, TE Nicol, CJ Fievet, C Staels, B Ward, JM Auwerx, J Lee, SST Gonzalez, FJ Peters, JM AF Akiyama, TE Nicol, CJ Fievet, C Staels, B Ward, JM Auwerx, J Lee, SST Gonzalez, FJ Peters, JM TI Peroxisome proliferator-activated receptor-alpha regulates lipid homeostasis, but is not associated with obesity - Studies with congenic mouse lines SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FATTY-ACID OXIDATION; PPAR-ALPHA; GENE-EXPRESSION; DEFICIENT MICE; TARGETED DISRUPTION; ADAPTIVE RESPONSE; TRANSGENIC MICE; BILE-ACID; NULL MICE; KAPPA-B AB Considerable controversy exists in determining the role of peroxisome proliferator-activated receptor-a (PPAR alpha) in obesity. Two purebred congenic strains of PPAR alpha -null mice were developed to study the role of this receptor in modulating lipid transport and storage. Weight gain and average body weight in wild-type and PPAR alpha -null mice on either an Sv/129 or a C57BL/6N background were not markedly different between genotypes from 3 to 9 months of age. However, gonadal adipose stores were significantly greater in both strains of male and female PPAR alpha -null mice. Hepatic accumulation of lipids was greater in both strains and sexes of PPAR alpha -null mice compared with wild-type controls. Administration of the peroxisome proliferator WY-14643 caused hepatomegaly, alterations in mRNAs encoding proteins that regulate lipid metabolism, and reduced serum triglycerides in a PPAR alpha -dependent mechanism. Constitutive differences in serum cholesterol and triglycerides in PPAR alpha -null mice were found between genetic backgrounds. Results from this work establish that PPAR alpha is a critical modulator of lipid homeostasis in two congenic mouse lines. This study demonstrates that disruption of the murine gene encoding PPAR alpha results in significant alterations in constitutive serum, hepatic, and adipose tissue lipid metabolism. However, an overt, obese phenotype in either of the two congenic strains was not observed. In contrast to earlier published work, this study establishes that PPAR alpha is not associated with obesity in mice. C1 Penn State Univ, Dept Vet Sci, Ctr Mol Toxicol, University Pk, PA 16802 USA. NCI, Met Lab, NIH, Bethesda, MD 20892 USA. Inst Pasteur, INSERM, Dept Atherosclerose, F-59019 Lille, France. NCI, Vet & Tumour Pathol Sect, Off Lab Anim Resources, Frederick Canc Res & Dev Ctr, Ft Detrick, MD 21702 USA. Univ Strasbourg 1, INSERM, CNRS, Inst Genet & Biol Mol & Cellulaire, F-67400 Illkirch Graffenstaden, France. Chinese Univ Hong Kong, Dept Biochem, Shatin, Hong Kong, Peoples R China. RP Peters, JM (reprint author), Penn State Univ, Dept Vet Sci, Ctr Mol Toxicol, 226 Fenske Lab, University Pk, PA 16802 USA. RI Peters, Jeffrey/D-8847-2011; Staels, Bart/N-9497-2016 OI Staels, Bart/0000-0002-3784-1503 NR 54 TC 88 Z9 90 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39088 EP 39093 DI 10.1074/jbc.M107073200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200099 PM 11495927 ER PT J AU Parry, DAD Marekov, LN Steinert, PM AF Parry, DAD Marekov, LN Steinert, PM TI Subfilamentous protofibril structures in fibrous proteins - Cross-linking evidence for protofibrils in intermediate filaments SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EPIDERMAL KERATIN FILAMENTS; HARD ALPHA-KERATIN; COLLAGEN FIBRILS; MOLECULAR PACKING; ASSEMBLED INVITRO; VIMENTIN; MODEL; MASS; POLYMORPHISM; MECHANISM AB The packing of the constituent molecules in some fibrous proteins such as collagen and intermediate filaments (IF) is thought to consist of several hierarchical levels, the penultimate of which is the organization of subfilamentous units termed protofibrils. However, to date only indirect evidence, such as electron microscopic images of unraveling fibers or the existence of mass quanta, has been adduced in support of the existence of protofibrils. We have reexamined this issue in IF. Cross-links have been induced in trichocyte keratin, cytokeratin, and vimentin IF proteins. Using improved experimental conditions, several additional and reproducible cross-links have been characterized. Notably, many of these link between columns of molecular strands four apart on two-dimensional surface lattices. These data provide robust support for the concept of an 8-chain (4-molecule) protofibril entity in IF. Further, their positions correspond to the axial displacements predicted for protofibrils in the different types of IF. Also, the data are consistent with intact IF containing four protofibrils. In addition, the positions of these novel cross-links suggest that there are multiple possible groupings of four molecular strands to form a protofibril, suggesting a promiscuous association of molecules to form a protofibril. This may underlie the reason that organized elongated protofibrils cannot be visualized by conventional microscopic methods. C1 NIAMS, Skin Biol Lab, NIH, Bethesda, MD 20892 USA. Massey Univ, Inst Fundamental Sci, Palmerston North, New Zealand. RP Steinert, PM (reprint author), NIAMS, Skin Biol Lab, NIH, Bldg 6,Rm 152, Bethesda, MD 20892 USA. NR 39 TC 28 Z9 30 U1 3 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39253 EP 39258 DI 10.1074/jbc.M104604200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200121 PM 11495907 ER PT J AU Chen, SQ Guttridge, DC Tang, E Shi, ST Guan, KL Wang, CY AF Chen, SQ Guttridge, DC Tang, E Shi, ST Guan, KL Wang, CY TI Suppression of tumor necrosis factor-mediated apoptosis by nuclear factor kappa B-independent bone morphogenetic protein/Smad signaling SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INDUCED CELL-DEATH; MICE LACKING; ACTIVATION; DIFFERENTIATION; OSTEOBLAST; RECEPTORS; THERAPY; SMADS; MITOCHONDRIA; INHIBITION AB The activation of nuclear factor kappaB (NF-kappa B) plays a pivotal role in the regulation of tumor necrosis factor (TNF)-mediated apoptosis. However, little is known about the regulation of TNF-mediated apoptosis by other signaling pathways or growth factors. Here, unexpectedly, we found that bone morphogenetic protein (BMP)-2 and BMP-4 inhibited TNF-mediated apoptosis by inhibition of caspase-8 activation in C2C12 cells, a pluripotent mesenchymal cell line that has the potential to differentiate into osteoblasts depending on BMP stimulation. Utilizing both a trans-dominant I kappaB alpha inhibitor of NF-kappaB expressed in C2C12 cells and I kappaB kinase beta -deficient embryonic mouse fibroblast, we show that BMP-mediated survival was independent of NF-kappaB activation. Rather, the antiapoptotic activity of BMPs functioned through the Smad signaling pathway. Thus, these findings provide the first report of a BMP/Smad signaling pathway that can inhibit TNF-mediated apoptosis, independent of the prosurvival activity of NF-kappaB. Our results suggest that BMPs not only stimulate osteoblast differentiation but can also promote cell survival during the induction of bone formation, offering new insight into the biological functions of BMPs. C1 Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Lab Mol Signaling & Apoptosis, Ann Arbor, MI 48109 USA. Univ Michigan, Program Mol & Cellular Biol, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Biol Chem, Ann Arbor, MI 48109 USA. Univ N Carolina, Ctr Comprehens Canc, Chapel Hill, NC 27599 USA. NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA. RP Wang, CY (reprint author), Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Lab Mol Signaling & Apoptosis, Rm 5223,Box 1078,1011 N Univ Ave, Ann Arbor, MI 48109 USA. FU NIDCR NIH HHS [DE13788, DE13848] NR 39 TC 53 Z9 61 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39259 EP 39263 DI 10.1074/jbc.M105335200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200122 PM 11500509 ER PT J AU Kovalsky, O Lung, FDT Roller, PP Fornace, AJ AF Kovalsky, O Lung, FDT Roller, PP Fornace, AJ TI Oligomerization of human Gadd45a protein SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-CYCLE CHECKPOINT; DNA-DAMAGE; NUCLEAR ANTIGEN; GROWTH; MYD118; REPAIR; GENES; PCNA; P53; ACCESSIBILITY AB Gadd45a is an 18-kDa acidic protein that is induced by genotoxic and certain other cellular stresses. The exact function of this protein is not known. However, there is evidence for its involvement in growth control, maintenance of genomic stability, DNA repair, cell cycle control, and apoptosis. Consistently, Gadd45a has previously been shown to interact in vitro and/or in vivo with a number of proteins playing central roles in these cellular processes: proliferating cell nuclear antigen, p21(Cip1/Waf1), Cdc2-CyclinB complex, MTK1, and histories. Adding to this complexity, we have found that Gadd45a self-associates in solution, both in vitro and when expressed in the cell. Moreover, Gadd45a can complex with the two other members of the Gadd45 family of stress-induced proteins, human Gadd45b (MyD118) and Gadd45g (CR6). Gel-exclusion chromatography, native gel electrophoretic analysis, enzyme-linked immunosorbent assay, and chemical cross-linking showed that recombinant Gadd45a forms dimeric, trimeric, and tetrameric species in vitro, the dimers being the predominant form. Deletion mutant and peptide scanning analyses suggest that Gadd45a has two self-association sites: within N-terminal amino acids 33-61 and within 40 C-terminal amino acids. Despite the low abundance of Gadd45a in the cell, oligomer-forming concentrations can probably be achieved in the foci-like nuclear structures formed by the protein upon overexpression. Evidence for a potential role of Gadd45a self-association in altering DNA accessibility on damaged nucleosomes is presented. C1 NCI, NIH, Gene Response Sect, Bethesda, MD 20892 USA. Frederick Canc Res Ctr, Med Chem Lab, Frederick, MD 21702 USA. RP Fornace, AJ (reprint author), NCI, NIH, Gene Response Sect, Bldg 37,9000 Rockville Pike, Bethesda, MD 20892 USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 35 TC 60 Z9 65 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 19 PY 2001 VL 276 IS 42 BP 39330 EP 39339 DI 10.1074/jbc.M105115200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200132 PM 11498536 ER PT J AU Schuetz, EG Strom, S Yasuda, K Lecureur, V Assem, M Brimer, C Lamba, J Kim, RB Ramachandran, V Komoroski, BJ Venkataramanan, R Cai, HB Sinal, CJ Gonzalez, FJ Schuetz, JD AF Schuetz, EG Strom, S Yasuda, K Lecureur, V Assem, M Brimer, C Lamba, J Kim, RB Ramachandran, V Komoroski, BJ Venkataramanan, R Cai, HB Sinal, CJ Gonzalez, FJ Schuetz, JD TI Disrupted bile acid homeostasis reveals an unexpected interaction among nuclear hormone receptors, transporters, and cytochrome p450 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SALT EXPORT PUMP; FAMILIAL INTRAHEPATIC CHOLESTASIS; RESISTANCE-ASSOCIATED PROTEIN-3; P-GLYCOPROTEIN; RAT-LIVER; IN-VIVO; URSODEOXYCHOLIC ACID; UP-REGULATION; GENE; EXPRESSION AB Sister of P-glycoprotein (SPGP) is the major hepatic bile salt export pump (BSEP). BSEP/SPGP expression varies dramatically among human livers. The potency and hierarchy of bile acids as ligands for the farnesyl/ bile acid receptor (FXR/BAR) paralleled their ability to induce BSEP in human hepatocyte cultures. FXR:RXR heterodimers bound to IR1 elements and enhanced bile acid transcriptional activation of the mouse and human BSEP/SPGP promoters. In FXR/BAR nullizygous mice, which have dramatically reduced BSEP/SPGP levels, hepatic CYP3A11 and CYP2B10 were strongly but unexpectedly induced. Notably, the rank order of bile acids as CYP3A4 inducers and activators of pregnane X receptor/steroid and xenobiotic receptor (PXR/SXR) closely paralleled each other but was markedly different from their hierarchy and potency as inducers of BSEP in human hepatocytes. Moreover, the hepatoprotective bile acid ursodeoxycholic acid, which reverses hydrophobic bile acid hepatotoxicity, activates PXR and efficaciously induces CYP3A4 (a bile-metabolizing enzyme) in primary human hepatocytes thus providing one mechanism for its hepatoprotection. Because serum and urinary bile acids increased in FXR/BAR -/- mice, we evaluated hepatic transporters for compensatory changes that might circumvent the profound decrease in BSEP/SPGP. We found weak MRP3 up-regulation. In contrast, MRP4 was substantially increased in the FXR/ BAR nullizygous mice and was further elevated by cholic acid. Thus, enhanced hepatocellular concentrations of bile acids, due to the down-regulation of BSEP/SPGP-mediated efflux in FXR nullizygous mice, result in an alternate but apparent compensatory up-regulation of CYP3A, CYP2B, and some ABC transporters that is consistent with activation of PXR/SXR by bile acids. C1 St Jude Childrens Res Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA. Univ Pittsburgh, Dept Pathol, Pittsburgh, PA 15261 USA. Univ Pittsburgh, Dept Pharmaceut Sci, Pittsburgh, PA 15261 USA. Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37203 USA. NIH, Lab Med, Bethesda, MD 20892 USA. RP Schuetz, JD (reprint author), St Jude Childrens Res Hosp, Dept Pharmaceut Sci, 332 N Lauderdale St, Memphis, TN 38105 USA. EM John.schuetz@stjude.org RI Strom, Stephen/A-6501-2008; Cline, Cynthia/F-7065-2012; LECUREUR, Valerie/J-9095-2015 FU NCI NIH HHS [P30 CA21745]; NIDDK NIH HHS [DK92310]; NIEHS NIH HHS [ES08648, ES05780, ES058571]; NIGMS NIH HHS [GM60346] NR 47 TC 289 Z9 294 U1 0 U2 8 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 OCT 19 PY 2001 VL 276 IS 42 BP 39411 EP 39418 DI 10.1074/jbc.M106340200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 484CT UT WOS:000171673200141 PM 11509573 ER PT J AU Steffan, JS Bodai, L Pallos, J Poelman, M McCampbell, A Apostol, BL Kazantsev, A Schmidt, E Zhu, YZ Greenwald, M Kurokawa, R Housman, DE Jackson, GR Marsh, JL Thompson, LM AF Steffan, JS Bodai, L Pallos, J Poelman, M McCampbell, A Apostol, BL Kazantsev, A Schmidt, E Zhu, YZ Greenwald, M Kurokawa, R Housman, DE Jackson, GR Marsh, JL Thompson, LM TI Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila SO NATURE LA English DT Article ID CREB-BINDING PROTEIN; HUNTINGTONS-DISEASE; EXPANDED POLYGLUTAMINE; MAMMALIAN-CELLS; TRANSGENIC MICE; LOCALIZATION; AGGREGATION; EXPRESSION; APOPTOSIS; GROWTH AB Proteins with expanded polyglutamine repeats cause Huntington's disease and other neurodegenerative diseases. Transcriptional dysregulation and loss of function of transcriptional coactivator proteins have been implicated in the pathogenesis of these diseases(1). Huntington's disease is caused by expansion of a repeated sequence of the amino acid glutamine in the abnormal protein huntingtin (Htt). Here we show that the polyglutamine-containing domain of Htt, Htt exon 1 protein (Httex1p), directly binds the acetyltransferase domains of two distinct proteins: CREB-binding protein (CBP) and p300/CBP-associated factor (P/CAF). In cell-free assays, Httex1p also inhibits the acetyltransferase activity of at least three enzymes: p300, P/CAF and CBP. Expression of Httex1p in cultured cells reduces the level of the acetylated histones H3 and H4, and this reduction can be reversed by administering inhibitors of histone deacetylase (HDAC). In vivo, HDAC inhibitors arrest ongoing progressive neuronal degeneration induced by polyglutamine repeat expansion, and they reduce lethality in two Drosophila models of polyglutamine disease. These findings raise the possibility that therapy with HDAC inhibitors may slow or prevent the progressive neurodegeneration seen in Huntington's disease and other polyglutamine-repeat diseases, even after the onset of symptoms. C1 Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92697 USA. Univ Calif Irvine, Dept Dev & Cell Biol, Irvine, CA 92697 USA. NINCDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. MIT, Dept Biol, Cambridge, MA 02139 USA. Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA. Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA. RP Thompson, LM (reprint author), Univ Calif Irvine, Dept Psychiat & Human Behav, Gillespie 2121, Irvine, CA 92697 USA. RI Bodai, Laszlo/A-9764-2012 OI Bodai, Laszlo/0000-0001-8411-626X NR 27 TC 764 Z9 783 U1 4 U2 31 PU MACMILLAN PUBLISHERS LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD OCT 18 PY 2001 VL 413 IS 6857 BP 739 EP 743 DI 10.1038/35099568 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 482ZK UT WOS:000171608000045 PM 11607033 ER PT J AU Musser, JM Kaplan, SL AF Musser, JM Kaplan, SL TI Pneumococcal research transformed. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material C1 NIAID, Hamilton, MT 59840 USA. Baylor Coll Med, Houston, TX 77030 USA. RP Musser, JM (reprint author), NIAID, Hamilton, MT 59840 USA. NR 6 TC 6 Z9 6 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 18 PY 2001 VL 345 IS 16 BP 1206 EP 1207 DI 10.1056/NEJM200110183451612 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 482YX UT WOS:000171605800011 PM 11642239 ER PT J AU Rogan, WJ Shaffer, TR Dietrich, KN AF Rogan, WJ Shaffer, TR Dietrich, KN CA Treatment Lead-Exposed Children Tr TI Chelation therapy in children exposed to lead. Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIEHS, Res Triangle Pk, NC 27709 USA. Dept Hlth & Human Serv, Perry Point, MD 21902 USA. Univ Cincinnati, Cincinnati, OH 45267 USA. RP Rogan, WJ (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. RI Rogan, Walter/I-6034-2012 OI Rogan, Walter/0000-0002-9302-0160 NR 5 TC 0 Z9 0 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 18 PY 2001 VL 345 IS 16 BP 1213 EP 1213 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 482YX UT WOS:000171605800022 ER PT J AU Forus, A D'Angelo, A Henriksen, J Merla, G Maelandsmo, GM Florenes, VA Olivieri, S Bjerkehagen, B Meza-Zepeda, LA Blanco, FD Muller, C Sanvito, F Kononen, J Nesland, JM Fodstad, O Reymond, A Kallioniemi, OP Arrigoni, G Ballabio, A Myklebost, O Zollo, M AF Forus, A D'Angelo, A Henriksen, J Merla, G Maelandsmo, GM Florenes, VA Olivieri, S Bjerkehagen, B Meza-Zepeda, LA Blanco, FD Muller, C Sanvito, F Kononen, J Nesland, JM Fodstad, O Reymond, A Kallioniemi, OP Arrigoni, G Ballabio, A Myklebost, O Zollo, M TI Amplification and overexpression of PRUNE in human sarcomas and breast carcinomas - a possible mechanism for altering the nm23-H1 activity SO ONCOGENE LA English DT Article DE PRUNE; nm23; sarcoma; breast ID COMPARATIVE GENOMIC HYBRIDIZATION; NUCLEOSIDE DIPHOSPHATE KINASE; HUMAN HEPATOCELLULAR-CARCINOMA; CELL-LINES; MOLECULAR CHARACTERIZATION; TISSUE MICROARRAYS; PROTEIN EXPRESSION; TUMOR PROGRESSION; GENE-EXPRESSION; DROSOPHILA AB PRUNE, the human homologue of the Drosophila gene, is located in 1q21.3, a region highly amplified in human sarcomas, malignant tumours of mesenchymal origin. Prune protein interacts with the metastasis suppressor nm23-H1, but shows impaired affinity towards the nm23-H1 S120G mutant associated with advanced neuroblastoma. Based on these observations, we previously suggested that prune may act as a negative regulator of nm23-H1 activity. We found amplification of PRUNE in aggressive sarcoma subtypes, such as leiomyosarcomas and malignant fibrous histiocytomas (NIFH) as well as in the less malignant liposarcomas. PRUNE amplification was generally accompanied by high mRNA and moderate to high protein levels. The sarcoma samples expressed nm23-H1 mostly at low or moderate levels, whereas mRNA and protein levels were moderate to high in breast carcinomas. For the more aggressive sarcoma subtypes, 9/13 patients with PRUNE amplification developed metastases. A similar situation was observed in all breast carcinomas with amplification of PRUNE. Infection of NIH3T3 cells with a PRUNE recombinant retrovirus increased cell proliferation. Possibly, amplification and overexpression of PRUNE has the same effect in the tumours. We suggest that amplification and overexpression of PRUNE could be a mechanism for inhibition of nm23-H1 activity that affect the development or progression of these tumours. C1 Telethon Inst Genet & Med, I-80131 Naples, Italy. Norwegian Radium Hosp, Dept Tumor Biol, Oslo, Norway. Norwegian Radium Hosp, Dept Pathol, Oslo, Norway. HSR Biomed Sci Pk, Dept Pathol, Milan, Italy. NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA. Univ Tampere, Inst Med Technol, Canc Genet Lab, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Tampere, Finland. Univ Geneva, Sch Med, Div Med Genet, CH-1211 Geneva, Switzerland. RP Zollo, M (reprint author), Telethon Inst Genet & Med, Via Pietro Castellino 111, I-80131 Naples, Italy. RI Myklebost, Ola/E-9335-2010; Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012; OI Myklebost, Ola/0000-0002-2866-3223; Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332; BALLABIO, Andrea/0000-0003-1381-4604 FU Telethon [TGM06S01] NR 61 TC 42 Z9 47 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 18 PY 2001 VL 20 IS 47 BP 6881 EP 6890 DI 10.1038/sj.onc.1204874 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 483NK UT WOS:000171641000009 PM 11687967 ER PT J AU Moss, J DeCastro, R Patronas, NJ Taveira-DeSilva, A AF Moss, J DeCastro, R Patronas, NJ Taveira-DeSilva, A TI Meningiomas in lymphangioleiomyomatosis SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID TUBEROUS SCLEROSIS COMPLEX; PULMONARY LYMPHANGIOLEIOMYOMATOSIS; PROGESTERONE RECEPTORS; TSC2; LYMPHANGIOMYOMATOSIS; EPIDEMIOLOGY; MUTATIONS; GROWTH; WOMEN; GENES AB Context Lymphangioleiomyomatosis (LAM), a cystic lung disease associated with progressive respiratory failure, is found predominantly in women of childbearing age and therefore has been treated with progesterone and other hormonal agents. However, meningiomas have progesterone receptors, and progesterone is believed to be a mitogen for meningioma cells in culture. Since 30% to 40% of patients with tuberous sclerosis complex (TSC) have LAM, we routinely screen patients with LAM for brain lesions found in TSC. Objective To determine the prevalence of meningiomas in women with LAM. Design and Setting Analysis of results from ongoing routine screening protocols initiated in December 1995 at the National Heart, Lung, and Blood Institute. Patients Two hundred fifty women with sporadic LAM who were referred for screening by magnetic resonance imaging (MRI) and/or computed tomography (CT) of the brain. Main Outcome Measures Presence of meningiomas on MRI and/or CT scans. Results Eight women with LAM (3 with and 5 without a diagnosis of TSC) had lesions on MRI scans compatible with meningiomas. Five of the patients had been treated with progesterone. Multiple meningiomas were observed in 2 patients. Conclusions Women with LAM appear to have a high prevalence of meningiomas. We recommend that patients with LAM be screened for meningiomas regardless of diagnosis of TSC. In view of the lack of a documented effect of progesterone on progression of lung disease in LAM and the reported mitogenic response of meningiomas to progesterone, we recommend that the drug not be given to LAM patients with an MRI result consistent with diagnosis of meningioma. C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA. RP Moss, J (reprint author), NHLBI, Pulm Crit Care Med Branch, NIH, Room 6D05,Bldg 10,MSC 1590, Bethesda, MD 20892 USA. NR 33 TC 29 Z9 30 U1 0 U2 1 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 OCT 17 PY 2001 VL 286 IS 15 BP 1879 EP 1881 DI 10.1001/jama.286.15.1879 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 482UH UT WOS:000171595300029 PM 11597290 ER PT J AU Hjalgrim, H Lind, I Rostgaard, K Melbye, M Frisch, M Stossel, A Reimann, K Biggar, RJ Whitby, D AF Hjalgrim, H Lind, I Rostgaard, K Melbye, M Frisch, M Stossel, A Reimann, K Biggar, RJ Whitby, D TI Prevalence of human herpesvirus 8 antibodies in young adults in Denmark (1976-1977) SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID SARCOMA-ASSOCIATED HERPESVIRUS; IMMUNODEFICIENCY-VIRUS TYPE-1; KAPOSIS-SARCOMA; HUMAN-HERPESVIRUS-8 INFECTION; SEXUAL TRANSMISSION; HOMOSEXUAL MEN; RISK-FACTORS; SEROEPIDEMIOLOGY; AIDS; SEROPOSITIVITY C1 Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen S, Denmark. Statens Serum Inst, ALMOS, DK-2300 Copenhagen, Denmark. NCI, Viral Epidemiol Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. NCI, Viral Epidemiol Branch, Bethesda, MD 20892 USA. RP Hjalgrim, H (reprint author), Statens Serum Inst, Dept Epidemiol Res, 5 Artillerivej, DK-2300 Copenhagen S, Denmark. RI Frisch, Morten/E-9206-2016; OI Frisch, Morten/0000-0002-3864-8860; Rostgaard, Klaus/0000-0001-6220-9414 FU NCI NIH HHS [N01CO56000] NR 21 TC 5 Z9 6 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 17 PY 2001 VL 93 IS 20 BP 1569 EP 1571 PG 3 WC Oncology SC Oncology GA 481RZ UT WOS:000171535000014 PM 11604481 ER PT J AU Gallo, SA Puri, A Blumenthal, R AF Gallo, SA Puri, A Blumenthal, R TI HIV-1 gp41 six-helix bundle formation occurs rapidly after the engagement of gp120 by CXCR4 in the HIV-1 Env-mediated fusion process SO BIOCHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; CELL-CELL FUSION; ENVELOPE GLYCOPROTEIN; MEMBRANE-FUSION; CORECEPTOR SPECIFICITY; SYNTHETIC PEPTIDE; ATOMIC-STRUCTURE; ENTRY; CD4; INHIBITOR AB The onset of cell fusion mediated by HIV-1 IIIB Env is preceded by a lag phase of 15-20 min. Fusion mediated by the CD4-independent HIV-1 Env 8x, which is capable, of interacting directly with CXCR4, proceeds with a greatly reduced lag phase. We probed the intermediate steps during the lag phase in HIV-1 IIIB Env-mediated fusion with Leu3-a, an inhibitor of attachment of gp120 to CD4, AMD3100, an inhibitor of attachment of gp120 to CXCR4, and C34, a synthetic peptide that interferes with the transition of gp41 to the fusion active state. Inhibitions of fusion as a function of time of addition of C34 and of AMD3100 were equivalent, indicating that engagement of gp120 by CXCR4 and formation of the gp41 six-helix bundle follow similar kinetics. The initial steps in fusion mediated by the CD4-independent Env 8x are too rapid for these inhibitors to interfere with. However, when 8x Env-expressing cells were incubated with target cells at 25 degreesC in the presence of AMD3100 or C34, prior to incubation at 37 degreesC, these inhibitors were capable of inhibiting 8x. Env-mediated fusion. To further examine engagement of gp120 by CXCR4 and exposure of binding sites for C34, we have reversibly arrested the fusion reaction at 37 degreesC by adding cytochalasin B to the medium. We show that CXCR4 engagement and six-helix bundle formation only occur after the release of the cytochalasin. arrest, indicating that a high degree of cooperativity is required to trigger the initial steps in HIV-1 Env-mediated fusion. C1 NCI, Lab Expt & Computat Biol, Ctr Canc Res, NIH, Frederick, MD 21702 USA. RP Blumenthal, R (reprint author), POB B,Bldg 469,Rm 216A,Miller Dr, Frederick, MD 21702 USA. OI Gallo, Stephen/0000-0001-6043-2153 NR 43 TC 108 Z9 108 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 16 PY 2001 VL 40 IS 41 BP 12231 EP 12236 DI 10.1021/bi0155596 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 482XC UT WOS:000171601700001 PM 11591141 ER PT J AU Ferrucci, L Furberg, CD Penninx, BWJH Di Bari, M Williamson, JD Guralnik, JM Chen, JG Applegate, WB Pahor, M AF Ferrucci, L Furberg, CD Penninx, BWJH Di Bari, M Williamson, JD Guralnik, JM Chen, JG Applegate, WB Pahor, M TI Treatment of isolated systolic hypertension is most effective in older patients with high-risk profile SO CIRCULATION LA English DT Article DE hypertension; aging; risk factors; cardiovascular diseases; trials ID BLOOD-PRESSURE AB Background-Although present guidelines suggest that treatment of hypertension is more effective in patients with multiple risk factors and higher risk of cardiovascular events, this hypothesis was never verified in older patients with systolic hypertension. Methods and Results-Using data from the Systolic Hypertension in the Elderly Program, we calculated the global cardiovascular risk score according to the American Heart Association Multiple Risk Factor Assessment Equation in 4,189 participants free of cardiovascular disease (CVD) and in 264 participants with CVD at baseline. In the placebo group, rates of cardiovascular events over 4.5 years were progressively higher according to higher quartiles of CVD risk. The protection conferred by treatment was similar across quartiles of risk. However, the numbers needed to treat (NNTs) to prevent one cardiovascular event were progressively smaller according to higher cardiovascular risk quartiles. In participants with baseline CVD, the NNTs to prevent one cardiovascular event were similar to those estimated for CVD-free participants in the highest-risk quartile. Conclusions-Treatment of systolic hypertension is most effective in older patients who, because of additional risk factors or prevalent CVD, are at higher risk of developing a cardiovascular event. These patients are prime candidates for antihypertensive treatment. C1 INRCA, Dept Geriatr, Lab Clin Epidemiol, I-50125 Florence, Italy. Wake Forest Univ, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. Wake Forest Univ, Sticht Ctr Aging, Sect Gerontol & Geriatr, Winston Salem, NC 27109 USA. Wake Forest Univ, Dept Internal Med, Winston Salem, NC 27109 USA. Azienda Osped Careggi, Dept Crit Care Med & Surg, Sect Gerontol & Geriatr Med, Florence, Italy. NIA, Epidemiol Demog & Biometry Program, NIH, Bethesda, MD 20892 USA. RP Ferrucci, L (reprint author), INRCA, Dept Geriatr, Lab Clin Epidemiol, Viale Michelangiolo 41, I-50125 Florence, Italy. RI DI BARI, MAURO/J-1524-2012 FU NHLBI NIH HHS [HLBI-R03-HL5995-01A1]; NIA NIH HHS [P60-AG 10484] NR 23 TC 28 Z9 33 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 16 PY 2001 VL 104 IS 16 BP 1923 EP 1926 DI 10.1161/hc4101.097520 PG 4 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 486QP UT WOS:000171828700012 PM 11602495 ER PT J AU Albert, PS Ratnasinghe, D Tangrea, J Wacholder, S AF Albert, PS Ratnasinghe, D Tangrea, J Wacholder, S TI Limitations of the case-only design for identifying gene-environment interactions SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE case-control studies; cohort studies; environment; genes; genetics ID LUNG-CANCER; RISK; SMOKING; SUSCEPTIBILITY; POLYMORPHISMS; EXPOSURE AB The case-only design, which requires only diseased subjects, allows for estimation of multiplicative interactions between factors known to be independent in the study population. The design is being used as an alternative to the case-control design to study gene-environment interactions. Estimates of gene-environment interactions have been shown to be very efficient relative to estimates obtained with a case-control study under the assumption of independence between the genetic and environmental factors. In this paper, the authors explore the robustness of this procedure to uncertainty about the independence assumption. By using simulations, they demonstrate that inferences about the multiplicative interaction with the case-only design can be highly distorted when there is departure from the independence assumption. They illustrate their results with a recent study of gene-environment interactions and risk of lung cancer incidence in a cohort of miners from the Yunnan Tin Corporation in southern China. Investigators should be aware that the increased efficiency of the case-only design is a consequence of a strong assumption and that this design can perform poorly if the assumption is violated. C1 NCI, Biometr Res Branch, Div Canc Treatment & Diagnosis, Bethesda, MD 20892 USA. NCI, Canc Prevent Studies Branch, Div Clin Sci, Bethesda, MD 20892 USA. NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Albert, PS (reprint author), 15158 Callohan Court, Silver Spring, MD 20906 USA. NR 16 TC 124 Z9 127 U1 1 U2 4 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 OCT 15 PY 2001 VL 154 IS 8 BP 687 EP 693 DI 10.1093/aje/154.8.687 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 482PV UT WOS:000171585200001 PM 11590080 ER PT J AU England, LJ Kendrick, JS Wilson, HG Merritt, RK Gargiullo, PM Zahniser, SC AF England, LJ Kendrick, JS Wilson, HG Merritt, RK Gargiullo, PM Zahniser, SC TI Effects of smoking reduction during pregnancy on the birth weight of term infants SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE birth weight; cotinine; nicotine; pregnancy; smoking; tobacco ID MATERNAL SMOKING; PRENATAL-CARE; CESSATION; EXPOSURE; COTININE AB This study was undertaken to determine 1) whether reducing tobacco exposure during pregnancy increases the birth weight of term infants and 2) the relative effects of early- and late-pregnancy exposure to tobacco on infant birth weight. Data were obtained from the Smoking Cessation in Pregnancy project, conducted in public clinics in three states (Colorado, Maryland, and Missouri) between 1987 and 1991. Self-reported cigarette use and urine cotinine concentration were collected from 1,583 pregnant smokers at study enrollment and in the third trimester. General linear models were used to generate mean adjusted birth weights for women who reduced their tobacco exposure by 50 percent or more and for those who did not change their exposure. Regression smoothing techniques were used to characterize the relation between birth weight and early exposure and birth weight and third-trimester exposure. Reducing cigarette use was associated with an increase in mean adjusted birth weight of only 32 g, which was not significant (p = 0.33). As third-trimester cigarette use increased, birth weight declined sharply but leveled off at more than eight cigarettes per day. Findings were similar when urine cotinine concentration was used. Women who smoke during pregnancy may need to reduce to low levels of exposure (less than eight cigarettes per day) to improve infant birth weight. C1 CDCP, Epidem Intelligence Serv, Div Appl Publ Hlth Training, Ctr Dis Control & Prevent Program Off, Atlanta, GA USA. CDCP, Pregnancy & Infant Hlth Branch, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA. CDCP, Stat & Comp Resources Branch, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA. CDCP, Program Serv & Dev Branch, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA. CDCP, Natl Immunizat Program, Epidemiol & Surveillance Div, Childhood Vaccine Preventable Dis Branch, Atlanta, GA USA. Ctr Dis Control & Prevent, Epidemiol Program Off, Div Appl Publ Hlth Training, Atlanta, GA USA. RP England, LJ (reprint author), NICHHD, 6100 Execut Blvd,Room 7B03, Bethesda, MD 20892 USA. NR 19 TC 83 Z9 86 U1 2 U2 5 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 OCT 15 PY 2001 VL 154 IS 8 BP 694 EP 701 DI 10.1093/aje/154.8.694 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 482PV UT WOS:000171585200002 PM 11590081 ER PT J AU Bell, EM Hertz-Picciotto, I Beaumont, JJ AF Bell, EM Hertz-Picciotto, I Beaumont, JJ TI Case-cohort analysis of agricultural pesticide applications near maternal residence and selected causes of fetal death SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE environmental exposure; fetal death; pesticides; pregnancy outcome; survival analysis ID EXPOSURE; PREGNANCY; STILLBIRTH; CHEMICALS; MORTALITY; HUMANS; STATE; RISK AB The potential association between fetal death and residential proximity to agricultural pesticide applications was examined in 10 California counties for 1984. A case-cohort analysis utilized 319 cases of selected causes of fetal death other than congenital anomalies and 611 noncases. A statewide database of all applications of restricted pesticides was linked to maternal address; residential proximity within 1 mile (1.6 km) provided a surrogate for daily exposure. Pesticides were grouped by chemical class and mechanism of acetylcholinesterase inhibition. Multivariate proportional hazards models using time-dependent exposure variables were fit for each pesticide grouping. Overall, pesticides showed no strong association with fetal death. Slightly elevated risks were observed for women who resided near applications of halogenated hydrocarbons, carbamates, estrogenic pesticides, and carbamate acetylcholinesterase inhibitors during the second trimester, with hazard ratios of 1.3 (95% confidence interval (CI): 1.0, 1.8), 1.3 (95% CI: 1.0, 1.8), 1.4 (95% CI: 0.8, 2.5), and 1.3 (95% CI: 1.0, 1.8), respectively. In a month-by-month analysis, elevated risks were observed when exposure occurred during gestational months 3 and 4 for carbamates and carbamate inhibitors and during months 4 and 5 for halogenated hydrocarbons. Since previous studies have relied on personal recall of exposure, major strengths of this study were the objective source for environmental pesticide exposure assessment and the use of data on the timing of exposure. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA. Univ Calif Davis, Dept Epidemiol & Prevent Med, Davis, CA 95616 USA. RP Bell, EM (reprint author), NCI, Occupat Epidemiol Branch, 6120 Execut Blvd,EPS 8111,MSC 7240, Bethesda, MD 20892 USA. FU NIEHS NIH HHS [ES03767] NR 33 TC 39 Z9 40 U1 0 U2 4 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 OCT 15 PY 2001 VL 154 IS 8 BP 702 EP 710 DI 10.1093/aje/154.8.702 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 482PV UT WOS:000171585200003 PM 11590082 ER PT J AU Nowaczyk, MJM Siu, VM Krakowiak, PA Porter, FD AF Nowaczyk, MJM Siu, VM Krakowiak, PA Porter, FD TI Adrenal insufficiency and hypertension in a newborn infant with Smith-Lemli-Opitz syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Smith-Lemli-Opitz syndrome; adrenal insufficiency; hypertension; 7-dehydrocholesterol; DHCR7 mutations ID DELTA-7-STEROL REDUCTASE GENE; MUTATIONS; PHENOTYPE; SPECTRUM AB Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive disorder caused by mutations in the 7-dehydrocholesterol reductase gene, DHCR7. The diagnosis is based on the biochemical findings of elevated plasma 7-dehydrocholesterol (7DHC) levels. Adrenal insufficiency with hyponatremia has been reported in 3 patients with severe SLOS; in those cases it was thought to be caused by aldosterone deficiency because it responded to mineralocorticoid replacement. We present a fourth patient with a severe form of SLOS and adrenal insufficiency who had unexplained persistent hypertension, a combination of signs that has not been reported previously in SLOS. (C) 2001 Wiley-Liss, Inc. C1 McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Hamilton, ON L8S 4J9, Canada. McMaster Univ, Dept Pediat, Hamilton, ON L8S 4J9, Canada. Hamilton Reg Lab Program, Hamilton, ON, Canada. Univ Western Ontario, Dept Pediat, London, ON N6A 3K7, Canada. Univ Western Ontario, Dept Biochem, London, ON N6A 3K7, Canada. Reg Med Genet Program SW Ontario, London, ON, Canada. NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD USA. RP Nowaczyk, MJM (reprint author), McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Room 3N16,1200 Main St W, Hamilton, ON L8S 4J9, Canada. NR 19 TC 7 Z9 7 U1 1 U2 1 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 OCT 15 PY 2001 VL 103 IS 3 BP 223 EP 225 DI 10.1002/ajmg.1545 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 477HC UT WOS:000171277000007 PM 11745994 ER PT J AU Cobbs, CS Samanta, M Harkins, LE Gillespie, GY Merrick, BA MacMillan-Crow, LA AF Cobbs, CS Samanta, M Harkins, LE Gillespie, GY Merrick, BA MacMillan-Crow, LA TI Evidence for peroxynitrite-mediated modifications to p53 in human gliomas: Possible functional consequences SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE tyrosine nitration; aggregation; p53; glioma; peroxynitrite; tumor suppressor ID WILD-TYPE P53; MANGANESE SUPEROXIDE-DISMUTASE; NITRIC-OXIDE SYNTHASE; TYROSINE NITRATION; RADICAL PRODUCTION; CELLS; PROTEIN; NITROTYROSINE; INACTIVATION; ACCUMULATION AB Based on previous findings of increased nitric oxide synthase (NOS) expression in human gliomas (4), we hypothesized that peroxynitrite, a highly reactive metabolite of nitric oxide (NO) and superoxide (O-2(.-)), might be increased in these tumors in vivo. Here we demonstrate that nitrotyrosine (a footprint of peroxynitrite protein modification) is present in human malignant gliomas. Furthermore, we show that p53, a key tumor suppressor protein, has evidence of peroxynitrite-mediated modifications in gliomas in vivo. Experiments in vitro demonstrate that peroxynitrite treatment of recombinant wildtype p53 at physiological concentrations results in formation of higher molecular weight aggregates, tyrosine nitration, and loss of specific DNA binding. Peroxynitrite treatment of human glioma cell lysates similarly resulted in selective tyrosine nitration of p53 and was also associated with loss of p53 DNA binding ability. These data indicate that tyrosine nitration of proteins occurs in human gliomas in vivo, that p53 may be a target of peroxynitrite in these tumors, and that physiological concentrations of peroxynitrite can result in a loss of p53 DNA binding ability in vitro. These findings raise the possibility that peroxynitrite may contribute to loss of wildtype p53 functional activity in gliomas by posttranslational protein modifications. (C) 2001 Academic Press. C1 Univ Alabama, Sch Med, Dept Surg, Div Neurol Surg, Birmingham, AL 35294 USA. Birmingham Vet Affairs Hosp, Birmingham, AL 35294 USA. NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. RP MacMillan-Crow, LA (reprint author), Univ Alabama, Sch Med, Dept Surg, Div Neurol Surg, Birmingham, AL 35294 USA. NR 20 TC 52 Z9 54 U1 0 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD OCT 15 PY 2001 VL 394 IS 2 BP 167 EP 172 DI 10.1006/abbi.2001.2540 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 486ME UT WOS:000171820900006 PM 11594730 ER PT J AU Schwartz, PJ Rosenthal, NE Wehr, TA AF Schwartz, PJ Rosenthal, NE Wehr, TA TI Band-specific electroencephalogram and brain cooling abnormalities during NREM sleep in patients with winter depression SO BIOLOGICAL PSYCHIATRY LA English DT Article DE seasonal affective disorder; sleep; EEG; circadian; thermoregulation ID SEASONAL AFFECTIVE-DISORDER; SLOW-WAVE SLEEP; HEALTHY CONTROL SUBJECTS; CORE BODY-TEMPERATURE; EEG POWER SPECTRA; CIRCADIAN PACEMAKER; LIGHT TREATMENT; HUMANS; DEPRIVATION; SUPPRESSION AB Background: We previously reported that delta wave activity and facial skin temperatures, an index of brain cooling activity, were both abnormal during sleep in patients with winter depression (SAD). Because other electroencephalographic (EEG) frequencies may also convey relevant thermal, homeostatic, and circadian information, we sought to spectrally analyze delta, theta, alpha, and sigma frequencies during sleep from 23 patients with SAD and 23 healthy control subjects. Methods: We computed means for delta, theta, alpha, and sigma power during both NREM and REM sleep. We also generated 22 cross-correlation functions for each group by crossing facial and rectal temperature with each other, as well as with delta, theta, alpha, and sigma frequencies. Results: We found that delta, theta, and alpha frequency activities were all increased during NREM, but not REM sleep, in patients with SAD. In addition, there were significant and abnormal cross-correlations between facial temperatures and delta and theta frequencies during NREM sleep in patients with SAD. Conclusion: Patients with winter depression exhibit correlated abnormalities of sleep homeostasis and brain cooling during NREM sleep. Their EEG profiles during NREM steep resemble the EEG profiles of subjects who have been sleep deprived. Further studies of NREM sleep homeostasis in patients with SAD seem warranted. (C) 2001 Society of Biological Psychiatry. C1 VA Med Ctr, Dept Psychiat, Dayton, OH 45428 USA. Georgetown Univ, Dept Psychiat, Washington, DC USA. NIMH, Sect Biol Rhythms, Bethesda, MD 20892 USA. RP Schwartz, PJ (reprint author), VA Med Ctr, Dept Psychiat, Bldg 302,2nd Floor,4100 W 3rd St, Dayton, OH 45428 USA. RI Sanguansri, Luz/B-6630-2011 OI Sanguansri, Luz/0000-0003-1908-7604 NR 38 TC 5 Z9 5 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD OCT 15 PY 2001 VL 50 IS 8 BP 627 EP 632 DI 10.1016/S0006-3223(01)01097-6 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 486HQ UT WOS:000171812700010 PM 11690599 ER PT J AU Gould, TD Bastain, TM Israel, ME Hommer, DW Castellanos, FX AF Gould, TD Bastain, TM Israel, ME Hommer, DW Castellanos, FX TI Altered performance on an ocular fixation task in attention-deficit/hyperactivity disorder SO BIOLOGICAL PSYCHIATRY LA English DT Article DE fixation; attention; Saccades; attention-deficit/hyperactivity disorder; eye movements ID DEFICIT HYPERACTIVITY DISORDER; PURSUIT EYE-MOVEMENTS; ADHD; SCHIZOPHRENIA; SACCADES; MEMORY; ADULTS; SAMPLE; GIRLS AB Background: Attention-deficit/hyperactivity disorder (ADHD) is a common psychiatric disorder without validated objective markers. Eye movement studies may be useful in providing objective criteria for characterizing the disorder. Methods: We compared 53 children (29 girls) with ADHD to 44 healthy control children (18 girls) on a 21-sec fixation task. Large saccades (> 4 degrees) away from the fixation point were analyzed. Results: Children with ADHD made more large saccades that interrupted fixation than did control children (p =.001). Mean scores of the ADHD group did not change significantly with subsequent retesting on placebo (p =.11); however, there was poor intrasubject correlation (r =.16). Conclusions: Both boys and girls with ADHD made significantly more intrusive saccades during fixation than did control subjects, possibly, reflecting intrinsic neurologic dysfunction; however, a probable "floor effect" obviates conclusions about the reliability, of this measure. (C) 2001 Society of Biological Psychiatry. C1 NIMH, Clin Psychiat Branch, Bethesda, MD 20892 USA. NIAAA, Clin Studies Lab, Bethesda, MD 20892 USA. RP Castellanos, FX (reprint author), NIMH, Clin Psychiat Branch, Bldg 10,Room 3B-19,10 Ctr Dr, Bethesda, MD 20892 USA. NR 21 TC 34 Z9 35 U1 2 U2 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD OCT 15 PY 2001 VL 50 IS 8 BP 633 EP 635 DI 10.1016/S0006-3223(01)01095-2 PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 486HQ UT WOS:000171812700011 PM 11690600 ER PT J AU Carballo, E Blackshear, PJ AF Carballo, E Blackshear, PJ TI Roles of tumor necrosis factor-alpha receptor subtypes in the pathogenesis of the tristetraprolin-deficiency syndrome SO BLOOD LA English DT Article ID FACTOR TNF RECEPTOR; TRANSGENIC MICE; MESSENGER-RNA; TRANSCRIPTION FACTOR; LIGAND; ARTHRITIS; PROTEIN; DEADENYLATION; PROLIFERATION; MONOCYTOGENES AB Tristetraprolin (TTP) is a member of the CCCH tandem zinc-finger class of proteins. It can bind to and destabilize mRNAs encoding tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Conversely, mice deficient in TTP develop a complex syndrome characterized by cachexia, myeloid hyperplasia, and joint and skin inflammation. Studies using anti-TNF-alpha neutralizing antibodies demonstrated that this syndrome, at least in part, is a consequence of the excess production of TNF-alpha in the absence of TTP. To evaluate the role played by each TNF-alpha receptor in the pathogenesis of this syndrome, mice were generated that were deficient in TTP and either or both of the known TNF-alpha receptors (TNFRs), type 1 (TNFR1) and type 2 (TNFR2). Mice deficient in TTP and TNFR1, or in TTP and both receptors, were protected from developing the TNF-alpha -induced cachexia and inflammation. In contrast, mice deficient in TNFR2 were more severely affected than mice deficient in TTP alone, suggesting that TNFR2 might play a protective role in the development of the syndrome. In cultured cells derived from these mice, apparent cooperation between the TNFRs was required to achieve normal TNF-alpha -induced expression of TTP, TNF-alpha, and GM-CSF mRNAs. Finally, the results showed that TNFR1 plays an important role in mediating TNF alpha -induced changes in TNF-alpha and GMCSF mRNA stability. (C) 2001 by The American Society of Hematology. C1 NIEHS, Off Clin Res, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 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, Off Clin Res, MD A2-05,POB 12233, Res Triangle Pk, NC 27709 USA. NR 31 TC 72 Z9 73 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 2001 VL 98 IS 8 BP 2389 EP 2395 DI 10.1182/blood.V98.8.2389 PG 7 WC Hematology SC Hematology GA 482PG UT WOS:000171584000017 PM 11588035 ER PT J AU Bleesing, JJH Brown, MR Straus, SE Dale, JK Siegel, RM Johnson, M Lenardo, MJ Puck, JM Fleisher, TA AF Bleesing, JJH Brown, MR Straus, SE Dale, JK Siegel, RM Johnson, M Lenardo, MJ Puck, JM Fleisher, TA TI Immunophenotypic profiles in families with autoimmune lymphoproliferative syndrome SO BLOOD LA English DT Article ID IMMUNOLOGICAL SELF-TOLERANCE; IMMUNOREGULATORY T-CELLS; FAS GENE-MUTATIONS; SYSTEMIC LUPUS-ERYTHEMATOSUS; CONVENTIONAL B-CELLS; LYMPHOCYTE APOPTOSIS; INTERLEUKIN-2 RECEPTOR; DEFECTIVE FAS; ALPHA-CHAIN; MICE AB Autoimmune lymphoproliferative syndrome (ALPS) type Ia is caused by inherited defects in apoptosis and is characterized by nonmalignant lymphoaccumulation, autoimmunity, and increased alpha/beta (+) double-negative T cells (alpha/beta (+)-DNT cells). This study reports immunophenotypic findings in 166 members of 31 families with ALPS type Ia, associated with genetic mutations in the TNFRSF6 gene encoding Fas. The ALPS type Ia probands (n = 31) and relatives having both a Fas mutation and clinically proven ALPS (n = 28) showed significant expansion of CD8(+) T cells, alpha/beta (+)-DNT cells, gamma/delta (+)-DNT cells, CD3(+)/HLA-DR+ T cells, CD8(+)/CD57(+) T cells, and CD5(+) B cells. Relatives with Fas mutations, but without all the required criteria for ALPS (n = 42), had expansions of CD8(+) T cells, alpha/beta (+)-DNT cells, and gamma/delta (+)-DNT cells. Interestingly, relatives without a Fas mutation and with no features of ALPS (n = 65) demonstrated a small but significant expansion of CD8(+) T cells, both DNT cell subsets, and CD5(+) B cells. As compared to unrelated healthy controls, lymphocyte subset alterations were greatest in the probands, followed by the relatives with mutations and ALPS. Probands and relatives with mutations and ALPS also showed a lower number of CD4(+)/CD25(+) T cells that, in combination with an independent increase in HLA-DR+ T cells, provided a profile predictive of the presence of clinical ALPS. Because quantitative defects in apoptosis were similar in mutation-positive relatives regardless of the presence of clinical ALPS, factors, other than modifiers of the Fas apoptosis pathway, leading to these distinctive immunophenotypic profiles most likely contribute to disease penetrance in ALPS. (Blood. 2001;98:2466-2473) (C) 2001 by The American Society of Hematology. C1 NIAID, Serv Immunol, Dept Lab Med, Clin Ctr,Lab Clin Invest,NIH, Bethesda, MD 20892 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. RP Bleesing, JJH (reprint author), Arkansas Childrens Hosp, Res Inst, 1120 Marshall St, Little Rock, AR 72202 USA. RI Siegel, Richard/C-7592-2009 OI Siegel, Richard/0000-0001-5953-9893 NR 45 TC 80 Z9 84 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 2001 VL 98 IS 8 BP 2466 EP 2473 DI 10.1182/blood.V98.8.2466 PG 8 WC Hematology SC Hematology GA 482PG UT WOS:000171584000026 PM 11588044 ER PT J AU Turville, SG Arthos, J Mac Donald, K Lynch, G Naif, H Clark, G Hart, D Cunningham, AL AF Turville, SG Arthos, J Mac Donald, K Lynch, G Naif, H Clark, G Hart, D Cunningham, AL TI HIV gp120 receptors on human dendritic cells SO BLOOD LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; EPIDERMAL LANGERHANS CELLS; C-TYPE LECTIN; MANNOSE RECEPTOR; T-CELLS; PRODUCTIVE INFECTION; LYMPHOCYTE SUBSETS; SURFACE-RECEPTOR; GENITAL-TRACT; MACROPHAGES AB Dendritic cells (DCs) are important targets for human immunodeficiency virus (HIV) because of their roles during transmission and also maintenance of immune competence. Furthermore, DCs are a key cell in the development of HIV vaccines. In both these settings the mechanism of binding of the HIV envelope protein gp120 to DCs is of importance. Recently a single C-type lectin receptor (CLR), DC-SIGN, has been reported to be the predominant receptor on monocyte-derived DCs (MD-DCs) rather than CD4. In this study a novel biotinylated gp120 assay was used to determine whether CLR or CD4 were predominant receptors on MDDCs and ex vivo blood DCs. CLR bound more than 80% of gp120 on MDDCs, with residual binding attributable to CD4, reconfirming that CLRs were the major receptors for gp120 on MDDCs. However, in contrast to recent reports, gp120 binding to at least 3 CLRs was observed: DC-SIGN, mannose receptor, and unidentified trypsin resistant CLR(s). In marked contrast, freshly isolated and cultured CD11c(+ve) and CD11c(-ve) blood DCs only bound gp120 via CD4. In view of these marked differences between MDDCs and blood DCs, HIV capture by DCs and transfer mechanisms to T cells as well as potential antigenic processing pathways will need to be determined for each DC phenotype. (Blood. 2001;98:2482-2488) (C) 2001 by The American Society of Hematology. C1 Westmead Millennium Inst, Sydney, NSW, Australia. NIAID, NIH, Bethesda, MD 20892 USA. Mater Med Res Inst, Brisbane, Qld, Australia. RP Cunningham, AL (reprint author), Westmead Millennium Inst, POB 412,Darcy Rd, Westmead, NSW 2145, Australia. RI Cunningham, Tony/B-7011-2013; MacDonald, Kelli/O-2722-2016; OI MacDonald, Kelli/0000-0003-3451-4221; Cunningham, Anthony/0000-0002-6744-5667 NR 42 TC 155 Z9 158 U1 2 U2 10 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 OCT 15 PY 2001 VL 98 IS 8 BP 2482 EP 2488 DI 10.1182/blood.V98.8.2482 PG 7 WC Hematology SC Hematology GA 482PG UT WOS:000171584000028 PM 11588046 ER PT J AU Faries, MB Bedrosian, I Xu, SW Koski, G Roros, JG Moise, MA Nguyen, HQ Engels, FHC Cohen, PA Czerniecki, BJ AF Faries, MB Bedrosian, I Xu, SW Koski, G Roros, JG Moise, MA Nguyen, HQ Engels, FHC Cohen, PA Czerniecki, BJ TI Calcium signaling inhibits interleukin-12 production and activates CD83(+) dendritic cells that induce Th2 cell development SO BLOOD LA English DT Article ID TUMOR-NECROSIS-FACTOR; T-HELPER CELL; MHC CLASS-II; MONOCYTE CHEMOTACTIC PROTEIN-1; PERIPHERAL-BLOOD MONOCYTES; LEVEL IL-12 PRODUCTION; VERSUS-HOST DISEASE; CHEMOKINE RECEPTORS; CYTOKINE PRODUCTION; INTERFERON-GAMMA AB Mature dendritic cells (DCs), in addition to providing costimulation, can define the Th1, in contrast to the Th2, nature of a T-cell response through the production of cytokines and chemokines. Because calcium signaling alone causes rapid DC maturation of both normal and transformed myeloid cells, it was evaluated whether calcium-mobilized DCs polarize T cells toward a Th1 or a Th2 phenotype. After human monocytes were cultured for 24 hours in serum-free medium and granulocyte-macrophage colony-stimulating factor to produce immature DCs, additional overnight culture with either calcium ionophore (CI) or interferon gamma (IFN gamma), tumor necrosis factor-alpha (TNF-alpha), and soluble CD40L resulted in phenotypically mature DCs that produced interleukin-8 (IL-8) and displayed marked expression of CD80, CD86, CD40, CD54, CD83, DC-LAMP, and ReIB. DCs matured by IFN-gamma, TNF-alpha, and soluble CD40L were additionally distinguished by undetectable CD4 expression, marked secretion of IL-12, IL-6, and MIP-1 beta, and preferential ability to promote Th1/Tc1 characteristics during T-cell sensitization. In contrast, DCs matured by CI treatment were distinguished by CD4 expression, modest or absent levels of IL-12, IL-6, and MIP-1 beta, and preferential ability to promote Th2/Tc2 characteristics. Calcium signaling selectively antagonized IL-12 production by mature DCs activated with IFN-gamma, TNF-alpha, and soluble CD40L. Although the activation of DCs by calcium signals is largely mediated through calcineurin phosphatase, the inhibition of IL-12 production by calcium signaling was independent of this enzyme. Naturally occurring calcium fluxes in immature DCs, therefore, negatively regulate Dc1 differentiation while promoting Dc2 characteristics and Th2/Tc2 polarization. Calcium-mobilized DCs may have clinical usefulness in treating disease states with excessive Th1/Tc1 activity, such as graft-versus-host disease or autoimmunity. (Blood. 2001;98: 2489-2497) (C) 2001 by The American Society of Hematology. C1 Univ Penn, Dept Surg, Philadelphia, PA 19104 USA. Univ Penn, Harrison Surg Res Ctr, Philadelphia, PA 19104 USA. NCI, Frederick Canc Res & Dev Ctr, Bethesda, MD 20892 USA. Cleveland Clin Fdn, Surg Res Ctr, Cleveland, OH USA. RP Czerniecki, BJ (reprint author), Univ Penn, Dept Surg, 4 Silverstein,3400 Spruce St, Philadelphia, PA 19104 USA. NR 66 TC 46 Z9 55 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 2001 VL 98 IS 8 BP 2489 EP 2497 DI 10.1182/blood.V98.8.2489 PG 9 WC Hematology SC Hematology GA 482PG UT WOS:000171584000029 PM 11588047 ER PT J AU Magnusson, MK Meade, KE Brown, KE Arthur, DC Krueger, LA Barrett, AJ Dunbar, CE AF Magnusson, MK Meade, KE Brown, KE Arthur, DC Krueger, LA Barrett, AJ Dunbar, CE TI Rabaptin-5 is a novel fusion partner to platelet-derived growth factor beta receptor in chronic myelomonocytic leukemia SO BLOOD LA English DT Article ID CELL MYELOPROLIFERATIVE DISORDER; ENDOCYTIC MEMBRANE-FUSION; ACUTE MYELOID-LEUKEMIA; MYELOGENOUS LEUKEMIA; GENE; PROTEIN; RAB5; TRANSLOCATION; PATHWAYS; EFFECTOR AB Chromosomal translocations involving the platelet-derived growth factor beta receptor (PDGF betaR) gene have been reported in some patients with chronic myelomonocytic leukemia (CMML). The resultant fusion proteins have constitutive PDGF betaR tyrosine kinase activity, but the partner genes previously reported (tel, Huntingtin interacting protein 1 [HIP-1], H4/D10S170) have poorly understood roles in the oncogenic activity of the fusion proteins. A novel PDGF betaR fusion protein has been characterized in a patient with CMML and an acquired t(5;17)(q33;p13). Southern blot analysis on patient leukemia cells demonstrated involvement of the PDGF betaR gene. Using 5' rapid amplification of complementary DNA ends-polymerase chain reaction (RACE-PCR) on patient RNA, rabaptin-5 was identified as a novel partner fused in-frame to the PDGF betaR gene. The new fusion protein includes more than 85% of the native Rabaptin-5 fused to the transmembrane and intracellular tyrosine kinase domains of the PDGF betaR. Transduction with a retroviral vector expressing rabaptin-5/PDGF betaR transformed the hematopoietic cell line Ba/F3 to growth factor independence and caused a fatal myeloproliferative disease in mice. Rabaptin-5 is a well-studied protein shown to be an essential and rate-limiting component of early endosomal fusion through interaction with the Ras family GTPases Rab5 and Rab4. The fusion protein includes 3 of 4 coiled-coil domains (involved in homodimerization of native rabaptin-5), 2 caspase-3 cleavage sites, and a binding site for the tumor suppressor gene tuberin (tuberous sclerosis complex-2). Early endosomal transport is critical in regulation of various growth factor receptors, through ligand-induced clathrin-mediated endocytosis, and thus this new fusion protein links together 2 important pathways of growth regulation. (Blood. 2001;98:2518-2525) (C) 2001 by The American Society of Hematology. C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NCI, Pathol Lab, Div Clin Sci, NIH, Bethesda, MD 20892 USA. RP Magnusson, MK (reprint author), NHLBI, Hematol Branch, Bldg 10,Rm 7C103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 39 TC 102 Z9 111 U1 0 U2 5 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 OCT 15 PY 2001 VL 98 IS 8 BP 2518 EP 2525 DI 10.1182/blood.V98.8.2518 PG 8 WC Hematology SC Hematology GA 482PG UT WOS:000171584000032 PM 11588050 ER PT J AU Loyevsky, M LaVaute, T Allerson, CR Stearman, R Kassim, OO Cooperman, S Gordeuk, VR Rouault, TA AF Loyevsky, M LaVaute, T Allerson, CR Stearman, R Kassim, OO Cooperman, S Gordeuk, VR Rouault, TA TI An IRP-like protein from Plasmodium falciparum binds to a mammalian iron-responsive element SO BLOOD LA English DT Article ID MESSENGER-RNA; REGULATORY PROTEINS; MALARIA PARASITES; EVOLUTIONARY CONSERVATION; HEMOGLOBIN DENATURATION; DROSOPHILA-MELANOGASTER; 5'-UNTRANSLATED REGION; MOLECULAR-CLONING; METABOLISM; ACONITASE AB This study cloned and sequenced the complementary DNA (cDNA) encoding of a putative malarial iron responsive element-binding protein (PfIRPa) and confirmed its identity to the previously identified iron-regulatory protein (IRP)-like cDNA from Plasmodium falciparum. Sequence alignment showed that the plasmodial sequence has 47% identity with human IRP1. Hemoglobin-free lysates obtained from erythrocyte-stage P falciparum contain a protein that binds a consensus mammalian iron-responsive element (IRE), indicating that a protein(s) with iron-regulatory activity was present in the lysates. IRE-binding activity was found to be iron regulated in the electrophoretic mobility shift assays. Western blot analysis showed a 2-fold increase in the level of PflRPa in the desferrioxamine-treated cultures versus control or iron-supplemented cells. Malarial IRP was detected by anti-PflRPa antibody in the IRE-protein complex from P falciparum lysates. Immunofluorescence studies confirmed the presence of PflRPa in the infected red blood cells. These findings demonstrate that erythrocyte P falciparum contains an iron-regulated IRP that binds a mammalian consensus IRE sequence, raising the possibility that the malaria parasite expresses transcripts that contain IREs and are iron-dependently regulated. (Blood. 2001;98:2555-2562) (C) 2001 by The American Society of Hematology. C1 Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA. NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. RP Loyevsky, M (reprint author), Howard Univ, Ctr Sickle Cell Dis, 2121 Georgia Ave NW, Washington, DC 20059 USA. FU NHLBI NIH HHS [5-UH1-HL03 679-02]; NIAID NIH HHS [R01 AI 44857-02] NR 43 TC 25 Z9 25 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 OCT 15 PY 2001 VL 98 IS 8 BP 2555 EP 2562 DI 10.1182/blood.V98.8.2555 PG 8 WC Hematology SC Hematology GA 482PG UT WOS:000171584000036 PM 11588054 ER PT J AU Brown, LM Gridley, G Diehl, SR Winn, DM Harty, LC Otero, EB Fraumeni, JF Hayes, RB AF Brown, LM Gridley, G Diehl, SR Winn, DM Harty, LC Otero, EB Fraumeni, JF Hayes, RB TI Family cancer history and susceptibility to oral carcinoma in Puerto Rico SO CANCER LA English DT Article DE alcohol; case-control studies; diet; family; head and neck neoplasms; Puerto Rico; tobacco ID SQUAMOUS-CELL CARCINOMA; AERODIGESTIVE TRACT CANCER; MUTAGEN SENSITIVITY; ESOPHAGEAL CANCER; NECK-CANCER; GENETIC POLYMORPHISMS; TOBACCO USE; ALCOHOL-USE; DNA-REPAIR; HEAD AB Background. Use of alcohol and tobacco are the major risk factors for cancers of the oral cavity and pharynx in most of the world. A heritable component to oral carcinoma risk also has been suggested, although only limited data are available on familial aggregation of this disease. Methods. A population-based case-control study of 342 subjects with carcinomas of the oral cavity and pharynx (oral carcinoma) and 521 controls was conducted in Puerto Rico. The relation between family history of carcinomas of the oral cavity, the upper aerodigestive tract (UADT), and other selected sites with risk of oral carcinoma was explored using logistic regression modeling techniques. Results. Risk of oral carcinoma was elevated for subjects reporting a first-degree relative with carcinoma of the oral cavity (odds ratio [OR], 2.5; 95%. confidence interval [CI], 0.8-8.0) or any UADT carcinoma (OR, 2.6; 95% Cl, 1.4-4.8). The increased risk associated with family history of UADT carcinoma tended to be greatest for subjects with known risk factors (i.e., heavy consumption of alcohol and/or tobacco and infrequent intake of raw fruits and vegetables) and with oral carcinoma diagnoses at ages younger than 65 years. Conclusions. These findings are consistent with a heritable component to oral carcinoma, although shared lifestyle risk factors may be partially involved. Cancer 2001;92:2102-8. (C) 2001 America Cancer Society. C1 NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Inst Dent & Craniofacial Res, Craniofacial Epidemiol & Genet Branch, Bethesda, MD USA. NCI, Epidemiol & Genet Res Program, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA. Univ Puerto Rico, San Juan, PR 00936 USA. RP Brown, LM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Execut Plaza S,Room 8026,6120 Execut Blvd MSC 724, Bethesda, MD 20892 USA. NR 38 TC 21 Z9 21 U1 1 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 2001 VL 92 IS 8 BP 2102 EP 2108 PG 7 WC Oncology SC Oncology GA 483DH UT WOS:000171618100014 PM 11596026 ER PT J AU Reid, BC Alberg, AJ Klassen, AG Samet, JM Rozier, RG Garcia, I Winn, DM AF Reid, BC Alberg, AJ Klassen, AG Samet, JM Rozier, RG Garcia, I Winn, DM TI Comorbidity and survival of elderly head and neck carcinoma patients SO CANCER LA English DT Article DE survival; head and neck neoplasms; comorbidity; epidemiology; SEER; age older than 65 ID SEVERITY STAGING SYSTEM; BREAST-CANCER PATIENTS; ADMINISTRATIVE DATA; PANCREATIC-CANCER; TUMOR-REGISTRY; CO-MORBIDITY; RISK-FACTORS; EPIDEMIOLOGY; INDEX; RATES AB Background. Alcohol and tobacco, the primary etiologic agents for head and neck carcinoma (HNCA), cause other chronic diseases and may contribute to the high prevalence of comorbid conditions and generally poor survival of persons with HNCA. Methods. The authors explored the prognostic role of comorbidity in persons with HNCA using Health Care Finance Administration Medicare (HCFA) files linked with the appropriate files of the Surveillance, Epidemiology, and End Results (SEER) Program. The Charlson comorbidity index was applied to in-patient data from the HCFA files. The SEER data were used to ascertain survival and identify persons with HNCA diagnosed from 1985 to 1993 (n=9386). Results. in a proportional hazards regression model adjusted for age and historic stage at diagnosis, race, gender, marital status, socioeconomic status, histologic grade, anatomic site, treatment, and pre-1991 diagnosis, Charlson index scores of 0, 1, and 2+ had estimated relative hazards (RHs) with 95 confidence intervals (Cls) of 1.00, 1.33 (95% CI, 1.21-1.47), and 1.83 (95% CI, 1.64-2.05), respectively (P value for trend <0.0001). The adjusted RH for a Charlson index score of 1 or more compared with 0, using stratified models, was found to be greater in whites (RH, 1.55; 95% CI, 1.43-1.67) than blacks (RH, 1.24; 95% CI, 0.96-1.60), local (RH, 1.72; 95% CI, 1.50-1.96) versus distant stage (RH, 1.25; 95% CI, 1.00-1.56), and age 65-74 years (RH, 1.53; 95% CI, 1.38-1.69) versus age 85+ years (RH, 1.42; 95% CI, 1.09-1.84). Conclusions. This study establishes comorbidity as a predictor of survival in an elderly HNCA population and lends support to the inclusion of comorbidity assessment in prognostic staging of patients with HNCA diagnosed after 65 years of age. Cancer 2001;92:2109-16. (C) 2001 American Cancer Society. C1 Univ Maryland, Sch Dent, Dept Oral Hlth Care Delivery, Baltimore, MD 21201 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD USA. Univ N Carolina, Sch Publ Hlth, Dept Hlth Policy & Adm, Chapel Hill, NC USA. Natl Inst Dent & Craniofacial Res, Off Director, NIH, Bethesda, MD USA. NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. RP Reid, BC (reprint author), Univ Maryland, Sch Dent, Dept Oral Hlth Care Delivery, Room 3E-04,666 W Baltimore St, Baltimore, MD 21201 USA. FU NCI NIH HHS [CA-73790]; NIDCR NIH HHS [T32 DE-7255] NR 49 TC 80 Z9 80 U1 1 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 2001 VL 92 IS 8 BP 2109 EP 2116 DI 10.1002/1097-0142(20011015)92:8<2109::AID-CNCR1552>3.0.CO;2-M PG 8 WC Oncology SC Oncology GA 483DH UT WOS:000171618100015 PM 11596027 ER PT J AU Gelber, E Granoth, R Fridkin, M Dreznik, Z Brenneman, DE Moody, TW Gozes, I AF Gelber, E Granoth, R Fridkin, M Dreznik, Z Brenneman, DE Moody, TW Gozes, I TI A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines SO CANCER LA English DT Article DE vasoactive intestinal peptide (VIP); stearyl-Nle(17)-neurotensin-VIP analog (SNH); NCI-H727; HT-29; chemotherapy; lipophilic peptides ID CYCLASE-ACTIVATING POLYPEPTIDE; CULTURED MOUSE EMBRYOS; VIP RECEPTORS; PANCREATIC-CANCER; GENE-EXPRESSION; GROWTH; TUMORS; ANTAGONIST; LOCALIZATION; MODULATION AB Background. Vasoactive intestinal peptide (VIP) is one of several small neuropeptides that affect cancer growth. A lipophilic VIP analog, stearyl-Nle(17)-neurotensin(6.11)VIP(7-28) (SNH) that inhibited lung carcinoma growth has been described previously. The experiments performed were clonogenic assays in vitro and tumor. xenografts in nude mice in vivo. These studies were now extended to colon carcinoma and to combination therapy with chemotherapeutic agents. Methods. Assays were performed with cell lines, and tumor proliferation was assessed using the (3-[4,5-dimetliylthiazol-2-yl-5]-[3-carboxmethoxyphenyl]-2[4-sulfophenyl]-2H-tetrazolium) (MTS) colorimetric assay for mitochondrial function of living cells. Results. The lipophilic analog (SNH) enhanced the antiproliferative activity of diverse chemotherapeutic agents: doxorubicine (antibiotic); vinorelbine (vinca alkaloid, antimicrotubule formation); paclitaxel (antimicrotubule agent); gemcitabine (antimetabolite); irinotecan (topoisomerase I inhibitor); and cisplatin (platinum compound acting as an alkylating agent). In all cases, the antiproliferative effect of SNH and the chemotheraputic agent was at least additive and for some combinations and concentrations even synergistic. For example, 2 muM of the antagonist that produced a 15-20% growth inhibition in the nonsmall cell lung carcinoma cell line reduced the IC50 by 2-4-fold for most of the chemotherapeutic agents tested. Higher analog concentrations were even more efficacious. Similar results were obtained with colon carcinoma cell lines. Conclusions. Chemotherapeutic treatment of advanced solid tumors, such as nonsmall cell lung carcinoma, colon carcinoma, or prostate carcinoma, achieves a response rate of between 10% and 30% with significant toxicity. Combination therapy with the lipophilic VIP analog SNH and the preferred chemotherapeutic agent may greatly enhance the response rate, and by permitting a dose reduction, should significantly reduce side effects. Cancer 2001;92:2172-80. (C) 2001 American Cancer Society. C1 Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Sackler Fac Med, Dept Surg, IL-69978 Tel Aviv, Israel. Weizmann Inst Sci, Dept Organ Chem, IL-76100 Rehovot, Israel. NICHHD, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA. NCI, Med Branch, Rockville, MD USA. RP Gozes, I (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NR 39 TC 28 Z9 28 U1 0 U2 6 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 2001 VL 92 IS 8 BP 2172 EP 2180 DI 10.1002/1097-0142(20011015)92:8<2172::AID-CNCR1560>3.0.CO;2-4 PG 9 WC Oncology SC Oncology GA 483DH UT WOS:000171618100023 PM 11596035 ER PT J AU Tomicic, MT Thust, R Sobol, RW Kaina, B AF Tomicic, MT Thust, R Sobol, RW Kaina, B TI DNA polymerase beta mediates protection of mammalian cells against ganciclovir-induced cytotoxicity and DNA breakage SO CANCER RESEARCH LA English DT Article ID THYMIDINE KINASE GENE; PURINE NUCLEOSIDE ANALOGS; BASE-EXCISION-REPAIR; CYTOGENETIC GENOTOXICITY; VIRUS; APOPTOSIS; PENCICLOVIR; MECHANISMS; EXPRESSION; ACYCLOVIR AB The efficacy of suicide herpes simplex virus-1 thymidine kinase (HSVtk)/ganciclovir (GCV) gene therapy is often limited by intrinsic resistance of tumor cells. Here we show that repair of GCV incorporated in DNA is a factor involved in GCV resistance. A protective role of DNA repair in GCV-induced cell killing is supported by the following findings: (a) GCV-exposed Chinese hamster ovary-HSVtk cells exhibited both reduced repair of GCV and cloning efficiency in the presence of a specific polymerase beta (beta -pol) inhibitor, prunasin; (b) DNA beta -pol-deficient mouse fibroblasts were more sensitive to the cytotoxic, apoptosis-inducing, and genotoxic (DNA breakage and chromosomal aberration-inducing) effects of GCV as compared with wild-type and beta -pol-complemented cell lines; (c) methoxyamine, an inhibitor of beta -pol-dependent short-patch base excision repair, sensitized wild-type and complemented P-pol cells to GCV, whereas it had no effect on the sensitivity of beta -pol-null cells to GCV. Because methoxyamine-mediated sensitization of beta -pol wild-type and beta -pol-complemented cells to GCV did not reach the level of null cells, we suggest that both beta -pol-dependent short- and long-patch base excision repair are involved in protection of cells to GCV. Some implications for HSVtk/GCV gene therapy are being discussed. C1 Univ Mainz, Inst Toxicol, Div Appl Toxicol, D-55131 Mainz, Germany. Univ Jena, Inst Antiviral Chemotherapy, D-07745 Jena, Germany. NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. RP Kaina, B (reprint author), Univ Mainz, Inst Toxicol, Div Appl Toxicol, Obere Zahlbacher Str 67, D-55131 Mainz, Germany. RI Sobol, Robert/E-4125-2013 OI Sobol, Robert/0000-0001-7385-3563 NR 22 TC 38 Z9 38 U1 0 U2 1 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 OCT 15 PY 2001 VL 61 IS 20 BP 7399 EP 7403 PG 5 WC Oncology SC Oncology GA 484UF UT WOS:000171707400007 PM 11606369 ER PT J AU Seker, H Butkiewicz, D Bowman, ED Rusin, M Hedayati, M Grossman, L Harris, CC AF Seker, H Butkiewicz, D Bowman, ED Rusin, M Hedayati, M Grossman, L Harris, CC TI Functional significance of XPD polymorphic variants: Attenuated apoptosis in human lymphoblastoid cells with the XPD 312 Asp/Asp genotype SO CANCER RESEARCH LA English DT Article ID NUCLEOTIDE EXCISION-REPAIR; DNA-REPAIR; TRANSCRIPTION FACTOR; TFIIH; P53; PROFICIENCY; MUTATIONS; HELICASE; DAMAGE; CANCER AB Recent molecular epidemiological studies have identified polymorphisms in the XPD gene that are associated with increased risk of brain gliomas and head, neck, lung, and skin cancers. However, the functional significance of these polymorphic variants in altering cell processes such as cell cycle checkpoints, DNA repair, and apoptosis is uncertain. We have cloned the XPD variants Lys751Gln, Asp312Asn, and Lys751Gln-Asp312Asn into a pcDNA-3.1-expression vector. Using these constructs, we did not rind any detectable difference in either in vitro binding with wild-type p53 or in DNA repair proficiency as measured by host cell reactivation assay. We then genotyped 34 different lymphoblastoid cell lines from six Centre d'Etude du Polymorphisme Humaine (CEPH)/Utah pedigree families and a CEPH/French pedigree family for polymorphisms at codons 751 and 312 and assessed their apoptotic response after either UV or ionized radiation exposure. The lymphoblastoid cell lines with homozygous or heterozygous Asp at codon 312 have similar apoptotic rates, whereas cell lines with homozygous Asn at codon 312 showed a 2.5-fold increased response to UV (P = 0.005; Student's t test). This is the first report known to us of a functional polymorphism in a gene involved in DNA damage-induced apoptosis. However, the presence of Lys or Gln at codon 751 did not influence the apoptotic response to UV. The diminished apoptotic response of cells containing the 312 Asp allele could both allow the survival and selective clonal expansion of carcinogen-damaged cells and be a mechanistic explanation for the increased risk of cancer at diverse tissue sites. C1 NCI, Human Carcinogenesis Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. Marie Curie Sklodowska Univ, Dept Tumor Biol, PL-44101 Gliwice, Poland. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biochem, Baltimore, MD 21205 USA. RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Canc Res Ctr, NIH, 37 Convent Dr,Bldg 37,Room 2C05, Bethesda, MD 20892 USA. NR 31 TC 100 Z9 105 U1 0 U2 1 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 OCT 15 PY 2001 VL 61 IS 20 BP 7430 EP 7434 PG 5 WC Oncology SC Oncology GA 484UF UT WOS:000171707400014 PM 11606376 ER PT J AU Green, JE Shibata, MA Shibata, E Moon, RC Anver, MR Kelloff, G Lubet, R AF Green, JE Shibata, MA Shibata, E Moon, RC Anver, MR Kelloff, G Lubet, R TI 2-difluoromethylornithine and dehydroepiandrosterone inhibit mammary tumor progression but not mammary or prostate tumor initiation in C3(1)/SV40 T/t-antigen transgenic mice SO CANCER RESEARCH LA English DT Article ID LARGE T-ANTIGEN; BREAST-CANCER; ORNITHINE DECARBOXYLASE; ALPHA-DIFLUOROMETHYLORNITHINE; 9-CIS-RETINOIC ACID; CARCINOMA MODEL; RAT; CHEMOPREVENTION; CARCINOGENESIS; NEOPLASIA AB Female transgenic mice that express SV40 T/t antigens under the regulatory control of the rat C3(1) gene spontaneously develop multifocal Mammary lesions that predictably evolve into invasive, hormone-independent carcinomas, whereas male mice are prone to develop prostate cancer. Chemo-preventive agents were administered to female C3(1)/SV40 large T-antigen mice from 7 to 19 weeks of age, during which time the mammary lesions developed and progressed to invasive carcinomas. No significant differences in the numbers of preinvasive mammary intraepithelial neoplasia lesions (histologically similar to human ductal carcinoma in situ) were observed after 2 or 8 weeks of treatment between mice receiving either vehicle alone, dehydroepiandrosterone (DHE A), or 2-difluoromethylornithine (DFMO). However, a dose-response reduction in invasive carcinoma growth was observed for both DFMO, an inhibitor of ornithine decarboxylase, and DHEA, the primary steroid precursor to both androgens and estrogens in primates. Despite unaltered expression of the transgene, tumor incidence was reduced approximately 20% by DFMO (8000 mg/kg) and 30% by DHEA (4000 mg/kg; P < 0.05). Tumor multiplicity was reduced by similar to 50% by both DFMO and DHEA (P < 0.05). DFMO had a dose-dependent effect on total tumor burden, which was reduced by 25% at low doses 4000 mg/kg) and 70% at high doses (8000 mg/kg). DHE A reduced tumor burden by 50% and 66% at low (2000 mg(kg) and high (4000 mg/kg) doses, respectively. Interestingly, despite its inhibitory effects on tumor development, DHEA caused a dose-dependent increase of serum estradiol levels that we have previously shown to increase mammary tumor formation in this model. No effect on the development of the prostate cancer precursor lesions (prostate intraepithelial neoplasia) was observed when mice were treated with DHEA, DFMO, tocopherol acetate, selenomethionine, or 9-cis-retinoic acid, although the effects on late-stage prostate cancer development were not determined. These results demonstrate that despite the expression of the highly transforming C3(1)/SV40 large T-antigen transgene, this transgenic model can be used to study the effects of chemopreventive agents on mammary cancer progression. The tumor-inhibitory effects of DHEA and DFMO on mammary cancer growth appear to occur after the development of preinvasive lesions, suggesting that these agents inhibit tumor progression but not initiation. C1 NCI, Lab Cell Regulat & Carcinogensis, NIH, Bethesda, MD 20892 USA. Univ Illinois, Coll Med, Dept Surg Oncol, Chicago, IL USA. NCI, Sci Applicat Int Corp, Pathol Histotechnol Lab, Frederick, MD 21702 USA. NCI, Div Canc Prevent, Rockville, MD 20892 USA. RP Green, JE (reprint author), NCI, Lab Cell Regulat & Carcinogensis, NIH, Bldg 41,Room C629,41 Lib Dr, Bethesda, MD 20892 USA. FU PHS HHS [N01-C0-56000] NR 35 TC 52 Z9 53 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 OCT 15 PY 2001 VL 61 IS 20 BP 7449 EP 7455 PG 7 WC Oncology SC Oncology GA 484UF UT WOS:000171707400017 PM 11606379 ER PT J AU Tsang, KY Zhu, MZ Even, J Gulley, J Arlen, P Schlom, J AF Tsang, KY Zhu, MZ Even, J Gulley, J Arlen, P Schlom, J TI The infection of human dendritic cells with recombinant avipox vectors expressing a costimulatory molecule transgene (CD80) to enhance the activation of antigen-specific cytolytic T cells SO CANCER RESEARCH LA English DT Article ID HUMAN CARCINOEMBRYONIC ANTIGEN; COLONY-STIMULATING FACTOR; VACCINIA VIRUS; GENE-TRANSFER; IN-VITRO; PHASE-I; ADENOVIRUS VECTORS; IMMUNE-RESPONSES; PRESENTING CELLS; CANCER-PATIENTS AB Human dendritic cells (DCs) express MHC class I and II molecules and several T-cell costimulatory molecules that contribute to their efficiency as antigen-presenting cells (APCs). Whereas most human DC populations uniformly express some costimulatory molecules such as B7-2 (CD86), previous studies have shown a wide variation in the expression of B7-1 (CD80) among different human DC preparations. In the studies reported here, we demonstrate that replication-defective avipox vectors expressing B7-1 can be used to rapidly and efficiently infect human DCs and can enhance the efficacy of human DCs to activate specific human T-cell populations. This has been demonstrated both in systems using peptide as a source of signal 1 and in systems using recombinant avipox vector to deliver signal 1. The antigen used in these studies was the tumor-associated human carcinoembryonic antigen (CEA). An immunodominant 9-mer CTL epitope for CEA (designated CAP-1) has been previously characterized (K. Y. Tsang et al., J. NatI. Cancer Inst. (Bethesda), 87: 982-990, 1995). The source of signal 1 used in these studies was (a) the CAP-1 peptide; (b) recombinant avipox-CEA; or (c) the dual transgene recombinant avipox-CEA/B7-1. These studies demonstrate that CEA-specific T cells are more efficiently activated using as APCs peptide-pulsed DCs infected with avipox-B7-1, as compared with peptide-pulsed DCs infected with wild-type vector, or with uninfected peptide-pulsed DCs. Greater activation of CEA-specific T cells was also obtained using as APCs DCs that were infected with avipox-CEA/B7-1 as compared with the use of DCs infected with avipox-CEA. A CEA tetramer was also used to isolate high- and low-tetramer-binding CEA-specific T-cell populations. Although both high- and low-tetramer-binding, T cells had the ability to lyse CEA peptide-pulsed targets, only the high-tetramer-binding T cells had the ability to lyse colon carcinoma cells expressing CEA, which suggests the existence of tetramer-binding populations with different T-cell receptor (TCR) affinities. The demonstrated safety of recombinant avipox vectors in humans and the previously demonstrated ability to administer them multiple times without host immune response limitations indicate that these vectors expressing B7-1 have a potential use in enhancing the efficacy of human DC immunotherapy protocols using either peptide or recombinant vector to deliver signal 1. C1 NCI, Tumor Immunol & Biol Lab, NIH, Bethesda, MD 20892 USA. Inst Pasteur, Dept Immunol, INSERM U277, F-75724 Paris 15, France. RP Schlom, J (reprint author), NCI, Tumor Immunol & Biol Lab, NIH, 10 Ctr Dr,Rm 8B09, Bethesda, MD 20892 USA. RI Gulley, James/K-4139-2016 OI Gulley, James/0000-0002-6569-2912 NR 54 TC 36 Z9 37 U1 0 U2 0 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 OCT 15 PY 2001 VL 61 IS 20 BP 7568 EP 7576 PG 9 WC Oncology SC Oncology GA 484UF UT WOS:000171707400034 PM 11606396 ER PT J AU Bradbury, CM Markovina, S Wei, SJ Rene, LM Zoberi, I Horikoshi, N Gius, D AF Bradbury, CM Markovina, S Wei, SJ Rene, LM Zoberi, I Horikoshi, N Gius, D TI Indomethacin-induced radiosensitization and inhibition of ionizing radiation-induced NF-kappa B activation in HeLa cells occur via a mechanism involving p38 MAP kinase SO CANCER RESEARCH LA English DT Article ID HEAT-SHOCK; TRANSCRIPTION FACTOR; DOWN-REGULATION; C-JUN; ALPHA; PHOSPHORYLATION; STRESS; SIGNAL; BETA; DNA AB Although ionizing radiation (IR) activates multiple cellular factors that vary depending on dose and tissue specificity, the activation of NF-kappaB appears to be a well-conserved response in tumor cells exposed to IR. Recently, it also has been demonstrated that nonsteroidal anti-inflammatory agents inhibit tumor necrosis factor and interleukin-1-induced NF-kappaB activation and act as radiosensitizing agents. These observations reinforce the growing notion that NF-kappaB may be a protective cellular factor responding to the cytotoxicity of IR and other damaging stimuli. As such, we addressed the idea and mechanism that NF-kappaB is a downstream target of the nonsteroidal anti-inflaminatory agent indomethacin and is involved in the process of radiosensitization. In this study, we report that indomethacin inhibited IR-induced activation of NF-kappaB and sensitized HeLa cells to IR-induced cytotoxicity at similar concentrations. Pretreatment of HeLa cells with SB 203580, a pyridinyl imidazole compound that specifically inhibits p38 mitogen-activated protein kinase (MAPK), abrogated the ability of indomethacin to inhibit IR-induced activation of NF-kappaB and diminished the indomethacin radiosensitizing effect. In addition, the transient genetic activation of p38(MAPK) inhibited IR induction of NF-kappaB gene expression in the absence of indomethacin. Finally, permanently transfected cell lines genetically unable to activate NF-kappaB, because of expression of a dominant negative I-kappaB alpha gene, demonstrated increased sensitivity to IR-induced cytotoxicity. Taken together, these results suggest that p38 MAPK is a target involved in indomethacin-induced radiosensitization and that NF-kappaB may be one downstream target in this process. C1 NCI, Radiat Oncol Branch, Radiat Oncol Sci Program, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. Washington Univ, Sch Med, Edward Mallinckrodt Inst Radiol, Radiat Oncol Ctr,Sect Canc Biol, St Louis, MO 63110 USA. RP NCI, Radiat Oncol Branch, Radiat Oncol Sci Program, Ctr Canc Res,NIH, Bldg 10,Room B3B69, Bethesda, MD 20892 USA. EM giusd@mail.nih.gov FU NCI NIH HHS [P01 CA75556, 1 K08 CA72602-01] NR 51 TC 60 Z9 63 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 2001 VL 61 IS 20 BP 7689 EP 7696 PG 8 WC Oncology SC Oncology GA 484UF UT WOS:000171707400051 PM 11606413 ER PT J AU Wersto, RP Chrest, FJ Leary, JF Morris, C Stetler-Stevenson, M Gabrielson, E AF Wersto, RP Chrest, FJ Leary, JF Morris, C Stetler-Stevenson, M Gabrielson, E TI Doublet discrimination in DNA cell-cycle analysis SO CYTOMETRY LA English DT Article DE G alpha/1 doublets; DNA cell cycle; flow cytometry; cylin B1; pulse width; pulse height; modeling ID S-PHASE FRACTION; FLOW CYTOMETRIC ANALYSIS; NEGATIVE BREAST-CANCER; QUALITY-CONTROL; SOLID TUMORS; HISTOGRAMS; CYTOKERATIN; PROGNOSIS; REPRODUCIBILITY; DISAGGREGATION AB Differences in doublet analysis have the potential to alter DNA cell-cycle measurements. The techniques for doublet determination are often used interchangeably without regard for the complexity in cell shapes and sizes of biological specimens. G(0/1) doublets were identified and quantitated using fluorescence height versus area and fluorescence width versus area pulse measurements, by enumerating the proportion of G(2) + M cells that lack cyclin BI immunoreactivity, and modeled in the DNA histograms by software algorithms. These techniques were tested on propidium iodide-stained whole epithelial cells or nuclei from asynchronous cultures, or after exposure to chemotherapeutic agents that induced cell-cycle arrest and were extended to human breast tumor specimens having DNA diploid patterns. G(0/1) doublets were easily discernible from G(2) + M singlets in cells or nuclei that are generally homogenous and spherical in shape. Doublet discrimination based on pulse processing or cyclin B1 measurements was nonconcordant in some nonspherical cell types and in cells following cell cycle arrest. Significant differences in G(0/1) doublet estimates were observed in breast tumor specimens (n = 50), with estimates based on pulse width twice those of pulse height and nearly five times greater than computer estimates. Differences between techniques are attributed to difficulties in the separation of the boundaries between G(0/1) doublets and G(2) + M singlet populations in biologically heterogeneous specimens. To improve reproducibility and enhance standardization among laboratories performing cell cycle analysis in experimental cell systems and in human breast tumors, doublet discrimination analysis should best be accomplished by computer modeling. Shape and size heterogeneity of tumor and arrested cells using pulse-processing can lead to errors and make interlaboratory comparison difficult. Published 2001 Wiley-Liss, Inc. C1 NIA, Flow Cytometry Unit, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. Univ Texas, Med Branch, Mol Cytometry Unit, Galveston, TX 77550 USA. NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. Johns Hopkins Sch Med, Dept Pathol, Baltimore, MD USA. RP Wersto, RP (reprint author), NIA, Flow Cytometry Unit, Gerontol Res Ctr, NIH, 5600 Nathan Shock DR, Baltimore, MD 21224 USA. RI Leary, James/H-8554-2014 OI Leary, James/0000-0002-0250-4427 NR 43 TC 81 Z9 82 U1 3 U2 9 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0196-4763 J9 CYTOMETRY JI Cytometry PD OCT 15 PY 2001 VL 46 IS 5 BP 296 EP 306 DI 10.1002/cyto.1171 PG 11 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 487WW UT WOS:000171902900005 PM 11746105 ER PT J AU Perfetto, S Roederer, M AF Perfetto, S Roederer, M TI Application of 12-color digital flow cytometry to the characterization and funtional measurements of hyperfine T cell subsets SO CYTOMETRY LA English DT Meeting Abstract C1 NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 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 0196-4763 J9 CYTOMETRY JI Cytometry PD OCT 15 PY 2001 VL 46 IS 5 MA 31 BP 322 EP 323 PG 2 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 487WW UT WOS:000171902900037 ER PT J AU Riordan, MJ Gahl, WA Rivera, CE AF Riordan, MJ Gahl, WA Rivera, CE TI Reduced expression of P-selectin and activated fibrinogen receptors on stimulated platelets in gray platelet syndrome (GPS) SO CYTOMETRY LA English DT Meeting Abstract C1 DLM, Serv Hematol, CC, Bethesda, MD USA. NR 0 TC 0 Z9 0 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 0196-4763 J9 CYTOMETRY JI Cytometry PD OCT 15 PY 2001 VL 46 IS 5 MA 39 BP 325 EP 325 PG 1 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 487WW UT WOS:000171902900045 ER PT J AU Couse, JF Dixon, D Yates, M Moore, AB Ma, L Maas, R Korach, KS AF Couse, JF Dixon, D Yates, M Moore, AB Ma, L Maas, R Korach, KS TI Estrogen receptor-alpha knockout mice exhibit resistance to the developmental effects of neonatal diethylstilbestrol exposure on the female reproductive tract SO DEVELOPMENTAL BIOLOGY LA English DT Article DE estrogen receptor; diethylstilbestrol; teratogenesis; uterus; Hox; Wnt ID HOX GENE-EXPRESSION; C-FOS PROTOONCOGENE; MOUSE UTERUS; ENVIRONMENTAL ESTROGENS; TRANSGENIC MICE; NULL MICE; WNT GENES; IN-UTERO; BETA; DES AB Data indicate that estrogen-dependent and -independent pathways are involved in the teratogenic/carcinogenic syndrome that follows developmental exposure to 17 beta -estradiol or diethylstilbestrol (DES), a synthetic estrogen. However, the exact role and extent to which each pathway contributes to: the resulting pathology remain unknown. We employed the alpha ERKO mouse, which lacks estrogen receptor-alpha (ER alpha)(r). to discern the role of ER alpha and estrogen signaling in mediating the effects of neonatal DES exposure. The aERKO provides the potential to expose DES actions mediated by the second known ER, ER beta, and those that are ER-independent. Wild-type and alpha ERKO females were treated with vehicle or DES (2 mug/pup/day for Days 1-5) and terminated after 5 days and 2, 4, 8, 12, and 20 months for biochemical and histomorphological analyses. Assays for uterine expression of the genes Hoxa10, Hoxa11, and Wnt7a shortly after treatment indicated significant decreases in DES-treated wild-type but no effect in the alpha ERKO. In contrast, the DES effect on uterine expression of Wnt4 and Wnt5a was preserved in both genotypes, suggesting a developmental role for ER beta. Adult aERKO mice exhibited complete resistance to the chronic effects of neonatal DES exposure exhibited in treated wild-type animals, including atrophy, decreased weight, smooth muscle disorganization, and epithelial squamous metaplasia in the uterus; proliferative lesions of the oviduct; and persistent vaginal cornification. Therefore, the lack of DES effects on gene expression and tissue differentiation in the alpha ERKO provides unequivocal evidence of, an obligatory role for ERa in mediating the detrimental actions of neonatal DES exposure in the murine reproductive tract. (C) 2001 Academic Press. C1 Natl Inst Environm Hlth Sci, Natl Inst Hlth, Receptor Biol Sect, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA. Natl Inst Environm Hlth Sci, Natl Inst Hlth, Comparat Pathobiol Sect, Lab Expt Pathol, Res Triangle Pk, NC 27709 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Genet, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. RP Korach, KS (reprint author), Natl Inst Environm Hlth Sci, Natl Inst Hlth, Receptor Biol Sect, Reprod & Dev Toxicol Lab, POB 12233,MD B3-02, Res Triangle Pk, NC 27709 USA. OI Korach, Kenneth/0000-0002-7765-418X NR 73 TC 111 Z9 117 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD OCT 15 PY 2001 VL 238 IS 2 BP 224 EP 238 DI 10.1006/dbio.2001.0413 PG 15 WC Developmental Biology SC Developmental Biology GA 486CU UT WOS:000171801500002 PM 11784006 ER PT J AU Brosh, RM von Kobbe, C Sommers, JA Karmakar, P Opresko, PL Piotrowski, J Dianova, I Dianov, GL Bohr, VA AF Brosh, RM von Kobbe, C Sommers, JA Karmakar, P Opresko, PL Piotrowski, J Dianova, I Dianov, GL Bohr, VA TI Werner syndrome protein interacts with human flap endonuclease 1 and stimulates its cleavage activity SO EMBO JOURNAL LA English DT Article DE flap endonuclease 1; genomic instability; helicase; replication; Wemer syndrome ID CELL NUCLEAR ANTIGEN; SYNDROME GENE-PRODUCT; DNA-POLYMERASE-DELTA; SINGLE-STRANDED-DNA; BASE EXCISION-REPAIR; SACCHAROMYCES-CEREVISIAE; FUNCTIONAL INTERACTION; REPLICATION FORK; SYNDROME FIBROBLASTS; HELICASE ACTIVITY AB Werner syndrome (WS) is a human premature aging disorder characterized by chromosomal instability. The cellular defects of WS presumably reflect compromised or aberrant function of a DNA metabolic pathway that under normal circumstances confers stability to the genome. We report a novel interaction of the WRN gene product with the human 5' flap endonuclease/5'-3' exonuclease (FEN-1), a DNA structure-specific nuclease implicated in DNA replication, recombination and repair. WS protein (WRN) dramatically stimulates the rate of FEN-1 cleavage of a 5' flap DNA substrate. The WRN-FEN-1 functional interaction is independent of WRN catalytic function and mediated by a 144 amino acid domain of WRN that shares homology with RecQ DNA helicases. A physical interaction between WRN and FEN-1 is demonstrated by their co-immunoprecipitation from HeLa cell lysate and affinity pull-down experiments using a recombinant C-terminal fragment of WRN. The underlying defect of WS is discussed in light of the evidence for the interaction between WRN and FEN-1. C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. MRC, Radiat & Genome Stabil Unit, Harwell OX11 0RD, Oxon, England. RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. OI Opresko, Patricia/0000-0002-6470-2189 NR 66 TC 193 Z9 197 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 15 PY 2001 VL 20 IS 20 BP 5791 EP 5801 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 485QP UT WOS:000171766300024 PM 11598021 ER PT J AU Stanulla, M Chhalliyil, P Wang, JJ Jani-Sait, SN Aplan, PD AF Stanulla, M Chhalliyil, P Wang, JJ Jani-Sait, SN Aplan, PD TI Mechanisms of MLL gene rearrangement: site-specific DNA cleavage within the breakpoint cluster region is independent of chromosomal context SO HUMAN MOLECULAR GENETICS LA English DT Article ID ACUTE MYELOID-LEUKEMIA; ORDER CHROMATIN FRAGMENTATION; SCAFFOLD ATTACHMENT REGIONS; EPSTEIN-BARR VIRUS; TOPOISOMERASE-II; 11Q23 TRANSLOCATIONS; DROSOPHILA-TRITHORAX; LOOP ANCHORAGE; ALL1 GENE; CELLS AB The MLL gene at chromosome band 11q23 is specifically cleaved at a unique site within its breakpoint cluster region (bcr) during the higher order chromatin fragmentation associated with apoptosis. We now show that the same specific DNA cleavage event can be detected in an exogenous MLL bcr fragment that is integrated into the genome outside of its normal chromosomal context, as well as in an extrachromosomal episome containing an MLL bcr fragment. We also show that episomal or randomly integrated copies of the MLL bcr behave similar to the endogenous MLL bcr when tested in a scaffold-associated region (SAR) assay. Furthermore, an episomal murine MLL bcr introduced into human cells is cleaved at the same site as the endogenous murine MLL bcr; this episomal murine MLL bcr also functions as a SAR in human cells. We conclude that both nuclear DNA scaffold attachment as well as site-specific DNA cleavage can be directed by sequences contained within the MLL bcr, and that it is feasible to study these events using episomal shuttle vectors. C1 NCI, Ctr Canc Res, Genet Branch, Gaithersburg, MD USA. Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY USA. Roswell Pk Canc Inst, Dept Clin Cytogenet, Buffalo, NY USA. Hannover Med Sch, Dept Pediat Hematol & Oncol, D-3000 Hannover, Germany. RP Aplan, PD (reprint author), NCI, Ctr Adv Technol, 8717 Grovemont Circle, Gaithersburg, MD 20877 USA. RI Stanulla, Martin/D-2528-2010; Aplan, Peter/K-9064-2016 FU NCI NIH HHS [CA73773] NR 44 TC 16 Z9 16 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD OCT 15 PY 2001 VL 10 IS 22 BP 2481 EP 2491 DI 10.1093/hmg/10.22.2481 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 497GD UT WOS:000172446300002 PM 11709535 ER PT J AU Broughton, BC Berneburg, M Fawcett, H Taylor, EM Arlett, CF Nardo, T Stefanini, M Menefee, E Price, VH Queille, S Sarasin, A Bohnert, E Krutmann, J Davidson, R Kraemer, KH Lehmann, AR AF Broughton, BC Berneburg, M Fawcett, H Taylor, EM Arlett, CF Nardo, T Stefanini, M Menefee, E Price, VH Queille, S Sarasin, A Bohnert, E Krutmann, J Davidson, R Kraemer, KH Lehmann, AR TI Two individuals with features of both xeroderma pigmentosum and trichothiodystrophy highlight the complexity of the clinical outcomes of mutations in the XPD gene SO HUMAN MOLECULAR GENETICS LA English DT Article ID DNA-REPAIR; COCKAYNE-SYNDROME; REPAIR/TRANSCRIPTION GENE; TRANSCRIPTION FACTOR; ITALIAN PATIENTS; FLOW-CYTOMETRY; POLYMORPHISMS; CANCER; DEFECT; ERCC2 AB The xeroderma pigmentosum group D (XPD) protein is a subunit of transcription factor TFIIH with DNA helicase activity. TFIIH has two functions, in basal transcription and nucleotide excision repair. Mutations in XPD that affect DNA repair but not transcription result in the skin cancer-prone disorder, xeroderma pigmentosum (XP). If transcription is also affected, the result is the multi-system disorder trichothiodystrophy (TTD), in which there is no skin cancer predisposition, or in rare cases, XP combined with Cockayne syndrome. Up till now there have been no reports of combined clinical features of XP and TTD. We have now identified two patients with some features of both these disorders. One of these, XP189MA, a 3-year-old girl with sun sensitivity, mental and physical developmental delay, has XPD mutations not previously reported, and barely detectable levels of nucleotide excision repair. The other, XP38BR, a 28-year-old woman with sun sensitivity, pigmentation changes and skin cancers typical of XP, has a mutation that has been identified previously, but only in TTD patients with no features of XP. The level of repair of UV damage in XP38BR is substantially higher than that in other patients with the same mutation. With both patients, polarized light microscopy revealed a 'tiger-tail' appearance of the hair, and amino acid analysis of the hairshafts show levels of sulfur-containing proteins intermediate between those of normal and TTD individuals. Our findings highlight the complexities of genotype-phenotype relationships in the XPD gene. C1 Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RR, E Sussex, England. Univ Dusseldorf, D-40225 Dusseldorf, Germany. CNR, Ist Genet Biochim & Evoluionist, I-27100 Pavia, Italy. Trichos Res, Richmond, CA 94805 USA. Mol Genet Lab, CNRS, UPR 2169, F-94801 Villejuif, France. Univ Heidelberg, Fac Klin Med Mannheim, D-68135 Mannheim, Germany. Yorkhill NHS Trust, Dept Med Genet, Glasgow G3 8SJ, Lanark, Scotland. NCI, Basic Res Lab, Bethesda, MD 20892 USA. RP Lehmann, AR (reprint author), Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RR, E Sussex, England. OI Taylor, Elaine M./0000-0003-3699-2999 FU Intramural NIH HHS [Z01 BC004517-31] NR 37 TC 64 Z9 65 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD OCT 15 PY 2001 VL 10 IS 22 BP 2539 EP 2547 DI 10.1093/hmg/10.22.2539 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 497GD UT WOS:000172446300008 PM 11709541 ER PT J AU McGlynn, KA Tsao, L Hsing, AW Devesa, SS Fraumeni, JF AF McGlynn, KA Tsao, L Hsing, AW Devesa, SS Fraumeni, JF TI International trends and patterns of primary liver cancer SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE hepatocellular carcinoma; hepatitis B; hepatitis C; aflatoxin B1 ID HEPATITIS-C VIRUS; REPUBLIC-OF-CHINA; HEPATOCELLULAR-CARCINOMA; UNITED-STATES; B VIRUS; HIGH PREVALENCE; HBV INFECTION; RISK FACTOR; FOLLOW-UP; ASSOCIATION AB Primary liver cancer (PLC) is common in many areas of the developing world, but uncommon in most of the developed world. Some evidence suggests, however, that the global pattern of PLC may be changing. To clarify this issue, we examined incidence rates for PLC over the 15-year time period, 1978-92, in selected cancer registries around the world. With some exceptions, developed countries have experienced PLC increases in incidence whereas developing countries have experienced declines. Although the reasons for the trends are not entirely clear, the increased seroprevalence of HCV in the developed world and the elimination of HBV-cofactors in the developing world are likely to have contributed to the patterns. Further progress against PLC may be seen in the developing world once the HBV-vaccinated segment of the population reaches adulthood. C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA. RP McGlynn, KA (reprint author), NCI, Div Canc Epidemiol & Genet, EPS-7060,6120 Execut Blvd, Rockville, MD 20852 USA. NR 85 TC 230 Z9 247 U1 1 U2 9 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 15 PY 2001 VL 94 IS 2 BP 290 EP 296 DI 10.1002/ijc.1456 PG 7 WC Oncology SC Oncology GA 473LT UT WOS:000171045900021 PM 11668511 ER PT J AU Landi, MT Baccarelli, A Calista, D Fears, TR Landi, G AF Landi, MT Baccarelli, A Calista, D Fears, TR Landi, G TI Glucocorticoid use and melanoma risk SO INTERNATIONAL JOURNAL OF CANCER LA English DT Letter ID SKIN; RECEPTORS; GROWTH; CELLS; DEXAMETHASONE; INHIBITION; CYCLE C1 NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Univ Milan, EPOCA, Epidemiol Res Ctr, Milan, Italy. Bufalini Hosp, Dermatol Unit, Cesena, Italy. NCI, Biostat Branch, Bethesda, MD 20892 USA. RP Landi, MT (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 7114, Bethesda, MD 20892 USA. FU PHS HHS [65558-01A2] NR 19 TC 4 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 15 PY 2001 VL 94 IS 2 BP 302 EP 303 DI 10.1002/ijc.1468 PG 2 WC Oncology SC Oncology GA 473LT UT WOS:000171045900023 PM 11668513 ER PT J AU Misteli, T AF Misteli, T TI The concept of self-organization in cellular architecture SO JOURNAL OF CELL BIOLOGY LA English DT Review DE self-organization; cytoskeleton; nucleus; Golgi complex; dynamics ID SACCHAROMYCES-CEREVISIAE; GOLGI-APPARATUS; COILED BODIES; NUCLEOLUS; RNA; TRANSCRIPTION; DIVISION; NUCLEUS; DOMAIN AB In vivo microscopy has recently revealed the dynamic nature of many cellular organelles. The dynamic properties of several cellular structures are consistent with a role for self-organization in their formation, maintenance, and function; therefore, self-organization might be a general principle in cellular organization. C1 NCI, NIH, Bethesda, MD 20892 USA. RP Misteli, T (reprint author), NCI, NIH, 41 Liberty Dr,Bldg 41-B, Bethesda, MD 20892 USA. NR 33 TC 308 Z9 315 U1 1 U2 17 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT 15 PY 2001 VL 155 IS 2 BP 181 EP 185 DI 10.1083/jcb.200108110 PG 5 WC Cell Biology SC Cell Biology GA 483TH UT WOS:000171651600001 PM 11604416 ER PT J AU Wu, XF Zhao, XH Baylor, L Kaushal, S Eisenberg, E Greene, LE AF Wu, XF Zhao, XH Baylor, L Kaushal, S Eisenberg, E Greene, LE TI Clathrin exchange during clathrin-mediated endocytosis SO JOURNAL OF CELL BIOLOGY LA English DT Article DE clathrin; exchange; FRAP; endocytosis; Hsc70 ID COATED VESICLE FORMATION; CONFORMATIONAL-CHANGES; PIT FORMATION; DYNAMIN; RECEPTOR; PROTEIN; CELLS; CHOLESTEROL; AUXILIN; BINDING AB During clathrin-mediated endocytosis, clathrin-coated pits invaginate to form clathrin-coated vesicles (CVs). Since clathrin-coated pits are planar structures, whereas CVs are spherical, there must be a structural rearrangement of clathrin as invagination occurs. This could occur through simple addition of clathrin triskelions to the edges of growing clathrin-coated pits with very little exchange occurring between clathrin in the pits and free clathrin in the cytosol, or it could occur through large scale exchange of free and bound clathrin. In the present study, we investigated this question by studying clathrin exchange both in vitro and in vivo. We found that in vitro clathrin in CVs and clathrin baskets do not exchange with free clathrin even in the presence of Hsc70 and ATP where partial uncoating occurs. However, surprisingly FRAP studies on clathrin-coated pits labeled with green fluorescent protein-clathrin light chains in HeLa cells show that even when endocytosis is blocked by expression of a dynamin mutant or depletion of cholesterol from the membrane, replacement of photobleached clathrin in coated pits on the membrane occurs at almost the same rate and magnitude as when endocytosis is-occurring. Furthermore, very little of this replacement is due to dissolution of old pits and reformation of new ones; rather, it is caused by a rapid ATP-dependent exchange of clathrin in the pits with free clathrin in the cytosol. On the other hand, consistent with the in vitro data both potassium depletion and hypertonic sucrose, which have been reported to transform clathrin-coated pits into clathrin cages just below the surface of the plasma membrane, not only block endocytosis but also block exchange of clathrin. Taken together, these data show that ATP-dependent exchange of free and bound clathrin is a fundamental property of clathrin-coated pits, but not clathrin baskets, and may be involved in a structural rearrangement of clathrin as clathrin-coated pits invaginate. C1 NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Greene, LE (reprint author), NHLBI, Cell Biol Lab, NIH, 50 South Dr,Rm 2537 MSC 8017, Bethesda, MD 20892 USA. NR 33 TC 125 Z9 126 U1 2 U2 13 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT 15 PY 2001 VL 155 IS 2 BP 291 EP 300 DI 10.1083/jcb.200104085 PG 10 WC Cell Biology SC Cell Biology GA 483TH UT WOS:000171651600013 PM 11604424 ER EF