FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Wei, GP Loktionova, NA Pegg, AE Moschel, RC AF Wei, GP Loktionova, NA Pegg, AE Moschel, RC TI beta-glucuronidase-cleavable prodrugs of O-6-benzylguanine and O-6-benzyl-2 '-deoxyguanosine SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HUMAN O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; CARMUSTINE PLUS O-6-BENZYLGUANINE; PROGRESSIVE MALIGNANT GLIOMA; BRAIN-TUMOR XENOGRAFTS; PHASE-I TRIAL; SELECTIVE CHEMOTHERAPY; ANTICANCER PRODRUGS; THERAPY ADEPT; DERIVATIVES; CANCER AB Glucuronic acid linked prodrugs of O-6-benzylguanine and O-6-benzyl-2'-deoxyguanosine were synthesized. The prodrugs were found to be quite stable at physiological pH and were more than 200-fold less active as inactivators of O-6-alkylguanine-DNA alkyltransferase (alkyltransferase) than either O-6-benzylguanine or O-6-benzyl-2'-deoxyguanosine. beta-Glucuronidase from both Escherichia coli and bovine liver cleaved the prodrugs efficiently to release O-6-benzylguanine and O-6-benzyl-2'-deoxyguanosine, respectively. In combination with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the prodrugs were not effective adjuvants for HT29 cell killing. However, as expected, incubation of these prodrugs with beta-glucuronidase in the culture medium led to much more efficient cell killing by BCNU as a result of the liberation of the more potent inactivators, O-6-benzylguanine and O-6-benzyl-2'-deoxyguanosine. These prodrugs may be useful for prodrug monotherapy of necrotic tumors that liberate beta-glucuronidase or for antibody-directed enzyme prodrug therapy with antibodies that can deliver beta-glucuronidase to target tumor cells. C1 Natl Canc Inst, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA. Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA. Penn State Univ, Coll Med, Dept Pharmacol, Hershey, PA 17033 USA. RP Moschel, RC (reprint author), Natl Canc Inst, Comparat Carcinogenesis Lab, POB B,Bldg 538, Frederick, MD 21702 USA. EM moschel@mail.ncifcrf.gov NR 33 TC 23 Z9 23 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JAN 13 PY 2005 VL 48 IS 1 BP 256 EP 261 DI 10.1021/jm0493865 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 886FS UT WOS:000226212900025 PM 15634019 ER PT J AU Mertz, EL AF Mertz, EL TI Anomalous microscopic dielectric response of dipolar solvents and water SO JOURNAL OF PHYSICAL CHEMISTRY A LA English DT Review ID MOLECULAR-DYNAMICS SIMULATION; NONEQUILIBRIUM POLARIZATION SYSTEMS; ACCURATE EXCITATION-ENERGIES; ELECTRON-TRANSFER PROCESSES; ORDER MULTIPOLAR CHARACTER; DENSITY-FUNCTIONAL THEORY; CHARGE-TRANSFER REACTIONS; POLAR SOLVATION DYNAMICS; SELF-CONSISTENT-FIELD; REORGANIZATION ENERGY AB This paper reports measurements of static microscopic dielectric response of several dipolar solvents to charge redistribution in a fluorescent probe. Contrary to recent predictions of dielectric theories and computer simulations of bulk liquids, the observed dielectric response of most solvents conforms to the macroscopic continuum description even at atomic distances, as if these solvents had no spatial intermolecular structure. Such conformance is observed for several probes when the contribution of specific probe-solvent interactions to the response is negligible. However, water, formamide, and glycerol exhibit anomalous responses even though such a probe is used. We discuss a possible reason for the macroscopic-like behavior and a connection between the anomaly and fluctuating structures formed by anomalous solvents near the hydrophobic surface of the probe. C1 NICHHD, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Mertz, EL (reprint author), NICHHD, NIH, Dept Hlth & Human Serv, Bldg 9,Rm 1E125, Bethesda, MD 20892 USA. EM mertze@mail.nih.gov NR 120 TC 11 Z9 11 U1 0 U2 7 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 JAN 13 PY 2005 VL 109 IS 1 BP 44 EP 56 DI 10.1021/jp047091x PG 13 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 886FT UT WOS:000226213000007 PM 16839088 ER PT J AU Teramoto, H Castellone, MD Malek, RL Letwin, N Frank, B Gutkind, JS Lee, NH AF Teramoto, H Castellone, MD Malek, RL Letwin, N Frank, B Gutkind, JS Lee, NH TI Autocrine activation of an osteopontin-CD44-Rac pathway enhances invasion and transformation by H-RasV12 SO ONCOGENE LA English DT Article DE Ras; NIH3T3; RNAi; siRNA; microarray; osteopontin ID DOWNSTREAM-REGULATED GENE-2; TUMOR-CELL-MIGRATION; HOMING RECEPTOR CD44; FAMILY SMALL GTPASES; NIH3T3 CELLS; COLON-CANCER; RAS; EXPRESSION; BINDING; IDENTIFICATION AB Activated forms of Ras family members are prevalent in many cancers where Ras mutants transduce signals essential for transformation, angiogenesis, invasion and metastasis. As a cancer progression model, we used NIH3T3 cells to explore the mechanism of Ras-induced tumorigenesis. Ras family mutants H-RasV12 and Rit79L strongly induced foci formation, while Rho family mutants RhoA-QL, Rac1-QL and Cdc42-QL were less effective. A comparison of downstream transcriptional targets of Ras and Rho family members using a 26 383 element cDNA microarray revealed that the osteopontin (OPN) gene exhibited the best correlation between magnitude of gene expression change and level of foci formation (r=0.96, P<0.001). In association with H-RasV12- and Rit79L-mediated transformation, foci secreted OPN protein and upregulated the OPN receptor CD44, suggesting the novel initiation of an aberrant OPN-CD44-Rac autocrine pathway. In support of this were the following observations. First, RGD-deficient OPN protein-binding activity was present in H-RasV12- transformed cells but not in control cells, and binding activity was inhibited by the CD44 blocking antibody. Second, foci formation, cell invasion and Rac activity were induced by H-RasV12 and inhibited by the CD44 blocking antibody. Third, foci formation by H-RasV12 was substantially reduced by a short interfering RNA ( siRNA) specifically targeting OPN expression for knockdown. Fourth, H-RasV12- mediated transformation was not blocked by the GRGDS peptide, suggesting that OPN effects were not mediated by the integrins. Lastly, OPN knockdown affected the downstream expression of 160 '2nd tier' genes, and at least a subset of these genes appears to be involved in transformation. Indeed, four genes were selected for knockdown, each resulting in a disruption of foci formation and/or invasion. These results underscore the role of aberrant autocrine signaling and transcriptional networking during tumorigenesis. C1 Inst Genom Res, Dept Funct Genom, Rockville, MD 20850 USA. NIDR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. George Washington Univ, Med Ctr, Dept Pharmacol, Washington, DC 20037 USA. RP Gutkind, JS (reprint author), Inst Genom Res, Dept Funct Genom, 9712 Med Ctr Dr, Rockville, MD 20850 USA. EM sg39v@nih.gov; nhlee@tigr.org RI Gutkind, J. Silvio/A-1053-2009; OI CASTELLONE, MARIADOMENICA/0000-0003-0507-8037 NR 55 TC 56 Z9 60 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 EI 1476-5594 J9 ONCOGENE JI Oncogene PD JAN 13 PY 2005 VL 24 IS 3 BP 489 EP 501 DI 10.1038/sj.onc.1208209 PG 13 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 887CH UT WOS:000226279700019 PM 15516973 ER PT J AU Saxinger, C Conrads, TP Goldstein, DJ Veenstra, TD AF Saxinger, C Conrads, TP Goldstein, DJ Veenstra, TD TI Fully automated synthesis of (phospho) peptide arrays in microtiter plate wells provides efficient access to protein tyrosine kinase characterization SO BMC IMMUNOLOGY LA English DT Article ID GROWTH-FACTOR RECEPTOR; ALTERED AUTOPHOSPHORYLATION SITES; EGF-RECEPTOR; BINDING-SITES; SUBSTRATE-SPECIFICITY; C-SRC; PHOSPHORYLATION; ENDOCYTOSIS; IDENTIFICATION; MUTANTS AB Background: Synthetic peptides have played a useful role in studies of protein kinase substrates and interaction domains. Synthetic peptide arrays and libraries, in particular, have accelerated the process. Several factors have hindered or limited the applicability of various techniques, such as the need for deconvolution of combinatorial libraries, the inability or impracticality of achieving full automation using two-dimensional or pin solid phases, the lack of convenient interfacing with standard analytical platforms, or the difficulty of compartmentalization of a planar surface when contact between assay components needs to be avoided. This paper describes a process for synthesis of peptides and phosphopeptides on microtiter plate wells that overcomes previous limitations and demonstrates utility in determination of the epitope of an autophosphorylation site phospho-motif antibody and utility in substrate utilization assays of the protein tyrosine kinase, p60(c-src). Results: The overall reproducibility of phospho-peptide synthesis and multiplexed EGF receptor (EGFR) autophosphorylation site (pY1173) antibody ELISA (9H2) was within 5.5 to 8.0%. Mass spectrometric analyses of the released (phospho) peptides showed homogeneous peaks of the expected molecular weights. An overlapping peptide array of the complete EGFR cytoplasmic sequence revealed a high redundancy of 9H2 reactive sites. The eight reactive phospopeptides were structurally related and interestingly, the most conserved antibody reactive peptide motif coincided with a subset of other known EGFR autophosphorylation and SH2 binding motifs and an EGFR optimal substrate motif. Finally, peptides based on known substrate specificities of c-src and related enzymes were synthesized in microtiter plate array format and were phosphorylated by c-Src with the predicted specificities. The level of phosphorylation was proportional to c-Src concentration with sensitivities below 0.1 Units of enzyme. Conclusions: The ability of this method to interface with various robotics and instrumentation is highly flexible since the microtiter plate is an industry standard. It is highly scalable by increasing the surface area within the well or the number of wells and does not require specialized robotics. The microtiter plate array system is well suited to the study of protein kinase substrates, antigens, binding molecules, and inhibitors since these all can be quantitatively studied at a single uniform, reproducible interface. C1 NCI, Ctr Canc Res, Ft Detrick, MD 21702 USA. SAIC Frederick Inc, Lab Proteom & Analyt Technol, Bethesda, MD 21702 USA. NCI, Ctr Canc Res, Bethesda, MD 20892 USA. RP Saxinger, C (reprint author), NCI, Ctr Canc Res, Bldg 1052, Ft Detrick, MD 21702 USA. EM csax@helix.nih.gov; conrads@ncifcrf.gov; goldsted@ncifcrf.gov; veenstra@ncifcrf.gov NR 41 TC 0 Z9 0 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2172 J9 BMC IMMUNOL JI BMC Immunol. PD JAN 12 PY 2005 VL 6 DI 10.1186/1471-2172-6-1 PG 15 WC Immunology SC Immunology GA 016XK UT WOS:000235657000001 ER PT J AU Catalano, A Rodilossi, S Caprari, P Coppola, V Procopio, A AF Catalano, A Rodilossi, S Caprari, P Coppola, V Procopio, A TI 5-Lipoxygenase regulates senescence-like growth arrest by promoting ROS-dependent p53 activation SO EMBO JOURNAL LA English DT Article DE 5-lipoxygenase; oncogenic ras; p53; reactive oxygen species; senescence ID INDUCED PREMATURE SENESCENCE; NORMAL HUMAN FIBROBLASTS; ARACHIDONIC-ACID; ONCOGENIC RAS; INDUCED APOPTOSIS; LUNG FIBROBLASTS; CELL SENESCENCE; TELOMERASE; EXPRESSION; CANCER AB 5- Lipoxygenase ( 5LO) is involved in the production of leukotrienes and reactive oxygen species ( ROS) from arachidonic acid. Its strong activation has been associated with several diseases like cancer and neurodegeneration. Here we show that 5LO activity increases during senescence-like growth arrest induced by oncogenic ras or culture history in both human and mouse embryo fibroblasts. Overexpression of 5LO promotes senescence- like growth arrest via a p53/ p21- dependent pathway, and this occurs independently of telomerase activity. 5LO stabilizes p53 through phosphorylation at Ser15 and increases expression of the p53- transcriptional target p21. This is achieved by regulating ROS production. Indeed, ROS are increased in 5LO- arrested cells. Antioxidants and a low oxygen environment prevent 5LO- induced growth arrest. Finally, 5LO inhibition reduces the growth arrest induced by oncogenic ras or culture history and these effects are neutralized by the addition of exogenous ROS. These data link the 5LO pathway to oxidative crises of primary fibroblast and suggest that the ability of 5LO to induce senescence- like growth arrest may be important in the pathogenesis of 5LO- associated disorders. C1 Univ Politecn Marche, Dipartimento Patol Mol & Terapie Innovat, I-60131 Ancona, Italy. Italian Natl Res Ctr Aging, Lab Cytol, Ancona, Italy. NCI, Neural Dev Grp, Mouse Canc Genet Program, Frederick, MD 21701 USA. RP Catalano, A (reprint author), Univ Politecn Marche, Dipartimento Patol Mol & Terapie Innovat, Via Ranieri, I-60131 Ancona, Italy. EM catgfp@yahoo.it RI Coppola, Vincenzo/E-2917-2011 OI Coppola, Vincenzo/0000-0001-6163-1779 NR 41 TC 65 Z9 67 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0261-4189 J9 EMBO J JI Embo J. PD JAN 12 PY 2005 VL 24 IS 1 BP 170 EP 179 DI 10.1038/sj.emboj.7600502 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 895AC UT WOS:000226832000017 PM 15616590 ER PT J AU Zheng, YL Kesavapany, S Gravell, M Hamilton, RS Schubert, M Amin, N Albers, W Grant, P Pant, HC AF Zheng, YL Kesavapany, S Gravell, M Hamilton, RS Schubert, M Amin, N Albers, W Grant, P Pant, HC TI A Cdk5 inhibitory peptide reduces tau hyperphosphorylation and apoptosis in neurons SO EMBO JOURNAL LA English DT Article DE Alzheimer's disease; Cdk5 inhibitory peptide ( CIP); hyperphosphorylation; p25; tau ID CYCLIN-DEPENDENT KINASE-5; ALZHEIMERS-DISEASE BRAIN; ACTIVATOR P35; NEUROFIBRILLARY TANGLES; IN-VIVO; P25; PHOSPHORYLATION; NEURODEGENERATION; PROTEIN; CLEAVAGE AB The extracellular aggregation of amyloid beta (Abeta) peptides and the intracellular hyperphosphorylation of tau at specific epitopes are pathological hallmarks of neurodegenerative diseases such as Alzheimer's disease ( AD). Cdk5 phosphorylates tau at AD- specific phospho- epitopes when it associates with p25. p25 is a truncated activator, which is produced from the physiological Cdk5 activator p35 upon exposure to Abeta peptides. We show that neuronal infections with Cdk5 inhibitory peptide ( CIP) selectively inhibit p25/ Cdk5 activity and suppress the aberrant tau phosphorylation in cortical neurons. Furthermore, Abeta(1-42)- induced apoptosis of these cortical neurons was also reduced by coinfection with CIP. Of particular importance is our finding that CIP did not inhibit endogenous or transfected p35/ Cdk5 activity, nor did it inhibit the other cyclin- dependent kinases such as Cdc2, Cdk2, Cdk4 and Cdk6. These results, therefore, provide a strategy to address, and possibly ameliorate, the pathology of neurodegenerative diseases that may be a consequence of aberrant p25 activation of Cdk5, without affecting ' normal' Cdk5 activity. C1 NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. NINDS, Lab Mol Virol & Neurogenet, NIH, Bethesda, MD 20892 USA. RP Pant, HC (reprint author), NINDS, Neurochem Lab, NIH, Bldg 36,Room 4D04,36 Convent Dr, Bethesda, MD 20892 USA. EM panth@ninds.nih.gov NR 46 TC 103 Z9 118 U1 3 U2 6 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0261-4189 J9 EMBO J JI Embo J. PD JAN 12 PY 2005 VL 24 IS 1 BP 209 EP 220 DI 10.1038/sj.emboj.7600441 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 895AC UT WOS:000226832000021 PM 15592431 ER PT J AU Chao, A Thun, MJ Connell, CJ McCullough, ML Jacobs, EJ Flanders, WD Rodriguez, C Sinha, R Calle, EE AF Chao, A Thun, MJ Connell, CJ McCullough, ML Jacobs, EJ Flanders, WD Rodriguez, C Sinha, R Calle, EE TI Meat consumption and risk of colorectal cancer SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID II NUTRITION COHORT; COLO-RECTAL CANCER; LARGE-BOWEL-CANCER; HETEROCYCLIC AMINES; UNITED-STATES; RED MEAT; FOOD GROUPS; N-NITROSATION; GASTROINTESTINAL CANCERS; GENETIC SUSCEPTIBILITY AB Context Consumption of red and processed meat has been associated with colorectal cancer in many but not all epidemiological studies; few studies have examined risk in relation to long-term meat intake or the association of meat with rectal cancer. Objective To examine the relationship between recent and long-term meat consumption and the risk of incident colon and rectal cancer. Design, Setting, and Participants A cohort of 148610 adults aged 50 to 74 years (median, 63 years), residing in 21 states with population-based cancer registries, who provided information on meat consumption in 1982 and again in 1992/1993 when enrolled in the Cancer Prevention Study II (CPS II) Nutrition Cohort. Follow-up from time of enrollment in 1992/1993 through August 31, 2001, identified 1667 incident colorectal cancers. Participants contributed person-years at risk until death or a diagnosis of colon or rectal cancer. Main Outcome Measure Incidence rate ratio (RR) of colon and rectal cancer. Results High intake of red and processed meat reported in 1992/1993 was associated with higher risk of colon cancer after adjusting for age and energy intake but not after further adjustment for body mass index, cigarette smoking, and other covariates. When long-term consumption was considered, persons in the highest tertile of consumption in both 1982 and 1992/1993 had higher risk of distal colon cancer associated with processed meat (RR, 1.50; 95% confidence interval [CI], 1.04-2.17), and ratio of red meat to poultry and fish (RR, 1.53; 95% Cl, 1.08-2.18) relative to those persons in the lowest tertile at both time points. Long-term consumption of poultry and fish was inversely associated with risk of both proximal and distal colon cancer. High consumption of red meat reported in 1992/1993 was associated with higher risk of rectal cancer (RR, 1.71; 95% Cl, 1.15-2.52; P=.007 for trend), as was high consumption reported in both 1982 and 1992/1993 (RR, 1.43; 95% Cl, 1.00-2.05). Conclusions Our results demonstrate the potential value of examining long-term meat consumption in assessing cancer risk and strengthen the evidence that prolonged high consumption of red and processed meat may increase the risk of cancer in the distal portion of the large intestine. C1 Amer Canc Soc, Atlanta, GA 30329 USA. Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA. NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. RP Thun, MJ (reprint author), Amer Canc Soc, 1599 Clifton Rd NE, Atlanta, GA 30329 USA. EM mthun@cancer.org RI Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 FU NCI NIH HHS [K07CA75062] NR 83 TC 273 Z9 290 U1 5 U2 56 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 JAN 12 PY 2005 VL 293 IS 2 BP 172 EP 182 DI 10.1001/jama.293.2.172 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 885QC UT WOS:000226171000033 PM 15644544 ER PT J AU Morcombe, CR Gaponenko, V Byrd, RA Zilm, KW AF Morcombe, CR Gaponenko, V Byrd, RA Zilm, KW TI C-13 CPMAS spectroscopy of deuterated proteins: CP dynamics, line shapes, and T-1 relaxation SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID SOLID-STATE NMR; NUCLEAR-MAGNETIC-RESONANCE; SPECTRIN SH3 DOMAIN; ANGLE-SPINNING NMR; ROTATING SOLIDS; MICROCRYSTALLINE UBIQUITIN; MULTIDIMENSIONAL NMR; ASSIGNMENTS; N-15; BACKBONE AB C-13 CPMAS NMR has been investigated in application to protein samples with a variety of deuteration patterns. Samples were prepared with protons in either all hydrogen positions, only in the exchangeable sites, or in the exchangeable sites plus select methyl groups. CP dynamics, T-1 relaxation times, and C-13 line widths have been compared. Using ubiquitin as a model system, reasonable H-1-C-13 CP transfer is observed for the extensively deuterated samples. In the absence of deuterium decoupling, the C-13 line widths observed for the deuterated samples are identical to those observed for the perprotio samples with a MAS rate of 20 kHz. Extensive deuteration has little effect on the T-1 of the exchangeable protons. On the basis of these observations, it is clear that there are no substantive compromises accompanying the use of extensive deuteration in the design of H-1, N-15, or C-13 solid-state NMR methods. C1 Yale Univ, Dept Chem, New Haven, CT 06520 USA. NCI, Struct Biophys Lab, Frederick, MD 21702 USA. RP Zilm, KW (reprint author), Yale Univ, Dept Chem, POB 208107, New Haven, CT 06520 USA. EM kurt.zilm@yale.edu RI Byrd, R. Andrew/F-8042-2015 OI Byrd, R. Andrew/0000-0003-3625-4232 NR 26 TC 29 Z9 29 U1 0 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD JAN 12 PY 2005 VL 127 IS 1 BP 397 EP 404 DI 10.1021/ja045581x PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA 886PN UT WOS:000226240900071 PM 15631490 ER PT J AU Pierce, MM Baxa, U Steven, AC Bax, A Wickner, RB AF Pierce, MM Baxa, U Steven, AC Bax, A Wickner, RB TI Is the prion domain of soluble Ure2p unstructured? SO BIOCHEMISTRY LA English DT Article ID FUNGUS PODOSPORA-ANSERINA; YEAST SUP35 PROTEIN; SACCHAROMYCES-CEREVISIAE; IN-VITRO; NUCLEAR-LOCALIZATION; 2-HYBRID SYSTEM; TOR PROTEINS; PROPAGATION; DETERMINANT; INCOMPATIBILITY AB The [URE3] prion is a self-propagating amyloid form of the Ure2 protein of Saccharomyces cerevisiae. Deletions in the C-terminal nitrogen regulation domain of Ure2p increase the frequency with which the N-terminal prion domain polymerizes into the prion form, suggesting that the C-terminus stabilizes the prion domain or that the structured C-terminal region sterically impairs amyloid formation. We find by in vivo two-hybrid analysis no evidence of interaction of prion domain and C-terminal domain. Furthermore, surface plasmon resonance spectrometry shows no evidence of interaction of prion domain and C-terminal domain, and cleavage at a specific site between the domains frees the two fragments. Our NMR analysis indicates that most residues of the prion domain are in fact disordered in the soluble form of Ure2p. Deleting the tether holding the C-terminal structured region to the amyloid core does not impair prion formation, arguing against steric impairment of amyloid formation. These results suggest that the N-terminal prion domain is unstructured in the soluble protein and does not have a specific interaction with the C-terminus. C1 NIDDKD, Lab Biochem & Genet, Struct Biol Lab, NIAMSD,NIH, Bethesda, MD 20892 USA. NIDDKD, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. RP Wickner, RB (reprint author), NIDDKD, Lab Biochem & Genet, Struct Biol Lab, NIAMSD,NIH, Bethesda, MD 20892 USA. EM wickner@helix.nih.gov NR 45 TC 40 Z9 43 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JAN 11 PY 2005 VL 44 IS 1 BP 321 EP 328 DI 10.1021/bi047964d PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 886GJ UT WOS:000226214600036 PM 15628874 ER PT J AU Gould, TD Manji, HK AF Gould, TD Manji, HK TI DARPP-32: A molecular switch at the nexus of reward pathway plasticity SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Editorial Material ID SYNAPTIC PLASTICITY; DOPAMINE; ADDICTION; PHOSPHORYLATION; NEUROBIOLOGY; ACTIVATION; STRIATUM; RECEPTOR; MEMORY; BRAIN C1 NIMH, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA. RP Gould, TD (reprint author), NIMH, Mol Pathophysiol Lab, NIH, Bldg 35,Room 1C-912, Bethesda, MD 20892 USA. NR 17 TC 25 Z9 26 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 JAN 11 PY 2005 VL 102 IS 2 BP 253 EP 254 DI 10.1073/pnas.0408700102 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 887OP UT WOS:000226315700001 PM 15632217 ER PT J AU Kawahara, A Che, YS Hanaoka, R Takeda, H Dawid, IB AF Kawahara, A Che, YS Hanaoka, R Takeda, H Dawid, IB TI Zebrafish GADD45 beta genes are involved in somite segmentation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE presomitic mesoderm; periodicity; patterning; knockdown ID BOUNDARY FORMATION; WAVE-FRONT; NO TAIL; SOMITOGENESIS; OSCILLATOR; EXPRESSION; ACTIVATION; PATHWAY; KINASE; HER1 AB Somites in vertebrates are periodic segmented structures that give rise to the vertebrae and muscles of body. Somites are generated from presomitic mesoderm (PSM), but it is not fully understood how cellular differentiation and segment formation are achieved in the anterior PSM. We report here that zebrafish gadd45beta1 and gadd45beta2 genes are periodically expressed as paired stripes adjacent to the neural tube in the anterior PSM region where presomitic cells mature. In mammals, it is known that GADD45 (growth arrest and DNA damage) family proteins play a role in cell-cycle control. We found that both knockdown and overexpression of gadd45beta genes caused somite defects with different consequences for marker gene expression. Knockdown of gadd45beta genes with antisense morpholino oligonucleotides caused a broad expansion of mesp-a in the PSM, and both cyclic expression of her1 and segmented expression of MyoD were disorganized. On the other hand, injection of gadd45beta1 or gadd45beta2 suppressed expression of mesp-a and her1 in anterior PSM and MyoD in paraxial mesoderm. These results indicate that regulated expression of gadd45beta genes in the anterior PSM is required for somite segmentation. C1 Kyoto Univ, Fac Med, Horizontal Med Res Org, Lab Dev Mol Genet,Sakyo Ku, Kyoto 6068501, Japan. Univ Tokyo, Grad Sch Sci, Dept Biol Sci, Bunkyo Ku, Tokyo 1130033, Japan. NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. RP Kawahara, A (reprint author), Kyoto Univ, Fac Med, Horizontal Med Res Org, Lab Dev Mol Genet,Sakyo Ku, Kyoto 6068501, Japan. EM atsuo@hmro.med.kyoto-u.ac.jp; idawid@nih.gov NR 31 TC 17 Z9 18 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 11 PY 2005 VL 102 IS 2 BP 361 EP 366 DI 10.1073/pnas.0408726102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 887OP UT WOS:000226315700020 PM 15623554 ER PT J AU Cai, Q Dmitrieva, NI Ferraris, JD Brooks, HL van Balkolm, BWM Burg, M AF Cai, Q Dmitrieva, NI Ferraris, JD Brooks, HL van Balkolm, BWM Burg, M TI Pax2 expression occurs in renal medullary epithelial cells in vivo and in cell culture, is osmoregulated, and promotes osmotic tolerance SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE apoptosis; osmotic stress; renal inner medulla ID TRANSCRIPTION ACTIVATION; COLOBOMA SYNDROME; COLLECTING DUCT; PROTEIN; HYPEROSMOLALITY; APOPTOSIS; KIDNEY; GENES; NACL; VASOPRESSIN AB Pax2 is a transcription factor that is crucial for kidney development, and it is also expressed in the normal adult kidney, where its physiological function is unknown. In the present study, we find by cDNA microarray analysis that Pax2 expression in second-passage mouse inner-medullary epithelial cells is increased by a high NaCl concentration, which is significant because NaCl levels are normally high in the inner medulla in vivo, and varies with urinary concentration. Furthermore, a high NaCl concentration increases Pax2 mRNA and protein expression in mouse inner medullary collecting duct (mIMCD3) cells, and its transcriptional activity. Pax2 mRNA and protein expression is high in normal adult mouse renal inner medulla but much lower in renal cortex. Pax2 protein is present in collecting duct cells in both renal medulla and cortex and in thin descending limbs of Henle's loop in inner medulla. Treating Brattleboro rats with desamino-Cys-1,D-Arg-8 vasopressin, which increases inner-medullary NaCl concentration, causes a 4-fold increase in inner-medullary Pax2 protein. Treatment with furosemide, which decreases inner-medullary NaCl, reduces inner-medullary Pax2 mRNA and protein. Pax2-specific short interfering RNA increases high NaCl concentration-induced activation of caspase-3 and apoptotic bodies in mIMCD3 cells. We thus conclude that (i) Pax2 is expressed in normal renal medulla, (ii) its expression is regulated there by the normally high and variable NaCl concentration, and (iii) it protects renal medullary cells from high NaCl concentration-induced apoptosis. C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Univ Arizona, Coll Med, Dept Physiol, Tucson, AZ 85724 USA. Univ Utrecht, Inst Vet Sci, Dept Biomol Mass Spectrometry, NL-3584 CA Utrecht, Netherlands. RP Burg, M (reprint author), Bldg 10,6N250,10 Ctr Dr, Bethesda, MD 20819 USA. EM maurice.burg@nih.gov RI Dmitrieva, Natalia/A-2924-2013 OI Dmitrieva, Natalia/0000-0001-8074-6950 NR 35 TC 39 Z9 40 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 11 PY 2005 VL 102 IS 2 BP 503 EP 508 DI 10.1073/pnas.0408840102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 887OP UT WOS:000226315700044 PM 15623552 ER PT J AU Jeang, KT AF Jeang, KT TI Progress, challenges, and responsibilities in retrovirology SO RETROVIROLOGY LA English DT Editorial Material AB In this editorial, Retrovirology's choice for best basic science "retrovirus paper of the year" and a perspective on challenges and responsibilities facing HIV-I and HTLV-I research are presented. C1 NIH, Bethesda, MD 20892 USA. RP Jeang, KT (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. EM kj7e@nih.gov RI Jeang, Kuan-Teh/A-2424-2008 NR 5 TC 1 Z9 1 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1742-4690 J9 RETROVIROLOGY JI Retrovirology PD JAN 11 PY 2005 VL 2 AR 1 DI 10.1186/1742-4690-2-1 PG 2 WC Virology SC Virology GA 031WE UT WOS:000236734700001 PM 15644139 ER PT J AU Brawley, OW Kramer, BS AF Brawley, OW Kramer, BS TI Cancer screening in theory and in practice SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID SERVICES-TASK-FORCE; COLORECTAL-CANCER; PROSTATE-CANCER; BREAST-CANCER; LUNG-CANCER; VIRTUAL COLONOSCOPY; OVARIAN-CANCER; FOLLOW-UP; CERVICAL NEOPLASIA; SERUM CA-125 AB Improvements in technology have led to a number of tests that can be used to suggest that a patient has a cancer. Advances in cancer biology and medical imaging have led to a number of cancer screening tests. Cancer screening is commonly advocated, but its complexity is often lost in guidelines that have sound-bite quality. It is commonly viewed as of no harm. when in fact there are harms associated with every known screening test. Indeed, many screening experts believe a screening test should only be used when the potential for benefit clearly outweighs the potential for harm. Cancer screening principles are classically within the realm of the epidemiologist. As more screening tests are developed, these principles have become more relevent to the pacticing clinician. What is known and what is unknown about screening is distincilly distinctly from what is believed by the public and many practicing clinicians. Many tests have both screening and diagnostic uses, and it is only the context in which these are used that determines whether they are screening or diagnostic. A screening test is done on asymptomatic individuals who receive the test principally because they are oil the age or sex at risk for the cancer. A diagnostic test is done on an individual because of clinical suspicion of disease. C1 Emory Univ, Winship Canc Inst, Atlanta, GA USA. NIH, Bethesda, MD 20892 USA. RP Brawley, OW (reprint author), Georgia Canc Ctr, 69 Jesse Hill Jr Dr,Glenn Mem Bldg, Atlanta, GA 30303 USA. EM otis_brawley@emoryhealthcare.org NR 47 TC 48 Z9 50 U1 1 U2 1 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN 10 PY 2005 VL 23 IS 2 BP 293 EP 300 DI 10.1200/JCO.2005.06.107 PG 8 WC Oncology SC Oncology GA 887XG UT WOS:000226338200005 PM 15637392 ER PT J AU Taylor, PR Greenwald, P AF Taylor, PR Greenwald, P TI Nutritional interventions in cancer prevention SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID VITAMIN MINERAL SUPPLEMENTATION; BETA-CAROTENE SUPPLEMENTATION; DISEASE-SPECIFIC MORTALITY; BASE-LINE CHARACTERISTICS; CONTROLLED-TRIAL FINLAND; RETINOL EFFICACY TRIAL; PROSTATE-CANCER; ALPHA-TOCOPHEROL; LUNG-CANCER; SELENIUM SUPPLEMENTATION AB The first generation of phase III nutritional intervention studies to prevent cancer has been completed. Nearly 150,000 total participants were studied in nine different interventions using randomized, double-blind, placebo-controlled designs that tested whether vitamins and/or minerals, given singly or in combination, could prevent total or site-specilic cancer. The primary agents tested include beta-carotene, alpha-tocopherol, selenium, and retinol. This review summarizes the findings from the first generation of human experimental studies that tested micronutrients in the prevention of cancer, discusses lessons learned from these studies, identifies the most promising leads, and describes future prospects in nutritional intervention research. C1 NCI, Canc Res Ctr, Bethesda, MD 20892 USA. NCI, Div Canc Prevent, Bethesda, MD USA. RP Taylor, PR (reprint author), NCI, Canc Res Ctr, 6116 Execut Blvd,Rm 705, Bethesda, MD 20892 USA. EM ptaylor@mail.nih.gov NR 69 TC 38 Z9 40 U1 0 U2 6 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN 10 PY 2005 VL 23 IS 2 BP 333 EP 345 DI 10.1200/JCO.2005.06.190 PG 13 WC Oncology SC Oncology GA 887XG UT WOS:000226338200009 PM 15637396 ER PT J AU Dunn, BK Wickerham, L Ford, LG AF Dunn, BK Wickerham, L Ford, LG TI Prevention of hormone-related cancers: Breast cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID ANDROGEN RECEPTOR GENE; ONCOLOGY TECHNOLOGY-ASSESSMENT; SURGICAL ADJUVANT BREAST; ESTROGEN PLUS PROGESTIN; HEALTHY POSTMENOPAUSAL WOMEN; RANDOMIZED CONTROLLED-TRIAL; BRCA2 MUTATION CARRIERS; PROSTATE-CANCER; AROMATASE INHIBITORS; REPLACEMENT THERAPY AB Carcinorgenesis in the breast is a hormonally dependent process. Evidence implicating estrogen as a key breast carcinogen comes from various lines of investigation. Traditional epidemiologic studies demonstrate associations between estrogen exposure, both exogenous and endogenous, and increased breast cancer risk. Ongoing genetic epidemiologic studies also show associations between specific polymorphisms in estrogen-metabolizing Genes and risk, albeit inconsistently. The application of these findings to the treatment and, more recently, the prevention of breast cancer has led to the development of agents that either (1) inhibit estrogen action at the estrogen receptor (selective estrogen receptor modulators (SERMs)); of (2) inhibit estrogen-synthesizing enzymes, thereby abrogating synthesis of this hormone (aromatase inhibitors). Large phase III trials have evaluated the ability of such agents to reduce the incidence of breast cancer in women at increased risk of the disease. The National Surgical Adjuvant Breast and Bowel Project (NSABP) P-1: Breast Cancer Prevention Trial (SCPT) demonstrated the superiority of the SERM tamoxifen to placebo in reducing breast cancer risk. leading to the Food and Drug Administration approval of tamoxifen 1 of risk reduction. The implementation of tamoxifen for this indication has not become widespread in clinical practice , however, for a variety of reasons that we discuss. Results from the NSABP Study of Tamoxifen and Raloxifene, which compares the risk-reducing efficacy as well as toxicity of these two SERMs in a similar high-risk population, will be available in the near future. Based on promising, data involving reduction of contralateral breast cancer risk in adjuvant studies. several aromatase inhibitors, including letrozole, anastrozole, and exemestane, are being incorporated in into trials evaluating their efficacy as preventive agents in women at increased risk. C1 NCI, Div Canc Prevent, Basic Prevent Sci Res Grp, Bethesda, MD 20892 USA. Allegheny Hosp, Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA. RP Ford, LG (reprint author), NCI, Div Canc Prevent, Basic Prevent Sci Res Grp, 6130 Execut Blvd,Room 2046, Bethesda, MD 20892 USA. EM lf5Oz@nih.gov NR 175 TC 41 Z9 42 U1 0 U2 0 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X EI 1527-7755 J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN 10 PY 2005 VL 23 IS 2 BP 357 EP 367 DI 10.1200/JCO.2005.08.028 PG 11 WC Oncology SC Oncology GA 887XG UT WOS:000226338200011 PM 15637398 ER PT J AU Parnes, HL Thompson, IM Ford, LG AF Parnes, HL Thompson, IM Ford, LG TI Prevention of hormone-related cancers: Prostate cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID ANDROGEN RECEPTOR GENE; SRD5A2 GENE; MOLECULAR EPIDEMIOLOGY; FINASTERIDE PROSCAR(R); AFRICAN-AMERICAN; RACIAL VARIATION; REPEAT LENGTHS; UNITED-STATES; HISPANIC MEN; CYP17 GENE AB Androgens are known to play an important role in normal prostate development, benign prostatic hyperplasia, established prostate cancer, and in prostate carcinogenesis. However, despite convincing experimental and clinical evidence, the epidemiologic data correlating sex steroid levels with disease risk is inconsistent. More recent work has focused on studies of polymorphisms in germ-line DNA in an effort to develop polygenic models of prostate cancer susceptibility and prognosis. Such models have the potential to aid in the selection of men for specific chemopreventive interventions and to help determine which men with localized prostate cancer are most likely to benefit from aggressive therapy. In this review, we will provide a brief summary of androgen metabolic pathways followed by an assessment of the epidemiology literature addressing the relationship between androgens and prostate cancer. Finally, we will address the two major questions that have arisen in response to the recently published results from the Prostate Cancer Prevention Trial: Who are the best candidates for finasteride chemoprevention, and what are the clinical implications of the high prevalence of prostate cancer that was detected in men with prostate-specific antigen levels in the so-called "normal" range? C1 NCI, Div Canc Prevent, Prostate & Urol Canc Res Grp, Bethesda, MD 20892 USA. NCI, Deputy Directors Off, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Dept Surg, Div Urol, San Antonio, TX USA. RP Ford, LG (reprint author), NCI, Div Canc Prevent, Prostate & Urol Canc Res Grp, 6130 Execut Blvd,Room 2046, Bethesda, MD 20892 USA. EM lf5Oz@nih.gov NR 85 TC 39 Z9 39 U1 1 U2 1 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN 10 PY 2005 VL 23 IS 2 BP 368 EP 377 DI 10.1200/JCO.2005.08.027 PG 10 WC Oncology SC Oncology GA 887XG UT WOS:000226338200012 PM 15637399 ER PT J AU Hawk, ET Levin, B AF Hawk, ET Levin, B TI Colorectal cancer prevention SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID FECAL-OCCULT-BLOOD; FAMILIAL ADENOMATOUS POLYPOSIS; ABERRANT CRYPT FOCI; RANDOMIZED CONTROLLED-TRIAL; ELEVATED CYCLOOXYGENASE-2 EXPRESSION; ESTROGEN REPLACEMENT THERAPY; INDUCED COLON CARCINOGENESIS; BIRK INHIBITOR CONCENTRATE; DNA MISMATCH REPAIR; BASE-LINE FINDINGS AB Colorectal cancer is the second leading cause of mortality in the United States. In the United States, the cumulative lifetime risk of developing colorectal cancer for both men and women is 6%. Despite advances in the management of this disease, the 5-year survival rate in the United States in only 62%. Because only 38% of patients are diagnosed when the cancers are localized to the bowel wall, it is likely that widespread implementation of screening could significantly improve the outcome. Colorectal cancer screening is cost effective, irrespective of the methods used. In addition to currently available methods (fecal occult blood, flexible sigmoidoscopy, colonoscopy, and double contrast barium enema), computed tomographic colonography (virtual colonoscopy) and stool-based molecular screening are under development. Four classes of chemopreventive compounds have demonstrated efficacy in reducing recurrent colorectal adenomas and/or cancer in randomized, controlled trials. They are selenium, calcium carbonate, hormone replacement therapy, and nonsteroidal anti-inflammatory drugs. The mechanisms of action of nonsteroidal anti-inflammatory drugs include inhibition of the cyclooxygenase system as well as cyclooxygenase-independent effects. Considerable effort is being expended to define chemopreventive activity, optimal dose, administration schedule, and toxicity for the coxibs in adenoma recurrence prevention trials. The threshold for tolerating toxicities is very low in asymptomatic individuals at minimally increased risk for colorectal neoplasia. C1 NCI, Gi & Other Canc Res Grp, Bethesda, MD 20892 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. RP Hawk, ET (reprint author), NCI, Gi & Other Canc Res Grp, 6130 Execut Blvd,Suite 2141, Bethesda, MD 20892 USA. EM eh51p@nih.gov FU NCI NIH HHS [R01 CA131378, R01 CA148817, R01 CA155638] NR 166 TC 122 Z9 132 U1 0 U2 3 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN 10 PY 2005 VL 23 IS 2 BP 378 EP 391 DI 10.1200/JCO.2005.08.097 PG 14 WC Oncology SC Oncology GA 887XG UT WOS:000226338200013 PM 15637400 ER PT J AU Lee, KS Park, JE Asano, S Park, CJ AF Lee, KS Park, JE Asano, S Park, CJ TI Yeast polo-like kinases: functionally conserved multitask mitotic regulators SO ONCOGENE LA English DT Review DE yeast; polo kinase; G2/M transition; anaphase onset; mitosis exit; cytokinesis ID SISTER-CHROMATID SEPARATION; CELL-CYCLE PROGRESSION; DNA-DAMAGE CHECKPOINT; ANAPHASE-PROMOTING COMPLEX; SACCHAROMYCES-CEREVISIAE CDC5; XENOPUS EGG EXTRACTS; COHESIN SUBUNIT SCC1; KINESIN-LIKE PROTEIN; IN-VITRO REGULATION; FISSION YEAST AB The polo-like kinases (Plks) are a conserved subfamily of Ser/Thr protein kinases that play pivotal roles in regulating various cellular and biochemical events at multiple stages of M phase. Genetic and biochemical data revealed that both the budding yeast and the fission yeast polo kinase homologs (Cdc5 and Plo1, respectively) bear remarkable functional similarities with those in metazoan organisms, suggesting that the role of Plks is largely conserved throughout evolution. Thus, studies on Plks in genetically amenable lower eucaryotic organisms may yield valuable insights into the function of Plks in higher eucaryotic organisms. In this review, common properties and distinct functions of Cdc5 and Plo1 will be discussed and compared to properties and functions of Plks in higher eucaryotic organisms. C1 NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Lee, KS (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, 9000 Rockville Pike,Bldg 37,Rm 3118, Bethesda, MD 20892 USA. EM kyunglee@mail.nih.gov NR 180 TC 42 Z9 42 U1 3 U2 3 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN 10 PY 2005 VL 24 IS 2 BP 217 EP 229 DI 10.1038/sj.onc.1208271 PG 13 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 885UR UT WOS:000226183100002 PM 15640837 ER PT J AU Saksena, R Zhang, H Kovac, P AF Saksena, R Zhang, H Kovac, P TI Immunogens from a synthetic hexasaccharide fragment of the O-SP of Vibrio cholerae O : 1, serotype Ogawa SO TETRAHEDRON-ASYMMETRY LA English DT Article ID SQUARIC ACID DIESTER; ANTIGENIC DETERMINANTS; ALTERNATIVE METHOD; C-13-NMR SPECTRA; DIETHYL SQUARATE; BLOCK SYNTHESIS; GLYCOSIDES; PROTEINS; CARRIER; OLIGOSACCHARIDES AB The known 5-(methoxycarbonyl)pentyl alpha-glycoside of the hexasaccharide of Vibrio cholerae O:1, serotype Ogawa 24 was newly prepared. The efficiency of construction of the hexasaccharide from the disaccharide glycosyl acceptor 6 and each of the two tetrasaccharide glycosyl donors 16, and 18, as an alternative to the iterative coupling of the disaccharide glycosyl donor 7 with 6, was evaluated. Compound 24 was treated with each of hydrazine hydrate, ethylenediamine. and hexamethylenediamine to give ligands 25, 27, and 29, respectively, equipped with different linkers. Reaction of the foregoing compounds with squaric acid diethyl ester. and the reactions of the thus formed monoesters 26, 28, and 30 with BSA were evaluated. The rate of formation of the corresponding monoester was higher with hydrazide 25 than with amines 27 and 29. whose reaction rates were virtually the same. Reactions of squaric acid derivatives 26, 28, and 30 with BSA were conducted under the same conditions (reaction temperature, ligand-BSA ratio, and concentration with respect to the hapten) and targeted for neoglycoconjugates with 24-BSA ratio of similar to5. Monitoring the conversions by SELDI-TOF mass spectrometry in conjunction with the ProteinChip(R) system made it possible to conduct the conjugations in controlled fashion, and to terminate the reactions when the desired carbohydrate-protein ratios were reached. Products from 26, 28, and 30, neoglycoconjugates 31-33, containing 4.9, 5.0, and 5.1 moles of 24/BSA, respectively, were obtained in 87-93% yields. When the conjugation started with the initial molar carbohydrate-protein ratio of 15:1, the final molar carbohydrate-BSA ratio reached after 14 days with ligands 26, 28, and 30 was 9.0, 11.0, and 9.1, respectively. (C) 2004 Elsevier Ltd. All rights reserved. C1 NIDDK, LMC, NIH, Bethesda, MD 20892 USA. RP Kovac, P (reprint author), NIDDK, LMC, NIH, Bethesda, MD 20892 USA. EM kpn@helix.nih.gov NR 24 TC 16 Z9 18 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0957-4166 J9 TETRAHEDRON-ASYMMETR JI Tetrahedron: Asymmetry PD JAN 10 PY 2005 VL 16 IS 1 BP 187 EP 197 DI 10.1016/j.tetasy.2004.11.021 PG 11 WC Chemistry, Inorganic & Nuclear; Chemistry, Organic; Chemistry, Physical SC Chemistry GA 892WP UT WOS:000226681000024 ER PT J AU Herce, DH Perera, L Darden, TA Sagui, C AF Herce, DH Perera, L Darden, TA Sagui, C TI Surface solvation for an ion in a water cluster SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID MOLECULAR-DYNAMICS SIMULATIONS; FREE-ENERGY CALCULATIONS; CHARGING FREE-ENERGIES; LIQUID WATER; AB-INITIO; PHOTOELECTRON-SPECTROSCOPY; BIOMOLECULAR SIMULATIONS; POTENTIAL FUNCTIONS; FLUCTUATING CHARGE; CHLORIDE-ION AB We have used molecular dynamics simulations to study the structural, dynamical, and thermodynamical properties of ions in water clusters. Careful evaluations of the free energy, internal energy, and entropy are used to address controversial or unresolved issues, related to the underlying physical cause of surface solvation, and the basic assumptions that go with it. Our main conclusions are the following. (i) The main cause of surface solvation of a single ion in a water cluster is both water and ion polarization, coupled to the charge and size of the ion. Interestingly, the total energy of the ion increases near the cluster surface, while the total energy of water decreases. Also, our analysis clearly shows that the cause of surface solvation is not the size of the total water dipole (unless this is too small). (ii) The entropic contribution is the same order of magnitude as the energetic contribution, and therefore cannot be neglected for quantitative results. (iii) A pure energetic analysis can give a qualitative description of the ion position at room temperature. (iv) We have observed surface solvation of a large positive iodinelike ion in a polarizable water cluster, but not in a nonpolarizable water cluster. (C) 2005 American Institute of Physics. C1 N Carolina State Univ, Dept Phys, Raleigh, NC 27695 USA. Univ N Carolina, ITS, High Performance Comp Grp, Chapel Hill, NC 27599 USA. NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. RP Herce, DH (reprint author), N Carolina State Univ, Dept Phys, Raleigh, NC 27695 USA. RI perera, Lalith/B-6879-2012 OI perera, Lalith/0000-0003-0823-1631 NR 70 TC 61 Z9 62 U1 3 U2 13 PU AMER INST PHYSICS PI MELVILLE PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1, MELVILLE, NY 11747-4501 USA SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD JAN 8 PY 2005 VL 122 IS 2 AR 024513 DI 10.1063/1.1829635 PG 10 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 893DH UT WOS:000226699000042 PM 15638604 ER PT J AU Matochik, JA Eldreth, DA Cadet, JL Bolla, KI AF Matochik, JA Eldreth, DA Cadet, JL Bolla, KI TI Altered brain tissue composition in heavy marijuana users SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE marijuana; imaging; gray matter; white matter; hippocampus ID VOXEL-BASED MORPHOMETRY; CANNABINOID RECEPTORS; MAGNETIC-RESONANCE; CEREBRAL ATROPHY; CHRONIC EXPOSURE; GRAY-MATTER; DELTA(9)-TETRAHYDROCANNABINOL; DELTA-9-TETRAHYDROCANNABINOL; SMOKERS; ULTRASTRUCTURE AB Marijuana is the most widely used illicit substance in the United States: however. previous imaging studies have not detected altered brain structure in marijuana users compared to non-users. Voxel-based morphometry was used to investigate possible differences in brain tissue composition in a group of 11 heavy marijuana users and a group of 8 non-users. All participants were male. Statistical comparisons were made at the voxel level on T1-weighted magnetic resonance images to determine differences in gray matter and white matter tissue density Compared to non-users, marijuana users had lower gray matter density in a cluster of voxels in the right parahippocampal gyrus (P = 0.0001). and greater density bilaterally near the precentral gyrus and the right thalamus (P < 0.0-4). Marijuana users also had lower white matter density, in the left parietal lobe (P = 0.03), and higher density around the parahippocampal and fusiform gyri on the left side compared to non-users (P < 0.002). Longer duration of marijuana use (in years) was significantly correlated with higher white matter tissue density in the left precentral gyrus (P = 0.045). Our preliminary results suggest evidence of possible structural differences in the brain of heaxy marijuana users. and localize regions for further investigation of the effects of marijuana in the brain. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Natl Inst Drug Abuse, Intramural Res Program, Neuroimaging Res Branch, NIH,DHHS, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21224 USA. Natl Inst Drug Abuse, Intramural Res Program, Mol Neuropsychiat Branch, NIH,DHHS, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21224 USA. RP Matochik, JA (reprint author), Natl Inst Drug Abuse, Intramural Res Program, Neuroimaging Res Branch, NIH,DHHS, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM jmatochi@intra.nida.nih.gov FU NCRR NIH HHS [M01 RR02719]; NIDA NIH HHS [DA 11426] NR 39 TC 133 Z9 137 U1 8 U2 45 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD JAN 7 PY 2005 VL 77 IS 1 BP 23 EP 30 DI 10.1016/j.drugalcdep.2004.06.011 PG 8 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 888TQ UT WOS:000226397500004 PM 15607838 ER PT J AU Takeuchi, H Kao, S Miyagi, E Khan, MA Buckler-White, A Plishka, R Strebel, K AF Takeuchi, H Kao, S Miyagi, E Khan, MA Buckler-White, A Plishka, R Strebel, K TI Production of infectious SIVagm from human cells requires functional inactivation but not viral exclusion of human APOBEC3G SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIMIAN IMMUNODEFICIENCY VIRUS; CROSS-SPECIES TRANSMISSION; VIF PROTEIN; HIV-1 VIF; ANTIVIRAL ACTIVITY; ENZYME APOBEC3G; DEGRADATION; DNA; REPLICATION; PROTEASOME AB The virus infectivity factor (Vif) is a protein encoded by most primate lentiviruses. Recent evidence suggests that HIV-1 Vif reduces the intracellular levels of the host cytidine deaminase APOBEC3G (Apo3G) and inhibits its packaging into virions. These functions of Vif are thought to be species-specific. Accordingly, HIV-1 Vif can target only human Apo3G (hApo3G), whereas, African green monkey simian immunodeficiency virus ( SIVagm) Vif can inhibit African green monkey but not human Apo3G. Consistent with this, we found that SIVagm Vif does not affect the stability of exogenously and endogenously expressed hApo3G and does not prevent packaging of exogenous and endogenous hApo3G into SIVagm virions. Nevertheless, SIVagm Vif supported spreading infection of SIVagm virus in the hApo3G-positive human A3.01 T cell line and rescued infectivity of viruses produced from Apo3G-expressing HeLa cells. Sequence analysis verified that SIVagm Vif inhibited the accumulation of hApo3G-induced mutations, suggesting that SIVagm Vif is indeed active in human cells. Our data suggest that SIVagm Vif can inhibit hApo3G activity without inducing its intracellular degradation or preventing its packaging into virions. C1 NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA. RP Strebel, K (reprint author), NIAID, Mol Microbiol Lab, NIH, Bldg 4,Rm 310,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA. EM kstrebel@nih.gov RI Takeuchi, Hiroaki/F-9728-2012 NR 36 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 375 EP 382 DI 10.1074/jbc.M408987200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100045 PM 15528183 ER PT J AU Ho, M Kreitman, RJ Onda, M Pastan, I AF Ho, M Kreitman, RJ Onda, M Pastan, I TI In vitro antibody evolution targeting germline hot spots to increase activity of an anti-CD22 immunotoxin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MIMICKING SOMATIC HYPERMUTATION; B-CELL LEUKEMIAS; PHAGE DISPLAY; RECOMBINANT IMMUNOTOXIN; AFFINITY MATURATION; CYTOTOXIC ACTIVITY; PSEUDOMONAS EXOTOXIN; DIRECTED EVOLUTION; BINDING-AFFINITY; FV FRAGMENT AB Recombinant immunotoxin BL22, containing the Fv portion of an anti-CD22 antibody, produced complete remissions in most patients with drug-resistant hairy cell leukemia but had less activity in leukemias with low CD22 expression. Complementarity-determining region (CDR) mutagenesis is used to increase antibody affinity but can be difficult to perform successfully. We previously showed that antibodies with increased affinity and immunotoxins with increased activity could be obtained by directing mutations at specific DNA residues called hot spots. Because hot spots can arise either by somatic mutation or be present in the germline, we examined which type of hot spot is preferred for increasing antibody affinity. Initially, a second generation antibody phage-display library targeting a germline hot spot (Ser(30)-Asn(31)) within CDR1 of the antibody light chain was mutated. Substitution of serine 30 or asparagine 31 with arginine produced mutant immunotoxins with an affinity (0.8 nM) increased 7-fold over BL22 (5.8 nM) and 3-fold over the first generation mutant HA22 (2.3 nM). More importantly, a 10-fold increase in activity over BL22 and a 2-3-fold increase over HA22 were observed in various B lymphoma cell lines including WSU-CLL that contains only 5500 CD22 sites per cell. For comparison, two phage-display libraries targeting non-germline hot spots in heavy chain CDR1 and CDR3 were generated but did not produce Fv with increased affinity. Our results demonstrate that germline hot spots but not non-germline hot spots are effective for in vitro antibody affinity maturation. C1 NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Pastan, I (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Rm 5106, Bethesda, MD 20892 USA. EM pastani@mail.nih.gov RI Ho, Mitchell/F-5059-2015 NR 44 TC 64 Z9 72 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 607 EP 617 DI 10.1074/jbc.M409783200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100072 PM 15491997 ER PT J AU Kim, JS Coon, SL Blackshaw, S Cepko, CL Moller, M Mukda, S Zhao, WQ Charlton, CG Klein, DC AF Kim, JS Coon, SL Blackshaw, S Cepko, CL Moller, M Mukda, S Zhao, WQ Charlton, CG Klein, DC TI Methionine adenosyltransferase: Adrenergic-cAMP mechanism regulates a daily rhythm in pineal expression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADENOSYL-L-METHIONINE; S-ADENOSYLMETHIONINE SYNTHETASE; MELATONIN SYNTHESIS; SK-N-BE(2)C CELLS; GLAND; RAT; GENE; TRANSCRIPTION; BIOSYNTHESIS; HYDROXYLASE AB (S)-Adenosylmethionine (SAM) is a critical element of melatonin synthesis as the methyl donor in the last step of the pathway, the O-methylation of N-acetyl 5-hydroxytryptamine by hydroxyindole-O-methyltransferase. The activity of the enzyme that synthesizes SAM, methionine adenosyltransferase (MAT), increases 2.5-fold at night in the pineal gland. In this study, we found that pineal MAT2A mRNA and the protein it encodes, MAT II, also increase at night, suggesting that the increase in MAT activity is caused by an increase in MAT II gene products. The night levels of MAT2A mRNA in the pineal gland were severalfold higher than in other neural and non-neural tissues examined, consistent with the requirement for SAM in melatonin synthesis. Related studies indicate that the nocturnal increase in MAT2A mRNA is caused by activation of a well described neural pathway that mediates photoneural-circadian regulation of the pineal gland. MAT2A mRNA and MAT II protein were increased in organ culture by treatment with norepinephrine ( NE), the sympathetic neurotransmitter that stimulates the pineal gland at night. NE is known to markedly elevate pineal cAMP, and here it was found that cAMP agonists elevate MAT2A mRNA levels by increasing MAT2A mRNA synthesis and that drugs that block cAMP activation of cAMP dependent protein kinase block effects of NE. Therefore, the NE-cAMP dependent increase in pineal MAT activity seems to reflect an increase in MAT II protein, which occurs in response to cAMP-->protein kinase-dependent increased MAT2A expression. The existence of this MAT regulatory system underscores the importance that MAT plays in melatonin biogenesis. These studies also point to the possibility that SAM production in other tissues might be regulated through cAMP. C1 NICHHD, Sect Neuroendocrinol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Univ Copenhagen, Panum Inst, Inst Med Anat, DK-2200 Copenhagen, Denmark. Mahidol Univ, Neurobehav Biol Ctr, Inst Sci & Technol Res & Dev, Nakhon Pathom 73170, Thailand. Meharry Med Coll, Nashville, TN 37208 USA. RP Klein, DC (reprint author), NICHHD, Sect Neuroendocrinol, Dev Neurobiol Lab, NIH, Bldg 49,Rm 6A82, Bethesda, MD 20892 USA. EM klein@helix.nih.gov FU NEI NIH HHS [EY08064] NR 35 TC 25 Z9 26 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 677 EP 684 DI 10.1074/jbc.M408438200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100080 PM 15504733 ER PT J AU Endo, Y Wolf, V Muraiso, K Kamijo, K Soon, L Uren, A Barshishat-Kupper, M Rubin, JS AF Endo, Y Wolf, V Muraiso, K Kamijo, K Soon, L Uren, A Barshishat-Kupper, M Rubin, JS TI Wnt-3a-dependent cell motility involves RhoA activation and is specifically regulated by dishevelled-2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CONVERGENT EXTENSION MOVEMENTS; WNT SIGNALING PATHWAY; NEURAL-TUBE CLOSURE; BETA-CATENIN; VERTEBRATE GASTRULATION; COLON-CARCINOMA; TUMOR-FORMATION; PROTEINS; POLARITY; WINGLESS AB Wnts stimulate cell migration, although the mechanisms responsible for this effect are not fully understood. To investigate the pathways that mediate Wnt-dependent cell motility, we treated Chinese hamster ovary cells with Wnt-3a-conditioned medium and monitored changes in cell shape and movement. Wnt-3a induced cell spreading, formation of protrusive structures, reorganization of stress fibers and migration. Although Wnt-3a stabilized beta-catenin, two inhibitors of the beta-catenin/canonical pathway, Dickkopf-1 and a dominant-negative T cell factor construct, did not reduce motility. The small GTPase RhoA also was activated by Wnt-3a. In contrast to beta-catenin signaling, inhibition of Rho kinase partially blocked motility. Because Dishevelled (Dvl) proteins are effectors of both canonical and noncanonical Wnt signaling, we used immunofluorescent analysis and small interference RNA technology to evaluate the role of Dvl in cell motility. Specific knock-down of Dvl-2 expression markedly reduced Wnt-3a-dependent changes in cell shape and movement, suggesting that this Dvl isoform had a predominant role in mediating Wnt-3a-dependent motility in Chinese hamster ovary cells. C1 NCI, LCMB, CCR, NIH, Bethesda, MD 20892 USA. NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20057 USA. RP Rubin, JS (reprint author), NCI, LCMB, CCR, NIH, Bldg 37,Rm 2042,37 Convent Dr,MSC 4256, Bethesda, MD 20892 USA. EM rubinj@helix.nih.gov NR 52 TC 65 Z9 66 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 777 EP 786 DI 10.1074/jbc.M406391200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100091 PM 15509575 ER PT J AU Cho, HS Kim, DU Kehrl, JH AF Cho, HS Kim, DU Kehrl, JH TI RGS14 is a centrosomal and nuclear cytoplasmic shuttling protein that traffics to promyelocytic leukemia nuclear bodies following heat shock SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GTPASE-ACTIVATING PROTEINS; G-ALPHA; LOCALIZATION SIGNALS; DOMAIN; TRANSCRIPTION; REGULATOR; REPRESSION; EXPRESSION; SUBUNITS; FEATURES AB RGS14, a member of the regulator of G-protein signaling (RGS) protein family, possesses an N-terminal RGS domain, two Raf-like Ras-binding domains, and a GoLoco motif, which has GDP dissociation inhibitor activity. In this study we show that unique among the known mammalian RGS proteins, RGS14 localizes in centrosomes. Its first Ras-binding domain is sufficient to target RGS14 to centrosomes. RGS14 also shuttles between the cytoplasm and nucleus, and its nuclear export depends on the CRM-1 nuclear export receptor. Mutation of a nuclear export signal or treatment with leptomycin B causes nuclear accumulation of RGS14 and its association with promyelocytic leukemia protein nuclear bodies. Furthermore, a point mutant defective in nuclear export fails to target to centrosomes, suggesting that nuclear cytoplasmic shuttling is necessary for its proper localization. Mild heat stress, but not proteotoxic or transcription-linked stresses, re-localizes the RGS14 from the cytoplasm to promyelocytic leukemia nuclear bodies. Expression of RGS14, but not point mutants that disrupt the functional activity of its RGS domain or GoLoco motif, enhances the reporter gene activity. The multifunctional domains and the dynamic subcellular localization of RGS14 implicate it in a diverse set of cellular processes including centrosome and nuclear functions and stress-induced signaling pathways. C1 NIAID, Immunoregulat Lab, NIH, B Cell Mol Immunol Sect, Bethesda, MD 20892 USA. RP Kehrl, JH (reprint author), NIAID, Immunoregulat Lab, NIH, B Cell Mol Immunol Sect, Bldg 10,Rm 11B08,10 Ctr Dr,MSC 1876, Bethesda, MD 20892 USA. EM jkehrl@niaid.nih.gov OI Kehrl, John/0000-0002-6526-159X NR 39 TC 24 Z9 25 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 805 EP 814 DI 10.1074/jbc.M408163200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100094 PM 15520006 ER PT J AU Akimova, OA Bagrov, AY Lopina, OD Kamernitsky, AV Tremblay, J Hamet, P Orlov, SN AF Akimova, OA Bagrov, AY Lopina, OD Kamernitsky, AV Tremblay, J Hamet, P Orlov, SN TI Cardiotonic steroids differentially affect intracellular Na+ and [Na+](i)/[K+](i)-independent signaling in C7-MDCK cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SMOOTH-MUSCLE-CELLS; SODIUM-PUMP; CARDIAC-GLYCOSIDES; OUABAIN; ATPASE; MARINOBUFAGENIN; NA+,K+-ATPASE; APOPTOSIS; LIGAND; NA,K-ATPASE AB Recently, we reported that ouabain kills renal epithelial and vascular endothelial cells independently of elevation of the [Na+](i)/[K+](i) ratio. These observations raised the possibility of finding cardiotonic steroids (CTS) that inhibit the Na+, K+ pump without attenuating cell survival and vice versa. To test this hypothesis, we compared CTS action on Na+, K+ pump, [Na+](i) content, and survival of Madin-Darby canine kidney cells. At a concentration of 1 muM, ouabain and other tested cardenolides, as well as bufadienolides such as bufalin, cinobufagin, cinobufotalin, and telobufotoxin, led to similar to10-fold inhibition of the Na+, K+ pump, a 2-3-fold decrease in staining with dimethylthiazol-diphenyltetrazolium (MTT), and massive death indicated by detachment of similar to80% of cells and caspase-3 activation. In contrast, Na+, K+ pump inhibition and elevation of [Na+](i) seen in the presence of 3 muM marinobufagenin (MBG) and marinobufotoxin did not affect MTT staining and cell survival. Inhibition of the Na+, Rb+ pump in K+-free medium was not accompanied by a decline of MTT staining and cell detachment but increased sensitivity to CTS. In K+-free medium, half-maximal inhibition of Rb-86 influx was observed in the presence of 0.04 muM ouabain and 0.1 muM MBG, whereas half-maximal detachment and decline of MTT staining were detected at 0.03 and 0.004 muM of ouabain versus 10 and 3 muM of MBG, respectively. Both ouabain binding and ouabain-induced [Na+](i),[K+](i)-independent signaling were suppressed in the presence of MBG. Thus, our results show that CTS exhibit distinctly different potency in Na+, K+ pump inhibition and triggering of [Na+](i)/[K+](i)-independent signaling, including cell death. C1 CHUM Hotel Dieu, Ctr Rech, Montreal, PQ H2W 1T7, Canada. Moscow MV Lomonosov State Univ, Fac Biol, Moscow 119899, Russia. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Russian Acad Sci, Zelinsky Inst Organ Chem, Moscow 119840, Russia. RP Orlov, SN (reprint author), CHUM Hotel Dieu, Ctr Rech, 3850 Rue St Urbain, Montreal, PQ H2W 1T7, Canada. EM sergei.n.orlov@umontreal.ca RI Tremblay, Johanne/E-2154-2013; ORLOV, SERGEI/I-4071-2013; Cossette, Suzanne/I-8008-2016 NR 34 TC 43 Z9 47 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 7 PY 2005 VL 280 IS 1 BP 832 EP 839 DI 10.1074/jbc.M411011200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 883PG UT WOS:000226025100097 PM 15494417 ER PT J AU Park, Y Sheetlin, S Spouge, JL AF Park, Y Sheetlin, S Spouge, JL TI Accelerated convergence and robust asymptotic regression of the Gumbel scale parameter for gapped sequence alignment SO JOURNAL OF PHYSICS A-MATHEMATICAL AND GENERAL LA English DT Article ID APPROXIMATE P-VALUES; LOCAL SEQUENCE; STATISTICAL SIGNIFICANCE; DATABASE SEARCHES; PSI-BLAST; SIMILARITIES; PROTEINS AB Searches through biological databases provide the primary motivation for studying sequence alignment statistics. Other motivations include physical models of annealing processes or mathematical similarities to, e.g., first-passage percolation and interacting particle systems. Here, we investigate sequence alignment statistics, partly to explore two general mathematical methods. First, we model the global alignment of random sequences heuristically with Markov additive processes. In sequence alignment, the heuristic suggests a numerical acceleration scheme for simulating an important asymptotic parameter (the Gumbel scale parameter lambda). The heuristic might apply to similar mathematical theories. Second, we extract the asymptotic parameter lambda from simulation data with the statistical technique of robust regression. Robust regression is admirably suited to 'asymptotic regression' and deserves to be better known for it. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. RP Park, Y (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. EM spouge@ncbi.nlm.nih.gov RI Park, Yonil/E-6075-2010 NR 36 TC 7 Z9 7 U1 1 U2 2 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND SN 0305-4470 J9 J PHYS A-MATH GEN JI J. Phys. A-Math. Gen. PD JAN 7 PY 2005 VL 38 IS 1 BP 97 EP 108 DI 10.1088/0305-4470/38/1/006 PG 12 WC Physics, Multidisciplinary; Physics, Mathematical SC Physics GA 892KG UT WOS:000226648800009 ER PT J AU Vethanayagam, JGG Flower, AM AF Vethanayagam, JGG Flower, AM TI Decreased gene expression from T7 promoters may be due to impaired production of active T7 RNA polymerase SO MICROBIAL CELL FACTORIES LA English DT Article ID ESCHERICHIA-COLI; CLONED GENES; PROTEIN AB Background: Protein expression vectors that utilize the bacteriophage T7 polymerase/promoter system are capable of very high levels of protein production. Frequently, however, expression from these vectors does not reliably achieve optimal levels of protein production. Strategies have been proposed previously that successfully maintain high expression levels, however we sought to determine the cause of induction failure. Results: We demonstrated that decreases in protein overproduction levels are not due to significant plasmid loss nor to mutations arising on the plasmid, but instead largely are attributable to chromosomal mutations that diminish the level of functional T7 RNA polymerase, resulting in decreased expression from the plasmid. Isolation of plasmid DNA from non-expressing strains and reintroduction of the plasmid into a T7 RNA polymerase-producing strain such as BL21(lambda DE3) reproducibly restored high level protein production. Conclusions: Our results suggest that a major contributing factor to decreased expression levels in T7 based systems is chromosomal mutation resulting in loss of functional T7 RNA polymerase. Consistent with this hypothesis, we found that optimal protein overproduction was obtained reproducibly from T7 promoters using freshly transformed cells that had not been subjected to outgrowth during which mutations could accumulate. C1 Univ N Dakota, Sch Med & Hlth Sci, Dept Microbiol & Immunol, Grand Forks, ND 58202 USA. NIAMS, Prot Express Lab, NIH, Bethesda, MD 20892 USA. RP Univ N Dakota, Sch Med & Hlth Sci, Dept Microbiol & Immunol, Grand Forks, ND 58202 USA. EM vethanaj@mail.nih.gov; aflower@medicine.nodak.edu NR 14 TC 22 Z9 22 U1 2 U2 9 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1475-2859 J9 MICROB CELL FACT JI Microb. Cell. Fact. PD JAN 7 PY 2005 VL 4 AR 3 DI 10.1186/1475-2859-4-3 PG 7 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA 975WC UT WOS:000232693800001 ER PT J AU Huppi, K Martin, SE Caplen, NJ AF Huppi, K Martin, SE Caplen, NJ TI Defining and assaying RNAi in mammalian cells SO MOLECULAR CELL LA English DT Editorial Material ID DOUBLE-STRANDED-RNA; SINGLE-NUCLEOTIDE POLYMORPHISMS; SHORT-INTERFERING RNAS; ENZYME COMPLEX; CAENORHABDITIS-ELEGANS; GENE-EXPRESSION; HUMAN DICER; IN-VIVO; SIRNAS; MICRORNA AB The investigation of protein function through the inhibition of activity has been critical to our understanding of many normal and abnormal biological processes. Until recently, functional inhibition in biological systems has been induced using a variety of approaches including small molecule antagonists, antibodies, aptamers, ribozymes, antisense oligonucleotides or transcripts, morpholinos, dominant-negative mutants, and knockout transgenic animals. Although all of these approaches have made substantial advances in our understanding of the function of many proteins, a lack of specificity or restricted applicability has limited their utility. Recently, exploitation of the naturally occurring posttranscriptional gene silencing mechanism triggered by double-stranded RNA (dsRNA), termed RNA interference (RNAi), has gained much favor as an alternative means for analyzing gene function. Aspects of the basic biology of RNAi, its application as a functional genomics tool, and its potential as a therapeutic approach have been extensively reviewed (Hannon and Rossi, 2004; Meister and Tuschl, 2004); however, there has been only limited discussion as to how to design and validate an individual RNAi effector molecule and how to interpret RNAi data overall, particularly with reference to experimentation in mammalian cells. This perspective will aim to consider some of the issues encountered when conducting and interpreting RNAi experiments in mammalian cells. C1 NCI, Gene Silencing Sect, Off Sci & Technol Partnerships,Off Director, Ctr Canc Res,Natl Inst Hlth, Bethesda, MD 20892 USA. RP Caplen, NJ (reprint author), NCI, Gene Silencing Sect, Off Sci & Technol Partnerships,Off Director, Ctr Canc Res,Natl Inst Hlth, Bldg 37,3128B 37 Convent Dr, Bethesda, MD 20892 USA. EM ncaplen@mail.nih.gov RI Caplen, Natasha/H-2768-2016 OI Caplen, Natasha/0000-0002-0001-9460 NR 56 TC 93 Z9 98 U1 2 U2 8 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD JAN 7 PY 2005 VL 17 IS 1 BP 1 EP 10 DI 10.1016/j.molcel.2004.12.017 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 888JV UT WOS:000226371100001 PM 15629712 ER PT J AU Dmitrieva, NI Burg, MB AF Dmitrieva, NI Burg, MB TI Hypertonic stress response SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Review DE DNA damage; apoptosis; NaCl concentration; cell cycle arrest; kidney ID DOUBLE-STRAND BREAKS; TONEBP TRANSCRIPTIONAL ACTIVATOR; MEDULLARY EPITHELIAL-CELLS; DNA-DAMAGE CHECKPOINT; MURINE KIDNEY-CELLS; HEAT-SHOCK PROTEINS; HISTONE H2AX; OSMOTIC-STRESS; HIGH NACL; MOLECULAR CHAPERONES AB Mammalian renal inner medullary cells are normally exposed to extremely high NaCl concentrations. Remarkably, under these normal conditions. the high NaCl causes DNA damage and inhibits its repair, yet the cells survive and function both in cell culture and in vivo. The interstitial NaCl concentration in parts of a normal renal medulla can be 500mM or more. depending on the species. Studies of how the cells survive and function despite this extreme stress have led to the discovery of protective adaptations. including accumulation of large amounts of organic osmolytes, which normalize cell volume and intracellular ionic strength, despite the hypertonicity of the high NaCl. Those adaptations, however, do not prevent DNA damage. High NaCl induces DNA breaks rapidly, and the DNA breaks persist even after the cells become adapted to the high NaCl. The adapted cells proliferate rapidly in cell culture and function adequately in vivo despite the DNA breaks. Both in cell culture and in vivo the breaks are rapidly repaired if the NaCl concentration is lowered. Although acute elevation of NaCl causes transient cell cycle arrest and, when the elevation is too extreme, apoptosis, proliferation of adapted cells is not arrested in culture and apoptosis is not evident either in culture or in vivo. Further. high NaCl impairs activation of several components of the classical DNA damage response such as Mre11, H2AX and Chk1 leading to inhibition of DNA repair. Nevertheless, other regular participants in the DNA damage response, such as Gadd45a, Gadd 153, p53: Hsp70, and ATM are still upregulated by high NaCl. How high NaCl causes the DNA breaks and how the cells survive them is conjectural at this point. We discuss possible answers to these questions, based on current knowledge about induction and processing of DNA breaks. (C) 2004 Elsevier B.V. All rights reserved. C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Burg, MB (reprint author), NHLBI, Kidney & Electrolyte Metab Lab, NIH, Dept Hlth & Human Serv, 10 Ctr Dr,Bldg 10,Room 6N260, Bethesda, MD 20892 USA. EM maurice_burg@nih.gov RI Dmitrieva, Natalia/A-2924-2013 OI Dmitrieva, Natalia/0000-0001-8074-6950 NR 65 TC 52 Z9 52 U1 1 U2 6 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 JAN 6 PY 2005 VL 569 IS 1-2 BP 65 EP 74 DI 10.1016/j.mrfmmm.2004.06.053 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 886FA UT WOS:000226211100005 PM 15603752 ER PT J AU Gonzalez, FJ AF Gonzalez, FJ TI Role of cytochromes P450 in chemical toxicity and oxidative stress: studies with CYP2E1 SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Review DE cytochromes P450; CYP2E1; gene knockout mice; acetaminophen; metabolic activation; carcinogens; reactive oxygm species; oxidative stress ERK; MAPK ID CONSTITUTIVE ANDROSTANE RECEPTOR; INDUCED HEPATIC NECROSIS; PREGNANE X-RECEPTOR; NONALCOHOLIC STEATOHEPATITIS; DRUG-METABOLISM; MICE LACKING; ACETAMINOPHEN HEPATOTOXICITY; PEROXISOME PROLIFERATORS; TARGETED DISRUPTION; MENADIONE TOXICITY AB Cytochromes P450 are responsible for metabolism of most xenobiotics and are required for the efficient elimination of foreign chemicals from the body. Paradoxically, these enzymes also metabolically activate biologically inert compounds to electrophilic derivatives that can cause toxicity, cell death and sometimes cellular transformation resulting in cancer. To establish the role of these enzymes in toxicity and carcinogenicity in vivo, gene knockout mice have been developed. To illustrate the role of P450s in toxicity, CYPM-null mice, were employed with the commonly used analgesic drug acetaminophen. CY-P2E1 is the rate-limiting enzyme that initiates the cascade of events leading to acetaminophen hepatotoxicity; in the absence of this P450. toxicity will only be apparent at high concentrations. Other enzymes and nuclear receptors are also involved in activation or inactivating chemicals. CYP2E1 is induced by alcohol and the primary P450 that carries out ethanol oxidation that can lead to the production of activated oxygen species and oxidative stress that elevate ERK 1/2 phosphorylation through EGRF/c-Raf signaling. Paradoxically, activation of this pathway inhibits apoptotic cell death stimulated by reactive oxygen generating chemicals but accelerates necrotic cell death produced by polyunsaturated fatty acids. CYP2E1 is thought to contribute to liver pathologies that result front alcoholic liver disease and non-alcoholic steatohepatitis. (C) 2004 Elsevier B.V. All rights reserved. C1 NCI, Lab Metab, Bethesda, MD 20892 USA. RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Bethesda, MD 20892 USA. EM fjgonz@helix.nih.gov NR 71 TC 260 Z9 288 U1 6 U2 44 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 JAN 6 PY 2005 VL 569 IS 1-2 BP 101 EP 110 DI 10.1016/j.mrfmmm.2004.04.021 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 886FA UT WOS:000226211100008 PM 15603755 ER PT J AU Grant, KA Raible, DW Piotrowski, T AF Grant, KA Raible, DW Piotrowski, T TI Regulation of latent sensory hair cell precursors by glia in the zebrafish lateral line SO NEURON LA English DT Article ID NEURAL-CREST; POSTEMBRYONIC DEVELOPMENT; CAGED FLUORESCEIN; NERVOUS-SYSTEM; SCHWANN-CELL; DANIO-RERIO; FATE; NEUROGENIN1; MUTATIONS; MIGRATION AB The lateral line is a placodally derived mechanosensory organ in anamniotes that detects the movement of water. In zebrafish embryos, a migrating primordium deposits seven to nine clusters of sensory hair cells, or neuromasts, at intervals along the trunk. Post-embryonically, neuromasts continue to be added. We show that some secondary neuromasts arise from a pool of latent precursors that are deposited by the primordium between primary neuromasts. Interneuromast cells lie adjacent to the lateral line nerve and associated glia. These cells remain quiescent while they are juxtaposed with the glia; however, when they move away from the nerve they increase proliferation and form neuromasts. If glia are manually removed or genetically ablated by mutations in cis/sox10, hypersensitive (hps), or rowgain (rog), neuromasts precociously differentiate. Transplantation of wt glia into mutants rescues the appropriate temporal differentiation of interneuromast cells. Our studies reveal a role for glia in regulating sensory hair cell precursors. C1 NICHD, NIH, LMG, Bethesda, MD 20892 USA. Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA. Univ Washington, Cell & Mol Biol Program, Seattle, WA 98195 USA. Univ Utah, Dept Anat & Neurobiol, Salt Lake City, UT 84132 USA. RP Raible, DW (reprint author), NICHD, NIH, LMG, Bethesda, MD 20892 USA. EM draible@u.washington.edu; piotrowski@neuro.utah.edu FU NICHD NIH HHS [5 T32 HD07183-25, T32 HD007183]; NIDCD NIH HHS [DC005987]; NINDS NIH HHS [NS35833] NR 56 TC 74 Z9 75 U1 1 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD JAN 6 PY 2005 VL 45 IS 1 BP 69 EP 80 DI 10.1016/j.neuron.2004.12.020 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 886HI UT WOS:000226217100010 PM 15629703 ER PT J AU Kaur, GP Reddy, DE Zimonjic, DB de Riel, JK Athwal, RS AF Kaur, GP Reddy, DE Zimonjic, DB de Riel, JK Athwal, RS TI Functional identification of a BAC clone from 16q24 carrying a senescence gene SEN16 for breast cancer cells SO ONCOGENE LA English DT Article DE cell senescence; breast cancer; BAC contig; BAC transfer; functional complementation ID CHROMOSOME ARM 16Q; IMMORTAL HUMAN FIBROBLASTS; TUMOR-SUPPRESSOR GENES; CARCINOMA IN-SITU; CELLULAR SENESCENCE; HEPATOCELLULAR-CARCINOMA; ALLELIC IMBALANCE; HETEROZYGOSITY REGION; OVARIAN-CANCER; FREQUENT LOSS AB We have identified an 85 kb BAC clone, 346J21, that carries a cell senescence gene (SEN16), previously mapped to 16q24.3. Transfer and retention of 346J21 in breast cancer cell lines leads to growth arrest after 8-10 cell doublings, accompanied by the appearance of characteristic senescent cell morphology and senescence-associated acid beta-galactosidase activity. Loss of transferred BAC results in reversion to the immortal growth phenotype of the parental cancer cell lines. BAC 346J21 restores senescence in the human breast cancer cell lines, MCF.7 and MDA-MB468, and the rat mammary tumor cell line LA7, but not in the human glioblastoma cell line T98G. We postulate that inactivation of both copies of SEN16 is required for the immortalization of breast epithelial cells at an early stage of tumorigenesis. Positional mapping of 346J21 shows that SEN16 is distinct from other candidate tumor suppressor genes reported at 16q24. C1 Temple Univ, Sch Med, Fels Inst Canc Res & Mol Biol, Philadelphia, PA 19140 USA. NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA. RP Kaur, GP (reprint author), Temple Univ, Sch Med, Fels Inst Canc Res, 3307 N Broad St,AHB Room 201, Philadelphia, PA 19140 USA. EM pkaur001@temple.edu FU NCI NIH HHS [CA74983] NR 44 TC 3 Z9 3 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN 6 PY 2005 VL 24 IS 1 BP 47 EP 54 DI 10.1038/sj.onc.1208175 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 884ZS UT WOS:000226125800007 PM 15558027 ER PT J AU Bhonde, MR Hanski, ML Magrini, R Moorthy, D Muller, A Sausville, EA Kohno, K Wiegand, P Daniel, PT Zeitz, M Hanski, C AF Bhonde, MR Hanski, ML Magrini, R Moorthy, D Muller, A Sausville, EA Kohno, K Wiegand, P Daniel, PT Zeitz, M Hanski, C TI The broad-range cyclin-dependent kinase inhibitor UCN-01 induces apoptosis in colon carcinoma cells through transcriptional suppression of the Bcl-x(L) protein SO ONCOGENE LA English DT Article DE colon carcinoma; chemotherapy; UCN-01; apoptosis; cell cycle arrest ID LUNG-CANCER CELLS; 7-HYDROXYSTAUROSPORINE UCN-01; SELECTIVE INHIBITOR; ANTITUMOR-ACTIVITY; UP-REGULATION; CONSTITUTIVE ACTIVATION; CHECKPOINT FUNCTION; GROWTH-INHIBITION; LEUKEMIA-CELLS; BCL-X AB The broad-range cyclin-dependent kinase inhibitor 7-hydroxystaurosporine (UCN-01) is known to induce both a G1 cell cycle arrest and apoptosis. The mechanism of UCN-01-induced apoptosis is largely unknown. We analysed the mechanism of cytotoxicity of UCN-01 in four established colon carcinoma cell lines. The cell lines SW48 and LS513 responded to UCN-01 treatment by undergoing apoptosis in a concentration-dependent manner while the cell lines HT-29 and WiDr were completely resistant. Apoptosis in LS513 and SW48 cell lines was concomitant with the suppression of Bcl-x(L) on mRNA and protein level. In contrast, in the apoptosis-resistant cell lines, Bcl-x(L) expression was not affected by UCN-01. Stable overexpression of the Bcl-x(L) protein abrogated UCN-01-triggered apoptosis, but only partially restored growth, indicating that both cell cycle arrest and apoptosis exert the anticancer effect in a coordinated manner. The inhibition of Akt phosphorylation did not correlate with the apoptotic phenotype. UCN-01 inhibited the activating STAT3 phosphorylations on Ser727 and, notably, on Tyr705, but STAT3 did not contribute to Bcl-x(L) expression in colon carcinoma cells. Moreover, we show for the first time that UCN-01 induces apoptosis by suppression of Bcl-x(L) expression. The inhibition of this pathway is a new aspect of cytotoxic and modulatory potential of UCN-01. C1 Charite Univ Med Berlin, Dept Gastroenterol, D-12200 Berlin, Germany. Dept Clin & Mol Oncol, Berlin, Germany. NCI, Rockville, MD USA. Univ Occupat & Environm Hlth, Sch Med, Kitakyushu, Fukuoka 807, Japan. Inst Forens Med, Ulm, Germany. RP Hanski, C (reprint author), Charite Univ Med Berlin, Dept Gastroenterol, Campus Benjamin Franklin,Hindenburgdamm 30, D-12200 Berlin, Germany. EM christoph.hanski@charite.de NR 51 TC 24 Z9 24 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN 6 PY 2005 VL 24 IS 1 BP 148 EP 156 DI 10.1038/sj.onc.1207842 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 884ZS UT WOS:000226125800017 PM 15467762 ER PT J AU Bobb, AJ Castellanos, FX Addington, AM Rapoport, JL AF Bobb, AJ Castellanos, FX Addington, AM Rapoport, JL TI Molecular genetic studies of ADHD: 1991 to 2004 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Review DE review; attention deficit disorder with hyperactivity; candidate gene; polymorphism ID ATTENTION-DEFICIT HYPERACTIVITY; DOPAMINE-D4 RECEPTOR GENE; CATECHOL-O-METHYLTRANSFERASE; SEROTONIN TRANSPORTER GENE; DEPENDENT PROTEIN-KINASE; CASE-CONTROL ASSOCIATION; MONOAMINE-OXIDASE-A; MAJOR HISTOCOMPATIBILITY COMPLEX; ALPHA-2A ADRENERGIC-RECEPTOR; PROMOTER REGION POLYMORPHISM AB Attention deficit hyperactivity disorder (ADHD) is highly heritable but is likely a complex disorder involving multiple genes of moderate effect (Smalley [1997: Am J Hum Genet 60:1276-1282]). Over 100 studies have examined the genetics of ADHD by linkage or association, though no article has presented a comprehensive overview of all published reports. We reviewed all ADHD studies, including 3 genome-wide linkage studies, and association studies of 94 polymorphisms in 33 candidate genes. To simplify comparisons across heterogeneous articles, demographics and comorbidity were ignored; analyses of subtype and haplotypes were excluded; and only the most positive finding for each polymorphism in a study was reported. Thirty-six percent of all findings were positive (P < 0.05), 17% were trends (0.05 < P < 0.15), and 47% were negative (P > 0. 15). Studies utilizing dimensional measures of ADHD tended to result in higher rates of positive findings than those using categorical diagnoses (x(2) = 5.6, P = 0.018), and case-control studies tended to result in higher rates of positive findings than 2 family-based studies (X = 18.8, P < 0.001). However, for either dichotomy, no significant difference remained when analyzing only studies using both methods within the same population and polymorphism. Evidence for association exists for four genes in ADHD: the dopamine D4 and D5 receptors, and the dopamine and serotonin transporters; others are promising but need further replication, including the dopamine D2 and serotonin 2A receptors. All candidate gene approaches continue to face the problem of relatively low power, given modest odds ratios for even the best replicated genes. Published 2004 Wiley-Liss, Inc. C1 NIMH, Child Psychiat Branch, IRP, NIH, Bethesda, MD 20892 USA. NYU, Ctr Child Study, New York, NY USA. RP Rapoport, JL (reprint author), NIMH, Child Psychiat Branch, IRP, NIH, 10 Ctr Dr,Bldg 10,Room 3N-202, Bethesda, MD 20892 USA. EM rapoport@helix.nih.gov NR 216 TC 107 Z9 109 U1 5 U2 15 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD JAN 5 PY 2005 VL 132B IS 1 BP 109 EP 125 DI 10.1002/ajmg.b.30086 PG 17 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 885UG UT WOS:000226181900023 PM 15700344 ER PT J AU Levine, RJ Thadhani, R Qian, C Lam, C Lim, KH Yu, KF Blink, AL Sachs, BP Epstein, FH Sibai, BM Sukhatme, VP Karumanchi, SA AF Levine, RJ Thadhani, R Qian, C Lam, C Lim, KH Yu, KF Blink, AL Sachs, BP Epstein, FH Sibai, BM Sukhatme, VP Karumanchi, SA TI Urinary placental growth factor and risk of preeclampsia SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID TYROSINE KINASE-1; FACTOR RECEPTOR; HYPERTENSION; CALCIUM; TRIAL; WOMEN AB Context Preeclampsia may be caused by an imbalance of angiogenic factors. We previously demonstrated that high serum levels of soluble fms-like tyrosine kinase 1 (sFlt1), an antiangiogenic protein, and low levels of placental growth factor (PIGF), a proangiogenic protein, predict subsequent development of preeclampsia. In the absence of glomerular disease leading to proteinuria, sFlt1 is too large a molecule to be filtered into the urine, while PIGF is readily filtered. Objective To test the hypothesis that urinary PIGF is reduced prior to onset of hypertension and proteinuria and that this reduction predicts preeclampsia. Design, Setting, and Patients Nested case-control study within the Calcium for Preeclampsia Prevention trial of healthy nulliparous women enrolled at 5 US university medical centers during 1992-1995. Each woman with preeclampsia was matched to 1 normotensive control by enrollment site, gestational age at collection of the first serum specimen, and sample Storage time at -70degreesC. One hundred twenty pairs of women were randomly chosen for analysis of serum and urine specimens obtained before labor. Main Outcome Measure Cross-sectional urinary PIGF concentrations, before and after normalization for urinary creatinine. Results Among normotensive controls, urinary PIGF increased during the first 2 trimesters, peaked at 29 to 32 weeks, and decreased thereafter. Among cases, before onset of preeclampsia the pattern of urinary PIGF was similar, but levels were significantly reduced beginning at 25 to 28 weeks. There were particularly large differences between controls and cases of preeclampsia with subsequent early onset of the disease or small-for-gestational-age infants. After onset of clinical disease, mean urinary PIGF in women with preeclampsia was 32 pg/mL, compared with 234 pg/mL in controls with fetuses of similar gestational age (P<.001). The adjusted odds ratio for the risk of preeclampsia to begin before 37 weeks of gestation for specimens obtained at 21 to 32 weeks, which were in the lowest quartile of control PIGF concentrations (<118 pg/mL), compared with all other quartiles, was 22.5 (95% confidence interval, 7.4-67.8). Conclusion Decreased urinary PIGF at mid gestation is strongly associated with subsequent early development of preeclampsia. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Renal Div, Boston, MA 02215 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Boston, MA 02215 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Allied Technol Grp, Rockville, MD USA. Univ Cincinnati, Coll Med, Dept Obstet & Gynecol, Cincinnati, OH 45267 USA. NICHHD, Div Epidemiol Stat & Prevent Res, US Dept HHS, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Obstet, Boston, MA 02114 USA. RP Karumanchi, SA (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Renal Div, Dana 517,330 Brookline Ave, Boston, MA 02215 USA. EM sananth@bidmc.harvard.edu FU NICHD NIH HHS [N01-HD-3154, N01-HD-1-3121, N01-HD-1-3122, N01-HD-1-3123, N01-HD-1-3124, N01-HD-1-3125, N01-HD-1-3126, N01-HD-5-3246, R01-HD-3-9223]; NIDDK NIH HHS [KO8-DK-002825] NR 20 TC 184 Z9 196 U1 2 U2 6 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 JAN 5 PY 2005 VL 293 IS 1 BP 77 EP 85 DI 10.1001/jama.293.1.77 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 884QY UT WOS:000226102100024 PM 15632339 ER PT J AU Banke, TG Dravid, SM Traynelis, SF AF Banke, TG Dravid, SM Traynelis, SF TI Protons trap NR1/NR2B NMDA receptors in a nonconducting state SO JOURNAL OF NEUROSCIENCE LA English DT Article DE NMDA receptor; protons; ion channel; ischemia; pH; glutamate ID CONE HORIZONTAL CELLS; ION-CHANNEL; GLUTAMATE-RECEPTOR; K+ CHANNELS; MOLECULAR DETERMINANTS; K(IR)1.1 CHANNELS; ZINC INHIBITION; LIGAND-BINDING; PH; MECHANISM AB NMDA receptors are highly expressed in the CNS and are involved in excitatory synaptic transmission, as well as synaptic plasticity. Given that overstimulation of NMDA receptors can cause cell death, it is not surprising that these channels are under tight control by a series of inhibitory extracellular ions, including zinc, magnesium, and H+. We studied the inhibition by extracellular protons of recombinant NMDA receptor NR1/NR2B single-channel and macroscopic responses in transiently transfected human embryonic kidney HEK293 cells using patch-clamp techniques. We report that proton inhibition proceeds identically in the absence or presence of agonist, which rules out the possibility that protonation inhibits receptors by altering coagonist binding. The response of macroscopic currents in excised patches to rapid jumps in pH was used to estimate the microscopic association and dissociation rates for protons, which were 1.4 x 10(9) M-1 sec(-1) and 110 - 196 sec(-1), respectively (K-d corresponds to pH 7.2). Protons reduce the open probability without altering the time course of desensitization or deactivation. Protons appear to slow at least one time constant describing the intra-activation shut-time histogram and modestly reduce channel open time, which we interpret to reflect a reduction in the overall channel activation rate and possible proton-induced termination of openings. This is consistent with a modest proton-dependent slowing of the macroscopic response rise time. From these data, we propose a physical model of proton inhibition that can describe macroscopic and single-channel properties of NMDA receptor function over a range of pH values. C1 NIH, Lab Cellular & Synapt Neurophysiol, Porter Neurosci Res Ctr, Bethesda, MD 20892 USA. Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA. RP Banke, TG (reprint author), NIH, Lab Cellular & Synapt Neurophysiol, Porter Neurosci Res Ctr, Bldg 35,Room 3C-705,35 Lincoln Dr, Bethesda, MD 20892 USA. EM banket@mail.nih.gov OI Banke, Tue/0000-0001-8417-4400 FU NINDS NIH HHS [NS36654] NR 62 TC 51 Z9 52 U1 0 U2 5 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JAN 5 PY 2005 VL 25 IS 1 BP 42 EP 51 DI 10.1523/JNEUROSCI.3154-04.2005 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 885BE UT WOS:000226130200007 PM 15634765 ER PT J AU Aoki, Y Tosato, G AF Aoki, Y Tosato, G TI Lymphatic regeneration: New insights from VEGFR-3 blockade SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID GROWTH-FACTOR RECEPTOR-3; LYMPHANGIOGENESIS; CELLS; ANGIOGENESIS; VASCULATURE; METASTASIS C1 NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Tosato, G (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM tosatog@mail.nih.gov NR 17 TC 10 Z9 12 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JAN 5 PY 2005 VL 97 IS 1 BP 2 EP 3 DI 10.1093/jnci/dji015 PG 2 WC Oncology SC Oncology GA 891RW UT WOS:000226599400001 PM 15632367 ER PT J AU Grundner, C Li, YX Louder, M Mascola, J Yang, XZ Sodroski, J Wyatt, R AF Grundner, C Li, YX Louder, M Mascola, J Yang, XZ Sodroski, J Wyatt, R TI Analysis of the neutralizing antibody response elicited in rabbits by repeated inoculation with trimeric HIV-1 envelope glycoproteins SO VIROLOGY LA English DT Article DE antibody; inoculation; glycoprotein ID IMMUNODEFICIENCY-VIRUS TYPE-1; MONOCLONAL-ANTIBODIES; SOLUBLE CD4; DEPENDENT ENHANCEMENT; IMMUNE-RESPONSES; PRIMARY ISOLATE; GP120; INFECTION; BINDING; PROTECTION AB The elicitation of broadly neutralizing antibodies directed against the human immunodeficiency virus type I (HIV-1) envelope glycoproteins, gp120 and gp41, remains a major challenge. Attempts to utilize monomeric gp120 as an immunogen to elicit high titers of neutralizing antibodies have been disappointing. Envelope glycoprotein constructs that better reflect the trimeric structutre of the functional envelope spike have exhibited improved immunogenicity compared with monomeric gp120. We have described soluble gp140 ectodomain constructs with a heterologous trimerization motif, these have previously been shown to elicit antibodies in mice that were able to neutralize a number of HIV-1 isolates. among them primary isolate viruses. Recently, solid-phase proteoliposomes retaining the envelope glycoproteins as trimeric spikes in a physiologic membrane setting have been described. Here, we compare the immunogenic properties of these two trimeric envelope glycoprotein formulations and monomeric gp120 in rabbits. Both trimeric envelope glycoprotein preparation generated neutralizing antibodies more effectively than gp120. In contrast to monomeric gp120 the trinieric envelope glycoproteins elicited neutralizing antibodies with some breadth of neutralization. Furthermore, repeated boosting with the soluble trimeric formulations resulted in an increase in potency that allowed neutralization of a subset of neutralization-resistant HIV-1 primary isolates. We demonstrated that the neutralization is concentration-dependent, is mediated by serum IgG and that the major portion of the neutralizing activity is not directed against the gp120 V3 loop. Thus, mimics of the trimeric envelope glycoprotein spike described here elicit HIV-1-neutralizing antibodies that could contribute to a protective immune response and provide platforms for further modifications to improve the efficiency of this process. Published by Elsevier Inc. C1 NIH, Struct Virol Sect, Vaccine Res Ctr, Bethesda, MD 20892 USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Div Aids, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Wyatt, R (reprint author), NIH, Struct Virol Sect, Vaccine Res Ctr, 40 Convent Dr,Bldg 40,Room 4512, Bethesda, MD 20892 USA. EM richardwyatt@nih.gov FU NIAID NIH HHS [1R21AI-44328-02, 5R21AI-44328-02, AI 27742, AI 31783, AI28691, AI49099] NR 42 TC 73 Z9 75 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 0042-6822 J9 VIROLOGY JI Virology PD JAN 5 PY 2005 VL 331 IS 1 BP 33 EP 46 DI 10.1016/j.virol.2004.09.022 PG 14 WC Virology SC Virology GA 886EU UT WOS:000226210500003 PM 15582651 ER PT J AU Gainer, JV Bellamine, A Dawson, EP Womble, KE Grant, SW Wang, YR Cupples, LA Guo, CY Demissie, S O'Donnell, CJ Brown, NJ Waterman, MR Capdevila, JH AF Gainer, JV Bellamine, A Dawson, EP Womble, KE Grant, SW Wang, YR Cupples, LA Guo, CY Demissie, S O'Donnell, CJ Brown, NJ Waterman, MR Capdevila, JH TI Functional variant of CYP4A11 20-hydroxyeicosatetraenoic acid synthase is associated with essential hypertension SO CIRCULATION LA English DT Article DE genetics; hypertension, renal; lipids; metabolism ID BLOOD-PRESSURE; ANGIOTENSINOGEN GENE; AFRICAN-AMERICANS; ARACHIDONIC-ACID; LINKAGE; MONOOXYGENASES; POLYMORPHISM; NATRIURESIS; METABOLITES; 20-HETE AB Background - The CYP4A11 arachidonic acid monooxygenase oxidizes endogenous arachidonic acid (AA) to 20-hydroxyeicosatetraenoic acid (20-HETE), a metabolite with renovascular and tubular functions. Mice with targeted disruption of Cyp4a14, a murine homologue of CYP4A11, have severe hypertension. We combined molecular and biochemical approaches to identify a functional variant of the CYP4A11 20-HETE synthase and determine its association with hypertensive status in 2 independent human populations. Methods and Results - A thymidine-to-cytosine polymorphism at nucleotide 8590 resulted in a phenylalanine-to-serine substitution at amino acid 434. Expression of cDNA with serine 434 resulted in a protein with a significantly reduced AA and lauric acid metabolizing activity. In a population of 512 whites from Tennessee, the age, body mass index, and gender-adjusted OR of having hypertension attributable to the 8590C variant was 2.31 (95% CI 1.41 to 3.78) compared with the reference 8590TT genotype. In subjects from the Framingham Heart Study, the adjusted ORs of hypertension associated with the 8590C variant were 1.23 (CI 0.94 to 1.59; n=1538) in all subjects and 1.33 (CI 1.01 to 1.77; n=1331) when subjects with diabetes were excluded. No association of the variant with hypertension was detected in a population of 120 blacks. Conclusions - We identified a variant of the human CYP4A11 (T8590C) that encodes for a monooxygenase with reduced 20-HETE synthase activity. The association of the T8590C variant with hypertension supports its role as a polygenic determinant of blood pressure control in humans, and results obtained from the large population database suggest that the relevance of the variant may vary according to hypertension comorbidity. C1 Vanderbilt Univ, Sch Med, Dept Biochem, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Dept Med, Div Clin Pharmacol, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Dept Med, Div Nephrol, Nashville, TN 37232 USA. BioVentures Inc, Murfreesboro, TN USA. Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA. NHLBI, Framingham Heart Study, Framingham, MA USA. RP Vanderbilt Univ, Sch Med, Dept Biochem, 607 Light Hall, Nashville, TN 37232 USA. EM michael.waterman@vanderbilt.edu OI Cupples, L. Adrienne/0000-0003-0273-7965 FU NCI NIH HHS [CA68485]; NCRR NIH HHS [RR00095]; NHLBI NIH HHS [N01-HC-25195, HL65193, HL67308, HL04221, HL60906]; NIDDK NIH HHS [DK28350, DK38226] NR 32 TC 116 Z9 127 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0009-7322 EI 1524-4539 J9 CIRCULATION JI Circulation PD JAN 4 PY 2005 VL 111 IS 1 BP 63 EP 69 DI 10.1161/01.CIR.0000151309.82473.59 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 884DR UT WOS:000226065300011 PM 15611369 ER PT J AU Wu, ZR Maderia, M Barchi, JJ Marquez, VE Bax, A AF Wu, ZR Maderia, M Barchi, JJ Marquez, VE Bax, A TI Changes in DNA bending induced by restricting nucleotide ring pucker studied by weak alignment NMR spectroscopy SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE conformational change; liquid crystal; nucleic acid ID RESIDUAL DIPOLAR COUPLINGS; HELIX STRUCTURE; B-DNA; MOLECULAR-DYNAMICS; BASE SEQUENCE; ADENINE-TRACT; DODECAMER; OLIGONUCLEOTIDES; MACROMOLECULES; BIOMOLECULES AB Changes in bending of the DNA helix axis caused by the introduction of conformationally locked nucleotide analogs into the center region of the palindromic Dickerson dodecamer, d(CGCGAAT-TCGCG)(2), have been studied by NMR measurement of residual one-bond C-13-H-1 dipolar couplings. Thymidine analogs, in which the deoxyribose was substituted by bicyclo[3.1.0]hexane, were incorporated in the T7, T8, and T7T8 positions. These nucleotide analogs restrict the ring pucker to the C2'-exo or "north" conformation, instead of C2'-endo or "south," which dominates in regular B-form DNA. For all three oligomers, bending toward the major groove is found relative to the native molecule. The effects are additive with bending of 5 +/- 1degrees per locked nucleotide. Measurement of the change in bending is more accurate than measurement of the bending angle itself and requires far fewer experimental data. C1 NIDDKD, Chem Phys Lab, Bethesda, MD 20892 USA. NCI, Ctr Canc Res, Med Chem Lab, Frederick, MD 21702 USA. RP Bax, A (reprint author), NIDDKD, Chem Phys Lab, Bethesda, MD 20892 USA. EM bax@nih.gov RI Barchi Jr., Joseph/N-3784-2014 NR 42 TC 17 Z9 17 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 4 PY 2005 VL 102 IS 1 BP 24 EP 28 DI 10.1073/pnas.0408498102 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 886HB UT WOS:000226216400006 PM 15618396 ER PT J AU Balbo, A Minor, KH Velikovsky, CA Mariuzza, RA Peterson, CB Schuck, P AF Balbo, A Minor, KH Velikovsky, CA Mariuzza, RA Peterson, CB Schuck, P TI Studying multiprotein complexes by multisignal sedimentation velocity analytical ultracentrifugation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE protein interactions; size distribution ID SIZE-DISTRIBUTION ANALYSIS; CELL ANTIGEN RECEPTOR; SIGNAL-TRANSDUCTION; ABSORPTION OPTICS; MACROMOLECULAR COMPLEXES; PROTEIN INTERACTIONS; INTERACTING SYSTEMS; SELF-ASSOCIATION; LAMM EQUATION; EQUILIBRIUM AB Protein interactions can promote the reversible assembly of multiprotein complexes, which have been identified as critical elements in many regulatory processes in cells. The biophysical characterization of assembly products, their number and stoichiometry, and the dynamics of their interactions in solution can be very difficult. A classical first-principle approach for the study of purified proteins and their interactions is sedimentation velocity analytical ultracentrifugation. This approach allows one to distinguish different protein complexes based on their migration in the centrifugal field without isolating reversibly formed complexes from the individual components. An important existing limitation for systems with multiple components and assembly products is the identification of the species associated with the observed sedimentation rates. We developed a computational approach for integrating multiple optical signals into the sedimentation coefficient distribution analysis of components, which combines the size-dependent hydrodynamic separation with discrimination of the extinction properties of the sedimenting species. This approach allows one to deduce the stoichiometry and to assign the identity of the assembly products without prior assumptions of the number of species and the nature of their interaction. Although chromophoric labels may be used to enhance the spectral resolution, we demonstrate the ability to work label-free for three-component protein mixtures. We observed that the spectral discrimination can synergistically enhance the hydrodynamic resolution. This method can take advantage of differences in the absorbance spectra of interacting solution components, for example, for the study of protein-protein, protein-nucleic acid or protein-small molecule interactions, and can determine the size, hydrodynamic shape, and stoichiometry of multiple complexes in solution. C1 NIH, Div Bioengn & Phys Sci, Off Res Serv, Off Director, Bethesda, MD 20892 USA. Univ Tennessee, Dept Biochem & Cellular & Mol Biol, Knoxville, TN 37996 USA. Univ Maryland, Maryland Biotechnol Inst, Ctr Adv Res Biotechnol, Rockville, MD 20850 USA. RP Schuck, P (reprint author), NIH, Div Bioengn & Phys Sci, Off Res Serv, Off Director, Bldg 10, Bethesda, MD 20892 USA. EM pschuck@helix.nih.gov OI Schuck, Peter/0000-0002-8859-6966 FU NIGMS NIH HHS [R01 GM052801, GM 52801] NR 45 TC 84 Z9 85 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 4 PY 2005 VL 102 IS 1 BP 81 EP 86 DI 10.1073/pnas.0408399102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 886HB UT WOS:000226216400016 PM 15613487 ER PT J AU Sugiyama, T Cam, H Verdel, A Moazed, D Grewal, SIS AF Sugiyama, T Cam, H Verdel, A Moazed, D Grewal, SIS TI RNA-dependent RNA polymerase is an essential component of a self-enforcing loop coupling heterochromatin assembly to siRNA production SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RNA interference; Schizosaccharomyces pombe ID HISTONE-H3 LYSINE-9 METHYLATION; FISSION YEAST; C-ELEGANS; CHROMOSOME SEGREGATION; EPIGENETIC CONTROL; GERM-LINE; GENE; INTERFERENCE; DNA; DROSOPHILA AB In fission yeast, factors involved in the RNA interference (RNAi) pathway including Argonaute, Dicer, and RNA-dependent RNA polymerase are required for heterochromatin assembly at centromeric repeats and the silent mating-type region. Previously, we have shown that RNA-induced initiation of transcriptional gene silencing (RITS) complex containing the Argonaute protein and small interfering RNAs (siRNAs) localizes to heterochromatic loci and collaborates with heterochromatin assembly factors via a self-enforcing RNAi loop mechanism to couple siRNA generation with heterochromatin formation. Here, we investigate the role of RNA-dependent RNA polymerase (Rdp1) and its polymerase activity in the assembly of heterochromatin. We find that Rdp1, similar to RITS, localizes to all known heterochromatic loci, and its localization at centromeric repeats depends on components of RITS and Dicer as well as heterochromatin assembly factors including Clr4/Suv39h and Swi6/HP1 proteins. We show that a point mutation within the catalytic domain of Rdp1 abolished its RNA-dependent RNA polymerase activity and resulted in the loss of transcriptional silencing and heterochromatin at centromeres, together with defects in mitotic chromosome segregation and telomere clustering. Moreover, the RITS complex in the rdp1 mutant does not contain siRNAs, and is delocalized from centromeres. These results not only implicate Rdp1 as an essential component of a self-enforcing RNAi loop but also ascribe a critical role for its RNA-dependent RNA polymerase activity in siRNA production necessary for heterochromatin formation. C1 NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. RP Grewal, SIS (reprint author), NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. EM grewals@mail.nih.gov RI Verdel, Andre/M-5201-2013; OI Sugiyama, Tomoyasu/0000-0001-5704-6606 NR 41 TC 177 Z9 185 U1 1 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 4 PY 2005 VL 102 IS 1 BP 152 EP 157 DI 10.1073/pnas.0407641102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 886HB UT WOS:000226216400028 PM 15615848 ER PT J AU Szabady, RL Peterson, JH Skillman, KM Bernstein, HD AF Szabady, RL Peterson, JH Skillman, KM Bernstein, HD TI An unusual signal peptide facilitates late steps in the biogenesis of a bacterial autotransporter SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE Escherichia coli; microbial pathogenesis; protein folding; protein translocation ID INNER MEMBRANE-PROTEINS; ESCHERICHIA-COLI; RECOGNITION PARTICLE; TRANSLOCATION; SECRETION; SEQUENCES; INSERTION; PROTEASE; DOMAIN; EXPRESSION AB Bacterial autotransporters are proteins that use a C-terminal porin-like domain to facilitate the transport of an upstream "passenger domain" across the outer membrane. Although autotransporters are translocated across the inner membrane (IM) via the Sec pathway, some of them contain exceptionally long signal peptides distinguished by a unique N-terminal sequence motif. In this study, we used the Escherichia coli O157:H7 autotransporter EspP as a model protein to investigate the function of the unusual signal peptides. We found that removal of the N-terminal motif or replacement of the EspP signal peptide did not affect translocation of the protein across the IM. Remarkably, modification of the signal peptide caused EspP to misfold in the periplasm and blocked transport of the passenger domain across the outer membrane. Further analysis suggested that the EspP signal peptide transits slowly through the Sec machinery. Based on these results, we propose that the unusual signal peptides not only function as targeting signals, but also prevent misfolding of the passenger domain in the periplasm by transiently tethering it to the IM. C1 NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA. RP Bernstein, HD (reprint author), NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA. EM harris_bernstein@nih.gov NR 28 TC 79 Z9 84 U1 1 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 4 PY 2005 VL 102 IS 1 BP 221 EP 226 DI 10.1073/pnas.0406055102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 886HB UT WOS:000226216400040 PM 15615856 ER PT J AU Lisziewicz, J Trocio, J Xu, JQ Whitman, L Ryder, A Bakare, N Lewis, MG Wagner, W Pistorio, A Arya, S Lori, F AF Lisziewicz, J Trocio, J Xu, JQ Whitman, L Ryder, A Bakare, N Lewis, MG Wagner, W Pistorio, A Arya, S Lori, F TI Control of viral rebound through therapeutic immunization with DermaVir SO AIDS LA English DT Article DE dendritic cells; HIV therapy; vaccine ID STRUCTURED TREATMENT INTERRUPTIONS; IMMUNODEFICIENCY-VIRUS-INFECTION; LYMPHOCYTES; VACCINE; HIV-1; AIDS AB Objective: To reconstitute immune responses capable of eliminating infected cells and suppressing viral load during chronic retroviral infection. Design: A topical, DNA-based therapeutic immunization (DermaVir) was designed to express most of the regulatory and structural viral genes in dendritic cells. Methods: DermaVir alone and in combination with antiretroviral drugs was tested in chronically SIV-infected macaques. Results: DermaVir provided virological, immunological and clinical benefit for SIV-infected macaques during chronic infection and AIDS. In combination with antiretroviral drugs, DermaVir augmented SIV-specific T-cell responses and enhanced control of viral load rebound during treatment interruptions. Conclusions: The results indicate the feasibility of therapeutic immunization even in immune compromised hosts, and suggest that DermaVir can complement antiretroviral drugs to sustain suppression of HIV-1 replication. (C) 2005 Lippincott Williams Wilkins. C1 RIGHT, Washington, DC 20007 USA. Genet Immunol LLC, Washington, DC USA. So Res Inst, Frederick, MD USA. IRCCS G Gaslini, Clin Epidemiol & Biometry Unit, Genoa, Italy. NCI, NIH, Bethesda, MD 20892 USA. RP Lisziewicz, J (reprint author), RIGHT, 2233 Wisconsin Ave NW,503, Washington, DC 20007 USA. EM lisziewj@geneticimmunity.com RI Pistorio, Angela/D-1375-2009 FU PHS HHS [N01 A165312] NR 11 TC 50 Z9 52 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD JAN 3 PY 2005 VL 19 IS 1 BP 35 EP 43 DI 10.1097/00002030-200501030-00004 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 887MR UT WOS:000226310700004 PM 15627031 ER PT J AU Nakagawa-Goto, K Chen, CX Hamel, E Wu, CC Bastow, KF Brossi, A Lee, KH AF Nakagawa-Goto, K Chen, CX Hamel, E Wu, CC Bastow, KF Brossi, A Lee, KH TI Antitumor agents. Part 236: Synthesis of water-soluble colchicine derivatives SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID THIOCOLCHICINE; CONGENERS; TUBULIN AB Water-soluble colchicine derivatives were synthesized from 2-demethylcolchicine and 2-demethylthiocolchicine and evaluated in vitro against human tumor cell replication and for inhibition of tubulin polymerization. The glycinate esters (4, 5) and their tartaric acid salts (4a, 5a) showed potent cytotoxic activity in three different tumor cell lines with IC50 values ranging from 0.02 to 0.88 mug/mL. The thiocolchicine analogs (5, 5a) were more potent than the colchicine analogs (4, 4a) in the tubulin polymerization assay. In particular, the water-soluble salt 5a merits preclinical development as an antitumor agent. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ N Carolina, Sch Pharm, Nat Prod Lab, Chapel Hill, NC 27599 USA. NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diagnosis, Ft Detrick, MD 21702 USA. RP Lee, KH (reprint author), Univ N Carolina, Sch Pharm, Nat Prod Lab, Chapel Hill, NC 27599 USA. EM khlee@unc.edu RI GOTO, Kyoko/D-8389-2015 OI GOTO, Kyoko/0000-0002-1642-6538 FU NCI NIH HHS [CA 17625] NR 11 TC 19 Z9 20 U1 0 U2 3 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 JAN 3 PY 2005 VL 15 IS 1 BP 235 EP 238 DI 10.1016/j.bmcl.2004.07.098 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA 880FE UT WOS:000225773600045 PM 15582446 ER PT J AU Wu, ZB Cocchi, F Gentles, D Ericksen, B Lubkowski, J DeVico, A Lehrer, RI Lu, WY AF Wu, ZB Cocchi, F Gentles, D Ericksen, B Lubkowski, J DeVico, A Lehrer, RI Lu, WY TI Human neutrophil alpha-defensin 4 inhibits HIV-1 infection in vitro SO FEBS LETTERS LA English DT Article DE HIV-1; defensin; CD4; gp120; surface plasmon resonance; peptide synthesis ID ALPHA-DEFENSINS; ANTIMICROBIAL PEPTIDES; DENDRITIC CELLS; THETA-DEFENSINS; RECEPTOR; RETROCYCLIN; LEUKOCYTES; ENTRY; BETA-DEFENSIN-2; MECHANISMS AB Human neutrophil alpha-defensin 4 (HNP4) is more effective than HNP1-3 in protecting human peripheral blood mononuclear cells from infection by both X4 and R5 HIV-1 strains. HNP4 binds to both CD4 and gp120 approximately two orders of magnitude weaker than does HNP1, and is less effectively sequestered by glycosylated serum proteins than HNP1. These results suggest that the HIV-1 inhibition by HNP4 stems at least partially from a unique and lectin-independent property of HNP4 with CD4 and/or gp120. Our finding identifies an anti-HIV-1 property of HNP4 and may have implications in the development of new antiviral agents for AIDS therapy. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. C1 Univ Maryland, Inst Biotechnol, Inst Human Virol, Baltimore, MD 21201 USA. NCI, Macromol Assembly Struct & Cell Signaling Sect, Frederick, MD 21702 USA. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90095 USA. RP Lu, WY (reprint author), Univ Maryland, Inst Biotechnol, Inst Human Virol, 725 W Lombard St, Baltimore, MD 21201 USA. EM luw@umbi.umd.edu RI Lu, Wuyuan/B-2268-2010; Ericksen, Bryan/F-9047-2012 FU NIAID NIH HHS [AI056264, AI058939] NR 35 TC 55 Z9 61 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD JAN 3 PY 2005 VL 579 IS 1 BP 162 EP 166 DI 10.1016/j.febslet.2004.11.062 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 885PT UT WOS:000226170100026 PM 15620707 ER PT J AU Chen, DY Dundr, M Wang, C Leung, A Lamond, A Misteli, T Huang, S AF Chen, DY Dundr, M Wang, C Leung, A Lamond, A Misteli, T Huang, S TI Condensed mitotic chromatin is accessible to transcription factors and chromatin structural proteins SO JOURNAL OF CELL BIOLOGY LA English DT Article ID RNA-POLYMERASE-I; LIVING HUMAN-CELLS; RIBOSOMAL GENE-TRANSCRIPTION; HISTONE H1; SACCHAROMYCES-CEREVISIAE; DYNAMIC INTERACTION; LINKER HISTONES; RAPID EXCHANGE; REMODELING COMPLEX; INTERPHASE CELLS AB During mitosis, chromosomes are highly condensed and transcription is silenced globally. One explanation for transcriptional repression is the reduced accessibility of transcription factors. To directly test this hypothesis and to investigate the dynamics of mitotic chromatin, we evaluate the exchange kinetics of several RNA polymerase I transcription factors and nucleosome components on mitotic chromatin in living cells. We demonstrate that these factors rapidly exchange on and off ribosomal DNA clusters and that the kinetics of exchange varies at different phases of mitosis. In addition, the nucleosome component H1c-GFP also shows phase-specific exchange rates with mitotic chromatin. Furthermore, core histone components exchange at detectable levels that are elevated during anaphase and telophase, temporally correlating with H3-K9 acetylation and recruitment of RNA polymerase II before the onset of bulk RNA synthesis at mitotic exit. Our findings indicate that mitotic chromosomes in general and ribosomal genes in particular, although highly condensed, are accessible to transcription factors and chromatin proteins. The phase-specific exchanges of nucleosome components during late mitotic phases are consistent with an emerging model of replication independent core histone replacement. C1 Northwestern Univ, Feinberg Sch Med, Dept Cell & Mol Biol, Chicago, IL 60611 USA. NCI, NIH, Bethesda, MD 20892 USA. Univ Dundee, Wellcome Trust Bioctr, Sch Life Sci, Div Gene Regulat & Express, Dundee DD1 5EH, Scotland. RP Huang, S (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Cell & Mol Biol, Chicago, IL 60611 USA. EM s-huang2@northwestern.edu FU NCI NIH HHS [CA77560, R01 CA077560]; Wellcome Trust [073980] NR 75 TC 127 Z9 130 U1 0 U2 3 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 JAN 3 PY 2005 VL 168 IS 1 BP 41 EP 54 PG 14 WC Cell Biology SC Cell Biology GA 893NW UT WOS:000226727500006 PM 15623580 ER PT J AU Yao, PJ Petralia, RS Bushlin, I Wang, Y Furukawa, K AF Yao, PJ Petralia, RS Bushlin, I Wang, Y Furukawa, K TI Synaptic distribution of the endocytic accessory proteins AP180 and CALM SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE synapse; clathrin adaptor; immunoelectron microscopy; subcellular localization ID CLATHRIN ASSEMBLY PROTEIN; VESICLE ENDOCYTOSIS; COATED VESICLES; RECEPTOR INTERNALIZATION; STRUCTURAL ORGANIZATION; MEDIATED ENDOCYTOSIS; APPENDAGE DOMAIN; TERMINAL DOMAIN; ENTH DOMAIN; BINDING AB Clathrin-coated vesicles mediate a variety of endocytosis pathways in cells, including endocytic events at synapses. AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation of clathrin-coated vesicles. Both proteins bind to membrane lipids through their epsin N-terminal homology domains and interact with clathrin and related protein components through their carboxyl-terminal peptide motifs. We examine their neuronal expression and synaptic distribution. We show that both proteins are detected in synapses but demonstrate different distribution patterns. AP180 is located predominantly in presynaptic profiles, whereas CALM is found nonselectively in pre- and postsynaptic profiles and also in perisynaptic processes. These observations reveal an unexpected relationship between AP180 and the presumed nonneuronal homologue CALM. We propose that both AP180 and CALM function as endocytic accessory proteins at synapses, but each may regulate distinct clathrin pathways. Published 2004 Wiley-Liss, Inc. C1 NIA, Neurosci Lab, NIH, Baltimore, MD 21224 USA. Natl Inst Deafness & Other Commun Disorders, Neurosci Lab, NIH, Bethesda, MD 20892 USA. RP Yao, PJ (reprint author), NIA, Neurosci Lab, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM yaopa@grc.nia.nih.gov NR 58 TC 31 Z9 32 U1 0 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 3 PY 2005 VL 481 IS 1 BP 58 EP 69 DI 10.1002/cne.20362 PG 12 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA 876SK UT WOS:000225517600005 PM 15558718 ER PT J AU Tomchik, SM Lu, ZM AF Tomchik, SM Lu, ZM TI Octavolateral projections and organization in the medulla of a teleost fish, the sleeper goby (Dormitator latifrons) SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE auditory; hearing; hindbrain; lateral line; otolithic organ; vestibular ID SOUND-PRODUCING FISH; LATERAL-LINE NERVES; ACOUSTIC RESPONSE PROPERTIES; GOLDFISH CARASSIUS-AURATUS; PRIMARY OCTAVAL NUCLEI; BRAIN-STEM; OPSANUS-TAU; INNER-EAR; HORSERADISH-PEROXIDASE; ASTRONOTUS-OCELLATUS AB This study is the first to employ simultaneous labeling with different colored fluorescent dyes and confocal microscopy to investigate the central projections of the octavolateral nerves in any fish. Three-dimensional reconstructions of the hindbrain octavolateral nuclei were made and overlap of octavolateral projections was assessed in a teleost, the sleeper goby (Dormitator latifrons). The octavolateral nerves, which innervate the otolithic organs, semicircular canals, and lateral lines, project to seven hindbrain nuclei in diverse, complex patterns. The medulla is generally organized with auditory regions dorsal to vestibular regions. The intermediate subdivision of the descending octaval nucleus (DON) receives interdigitating projections from the otolithic organs, and the dorsomedial DON likely integrates multiple auditory inputs. Afferents from the three otolithic organs (the utricle, saccule, and lagena) project to the intermediate DON in approximately equal proportion, supporting physiological evidence that suggests auditory roles for all three otolithic organs in the sleeper goby. The anterior octaval nucleus receives partially segregated inputs from the octavolateral organs. The dorsal division of the magnocellular octaval nucleus (MgON) receives highly overlapping otolithic organ and semicircular canal input, and we propose that this region is a major octaval integration center. Regions in the ventral medulla (the tangential octaval nucleus, ventral DON, and ventral MgON) receive mainly utricular and semicircular canal inputs, suggesting vestibular roles. Each semicircular canal nerve projects to distinct regions of the hindbrain, with little overlap in most octaval nuclei. Efferent neurons receive bilateral input and project unilaterally to the octavolateral organs. (C) 2004 Wiley-Liss, Inc. C1 Univ Miami, Dept Biol, Coral Gables, FL 33146 USA. Univ Miami, Program Neurosci, Miami, FL 33101 USA. Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, NIEHS, Marine & Freshwater Biomed Sci Ctr, Miami, FL 33149 USA. RP Lu, ZM (reprint author), Univ Miami, Dept Biol, 1301 Mem Dr,Room 4, Coral Gables, FL 33146 USA. EM zlu@miami.edu FU NIDCD NIH HHS [R29DC03275, R01DC03275] NR 69 TC 25 Z9 26 U1 0 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 3 PY 2005 VL 481 IS 1 BP 96 EP 117 DI 10.1002/cne.20363 PG 22 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA 876SK UT WOS:000225517600008 PM 15558734 ER PT J AU Tscharke, DC Karupiah, G Zhou, J Palmore, T Irvine, KR Haeryfar, SMM Williams, S Sidney, J Sette, A Bennink, JR Yewdell, JW AF Tscharke, DC Karupiah, G Zhou, J Palmore, T Irvine, KR Haeryfar, SMM Williams, S Sidney, J Sette, A Bennink, JR Yewdell, JW TI Identification of poxvirus CD8(+) T cell determinants to enable rational design and characterization of smallpox vaccines SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MHC CLASS-I; VIRUS CHALLENGE; PEPTIDE BINDING; DENDRITIC CELLS; PROTECTS MICE; RESPONSES; EXPRESSION; INFECTION; IMMUNODOMINANCE; MOUSEPOX AB The large size of poxvirus genomes has stymied attempts to identify determinants recognized by CD8(+) T cells and greatly impeded development of mouse smallpox vaccination models. Here, we use a vaccinia virus (VACV) expression library containing each of the predicted 258 open reading frames to identify five peptide determinants that account for approximately half of the VACV-specific CD8(+) T cell response in C57BL/6 mice. We show that the primary immunodominance hierarchy is greatly affected by the route of VACV infection and the poxvirus strain used. Modified vaccinia virus ankara (MVA), a candidate replacement smallpox vaccine, failed to induce responses to two of the defined determinants. This could not be predicted by genomic comparison of viruses and is not due strictly to limited MVA replication in mice. Several determinants are immunogenic in cowpox and ectromelia (mousepox) virus infections, and immunization with the immunodominant determinant provided significant protection against lethal mousepox. These findings have important implications for understanding poxvirus immunity in animal models and bench-marking immune responses to poxvirus vaccines in humans. C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. Queensland Inst Med Res, EBV Biol Lab, Div Immunol & Infect Dis, Herston, Qld 4006, Australia. Australian Natl Univ, John Curtin Sch Med Res, Div Immunol & Genet, Canberra, ACT 2601, Australia. La Jolla Inst Allergy & Immunol, Div Translat Immunol & Biodef, San Diego, CA 92121 USA. RP Tscharke, DC (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. EM davidT@qimr.edu.au; jyewdell@niaid.nih.gov RI yewdell, jyewdell@nih.gov/A-1702-2012; Karupiah, Gunasegaran/J-4707-2013; Tscharke, David/C-9133-2009 OI Tscharke, David/0000-0001-6825-9172 FU NIAID NIH HHS [N01AI40023, R01 AI056268, R01 AI56268] NR 43 TC 206 Z9 206 U1 1 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 3 PY 2005 VL 201 IS 1 BP 95 EP 104 DI 10.1084/jem.20041912 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 887LA UT WOS:000226306400014 PM 15623576 ER PT J AU Zeng, R Spolski, R Finkelstein, SE Oh, SK Kovanen, PE Hinrichs, CS Pise-Masison, CA Radonovich, MF Brady, JN Restifo, NP Berzofsky, JA Leonard, WJ AF Zeng, R Spolski, R Finkelstein, SE Oh, SK Kovanen, PE Hinrichs, CS Pise-Masison, CA Radonovich, MF Brady, JN Restifo, NP Berzofsky, JA Leonard, WJ TI Synergy of IL-21 and IL-15 in regulating CD8(+) T cell expansion and function SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID VIVO ANTITUMOR-ACTIVITY; IN-VIVO; LYMPHOID HOMEOSTASIS; CYTOKINE RECEPTOR; ADAPTIVE IMMUNITY; IMMUNODEFICIENCY; INTERLEUKIN-15; LYMPHOCYTES; EXPRESSION; AUTOIMMUNITY AB Interleukin (IL)-21 is the most recently recognized of the cytokines that share the common cytokine receptor gamma chain (gamma(c)), which is mutated in humans with X-linked severe combined immunodeficiency. We now report that IL-21 synergistically acts with IL-15 to potently promote the proliferation of both memory (CD44(high)) and naive (CD44(low)) phenotype CD8(+) T cells and augment interferon-gamma production in vitro. IL-21 also cooperated, albeit more weakly, with IL-7, but not with IL-2. Correspondingly, the expansion and cytotoxicity of CD8(+) T cells were impaired in IL-21R(-/-) mice. Moreover, in vivo administration of IL-21 in combination with IL-15 boosted antigen-specific CD8(+) T cell numbers and resulted in a cooperative effect on tumor regression, with apparent cures of large, established B16 melanomas. Thus, our studies reveal that IL-21 potently regulates CD8(+) T cell expansion and effector function, primarily in a synergistic context with IL-15. C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. NIH, Surg Branch, Bethesda, MD 20892 USA. NIH, Vaccine Branch, Bethesda, MD 20892 USA. NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA. RP Leonard, WJ (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. EM wjl@helix.nih.gov RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999] NR 34 TC 418 Z9 435 U1 3 U2 15 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 3 PY 2005 VL 201 IS 1 BP 139 EP 148 DI 10.1084/jem.20041057 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 887LA UT WOS:000226306400018 PM 15630141 ER PT J AU Furman, S Hill, JM Vulih, I Zaltzman, R Hauser, JM Brenneman, DE Gozes, I AF Furman, S Hill, JM Vulih, I Zaltzman, R Hauser, JM Brenneman, DE Gozes, I TI Sexual dimorphism of activity-dependent neuroprotective protein in the mouse arcuate nucleus SO NEUROSCIENCE LETTERS LA English DT Article DE ADNP; sexual dimorphism; hypothalamus; VIP ID VASOACTIVE-INTESTINAL-PEPTIDE; ESTROUS-CYCLE; MESSENGER-RNA; FEMALE RATS; NEUROPEPTIDE-Y; ELECTRICAL-ACTIVITY; NEURONAL SURVIVAL; GENE-EXPRESSION; PREOPTIC AREA; CELLS AB Activity-dependent neuroprotective protein (ADNP) is a highly conserved vasoactive intestinal peptide (VIP) responsive gene that is expressed abundantly in the brain and in the body and is essential for brain formation and embryonic development. Since, VIP exhibits sexual dimorphism in the hypothalamus, the potential differential expression of ADNP in mate and female mice was investigated. Real-time polymerase chain reaction revealed sexual dimorphism in ADNP mRNA expression as well as fluctuations within the estrus cycle. Immunohistochemistry with an antibody to ADNP showed specific staining in the arcuate nucleus of the hypothalamus. ADNP-like immunoreactivity in the arcuate nucleus also exhibited fluctuations during the estrus cycle. Here, brain sections at proestrus were the most immunoreactive and brain sections at estrus-the least. Furthermore, male arcuate nucleus ADNP-like immunoreactivity was significantly lower than that of the female estrus. Many neuropeptides, neurotransmitters and proteins are localized to the arcuate nucleus where they contribute to the regulation of reproductive cyclicity and energy homeostasis. The results presented here suggest that ADNP has a part in the estrus cycle as an affecter or an effector. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NICHHD, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA. RP Gozes, I (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. EM igozes@post.tau.ac.il NR 53 TC 32 Z9 34 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD JAN 3 PY 2005 VL 373 IS 1 BP 73 EP 78 DI 10.1016/j.neulet.2004.09.077 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 881DF UT WOS:000225842900015 PM 15555780 ER PT S AU Vahabzadeh, M Lin, JL Mezghanni, M Gupman, AE Schmittner, J Preston, KL AF Vahabzadeh, M Lin, JL Mezghanni, M Gupman, AE Schmittner, J Preston, KL GP IEEE Comp Soc TI An adaptable assessment generation system for clinical trials complementing human research information system SO 18TH IEEE SYMPOSIUM ON COMPUTER-BASED MEDICAL SYSTEMS, PROCEEDINGS SE IEEE International Symposium on Computer-Based Medical Systems LA English DT Proceedings Paper CT 18th IEEE Symposium on Computer-Based Medical Systems CY JUN 23-24, 2005 CL Dublin, IRELAND SP IEEE Comp Soc Tech Comm Computat Med, Trinity Coll Dublin, Dept Comp Sci, Sci Fdn Ireland AB Computerized testing methods have long been used for presenting clinical questionnaires and are regarded as an efficient and accurate data collection mechanism in human research settings. In order to adapt to the constant addition of new research protocols and incorporate the new data collection forms and questionnaires into our computerized medical information environment, it is necessary to have a solution that requires no modifications to the source code for creating new questionnaires and renders the results in a web browser-based format that can be seamlessly integrated into our patient records system. In this paper we describe our Test and Questionnaire System (TQS) that addresses our requirements and provides full-page browser-based assessments. In addition to managing the new questionnaires, TQS seamlessly communicates and incorporates the clinician-generated assessments built on and for a handheld electronic diary system and provides a powerful and user-friendly data extraction mechanism that allows full or selective data export for further analysis. This solution not only employs both a generic building tool and a flexible data model, but also renders the required questionnaires in a web browser-based environment making it possible for the collected data to become an integral part of our browser-based human research information system. Since its implementation 4 years ago, this system has been used to generate approximately 300 questionnaires at our site and is designed to provide the necessary adaptability and flexibility required for all of the current and potentially a very high percentage of future protocols. C1 NIDA, DHHS, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP NIDA, DHHS, Intramural Res Program, NIH, POB 5180, Baltimore, MD 21224 USA. EM massoudv@nih.gov RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 NR 10 TC 2 Z9 2 U1 1 U2 1 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA SN 2372-9198 BN 0-7695-2355-2 J9 COMP MED SY PY 2005 BP 191 EP 196 DI 10.1109/CBMS.2005.23 PG 6 WC Computer Science, Interdisciplinary Applications; Medical Informatics; Medicine, Research & Experimental; Radiology, Nuclear Medicine & Medical Imaging SC Computer Science; Medical Informatics; Research & Experimental Medicine; Radiology, Nuclear Medicine & Medical Imaging GA BCS05 UT WOS:000230987800031 ER PT S AU McCreedy, ES Cheng, R Hemler, PF Viswanathan, A Wood, BJ McAuliffe, MJ AF McCreedy, ES Cheng, R Hemler, PF Viswanathan, A Wood, BJ McAuliffe, MJ GP IEEE Comp Soc TI Radio frequency ablation registration, segmentation, and fusion tool SO 18TH IEEE SYMPOSIUM ON COMPUTER-BASED MEDICAL SYSTEMS, PROCEEDINGS SE IEEE International Symposium on Computer-Based Medical Systems LA English DT Proceedings Paper CT 18th IEEE Symposium on Computer-Based Medical Systems CY JUN 23-24, 2005 CL Dublin, IRELAND SP IEEE Comp Soc Tech Comm Computat Med, Trinity Coll Dublin, Dept Comp Sci, Sci Fdn Ireland AB The Radio Frequency Ablation Segmentation Tool (RFAST) is a software application developed using NIH's Medical Image Processing Analysis and Visualization (MIPAV) API for the specific purpose of assisting physicians in the planning of radio frequency ablation (RFA) procedures. The RFAST application sequentially leads the physician through the steps necessary to register, fuse, segment, visualize and plan the RFA treatment. Three-dimensional volume visualization of the CT dataset with segmented 3D surface models enables the physician to interactively position the ablation probe to simulate burns and to semi-manually simulate sphere packing in an attempt to optimize probe placement. C1 NIH, Bethesda, MD 20892 USA. RP NIH, Bldg 10, Bethesda, MD 20892 USA. EM mccreedy@mail.nih.gov; ruida@mail.nih.gov; phemler@hse.edu; viswanathana@cc.nih.gov; bwood@cc.nih.gov; mcmatt@mail.nih.gov OI Viswanathan, Anand/0000-0003-3810-6217 NR 8 TC 0 Z9 0 U1 0 U2 0 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA SN 2372-9198 BN 0-7695-2355-2 J9 COMP MED SY PY 2005 BP 259 EP 264 DI 10.1109/CBMS.2005.92 PG 6 WC Computer Science, Interdisciplinary Applications; Medical Informatics; Medicine, Research & Experimental; Radiology, Nuclear Medicine & Medical Imaging SC Computer Science; Medical Informatics; Research & Experimental Medicine; Radiology, Nuclear Medicine & Medical Imaging GA BCS05 UT WOS:000230987800042 ER PT J AU Hadj-Bouziane, F Frankowska, H Meunier, M Boussaoud, D AF Hadj-Bouziane, Fadila Frankowska, Helene Meunier, Martine Boussaoud, Driss BE Kaelbling, LP Saffotti, A TI CONDITIONAL VISUOMOTOR LEARNING AND VIABILITY THEORY SO 19TH INTERNATIONAL JOINT CONFERENCE ON ARTIFICIAL INTELLIGENCE (IJCAI-05) LA English DT Proceedings Paper CT 19th International Joint Conference on Artificial Intelligence (IJCAI 05) CY JUL 30-AUG 05, 2005 CL Edinburgh, SCOTLAND SP BCS, Scottish Enterprise, QinetiQ, BTO, Foresight, Microsoft Research, ERCIM, Intelligent Applications Ltd, IBM, CologNET, Intel, Google DE Basal ganglia; striatum; visuomotor learning; viability theory; electrophysiology; monkey; learning strategy ID BASAL GANGLIA AB In conditional visuomotor learning, several arbitrary associations between visual cues and motor responses have to be learned by trial and error at the same time. Monkeys, as humans, do not achieve this task by randomly trying each possible association. Rather, they use a strategy that organizes sequentially the acquisition of individual stimulus-response associations. Accordingly, neuronal recordings in the monkey striatum, the main basal ganglia structure, reveals two forms of plasticity during learning, a transient one that could constitute the neuronal correlate of the strategy, and a long-lasting one that could reflect the slow neuronal implementation of individual associations. Existing models of basal ganglia function based on reinforcement learning cannot account for this dual process. Hence, we developed a mathematical model of conditional visuomotor learning, inspired from viability theory, which implements both the formation of individual associations and the use of strategies to organize learning. C1 [Hadj-Bouziane, Fadila] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA. RP Hadj-Bouziane, F (reprint author), NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA. EM hadjf@mail.nih.gov; franko@shs.polytechnique.fr; meunier@incm.cnrs-mrs.fr; boussaoud@incm.cnrs-mrs.fr NR 8 TC 0 Z9 0 U1 0 U2 0 PU IJCAI-INT JOINT CONF ARTIF INTELL PI FREIBURG PA ALBERT-LUDWIGS UNIV FREIBURG GEORGES-KOHLER-ALLEE, INST INFORMATIK, GEB 052, FREIBURG, D-79110, GERMANY PY 2005 BP 1602 EP 1603 PG 2 WC Computer Science, Artificial Intelligence SC Computer Science GA BUS48 UT WOS:000290233000280 ER PT S AU Gandjbakhche, AH Vogel, A Amyot, F Chernomordik, V Demos, S Aleman, K Little, R Yarchoan, R Hassan, M AF Gandjbakhche, Amir H. Vogel, Abby Amyot, Franck Chernomordik, Victor Demos, Stavros Aleman, Karen Little, Richard Yarchoan, Robert Hassan, Moinuddin GP IEEE TI Noninvasive multimodality imaging techniques to assess Kaposi's sarcoma SO 2005 27th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vols 1-7 SE PROCEEDINGS OF ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY LA English DT Proceedings Paper CT 27th Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society CY AUG 31-SEP 03, 2005 CL Shanghai, PEOPLES R CHINA SP IEEE Engn Med & Biol Soc, Chinese Acad Engn Sci DE multi-modality imaging; laser Doppler imaging; temperature; multi-spectral imaging; angiogenesis ID ENDOTHELIAL GROWTH-FACTOR AB We evaluated three non-invasive method, thermography, laser Doppler imaging and near infrared multi-spectral imaging to quantitatively assess parameters of vascularity in Kaposi's sarcoma. The KS lesion generally has increased temperature, blood velocity and blood deoxy-hemoglobin. There is a strong correlation between temperature and blood velocity (R= 81, p < 0.001). After treatment with experimental drug (liposomal doxorubicin and interleukin-12), temperature, blood velocity, blood volume and deoxy-hemoglobin of the lesions are reduced from the baseline at week 18. The techniques are objective, easy to perform, and appear to be very sensitive in assessing improvement in the lesions upon administration of therapy. C1 NICHHD, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA. RP Gandjbakhche, AH (reprint author), NICHHD, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1094-687X BN 0-7803-8740-6 J9 P ANN INT IEEE EMBS PY 2005 BP 694 EP 696 DI 10.1109/IEMBS.2005.1616508 PG 3 WC Engineering, Biomedical SC Engineering GA BER00 UT WOS:000238998400182 ER PT S AU Martino, RL Russ, DE Johnson, CA AF Martino, R. L. Russ, D. E. Johnson, C. A. GP IEEE TI Assessing the codetermination of gene transcriptional states using both superscalar and vector multiple processor systems SO 2005 27th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vols 1-7 SE PROCEEDINGS OF ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY LA English DT Proceedings Paper CT 27th Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society CY AUG 31-SEP 03, 2005 CL Shanghai, PEOPLES R CHINA SP IEEE Engn Med & Biol Soc, Chinese Acad Engn Sci DE computational biology; gene expression analysis; microarray analysis; multiple processors; parallel computing; vector processing AB An important goal of functional genomics is to develop methods for determining ways in which individual actions of genes are integrated in the cell. One way of gaining insight into a gene's role in cellular activity is to study its expression pattern in a variety of circumstances and contexts, as it responds to its environment and to the action of other genes. Microarrays provide large-scale surveys of gene expression in which transcript levels can be determined for thousands of genes simultaneously. The coefficient of determination (CoD) has been proposed for the analysis of gene interaction via multivariate expression arrays. Parallel computing is essential to the application of the CoD to a large set of genes because of the large number of expression-based functions that must be statistically designed and compared. The results of the calculation of the CoD for a large set of genes with multiple superscalar processors are presented. A proposal for calculating the CoD,with multiple vector processors is described. Multiple vector processor systems offer the potential to greatly reduce the time to calculate the CoD for a large set of genes. C1 NIH, Dept Hlth & Human Serv, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Martino, RL (reprint author), NIH, Dept Hlth & Human Serv, Div Computat Biosci, Ctr Informat Technol, Bldg 10, Bethesda, MD 20892 USA. OI Russ, Daniel/0000-0003-4040-4416 NR 8 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1094-687X BN 0-7803-8740-6 J9 P ANN INT IEEE EMBS PY 2005 BP 4779 EP 4782 DI 10.1109/IEMBS.2005.1615540 PG 4 WC Engineering, Biomedical SC Engineering GA BER00 UT WOS:000238998404082 ER PT S AU Wu, CWH AF Wu, Carolyn W. -H. GP IEEE TI Peripheral somatosensory stimulation induced cortical plasticity and its clinical application on functional restoration in chronic stroke. SO 2005 27th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vols 1-7 SE PROCEEDINGS OF ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY LA English DT Proceedings Paper CT 27th Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society CY AUG 31-SEP 03, 2005 CL Shanghai, PEOPLES R CHINA SP IEEE Engn Med & Biol Soc, Chinese Acad Engn Sci ID HAND FUNCTION-TEST; MOTOR CORTEX; MOVEMENTS; PERFORMANCE; INPUT AB -Somatosensory input is required for motor control(1-4) and motor learning(5). It has been shown that a short period of peripheral somatosensory stimulation (PSS), leads to increases in motor cortical excitability and enhancement of motor memory encoding that outlast the stimulation period(6-9). However, the mechanisms by which PSS modulates cortical activites and its clinical application in restoring functions after brain injuries are not completely understood. Here, we conduced two sets of experiments to address these issues. C1 NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA. RP Wu, CWH (reprint author), NINDS, Human Cort Physiol Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 15 TC 0 Z9 0 U1 1 U2 1 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1094-687X BN 0-7803-8740-6 J9 P ANN INT IEEE EMBS PY 2005 BP 5230 EP 5233 DI 10.1109/IEMBS.2005.1615658 PG 4 WC Engineering, Biomedical SC Engineering GA BER00 UT WOS:000238998404200 ER PT S AU Weinrich, M AF Weinrich, M GP IEEE TI Engineering new approaches to rehabilitation SO 2005 2ND INTERNATINOAL IEEE/EMBS CONFERENCE ON NEURAL ENGINEERING SE International IEEE EMBS Conference on Neural Engineering LA English DT Proceedings Paper CT 2nd International IEEE/EMBS Conference on Neural Engineering CY MAR 16-20, 2005 CL Arlington, VA SP IEEE, EMBS, Natl Sci Fdn, Inst Phys, Off Naval Res Global C1 NICHHD, Natl Ctr Rehabil Res, NIH, Bethesda, MD 20892 USA. RP Weinrich, M (reprint author), NICHHD, Natl Ctr Rehabil Res, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1948-3546 BN 0-7803-8709-0 J9 I IEEE EMBS C NEUR E PY 2005 BP 61 EP 61 PG 1 WC Computer Science, Artificial Intelligence; Computer Science, Interdisciplinary Applications; Engineering, Biomedical SC Computer Science; Engineering GA BCI92 UT WOS:000229610400017 ER PT S AU He, Y Fu, MC Marcus, SI AF He, Ying Fu, Michael C. Marcus, Steven I. GP IEEE TI A two-timescale simulation-based gradient algorithm for weighted cost Markov Decision Processes SO 2005 44th IEEE Conference on Decision and Control & European Control Conference, Vols 1-8 SE IEEE CONFERENCE ON DECISION AND CONTROL - PROCEEDINGS LA English DT Proceedings Paper CT 44th IEEE Conference on Decision Control/European Control Conference (CCD-ECC) CY DEC 12-15, 2005 CL Seville, SPAIN SP IEEE Control Syst Soc, European Union Control Assoc, IFAC, INFORMS, SIAM, SICE, Honeywell, MathWorks ID STOCHASTIC-APPROXIMATION; PARAMETRIC OPTIMIZATION; REWARD PROCESSES; MODELS AB We develop a novel two-timescale simulation-based gradient algorithm for weighted cost Markov Decision Process (MDP) problems, illustrate the effectiveness of this algorithm by carrying out numerical experiments on a parking example, and compare the algorithm with two other algorithms in the literature. C1 Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA. RP He, Y (reprint author), Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA. NR 14 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 0191-2216 BN 0-7803-9567-0 J9 IEEE DECIS CONTR P PY 2005 BP 8022 EP 8027 PG 6 WC Automation & Control Systems SC Automation & Control Systems GA BFB21 UT WOS:000240653707114 ER PT S AU Le Meunier, L Hadi, M de Silva, R Carson, JM Dieckmann, W Bacharach, SL AF Le Meunier, Ludovic Hadi, Mohiuddin de Silva, Ranil Carson, Joann M. Dieckmann, William Bacharach, Stephen L. BE Yu, B TI Comparison of three methods of partial volume correction in dynamic PET cardiac imaging - A phantom and a pig study SO 2005 IEEE Nuclear Science Symposium Conference Record, Vols 1-5 SE IEEE NUCLEAR SCIENCE SYMPOSIUM - CONFERENCE RECORD LA English DT Proceedings Paper CT Nuclear Science Symposium/Medical Imaging Conference CY OCT 23-29, 2005 CL Fajardo, PR SP IEEE Nucl & Plasma Sci Soc, Brookhaven Natl Lab, CEA Saclay, DOE, CERN, Lawrence Berkeley Natl Lab, Lawrence Livermore Natl Lab, Stanford Linear Accelerator Ctr, Univ Calif Davis, Univ Washington ID POSITRON EMISSION; TOMOGRAPHY AB We compared 3 methods of correcting the underestimation in measurements of myocardial radiotracer uptake due to partial volume (PV) effects in cardiac PET. Methods: Measurements were made on a static heart phantom and on 12 pigs undergoing gated cardiac MRI and 2 dynamic (H2O)-O-15 PET. The 3 methods to compute PV correction factors (PVCF) were: 1. a gated MRI myocardial mask temporally and spatially blurred to the PET resolution; 2. an extra-vascular image (EV) created by subtracting the arterial phase of the (H2O)-O-15 bolus from a transmission image; 3. kinetic modeling (Fit) of the water data. Results: The phantom study confirmed that 7.0 mm Gaussian blurring simulated the scanner resolution, and that the water subtraction correctly determined PVCF from EV (vs theory and vs blurred MRI). PVCF for 60 regions were computed from the 12 pigs using each method. There was no significant systematic difference between PVCF obtained from the 3 methods. When we used only one water acquisition, all the slopes (intercepts) except EV vs MRI were not significantly lower than unity (greater than zero) but there is large variability in the data. When we used two water acquisitions summed together, we saw a slight improvement in the correlations between the methods although the variability did not go down as much its expected. Several factors may contribute to the remaining variability, and to any potential systematic differences which may be present but which we were unable to detect. Conclusion: in general we found a good agreement between the three methods. We believe our data show that accurate partial volume corrections can be made in the myocardium. C1 NIH, Bethesda, MD 20892 USA. RP Le Meunier, L (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1082-3654 BN 0-7803-9221-3 J9 IEEE NUCL SCI CONF R PY 2005 BP 2359 EP 2363 PG 5 WC Instruments & Instrumentation; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Instruments & Instrumentation; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA BFH22 UT WOS:000241851903120 ER PT S AU Gottlieb, EJ Lai, B Xu, XC Cannata, J Yen, J Zhou, QF Han, PD Ameri, H Ratanapakorn, T Barnes, A Humayun, M Shung, KK AF Gottlieb, EJ Lai, B Xu, XC Cannata, J Yen, J Zhou, QF Han, PD Ameri, H Ratanapakorn, T Barnes, A Humayun, M Shung, KK GP IEEE TI PMN-PT high frequency ultrasonic needle transducers for pulsed wave Doppler in the eye SO 2005 IEEE Ultrasonics Symposium, Vols 1-4 SE ULTRASONICS SYMPOSIUM LA English DT Proceedings Paper CT IEEE International Ultrasonics Symposium CY SEP 18-21, 2005 CL Rotterdam, NETHERLANDS SP IEEE AB The purpose of this study is to develop miniature intraocular transducers for pulsed wave Doppler. The intended use of this device is for in-vivo high frequency pulsed wave Doppler detection of blood flow in the posterior portion of the eye. High frequency ultrasonic needle transducers were fabricated using lead magnesium niobate-lead titanate (PMN-33%PT) as the active piezoelectric material. The measured center frequency and bandwidth of the device was 44 MHz and 36 % respectively. The electrical impedance magnitude and phase were 74 Omega and - 58 degrees respectively. A custom high frequency pulsed wave Doppler system has been developed based on the coherent demodulation and sample and hold techniques. An intial in-vivo Doppler measurement was performed on the retinal arterial blood flow of a New England Cottontail rabbit. A pulse repetition frequency of 44 kHz has shown a Doppler shift frequency of 2 kHz corresponding to an approximate velocity of 38.5 mm/s for a vessel diameter of less than 1 nun in the retina. C1 Univ So Calif, Dept Biomed Engn, NIH, Resource Med Ultrason Technol, Los Angeles, CA 90089 USA. RP Gottlieb, EJ (reprint author), Univ So Calif, Dept Biomed Engn, NIH, Resource Med Ultrason Technol, Los Angeles, CA 90089 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1051-0117 BN 0-7803-9382-1 J9 ULTRASON PY 2005 BP 2227 EP 2230 PG 4 WC Acoustics; Engineering, Biomedical; Physics, Applied SC Acoustics; Engineering; Physics GA BDY24 UT WOS:000236090703090 ER PT S AU Mao, S Nie, L Thoma, GR AF Mao, S Nie, L Thoma, GR GP IEEE TI Unsupervised style classification of document page images SO 2005 International Conference on Image Processing (ICIP), Vols 1-5 SE IEEE International Conference on Image Processing (ICIP) LA English DT Proceedings Paper CT IEEE International Conference on Image Processing (ICIP 2005) CY SEP 11-14, 2005 CL Genoa, ITALY SP IEEE AB Style classification of document page images is crucial for logical structure analysis of heterogeneous collections of documents. Both layout and contextual features contain significant information about document styles. Most existing methods. are supervised methods in which specific document models or classifiers are learned from a training set of document page images with known class labels. In this paper, we propose an unsupervised classification method that involves no training or manual selection of algorithm parameters. In particular, we first represent each document page as an ordered labeled X-Y tree. A tree matching algorithm is then used to compute style dissimilarity between two document pages. We propose a set of tree edit cost functions based on Karl Pearson distance between two multivariate feature observations, which is robust to the over-segmentation problem and zone length variations of same logical entities. Finally, the K-medoids algorithm is used to find an optimal grouping of the trees into K clusters, each of which corresponds to a distinct document style. We evaluate our algorithm on test datasets with different cluster sizes and degrees of style similarity. Experimental results show our algorithm achieved an average classification accuracy of 95.69% over six datasets consisting of 150 pages of 11 different styles. C1 US Natl Lib Med, Bethesda, MD 20894 USA. RP Mao, S (reprint author), US Natl Lib Med, Bethesda, MD 20894 USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1522-4880 BN 0-7803-9134-9 J9 IEEE IMAGE PROC PY 2005 BP 1245 EP 1248 PG 4 WC Computer Science, Artificial Intelligence; Imaging Science & Photographic Technology SC Computer Science; Imaging Science & Photographic Technology GA BDW08 UT WOS:000235773301118 ER PT J AU Rapaka, RS Sadee, W AF Rapaka, RS Sadee, W TI Editorial: Theme issue "Drug addiction - From basic research to therapies SO AAPS JOURNAL LA English DT Editorial Material C1 NIDA, Bethesda, MD 20892 USA. Ohio State Univ, Coll Med & Publ Hlth, Columbus, OH 43210 USA. RP Rapaka, RS (reprint author), NIDA, Bethesda, MD 20892 USA. EM rrapaka@nida.nih.gov; sadee-1@medctr.osu.edu NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC PHARMACEUTICAL SCIENTISTS PI ALEXANDRIA PA 1650 KING ST, STE 200, ALEXANDRIA, VA 22314-2747 USA SN 1550-7416 J9 AAPS J PY 2005 VL 7 IS 2 AR UNSP 33 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 007SX UT WOS:000234991100008 ER PT J AU Sobczak, A Blazejczyk, M Piszczek, G Zhao, G Kuznicki, J Wojda, U AF Sobczak, A Blazejczyk, M Piszczek, G Zhao, G Kuznicki, J Wojda, U TI Calcium-binding calmyrin forms stable covalent dimers in vitro, but in vivo is found in monomeric form SO ACTA BIOCHIMICA POLONICA LA English DT Article; Proceedings Paper CT 29th Congress of the Federation-of-European-Biochemical-Societies Celebrating the 40th Anniversary of FEBS CY JUN 26-JUL 01, 2004 CL Warsaw, POLAND SP Federat European Biochem Soc, Polish Biochem Soc DE EF-hand calcium-binding proteins; calmyrin monomer; covalent dimer; human lymphocytes ID ALPHA(IIB) CYTOPLASMIC DOMAIN; PROTEIN-KINASE; CA2+-BINDING PROTEINS; CIB BINDING; DNA-BINDING; CALCYCLIN; FAMILY; INTERACTS; S100; ACTIVATION AB The EF-hand Ca2+-binding protein calmyrin is expressed in many tissues and can interact with multiple effector proteins, probably as a sensor transferring Ca2+ signals. As oligomerization may represent one of Ca2+-signal transduction mechanisms, we characterised recombinant calmyrin forms using non-reducing SDS/PAGE, analytical ultracentrifugation and gel filtration. We also aimed at identification of biologically active calmyrin forms. Non-reducing SDS/PAGE showed that in vitro apo- and Ca2+-bound calmyrin oligomerizes forming stable intermolecular disulfide bridges. Ultracentrifugation indicated that at a 220 mu M initial protein concentration apo-calmyrin existed in an equilibrium of a 21.9 kDa monomer and a 43.8 kDa dimer (trimeric or tetrameric species were not detected). The dimerization constant was calculated as K-a = 1.78 x 10(3) M-1 at 6 degrees C. Gel filtration of apo- and Ca2+-bound calmyrin at a 100 mu M protein concentration confirmed an equilibrium of a monomer and a covalent dimer state. Importantly, both monomer and dimer underwent significant conformational changes in response to binding of Ca2+. However, when calmyrin forms were anal lyzed under non-reducing conditions in cell extracts by Western blotting, only monomeric calmyrin was detected inhuman platelets and lymphocytes, and in rat brain. Moreover, in contrast to recombinant calmyrin, crosslinking did not preserve any dimeric species of calmyrin regardless of Ca2+ concentrations. In summary, our data indicate that although calmyrin forms stable covalent dimers in vitro, it most probably functions as a monomer in vivo. C1 Int Inst Mol & Cell Biol, Lab Neurodegenerat, Warsaw, Poland. NHLBI, NIH, Biochem Lab, Bethesda, MD 20892 USA. M Nencki Inst Expt Biol, Lab Calcium Binding Prot, Warsaw, Poland. RP Wojda, U (reprint author), Int Inst Mol & Cell Biol, Lab Neurodegenerat, Warsaw, Poland. EM ulawojda@iimcb.gov.pl RI Wojda, Urszula/M-6079-2015 OI Wojda, Urszula/0000-0002-4525-2004 NR 45 TC 6 Z9 14 U1 0 U2 8 PU ACTA BIOCHIMICA POLONICA PI WARSAW PA PASTEURA 3, 02-093 WARSAW, POLAND SN 0001-527X J9 ACTA BIOCHIM POL JI Acta Biochim. Pol. PY 2005 VL 52 IS 2 BP 469 EP 476 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 942JV UT WOS:000230279600023 PM 15933764 ER PT J AU Sekar, K Rajakannan, V Gayathri, D Velmurugan, D Poi, MJ Dauter, M Dauter, Z Tsai, MD AF Sekar, K Rajakannan, V Gayathri, D Velmurugan, D Poi, MJ Dauter, M Dauter, Z Tsai, MD TI Atomic resolution (0.97 angstrom) structure of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A(2) SO ACTA CRYSTALLOGRAPHICA SECTION F-STRUCTURAL BIOLOGY AND CRYSTALLIZATION COMMUNICATIONS LA English DT Article ID X-RAY STRUCTURE; CRYSTAL-STRUCTURES; FUNCTIONAL ROLES; CALCIUM-ION; REFINEMENT; INHIBITOR; INTERFACE; MECHANISM; COMPLEX C1 Indian Inst Sci, Bioinformat Ctr, Bangalore 560012, Karnataka, India. Indian Inst Sci, Supercomp Educ & Res Ctr, Bangalore 560012, Karnataka, India. Univ Madras, Dept Crystallog & Biophys, Madras 600025, Tamil Nadu, India. Ohio State Univ, Dept Chem & Biochem, Columbus, OH 43210 USA. Ohio State Univ, Ohio State Biotechnol Program, Columbus, OH 43210 USA. Acad Sinica, Taipei, Taiwan. Brookhaven Natl Lab, SAIC Frederick Inc, Basic Res Program, Upton, NY 11973 USA. NCI, Macromol Crystallog Lab, Synchrotron Radiat Res Sect, Upton, NY 11973 USA. Brookhaven Natl Lab, Upton, NY 11973 USA. RP Sekar, K (reprint author), Indian Inst Sci, Bioinformat Ctr, Bangalore 560012, Karnataka, India. EM sekar@physics.iisc.ernet.in FU NIGMS NIH HHS [R01 GM057568, GM 41788, GM 57568] NR 29 TC 9 Z9 9 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1744-3091 J9 ACTA CRYSTALLOGR F JI Acta Crystallogr. F-Struct. Biol. Cryst. Commun. PD JAN PY 2005 VL 61 BP 3 EP 7 DI 10.1107/S1744309104021748 PN 1 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics; Crystallography SC Biochemistry & Molecular Biology; Biophysics; Crystallography GA 968IX UT WOS:000232157000002 PM 16508077 ER PT J AU Okujava, V Natishvili, T Mishkin, M Gurashvili, T Chipashvili, S Bagashvili, T Andronikashvili, G Kvernadze, G AF Okujava, V Natishvili, T Mishkin, M Gurashvili, T Chipashvili, S Bagashvili, T Andronikashvili, G Kvernadze, G TI One-trial visual recognition in cats SO ACTA NEUROBIOLOGIAE EXPERIMENTALIS LA English DT Article DE visual nonspatial memory; visuospatial memory; delayed matching-to-sample; delayed nonmatching-to-sample; manipulatory and locomotor responses ID MEMORY; MONKEYS AB The ability of normal cats to perform delayed matching- and nonmatching-to-sample with trial-unique stimuli was investigated both in a modified Wisconsin General Testing Apparatus requiring manipulatory responses and in a Nencki-type testing room requiring locomotor responses. Cats trained in the WGTA learned the two tasks at about the same rate, on average, as that reported for monkeys. However, unlike monkeys, whose strong preference for novelty facilitates their learning of the nonmatching rule and retards their learning of the matching rule, the cats learned the two different rules at about the same rate, suggesting that cats do not share the monkey's strong preference for novelty. In contrast to their relatively rapid learning of the manipulatory versions of the two tasks, cats learned the locomotor versions only slowly or even failed to learn. Experimental analysis indicated that a major source of the cats' difficulty on these locomotor versions was interference from a strong tendency in the large testing room to use visuospatial strategies. Nevertheless, once the matching or nonmatching rule was learned at short delays, whether in the WGTA or the testing room, the cats performed at criterion levels without further training even at delays of 10 minutes, indicating that this species, like monkeys, has a highly developed long-term recognition memory ability. C1 Res Ctr Expt Neurol, GE-0192 Tbilisi, Rep of Georgia. NIMH, NIH, Bethesda, MD 20892 USA. RP Okujava, V (reprint author), Res Ctr Expt Neurol, 2-A Gudamakari Str, GE-0192 Tbilisi, Rep of Georgia. EM okujava@geo.net.ge NR 16 TC 10 Z9 10 U1 1 U2 3 PU NENCKI INST EXPERIMENTAL BIOLOGY PI WARSAW PA UL PASTEURA 3, 02-093 WARSAW, POLAND SN 0065-1400 J9 ACTA NEUROBIOL EXP JI Acta Neurobiol. Exp. PY 2005 VL 65 IS 2 BP 205 EP 211 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 932YM UT WOS:000229590700014 PM 15960308 ER PT J AU Steinhoff, MC Walker, CF Rimoin, AW Hamza, HS AF Steinhoff, MC Walker, CF Rimoin, AW Hamza, HS TI A clinical decision rule for management of streptococcal pharyngitis in low-resource settings SO ACTA PAEDIATRICA LA English DT Article DE streptococcus; pharyngitis; pediatrics; diagnosis; clinical decision ID GUIDELINES; DIAGNOSIS; THROAT AB Background: Most of the world's children live in regions where laboratory facilities are not available. In these regions, clinical prediction rules can be useful to guide clinicians' decisions on antibiotic therapy for streptococcal pharyngitis, and to reduce routine presumptive antibiotic therapy for all pharyngitis. Methods: Prospective cohort study to assess diagnostic signs and develop a prediction rule. Bivariate and multivariate analyses were used to develop clinical rules. Participants were 410 children in Cairo, Egypt, aged from 2 to 12 y, presenting with complaint of sore throat and whose parents provided consent. Main outcome measures included presence of signs and symptoms, and positive group A beta hemolytic streptococcal (GABHS) culture. Results: 101 (24.6%) children had positive GABHS culture. Pharyngeal exudate, tender or enlarged anterior cervical lymph nodes, season, absence of rash, or cough or rhinitis were associated with positive culture in bivariate and multivariate analyses. Three variables ( enlarged nodes, no rash, no rhinitis), when used in a cumulative score, showed 92% sensitivity and 38% specificity in these children. Conclusions: The proposed three-variable clinical prediction rule for GABHS may be useful when diagnostic laboratories are not available. In this setting, the rule identified more than 90% of true cases. Compared to universal treatment of all pharyngitis, the rule will reduce antibiotic use in GABHS-negative cases by about 40%. C1 Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. NICHHD, NIH, Rockville, MD USA. Cairo Univ, Dept Pediat, Cairo, Egypt. Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA. RP Steinhoff, MC (reprint author), 615 N Wolfe St,Rm E5521, Baltimore, MD 21205 USA. EM msteinho@jhsph.edu NR 18 TC 15 Z9 16 U1 1 U2 2 PU TAYLOR & FRANCIS AS PI OSLO PA PO BOX 12 POSTHUSET, NO-0051 OSLO, NORWAY SN 0803-5253 J9 ACTA PAEDIATR JI Acta Paediatr. PY 2005 VL 94 IS 8 BP 1038 EP 1042 DI 10.1080/08035250510027994 PG 5 WC Pediatrics SC Pediatrics GA 957SP UT WOS:000231393900009 PM 16188846 ER PT J AU Breman, J Rosen, J Manclark, C Meade, B Collins, W Lobel, H Saliou, P Robert, J Campaore, P Miller, M AF Breman, J. Rosen, J. Manclark, C. Meade, B. Collins, W. Lobel, H. Saliou, P. Robert, J. Campaore, P. Miller, M. TI Malaria chemoprophylaxis and the serologic response to measles and diphtheria-tetanus-whole-cell pertussis vaccines [MIM-JB-140947] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA. NIH, Howard Hughes Med Inst, Res Program, Bethesda, MD 20892 USA. US FDA, Div Bacterial Prod, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA. Ctr Dis Control & Prevent, Div Parasit Dis, Natl Ctr Infect Dis, Atlanta, GA USA. Aventis Pasteur, Paris, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S233 EP S234 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600371 ER PT J AU Chelimo, K Ofulla, A Narum, D Kazura, J Lanar, D John, C AF Chelimo, K. Ofulla, A. Narum, D. Kazura, J. Lanar, D. John, C. TI Antibodies to Plasmodium falciparum antigens vary by age and antigen in children in a malaria holoendemic area of Kenya [MIM-KC-31452] SO ACTA TROPICA LA English DT Meeting Abstract C1 [Chelimo, K.] Kenya Govt Med Res Ctr, Kisian, Kenya. [Ofulla, A.] Maseno Univ, Maseno, Kenya. [Narum, D.] NIH, Bethesda, MD 20892 USA. [Kazura, J.] Case Western Reserve Univ, Cleveland, OH 44106 USA. [Lanar, D.] Walter Reed Army Med Ctr, Walter Reed Army Inst Res, Washington, DC 20307 USA. [John, C.] Univ Minnesota, Minneapolis, MN USA. RI Lanar, David/B-3560-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S149 EP S150 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600233 ER PT J AU Dicko, A Diemert, D Sagara, I Sogoba, M Dolo, A Long, C Diallo, D Saul, A Miller, L Doumbo, O AF Dicko, A. Diemert, D. Sagara, I. Sogoba, M. Dolo, A. Long, C. Diallo, D. Saul, A. Miller, L. Doumbo, O. TI Phase 1 study of the safety and immunogenicity of the AMA1-C1/Alhydrogel (R) Vaccine for Plasmodium falciparum malaria in semi-immune malian adults [MIM-DD-109020] SO ACTA TROPICA LA English DT Meeting Abstract C1 Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali. NIAID, Malaria Vaccine Dev Branch, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S85 EP S86 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600130 ER PT J AU Fay, M Halloran, M Follmann, D Diemert, D Dicko, A Thera, M Sagara, I Klion, A Doumbo, O Saul, A AF Fay, M. Halloran, M. Follmann, D. Diemert, D. Dicko, A. Thera, M. Sagara, I. Klion, A. Doumbo, O. Saul, A. TI The design of a phase 2 malaria vaccine trial based on a cohort study [MIM-MF-125074] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIAID, Bethesda, MD 20892 USA. Emory Univ, Atlanta, GA 30322 USA. Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S419 EP S420 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600677 ER PT J AU Fouda, G Leke, R Sama, G Long, C Taylor, D Johnson, A AF Fouda, G. Leke, R. Sama, G. Long, C. Taylor, D. Johnson, A. TI Characterization of the malarial antibody response of Cameroonian infants throughout the first year of life using a multiplex assay [MIM-GF-181010] SO ACTA TROPICA LA English DT Meeting Abstract C1 Georgetown Univ, Dept Biol, Washington, DC 20057 USA. Ctr Biotechnol, Immunol Lab, Yaounde, Cameroon. Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S14 EP S14 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600020 ER PT J AU Heinrichs, V Mundorff, E Makobongo, M Gratepanche, S Bass, S Whalen, R Locher, C AF Heinrichs, V. Mundorff, E. Makobongo, M. Gratepanche, S. Bass, S. Whalen, R. Locher, C. TI Improved cross-strain recognition of polymorphic Plasmodium falciparum PfEMPI CIDR1-as induced by shuffled PfEMPI CIDR1-a vaccine antigens [MIM-VH-19182] SO ACTA TROPICA LA English DT Meeting Abstract C1 Maxygen, Dept Mol Biol, Redwood City, CA 94063 USA. Maxygen, Dept Infect Dis, Redwood City, CA 94063 USA. NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S310 EP S310 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600498 ER PT J AU Kone, A Dijmde, A Mu, J Plowe, C Doumbo, O Wellems, T AF Kone, A. Dijmde, A. Mu, J. Plowe, C. Doumbo, O. Wellems, T. TI Association of PfNHE polymorphisms and quinine usage in Mali [MIM-AK-15020] SO ACTA TROPICA LA English DT Meeting Abstract C1 Univ Bamako, Mol Epidemiol & Drug Resistance Unit, Malaria Res & Training Ctr, Dept Epidemiol Parasit Dis,Fac Med Pharm & Odonto, Bamako, Mali. Univ Maryland, Malaria Sect, Ctr Vaccine Dev, College Pk, MD 20742 USA. NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S87 EP S87 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600132 ER PT J AU Long, C Miura, K Zhou, H Moretz, S Torres, S Miles, A Miller, L Saul, A Mahanty, S AF Long, C. Miura, K. Zhou, H. Moretz, S. Torres, S. Miles, A. Miller, L. Saul, A. Mahanty, S. TI Development, standardization, and application of an in vitro Plasmodium falciparum growth inhibition assay [MIM-CL-245672] SO ACTA TROPICA LA English DT Meeting Abstract C1 [Long, C.; Miura, K.; Zhou, H.; Moretz, S.; Torres, S.; Miles, A.; Miller, L.; Saul, A.; Mahanty, S.] NIAID, Malaria Vacine Dev Branch, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S312 EP S313 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600502 ER PT J AU Makobongo, M Gratepanche, S Long, C Miller, L AF Makobongo, M. Gratepanche, S. Long, C. Miller, L. TI Rapid and robust induction of anti-PfEMP1 CIDR1-alpha antibodies protects against Plasmodium falciparum-FVO challenge in Aotus monkeys [MIM-MM-267168] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIAID, Malaria Vaccine Dev Branch, NIH, Bethesda, MD 20892 USA. Inst Pasteur, Paris, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S58 EP S58 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600088 ER PT J AU Martin, L Malkin, E Medina, S Orcutt, A Tierney, E Moorthy, V Long, C Mahanty, S Miller, L Saul, A AF Martin, L. Malkin, E. Medina, S. Orcutt, A. Tierney, E. Moorthy, V. Long, C. Mahanty, S. Miller, L. Saul, A. TI Improving the immunogenicity of MSP1.42 Alhydrogel vaccines by the addition of CPG 7909 [MIM-LM-72314] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIH, Malaria Vaccine Dev Branch, Rockville, MD USA. PATH, Malaria Vaccine Initiat, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S57 EP S57 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600087 ER PT J AU Metenou, S Suguitan, A Fouda, G Tako, E Long, C Leke, R Taylor, D AF Metenou, S. Suguitan, A. Fouda, G. Tako, E. Long, C. Leke, R. Taylor, D. TI Fetal immune response to malarial antigens in Yaounde, Cameroon [MIM-SM-68328] SO ACTA TROPICA LA English DT Meeting Abstract C1 Georgetown Univ, Dept Biol, Washington, DC 20057 USA. NIAID, Malaria Vaccine Dev Unit, NIH, Rockville, MD 20852 USA. Univ Yaounde 1, Ctr Biotechnol, Fac Med & Biomed Sci, Yaounde, Cameroon. RI Metenou, Simon/C-1101-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S160 EP S160 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600249 ER PT J AU Ogutu, B Kawuondo, K Prudhome, W Remich, S Nanakorn, A Ohrt, C AF Ogutu, B. Kawuondo, K. Prudhome, W. Remich, S. Nanakorn, A. Ohrt, C. TI Microscopy for clinical trials [MIM-KK-38600] SO ACTA TROPICA LA English DT Meeting Abstract C1 Kenya Govt Med Res Ctr, Clin Res Ctr, Walter Read Project, Nairobi, Kenya. Walter Reed Army Inst Res, Silver Spring, MD USA. IDC, Bangkok, Thailand. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S301 EP S302 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600483 ER PT J AU Prudhomme, W Smith, D Breman, J McKenzie, F AF Prudhomme, W. Smith, D. Breman, J. McKenzie, F. TI Predicting the impact of intermittent preventive treatment for infants on the spread of drug resistant malaria [MIM-WP-321425] SO ACTA TROPICA LA English DT Meeting Abstract C1 [Prudhomme, W.; Smith, D.; Breman, J.; McKenzie, F.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA. RI Smith, David/L-8850-2013 OI Smith, David/0000-0003-4367-3849 NR 0 TC 0 Z9 0 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S135 EP S135 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600208 ER PT J AU Saul, A Miles, A Aebig, J Mcclellan, H Rausch, K Zhu, D Mullen, G Long, C Miller, L AF Saul, A. Miles, A. Aebig, J. Mcclellan, H. Rausch, K. Zhu, D. Mullen, G. Long, C. Miller, L. TI Adjuvant formulations for recombinant malaria vaccines [MIM-AS-77610] SO ACTA TROPICA LA English DT Meeting Abstract C1 [Saul, A.; Miles, A.; Aebig, J.; Mcclellan, H.; Rausch, K.; Zhu, D.; Mullen, G.; Long, C.; Miller, L.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S315 EP S315 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600506 ER PT J AU Simard, F Licht, M Lehmann, T AF Simard, F. Licht, M. Lehmann, T. TI Molecular evidence for selection acting on the Defensin gene in the Anopheles gambiae complex [MIM-FS-115040] SO ACTA TROPICA LA English DT Meeting Abstract C1 OCEAC IRD, Yaounde, Cameroon. CDC, Atlanta, GA 30333 USA. NIAID, NIH, Rockville, MD USA. RI SIMARD, Frederic/J-9489-2016 OI SIMARD, Frederic/0000-0002-2871-5329 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S107 EP S107 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600164 ER PT J AU Thera, M Dicko, A Coulibaly, D Sogoba, M Sagara, I Baby, M Diallo, D Plowe, C Diemert, D Doumbo, O AF Thera, M. Dicko, A. Coulibaly, D. Sogoba, M. Sagara, I. Baby, M. Diallo, D. Plowe, C. Diemert, D. Doumbo, O. TI Implementing phase I trials of malaria vaccine candidates in Mali, West Africa [MIM-DC-135470] SO ACTA TROPICA LA English DT Meeting Abstract C1 Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali. Univ Maryland, Sch Med, Ctr Vaccine Dev, Baltimore, MD 21201 USA. NIH, Malaria Vaccine Dev Branch, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S421 EP S422 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600680 ER PT J AU Wellems, T Diallo, D Guindo, A Fairhurst, R Doumbo, O AF Wellems, T. Diallo, D. Guindo, A. Fairhurst, R. Doumbo, O. TI A mechanism of malaria protection by hemoglobin C [MIM-TW-8570] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIAID, NIH, Bethesda, MD 20892 USA. Univ Bamako, Fac Med Pharm & Odontostomatol, Bamako, Mali. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S90 EP S90 PG 1 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600137 ER PT J AU Wu, Y Miles, A Lambert, L Muratova, O Orcutt, A Sattabongkot, J Keister, D Miller, L Long, C Saul, A AF Wu, Y. Miles, A. Lambert, L. Muratova, O. Orcutt, A. Sattabongkot, J. Keister, D. Miller, L. Long, C. Saul, A. TI Aiming for sustained high-level antibody responses-Formulation of Pfs25 and Pvs25 transmission blocking vaccines [MIM-YW-345345] SO ACTA TROPICA LA English DT Meeting Abstract C1 NIAID, Malaria Vaccine Dev Branch, Rockville, MD USA. Armed Forces Res Inst Med Sci, Dept Entomol, Bangkok 10400, Thailand. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PY 2005 VL 95 BP S317 EP S318 PG 2 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA V80CY UT WOS:000205415600510 ER PT J AU Strasser, AA Kaufmann, V Jepson, C Perkins, KA Pickworth, WB Wileyto, EP Rukstalis, M Audrain-McGovern, J Lerman, C AF Strasser, AA Kaufmann, V Jepson, C Perkins, KA Pickworth, WB Wileyto, EP Rukstalis, M Audrain-McGovern, J Lerman, C TI Effects of different nicotine replacement therapies on postcessation psychological responses SO ADDICTIVE BEHAVIORS LA English DT Article DE nicotine replacement therapy; postcessation; psychological ID SMOKING WITHDRAWAL DYNAMICS; NEGATIVE AFFECT; NASAL SPRAY; TRANSDERMAL NICOTINE; TOBACCO WITHDRAWAL; CIGARETTE-SMOKING; CESSATION; MOTIVATION; RELAPSE; TRIAL AB Transdermal nicotine patch (TN) and nicotine nasal spray (NS) are both efficacious forms of smoking cessation treatment, but have different pharmacokinetic properties and modes of action. To understand better psychological responses to treatment, we investigated the effects of TN versus NS on positive affect, negative affect, and withdrawal symptoms during treatment. Participants were randomly assigned to receive TN (n = 172) or NS (n = 163) plus seven sessions of behavioral counseling, and completed self-report questionnaires at pretreatment and during treatment. TN participants, but not NS participants, reported significant increases in positive affect during treatment. Increases in negative affect and withdrawal were observed, independent of treatment. Only changes in negative affect predicted relapse by the end of the treatment phase. These findings indicate that, although TN may enhance positive affect for smokers in treatment compared with NS, only changes in negative affect predict treatment outcome. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Penn, Dept Psychiat, Tobacco Use Res Ctr, Philadelphia, PA 19140 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA. Natl Inst Drug Abuse, Intramural Res Program, Baltimore, MD 21224 USA. RP Strasser, AA (reprint author), Univ Penn, Dept Psychiat, Tobacco Use Res Ctr, 3535 Market St,Suite 4110, Philadelphia, PA 19140 USA. EM strasse3@mail.med.upenn.edu FU NCRR NIH HHS [M01-RR0040]; NIDA NIH HHS [P50DA84718] NR 34 TC 20 Z9 20 U1 4 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PD JAN PY 2005 VL 30 IS 1 BP 9 EP 17 DI 10.1016/j.addbeh.2004.04.005 PG 9 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA 886IE UT WOS:000226219500002 PM 15561445 ER PT J AU Nava, VE Jaffe, ES AF Nava, VE Jaffe, ES TI The pathology of NK-Cell lymphomas and leukemias SO ADVANCES IN ANATOMIC PATHOLOGY LA English DT Review DE natural killer cell; T cell; Epstein-Barr virus; lymphoma; leukemia; hemophagocytic syndrome; dendritic cell; cytogenetics ID EPSTEIN-BARR-VIRUS; LETHAL MIDLINE GRANULOMA; PLASMACYTOID DENDRITIC CELLS; CUTANEOUS LYMPHOPROLIFERATIVE DISORDERS; DELTA T-CELL; HYDROA VACCINIFORME; HEMOPHAGOCYTIC SYNDROME; LYMPHOBLASTIC LYMPHOMA; MALIGNANT HISTIOCYTOSIS; POLYMORPHIC RETICULOSIS AB Natural killer (NK) cell lymphomas and leukemias are a rare but clinically important group of neoplasms. Most of these tumors are aggressive. with a high rate of mortality. They include extranodal NK/T-cell lymphomas of nasal type and aggressive NK-cell leukemias. Both are Epstein-Barr virus (EBV) associated and show, similar epidemiologic features. A closely related entity seen mainly in children is hydroa vacciniforme-like lymphoma, which also is EBV positive. EBV influences the pathophysiology of these tumors, through the induction of cytokines and chemokines. Tile differential diagnosis of NK-cell malignancies includes fulminant EBV-associated T-cell lymphoproliferative disorder, a condition referred to in the past as fatal infectious mononucleosis. Benign proliferations of NK cells can be seen in association with viral infection. The disease formerly referred to as blastic NK-cell lyrnphoma is now considered to be a malignancy derived from a dendritic cell precursor. C1 NCI, Hematopathol Sect, Pathol Lab, Bethesda, MD 20892 USA. RP Jaffe, ES (reprint author), 10 Ctr Dr ,MSC 1500,Bldg 10,Rm 2N-202, Bethesda, MD 20892 USA. EM elainejaffe@nih.gov NR 89 TC 49 Z9 54 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1072-4109 J9 ADV ANAT PATHOL JI Adv. Anat. Pathol. PD JAN PY 2005 VL 12 IS 1 BP 27 EP 34 DI 10.1097/01.pap.0000151318.34752.80 PG 8 WC Pathology SC Pathology GA 885IW UT WOS:000226151300005 PM 15614162 ER PT S AU Staudt, LM Dave, S AF Staudt, LM Dave, S BE Alt, FW TI The biology of human lymphoid malignancies revealed by gene expression profiling SO ADVANCES IN IMMUNOLOGY, VOL 87 SE Advances in Immunology LA English DT Review; Book Chapter ID B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMA; ANTI-CD20 MONOCLONAL-ANTIBODY; NF-KAPPA-B; GERMINAL-CENTER FORMATION; SECRETING PLASMA-CELLS; REED-STERNBERG CELLS; FOLLICULAR LYMPHOMA; C-MYC; CYCLIN D1 AB Gene expression profiling provides a quantitative molecular framework for the study of human lymphomas. This genomic technology has revealed that existing diagnostic categories are comprised of multiple molecularly and clinically distinct diseases. Diffuse large B-cell lymphoma (DLBCL), for example, consists of three gene expression subgroups, termed germinal center B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBL). These DLBCL subgroups arise from different stages of normal B-cell differentiation, utilize distinct oncogenic mechanisms, and differ in their ability to be cured by chemotherapy. Key regulatory factors and their target genes are differentially expressed among these subgroups, including BCL-6, Blimp-1, and XBP1. ABC DLBCL and PMBL depend upon constitutive activation of the NF-kappa B pathway for their survival but GCB DLBCL does not, demonstrating that this pathway is a potential therapeutic target for certain DLBCL subgroups. In DLBCL, mantle cell lymphoma, and follicular lymphoma, gene expression profiling has also been used to create gene expression-based models of survival, which have identified the biological characteristics of the tumors that influence their clinical behavior. In mantle cell lymphoma, the length of survival following diagnosis is primarily influenced by the tumor proliferation rate, which can be quantitatively measured by a proliferation gene expression "signature." Based on this accurate measure, the proliferation rate can now be viewed as an integration of several oncogenic lesions that each increase progression from the G1 to the S phase of the cell cycle. In DLBCL and follicular lymphoma, gene expression profiling has revealed that the molecular characteristics Of non-malignant tumor-infiltrating immune cells have a major influence on the length of survival. The implications of these insights for the diagnosis and treatment of non-Hodgkin lymphomas are discussed. C1 NCI, Metab Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. RP Staudt, LM (reprint author), NCI, Metab Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. FU NCI NIH HHS [Z01 SC004024-18] NR 154 TC 143 Z9 146 U1 1 U2 11 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-2776 BN 0-12-022487-9 J9 ADV IMMUNOL JI Adv.Immunol. PY 2005 VL 87 BP 163 EP + DI 10.1016/S0065-2776(05)87005-1 PG 51 WC Immunology SC Immunology GA BCU34 UT WOS:000231260200005 PM 16102574 ER PT S AU Carosi, M Linn, GS Visalberghi, E AF Carosi, M Linn, GS Visalberghi, E BE Slater, PJB Snowdon, CT Brockmann, HJ Roper, TJ Naguib, M TI The sexual behavior and breeding system of tufted capuchin monkeys (Cebus apella) SO ADVANCES IN THE STUDY OF BEHAVIOR, VOL 35 SE Advances in the Study of Behavior LA English DT Review; Book Chapter ID SPERM COMPETITION; REPRODUCTIVE-CYCLE; SEASONAL-VARIATION; FOOD COMPETITION; MENSTRUAL-CYCLE; MATING SYSTEM; WORLD MONKEY; TESTES SIZE; PRIMATES; NIGRITUS C1 CNR, Inst Cognit Sci & Technol, Unit Cognit Primatol, Rome, Italy. CNR, Inst Cognit Sci & Technol, Primate Ctr, Rome, Italy. NICHHD, Comparat Ethol Lab, NIH, Anim Ctr, Poolesville, MD 20837 USA. Nathan S Kline Inst Psychiat Res, Program Cognit Neurosci & Schizophrenia, NYSOMH, Orangeburg, NY 10962 USA. NYU, Sch Med, Dept Psychiat, Orangeburg, NY 10962 USA. RP Carosi, M (reprint author), CNR, Inst Cognit Sci & Technol, Unit Cognit Primatol, Rome, Italy. RI Carosi, Monica/C-9683-2014; OI Visalberghi, Elisabetta/0000-0001-7407-5468 NR 110 TC 10 Z9 11 U1 4 U2 13 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-3454 BN 0-12-004535-4 J9 ADV STUD BEHAV JI Advan. Study Behav. PY 2005 VL 35 BP 105 EP 149 DI 10.1016/S0065-3454(05)35003-0 PG 45 WC Behavioral Sciences SC Behavioral Sciences GA BDN21 UT WOS:000234422200003 ER PT S AU Brown, P AF Brown, P BE Vyas, GN Williams, AE TI Pathogenesis and transfusion risk of transmissible spongiform encephalopathies SO ADVANCES IN TRANSFUSION SAFETY SE DEVELOPMENTS IN BIOLOGICALS LA English DT Proceedings Paper CT 3rd Symposium on Advances in Transfusion Safety CY JUN 04-06, 2003 CL Natl Inst Hlth, Bethesda, MD SP US FDA, Amer Assoc Blood Banks, Natl Heart, Lung & Blood Inst, US Dept Defense, Int Assoc Biol HO Natl Inst Hlth DE transmissible spongiform encephalopathy; Creutzfeldt-Jakob disease; variant Creutzfeldt-Jakob disease; prion disease; transfusion risk ID CREUTZFELDT-JAKOB-DISEASE; PRION PROTEIN; BLOOD-TRANSFUSION; SCRAPIE VIRUS; HUMAN PLASMA; INFECTION; SPREAD; TISSUES; BRAIN; MOUSE AB The genesis (and pathogenesis) of sporadic and familial forms of human transmissible spongiform encephalopathy (TSE) is unknown, but the disease process may originate spontaneously in the brain as a statistically random event involving misfolding and amyloid formation of the '' prion '' protein. The pathogenesis of environmentally acquired TSE depends on the route of infection and is likely to involve both neural and haematogenous paths of neuro-invasion. Blood infectivity is well documented in experimental rodent models of TSE and in natural scrapie infections, but has not yet been proved to occur in humans. The knowledge that many plasma pools have included donations from individuals who later died of sporadic Creutzfeldt-Jakob disease (sCJD), together with the failure to identify any affected recipients, implies that the risk is either negligible or absent. In sharp contrast, two out of 26 recipients of labile blood products from individuals who later died from the variant form of CJD (vCJD) have became infected, and the still-living at-risk recipients are under continuing surveillance. C1 NINDS, NIH, Bethesda, MD 20814 USA. RP Brown, P (reprint author), NINDS, NIH, 7815 Exeter Rd, Bethesda, MD 20814 USA. EM paulbrown@comcast.net NR 27 TC 5 Z9 5 U1 0 U2 2 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1424-6074 BN 3-8055-7935-7 J9 DEV BIOLOGICALS JI Dev. Biols PY 2005 VL 120 BP 27 EP 33 PG 7 WC Biotechnology & Applied Microbiology; Hematology; Public, Environmental & Occupational Health SC Biotechnology & Applied Microbiology; Hematology; Public, Environmental & Occupational Health GA BDW89 UT WOS:000235894600004 PM 16050152 ER PT S AU Klein, HG AF Klein, HG BE Vyas, GN Williams, AE TI Blood substitutes: How close to a solution? SO ADVANCES IN TRANSFUSION SAFETY SE DEVELOPMENTS IN BIOLOGICALS LA English DT Proceedings Paper CT 3rd Symposium on Advances in Transfusion Safety CY JUN 04-06, 2003 CL Natl Inst Hlth, Bethesda, MD SP US FDA, Amer Assoc Blood Banks, Natl Heart, Lung & Blood Inst, US Dept Defense, Int Assoc Biol HO Natl Inst Hlth ID BOVINE HEMOGLOBIN; TRANSFUSIONS; OXYGENATION; EFFICACY; EMULSION; SURGERY; ANEMIA; TRIAL AB The term '' blood substitute '' is commonly misused when '' red cell substitute (RCS) is meant. The ideal RCS should deliver (i) oxygen; (ii) require no compatibility testing; (iii) cause few side effects; (iv) have prolonged storage qualities; (v) persist in the circulation and (vi) be available at reasonable cost. While no drug with all these qualities is on the near horizon, several early generation RCS are approaching submission for licensing, at least for limited indications. Haemoglobin-derived RCS from human, bovine and recombinant sources, as well as perfluorochemicals that dissolve O2 are in different stages of development. While each formulation has its own physical characteristics, biological activities, and adverse reaction profile, all share one characteristic: the physiological consequences of delivering O2 with small molecules is poorly understood and may both account for problems seen in the clinical trials and provide therapeutic opportunities for the cancer patient. Those RCS in phase III trials all have a half-life measured in hours and are unlikely to replace transfusions or drugs that stimulate erythropoiesis for chronic anaemia, but they may play a role (i) in military and civilian trauma as resuscitation solutions, (ii) as a bridge to transfusion when no compatible blood is immediately available, (iii) as an adjunct to the autologous haemodilution management of surgery or even (iv) in radiation therapy or the management of cancer-related vascular occlusive syndromes. C1 NIH, Warren G Magnuson Clin Ctr, Dept Transfus Med, Bethesda, MD 20892 USA. RP Klein, HG (reprint author), NIH, Warren G Magnuson Clin Ctr, Dept Transfus Med, Bldg 10,Rm 1C-711, Bethesda, MD 20892 USA. EM hk29h@nih.gov NR 22 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1424-6074 BN 3-8055-7935-7 J9 DEV BIOLOGICALS JI Dev. Biols PY 2005 VL 120 BP 45 EP 52 PG 8 WC Biotechnology & Applied Microbiology; Hematology; Public, Environmental & Occupational Health SC Biotechnology & Applied Microbiology; Hematology; Public, Environmental & Occupational Health GA BDW89 UT WOS:000235894600007 PM 16050155 ER PT B AU Phillips, CM AF Phillips, Clarenda M. BE Brown, TL Parks, GS Phillips, CM TI Sisterly Bonds African American Sororities Rising to Overcome Obstacles SO AFRICAN AMERICAN FRATERNITIES AND SORORITIES: THE LEGACY AND THE VISION, 2ND EDITION LA English DT Article; Book Chapter C1 [Phillips, Clarenda M.] Morehead State Univ, Interdisciplinary Womens Studies Program, Morehead, KY 40351 USA. RP Phillips, CM (reprint author), NIMH, Bethesda, MD 20892 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU UNIV PRESS KENTUCKY PI LEXINGTON PA 102 LAFFERTY HALL, UNIVERSITY OF KENTUCKY, LEXINGTON, KY 40506 USA BN 978-0-8131-2965-5 PY 2005 BP 341 EP 359 PG 19 WC Cultural Studies; Ethnic Studies SC Cultural Studies; Ethnic Studies GA BXS40 UT WOS:000296902000013 ER PT J AU Dwyer, J AF Dwyer, J TI Nutrition and cardiovascular disease prevention in children and adolescents Part 2: Nutritional measures to reduce cardiovascular risk SO AGRO FOOD INDUSTRY HI-TECH LA English DT Article ID BLOOD-PRESSURE; PLANT STANOL; STEROL ESTERS; SODIUM-INTAKE; CHOLESTEROL; INTERVENTION AB Nutrition is important in cardiovascular disease prevention in children and adolescents. Part 1 briefly reviewed diet related cardiovascular disease (CVD) risk factors that are often present in childhood and adolescence, and standards for screening and assessment now available from expert groups'. Part 2 discusses nutritional measures that are recommended by expert groups to reduce diet-related CVD risks in children and adolescents. These include maintaining or achieving a healthy body weight, and adoption of family dietary patterns that promote heart health that conform to the Dietary Guidelines for Americans, the National Cholesterol Education Program and National High Blood Pressure Education Program. These patterns emphasize fresh fruits, vegetables, and low fat dairy foods with moderation in other animal foods. Such as diet is relatively low in saturated fat, total fat and cholesterol and in sodium, and high in potassium. Dietary supplements are not regarded as necessary. Eating patterns and foods provided in schools and other institutions where children and adolescents spend a good deal of time also need to be heart healthy. In addition, a physically active life with at least 30-60 minutes or aerobic physical activity per day, preferably more, is recommended. Child microenvironments such as the family and school should foster healthful food consumption practices and a physically active life, and monitoring of physical activity and sedentary activities can encourages it. Smoking is a potent CVD risk that should also be avoided. C1 NIH, Off Dietary Supplements, Bethesda, MD 20892 USA. Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA USA. Tufts Univ, Sch Med, Boston, MA USA. Tufts Univ, Jean Mayer US Dept Agr Human Nutr Res Ctr Aging, Boston, MA USA. RP Dwyer, J (reprint author), NIH, Off Dietary Supplements, 6100 Execut Blvd,Room 3B01,MSC 7517, Bethesda, MD 20892 USA. OI Dwyer, Johanna/0000-0002-0783-1769 NR 32 TC 0 Z9 0 U1 1 U2 6 PU TEKNOSCIENZE PUBL PI MILAN PA VIA AURELIO SAFFI 23, 20123 MILAN, ITALY SN 1722-6996 J9 AGRO FOOD IND HI TEC JI Agro Food Ind. Hi-Tech PD JAN-FEB PY 2005 VL 16 IS 1 BP 46 EP + PG 4 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 916FN UT WOS:000228370900032 ER PT J AU Mannheimer, SB Matts, J Telzak, E Chesney, M Child, C Wu, AW Friedland, G AF Mannheimer, SB Matts, J Telzak, E Chesney, M Child, C Wu, AW Friedland, G CA Terry Beirn Community Programs TI Quality of life in HIV-infected individuals receiving antiretroviral therapy is related to adherence SO AIDS CARE-PSYCHOLOGICAL AND SOCIO-MEDICAL ASPECTS OF AIDS/HIV LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HEALTH-STATUS QUESTIONNAIRE; SELF-REPORTED ADHERENCE; PROTEASE INHIBITORS; ZIDOVUDINE THERAPY; MEDICAL OUTCOMES; RANDOMIZED-TRIAL; CLINICAL-TRIALS; SURVEY SF-36; VIRAL LOAD AB This study assesses changes in quality of life (QoL) over time among HIV-infected individuals receiving antiretroviral therapy (ART) and evaluates how this relates to ART adherence. Prospective, longitudinal data were examined from 1050 participants in two large, randomized, multi-centre antiretroviral clinical trials. QoL was assessed by the SF-12; adherence by the Terry Beirn Community Programs for Clinical Research on AIDS Antiretroviral Medication Self-report. Participants included 20% women, 53% African Americans, 16% Latinos; mean age was 39 years; mean baseline CD4+ cell count 230 cells/mm(3); 89% were ART-naive at entry. Baseline physical and mental health summary QoL scores were 45.4 and 42.9, comparable to scores reported in other advanced HIV populations. Significant improvements in mean QoL scores were seen for the group as a whole after 1 to 4 months on new ART regimens, and persisted for 12 months. Participants reporting 100% ART adherence achieved significantly higher QoL scores at 12 months compared to those with poorer adherence, particularly if 100% adherence was consistent (p< 0.001). Those with at least 80% ART adherence had smaller gains in QoL at 12 months when compared to baseline, while those with < 80% adherence had worsening of QoL. In this analysis, ART adherence was associated with improved QoL, particularly if adherence was sustained. C1 Columbia Univ, Coll Phys & Surg, New York, NY USA. Univ Minnesota, Div Biostat, Minneapolis, MN USA. Albert Einstein Coll Med, Dept Med, New York, NY USA. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, New York, NY USA. Bronx Lebanon Hosp Ctr, New York, NY USA. NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA. Johns Hopkins Univ, Dept Med, Baltimore, MD USA. Yale Univ, Yale Sch Med, Yale New Haven Hosp, New Haven, CT USA. RP Mannheimer, SB (reprint author), 506 Lenox Ave,Room 3101-A, New York, NY 10037 USA. EM sbm20@columbia.edu FU NIAID NIH HHS [5U01AI042170-10] NR 59 TC 135 Z9 137 U1 1 U2 10 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0954-0121 J9 AIDS CARE JI Aids Care-Psychol. Socio-Med. Asp. Aids/Hiv PD JAN PY 2005 VL 17 IS 1 BP 10 EP 22 DI 10.1080/09540120412331305098 PG 13 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychology, Multidisciplinary; Respiratory System; Social Sciences, Biomedical SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychology; Respiratory System; Biomedical Social Sciences GA 880CA UT WOS:000225764800002 PM 15832830 ER PT J AU Wielgosz, MM Rauch, DA Jones, KS Ruscetti, FW Ratner, L AF Wielgosz, MM Rauch, DA Jones, KS Ruscetti, FW Ratner, L TI Cholesterol dependence of HTLV-I infection SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID LEUKEMIA-VIRUS TYPE-1; LIPID RAFT MICRODOMAINS; MEMBRANE DOMAINS; T-CELLS; TRANSMEMBRANE DOMAIN; DETERGENT-RESISTANT; PLASMA-MEMBRANE; DENDRITIC CELLS; RECEPTOR; ENTRY AB Cholesterol- rich plasma membrane microdomains are important for entry of many viruses, including retroviruses. Depletion of cholesterol with 2- hydroxypropyl- beta- cyclodextrin inhibits entry of human T cell leukemia virus type I ( HTLV- 1) and HTLV- I envelope pseudotyped lentivirus particles. Using a soluble fusion protein of the HTLV- I surface envelope protein with the immunoglobulin Fc domain, the HTLV- I receptor was found to colocalize with a raft- associated marker and to cluster in specific plasma membrane microdomains. Depletion of cholesterol did not alter receptor binding activity, suggesting a requirement for cholesterol in a postbinding virus entry step. C1 Washington Univ, Sch Med, Dept Med & Mol Microbiol, St Louis, MO 63110 USA. Natl Canc Inst, Basic Res Lab, Frederick, MD 21702 USA. RP Ratner, L (reprint author), Washington Univ, Sch Med, Dept Med & Mol Microbiol, Box 8069,660 S Euclid Ave, St Louis, MO 63110 USA. EM lratner@im.wustl.edu FU NCI NIH HHS [P01 CA100730-01, P01 CA100730-02, R01 CA063417, R01 CA063417-09, R21 CA093062, R21 CA093062-02] NR 54 TC 18 Z9 18 U1 0 U2 0 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 2005 VL 21 IS 1 BP 43 EP 50 DI 10.1089/aid.2005.21.43 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 895AE UT WOS:000226832200006 PM 15665643 ER PT J AU Cox, JH Ferrari, G Kalams, SA Lopaczynski, W Oden, N D'Souza, MP AF Cox, JH Ferrari, G Kalams, SA Lopaczynski, W Oden, N D'Souza, MP CA ELISPOT Collaborative Study Grp TI Results of an ELISPOT proficiency panel conducted in 11 laboratories participating in international human immunodeficiency virus type 1 vaccine trials SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID T-CELL RESPONSES; LINKED-IMMUNOSORBENT-ASSAY; IMMUNE-RESPONSES; AIDS VACCINE; HIV VACCINES; SERONEGATIVE VOLUNTEERS; MONONUCLEAR-CELLS; PEPTIDE ANTIGENS; PERIPHERAL-BLOOD; CLINICAL-TRIALS AB We used an external quality assurance ( EQA) panel to assess laboratory competency and comparability when performing ELISPOT assays in support of human immunodeficiency virus type 1 ( HIV- 1) vaccine trials. Cell recovery, viability, and frequency of interferon-gamma ( IFN-gamma)- secreting cells after antigen stimulation were obtained from 11 laboratories on a coded panel of 11 peripheral blood mononuclear cell samples. The median recovery and viability before plating for all samples were 35% and 86%, respectively, with notable interlaboratory and intrasample variability. Empirical as well as statistical analysis methods were used to define positive ELISPOT responses. Remarkable concordance between laboratories was obtained in defining a qualitative assessment of responder/ nonresponder status to antigens, but the frequency of responding cells varied among the laboratories. This study highlights the need for better standardization of protocols and reagents to obtain reliable and reproducible data that may support immunogenicity studies, vaccine regulatory submissions, and licensure. C1 US Mil HIV Res Program, Rockville, MD 20850 USA. Duke Univ, Dept Surg, Durham, NC 27710 USA. Vanderbilt Univ, Med Ctr, Nashville, TN 37232 USA. BBI Biotech Res Labs Inc, Gaithersburg, MD 20877 USA. EMMES Corp, Rockville, MD 20850 USA. NIAID, Div AIDS, NIH, Bethesda, MD 20892 USA. RP US Mil HIV Res Program, Suite 200,13 Taft Court, Rockville, MD 20850 USA. EM jcox@hivresearch.org RI Ferrari, Guido/A-6088-2015 FU NIAID NIH HHS [N01-AI-85341, R01 AI047756-01, R01 AI047756-02, R01 AI047756-03, R01 AI047756-04, R01 AI047756-05] NR 69 TC 54 Z9 59 U1 1 U2 1 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 2005 VL 21 IS 1 BP 68 EP 81 DI 10.1089/aid.2005.21.68 PG 14 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 895AE UT WOS:000226832200009 PM 15665646 ER PT J AU Hu, XZ Oroszi, G Chun, J Smith, TL Goldman, D Schuckit, MA AF Hu, XZ Oroszi, G Chun, J Smith, TL Goldman, D Schuckit, MA TI An expanded evaluation of the relationship of four alleles to the level of response to alcohol and the alcoholism risk SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE alcoholism; genetics; association studies ID SEROTONIN TRANSPORTER GENE; NEUROPEPTIDE-Y; PROMOTER POLYMORPHISM; GABA(A) RECEPTOR; FAMILY-HISTORY; BEHAVIORAL DISINHIBITION; REGULATORY REGION; CONDUCT DISORDER; SUICIDE ATTEMPTS; SIGNAL PEPTIDE AB Background: Alcoholism is a complex, genetically influenced disorder the cause of which may be better understood through the study of genetically influenced phenotypes that mediate the risk. One such intermediate phenotype is the low level of response (LR) to alcohol. This project used a case-control approach to search for genes that may contribute to LR. Methods: Data were available from alcohol challenges at approximately age 20 and regarding the development of alcohol use disorders over the subsequent 20 years for 85 men, including 40 reported in a previous genetic analysis. LR was evaluated using oral consumption of 0.75 ml/kg of alcohol, after which changes in subjective feelings of intoxication and body sway were measured. Alcohol abuse and dependence were diagnosed by DSM-III-R criteria through structured interviews administered to both the participant and an informant (usually the spouse) 10, 15, and 20 years after initial testing. Four polymorphisms were evaluated, including the serotonin transporter HTTLPR promoter ins/del, GABA(Aalpha6) Pro385Ser, NPY Leu7Pro, and catalase 262C>T. Two of these, HTTLPR and GABA(Aalpha6) Pro385Ser, had been previously associated with LR and alcoholism in a preliminary study. Results: The HTTLPR L allele was significantly related to both the LR and alcoholism in an allele-dosage (stepwise) manner. Furthermore, the association remained when L alleles were subdivided into recently reported functional subtypes: the lowest LR was associated with genotypes correlated with the highest serotonin transporter expression. The GABA(Aalpha6) Ser385 allele showed a nonsignificant trend for association to a low LR, as had been previously observed, although the Ser385 allele is uncommon, and only 18 heterozygotes were in the current group. However, the six men with both LL and Pro385/Ser385 genotypes had the lowest LR, and each had developed alcoholism during follow-up. Neither NPY nor catalase was associated with either LR or alcoholic outcomes, although the sample did not have sufficient power for definitive conclusions. Conclusions: This report strengthens the support for a relationship between the HTTLPR L and GABA(Aalpha6) Ser385 alleles to low alcohol LR and to alcoholism in a prospectively studied cohort evaluated for LR in young adulthood and before the onset of alcohol dependence. C1 Univ Calif San Diego, Dept Psychiat, San Diego, CA 92161 USA. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. VA San Diego Healthcare Syst, San Diego, CA 92161 USA. RP Schuckit, MA (reprint author), Univ Calif San Diego, Dept Psychiat, 116A,3350 La Jolla Village Dr, San Diego, CA 92161 USA. EM mschuckit@ucsd.edu RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 FU PHS HHS [05526] NR 94 TC 332 Z9 338 U1 2 U2 20 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD JAN PY 2005 VL 29 IS 1 BP 8 EP 16 DI 10.1097/01.ALC.0000150008.68473.62 PG 9 WC Substance Abuse SC Substance Abuse GA 889QJ UT WOS:000226457200002 PM 15654286 ER PT J AU Stark, KD Beblo, S Murthy, M Whitty, JE Buda-Abela, M Janisse, J Rockett, H Martier, SS Sokol, RJ Hannigan, JH Salem, N AF Stark, KD Beblo, S Murthy, M Whitty, JE Buda-Abela, M Janisse, J Rockett, H Martier, SS Sokol, RJ Hannigan, JH Salem, N TI Alcohol consumption in pregnant, black women is associated with decreased plasma and erythrocyte docosahexaenoic acid SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE fatty acids; fetal alcohol syndrome; prenatal alcohol; arachidonic acid; docosahexaenoic acid; black women ID POLYUNSATURATED FATTY-ACIDS; SCREENING QUESTIONNAIRES; MATERNAL PLASMA; NUTRIENT INTAKE; FOOD FREQUENCY; RHESUS-MONKEYS; ENERGY-INTAKE; TERM INFANTS; ETHANOL; EXPOSURE AB Background: Inner-city, black women are among those groups that are at higher risk for having infants with fetal alcohol spectrum disorders that can include life-long neurobehavioral and cognitive impairments. Chronic alcohol consumption can decrease amounts of docosahexaenoic acid (DHA), a fatty acid that is essential for optimal infant neural and retinal development in a variety of tissues. Methods: Black women who presented at an inner-city antenatal clinic for their first prenatal visit were recruited into a longitudinal, observational study. Alcohol intake was determined by a structured interview. Participants provided blood specimens and completed food frequency surveys at 24 weeks of gestation, infant delivery, and 3 months postpartum. Fatty acid composition analyses were completed on 307, 260, and 243 for plasma and 278, 261, and 242 erythrocyte specimens at 24 weeks of gestation, delivery, and 3 months postpartum, respectively. Results: Proportion of drinking days at the first prenatal visit was associated with decreased DHA in plasma and erythrocytes throughout the study. This association was the strongest at 24 weeks of gestation. In addition, an interaction between proportion of drinking days at the time of conception and ounces of absolute alcohol per drinking day at the time of conception was detected and demonstrated that, in daily drinkers, high intakes of alcohol are associated with decreased DHA and arachidonic acid (AA) concentrations in plasma. Conclusions: Frequent and high intakes of alcohol that have been previously associated with fetal alcohol spectrum disorders are also associated with decreased maternal DHA and AA plasma concentrations. The present findings indicate that maternal DHA deficiency is associated with high-risk drinking and may contribute to the mechanism(s) of alcohol-related neurodevelopmental disorders. C1 NIAAA, LMBB, NIH, Rockville, MD 20852 USA. NIAAA, Div Intramural Clin & Biol Res, NIH, Rockville, MD 20852 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA. Wayne State Univ, Dept Psychol, Detroit, MI 48202 USA. RP Salem, N (reprint author), NIAAA, LMBB, NIH, 5625 Fisher Lane,Room 3C-07, Rockville, MD 20852 USA. EM nsalem@niaaa.nih.gov RI Stark, Ken/I-1347-2016 OI Stark, Ken/0000-0001-7828-4072 FU NIAAA NIH HHS [N01-AA83019] NR 74 TC 22 Z9 22 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD JAN PY 2005 VL 29 IS 1 BP 130 EP 140 DI 10.1097/01.ALC.0000150013.65416.06 PG 11 WC Substance Abuse SC Substance Abuse GA 889QJ UT WOS:000226457200017 PM 15654301 ER PT J AU Daurignac, E Toga, AW Jones, DK Aronen, HJ Hommer, DW Jernigan, TL Krystal, JH Mathalon, DH AF Daurignac, E Toga, AW Jones, DK Aronen, HJ Hommer, DW Jernigan, TL Krystal, JH Mathalon, DH TI Applications of morphometric and diffusion tensor magnetic resonance imaging to the study of brain abnormalities in the alcoholism spectrum SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE magnetic resonance imaging; diffusion tensor imaging; alcoholism; fetal alcohol syndrome; hippocampus; gray matter; white matter ID WHITE-MATTER; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; GRAY-MATTER; CORPUS-CALLOSUM; FETAL ALCOHOL; IN-VIVO; PROBABILISTIC ATLAS; HIPPOCAMPAL VOLUME; PRENATAL EXPOSURE AB Background: The International Conference on Applications of Neuroimaging to Alcoholism was held at Yale University in New Haven, CT, in January 2004. The following is a brief summary of the contributions of five speakers who presented their work during the magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) session. Methods: This session addressed how MRI and DTI are used to assess macro- and microstructural brain alterations in alcoholism. Structural MRI methods can address regional gray and white matter volumetric/ morphometric abnormalities, and DTI methods can address microstructural disruptions of white matter tracts. These methods can be applied across the spectrum of alcoholism to elucidate distinct brain abnormalities underlying clinical subtypes, to disentangle brain volume deficits that precede, from those that follow, the onset of alcoholic drinking in chronic alcoholics, and to examine effects of prenatal alcohol exposures on brain development in children. The presentations highlighted recent scientific findings and methodological advances in these areas. Results: Disease-specific probabilistic atlases, designed to reflect the unique anatomy and physiology of particular clinical subpopulations, can be developed for alcoholism. Such an atlas can be used to identify efficiently patterns of altered structure or function in alcoholism and can guide algorithms for knowledge-based image analysis. DTI is sensitive to constraints on the random diffusion of water molecules in axons, allowing assessment of white matter tract integrity in neuropsychiatric diseases, including alcoholism. Recent MRI and DTI data were presented showing region-specific brain abnormalities at both macro- and microstructural levels that varied differentially according to sex, time of alcohol exposure in life, and alcoholism subtype. Conclusion: The International Conference on Applications of Neuroimaging to Alcoholism brought together leading experts in MRI and DTI techniques to discuss their applications to the study of alcoholism. The extant and new imaging technologies provide us with multiple modalities to study the brain in vivo. These noninvasive tools enable us to monitor the time course of alcohol effects on the brain and to characterize macro- and microstructural brain abnormalities across the full spectrum of alcoholism, including its precursors and its sequelae. C1 Yale Univ, Sch Med, Psychiat Serv 116A, VA Connecticut Healthcare Syst,Dept Psychiat, West Haven, CT 06516 USA. Univ Calif Los Angeles, Sch Med, Dept Neurol, Los Angeles, CA 90024 USA. NICHHD, Lab Integrat Med & Biophys, NIH, Bethesda, MD 20892 USA. Univ Helsinki, Helsinki Brain Res Ctr, FIN-00014 Helsinki, Finland. NIAAA, Clin Studies Lab, NIH, Bethesda, MD 20892 USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. RP Mathalon, DH (reprint author), Yale Univ, Sch Med, Psychiat Serv 116A, VA Connecticut Healthcare Syst,Dept Psychiat, 950 Campbell Ave, West Haven, CT 06516 USA. EM daniel.mathalon@yale.edu RI Jones, Derek/D-1460-2009; OI Mathalon, Daniel/0000-0001-6090-4974; Jones, Derek/0000-0003-4409-8049 NR 76 TC 2 Z9 2 U1 3 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD JAN PY 2005 VL 29 IS 1 BP 159 EP 166 DI 10.1097/01.ALC.0000150891.72900.62 PG 8 WC Substance Abuse SC Substance Abuse GA 889QJ UT WOS:000226457200020 PM 15895490 ER PT J AU Kilada, S Gamaldo, L Grant, EA Moghekar, A Morris, JC O'Brien, RJ AF Kilada, S Gamaldo, L Grant, EA Moghekar, A Morris, JC O'Brien, RJ TI Brief screening tests for the diagnosis of dementia: Comparison with the mini-mental state exam SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE blessed memory task; dementia screening; verbal fluency; MMSE ID MILD COGNITIVE IMPAIRMENT; MEMORY-CONCENTRATION TEST; ALZHEIMERS-DISEASE; CLINICAL-DIAGNOSIS; VASCULAR DEMENTIA; ELDERLY-PATIENTS; CONTROLLED TRIAL; CARE; PREVALENCE; HEALTH AB Dementia is a common and under-diagnosed problem among the elderly. An accurate screening test would greatly aid the ability of physicians to evaluate dementia and memory problems in clinical practice. We sought to determine whether simple and brief psychometric tests perform similarly to the Mini-Mental State Examination (MMSE) in screening for dementia. Using a retrospective analysis, a series of standard, brief, psychometric tests were compared with each other and to the MMSE as screening tests for very mild dementia, using DSM-III-R criterion as the gold standard. Two independent cohorts from the Baltimore Longitudinal Study of Aging and the Washington University Alzheimer's Disease Research Center were evaluated. We found that two brief and simple-to-administer tests appear to offer similar degrees of sensitivity and specificity to the MMSE. These are the recall of a five-item name and address, "John Brown 42 Market Street Chicago" and the one-minute verbal fluency for animals. Combining these two tests further improves sensitivity and specificity, surpassing the MMSE, to detect dementia in individuals with memory complaints. C1 Johns Hopkins Univ Hosp, Dept Neurol, Baltimore, MD 21287 USA. NIA, Intramural Res Program, Lab Personal & Cognit, NIH, Bethesda, MD 20892 USA. Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. RP O'Brien, RJ (reprint author), Johns Hopkins Bayview Med Ctr, Mason F Lord Ctr Tower,Suite 5100,5200 Eastern Av, Baltimore, MD 21224 USA. EM robrien@jhmi.edu RI Morris, John/A-1686-2012 FU NIA NIH HHS [P50 AG03991, P50 AG05146, P50 AG05681] NR 74 TC 34 Z9 36 U1 4 U2 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD JAN-MAR PY 2005 VL 19 IS 1 BP 8 EP 16 DI 10.1097/01.wad.0000155381.01350.bf PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA 909IQ UT WOS:000227854000002 PM 15764865 ER PT J AU Carmona, RH Wattendorf, DJ AF Carmona, RH Wattendorf, DJ TI Personalizing prevention: The US Surgeon General's family history initiative SO AMERICAN FAMILY PHYSICIAN LA English DT Editorial Material C1 NHGRI, NIH, Bethesda, MD 20892 USA. US PHS, Commissioned Corps, US Dept Hlth & Human Serv, Washington, DC USA. RP Wattendorf, DJ (reprint author), NHGRI, NIH, Bldg 31,Room 4B09, Bethesda, MD 20892 USA. EM dwatten@mail.nih.gov NR 5 TC 16 Z9 16 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 USA SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD JAN 1 PY 2005 VL 71 IS 1 BP 36 EP + PG 2 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 886UT UT WOS:000226258900003 PM 15663022 ER PT J AU Jenkins, LS AF Jenkins, LS CA The AFFIRM Investigators TI Quality of life in atrial fibrillation: The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study SO AMERICAN HEART JOURNAL LA English DT Article ID INDEX AB Objective The objective of this prespecified substudy of the AFFIRM study, in which no differences in survival or event rates were found in patients with atrial fibrillation (AF) randomized to either rate control or rhythm control, was to test the null hypothesis that quality of life (QoL) is equal with rate- versus rhythm-control treatment strategies in AF. Methods Fifty-six (25%) of AFFIRM sites were randomly selected to recruit AFFIRM patients for the QoL substudy. Instruments used in the QoL assessment were (1) Perceived Health; (2) the Cantril Ladder of Life; (3) the Short Form 36 survey; (4) the QoL Index; and (5) the Symptom Checklist: Frequency and Severity. Data were collected at baseline, 2 months, 12 months, and annually; data are reported through 4 years of follow-up. Results Baseline characteristics of the AFFIRM QoL patients (n = 716) were generally similar to those of the rest of AFFIRM patients. Quality-of-life scores were similar in rate- and rhythm-control assignment groups at all time points. Quality-of life scores were similar whether the actual rhythm was sinus or AF. Scores increased from baseline to subsequent time points similarly for both groups; these improvements were not additive over time. Conclusions Quality of life was comparable between rate- and rhythm-control treatment strategies. In addition, QoL was similar with sinus rhythm versus AF. Attempts to improve QoL by restoring sinus rhythm will usually be unsuccessful. C1 Axio Res Corp, Seattle, WA USA. NHLBI, Seattle, WA USA. RP Jenkins, LS (reprint author), Univ Maryland, Sch Nursing, Suite 375,655 W Lombard St, Baltimore, MD 21201 USA. EM Jenkins@son.umaryland.edu NR 16 TC 136 Z9 140 U1 0 U2 2 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD JAN PY 2005 VL 149 IS 1 BP 112 EP 120 DI 10.1016/j.ahj.2004.03.065 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 888PP UT WOS:000226387000017 PM 15660042 ER PT J AU Miller, FG AF Miller, FG TI Does research ethics rest on a mistake? SO AMERICAN JOURNAL OF BIOETHICS LA English DT Editorial Material ID CLINICAL-TRIALS C1 Natl Inst Hlth, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Miller, FG (reprint author), Natl Inst Hlth, Dept Clin Bioeth, Bethesda, MD 20892 USA. NR 9 TC 8 Z9 8 U1 0 U2 2 PU ROUTLEDGE TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD JAN-FEB PY 2005 VL 5 IS 1 BP 34 EP 36 DI 10.1080/15265160590927705 PG 3 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 920CX UT WOS:000228667800006 PM 16036654 ER PT J AU Weinberg, CR AF Weinberg, CR TI Invited commentary: Barker meets Simpson SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Editorial Material ID BIRTH-WEIGHT; FETAL ORIGINS; DISEASE; TWIN C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. RP Weinberg, CR (reprint author), NIEHS, Biostat Branch, MD A3-03,POB 12233, Res Triangle Pk, NC 27709 USA. EM weinberg@niehs.nih.gov OI Tu, Yu-Kang/0000-0002-2461-474X NR 11 TC 27 Z9 27 U1 0 U2 1 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 JAN 1 PY 2005 VL 161 IS 1 BP 33 EP 35 DI 10.1093/aje/kwi003 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 884OK UT WOS:000226094700004 PM 15615911 ER PT J AU Lee, WJ Hoppin, JA Blair, A Lubin, JH Dosemeci, M Sandler, DP Alavanja, MCR AF Lee, WJ Hoppin, JA Blair, A Lubin, JH Dosemeci, M Sandler, DP Alavanja, MCR TI Re: Cancer incidence among pesticide applicators exposed to alachlor in the agricultural health study - The authors reply SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NIH, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Lee, WJ (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 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 JAN 1 PY 2005 VL 161 IS 1 BP 102 EP 103 DI 10.1093/aje/kwi010 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 884OK UT WOS:000226094700015 ER PT J AU Brenes, GA Guralnik, JM Williamson, J Fried, LP Penninx, BWJH AF Brenes, GA Guralnik, JM Williamson, J Fried, LP Penninx, BWJH TI Correlates of anxiety symptoms in physically disabled older women SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article ID PRIMARY-CARE PATIENTS; FUNCTIONAL STATUS; MAJOR DEPRESSION; ELDERLY-PATIENTS; SOCIAL SUPPORT; LATER LIFE; DISORDERS; DISABILITY; HEALTH; ADULTS AB objective: The authors describe characteristics that are associated with chronic anxiety symptoms and examine the use of anxiolytic and antidepressant medications in physically disabled women with and without symptoms of anxiety. Methods: Participants were 791 physically disabled women age 65 + years who participated in the Women's Health and Aging Study for 2-3 years. Anxiety symptoms were measured with four questions from the Hopkins Symptom Checklist, and women were categorized as having no anxiety, intermittent anxiety, and chronic anxiety symptoms. Health-related characteristics, medications, physical functioning, physical activity, and psychosocial variables were also measured. Results: Forty-nine percent of women reported no anxiety symptoms; 41% reported intermittent symptoms; and 10% reported chronic symptoms of anxiety Depressive symptoms and lack of emotional support were significant correlates of intermittent anxiety symptoms, whereas depressive symptoms, negative life events, and lack of emotional support were significant correlates of chronic anxiety symptoms. Over the course of 3 years, 20.3% of women with no anxiety, 33.0% of women with intermittent anxiety, and 48.7% of women with chronic anxiety symptoms took anxiolytic and/or antidepressant medications. Conclusion: Anxiety symptoms are common among disabled older women. Psychosocial variables were significantly different in women with intermittent or chronic anxiety symptoms, versus women without anxiety. C1 Wake Forest Univ, Sch Med, Dept Psychiat, Winston Salem, NC USA. Wake Forest Univ, Sch Med, Dept Behav Med, Winston Salem, NC USA. NIA, Dept Epidemiol, Bethesda, MD 20892 USA. NIA, Dept Demog, Bethesda, MD 20892 USA. NIA, Biometry Program, Bethesda, MD 20892 USA. Wake Forest Univ, Sch Med, Sticht Ctr Aging, Winston Salem, NC 27109 USA. RP Brenes, GA (reprint author), Wake Forest Univ, Sch Med, Dept Psychiat, Med Ctr Blvd, Winston Salem, NC USA. EM gbrenes@wfubmc.edu FU NIA NIH HHS [N01-AG-1-2112, AG-09834, R01 AG009834]; NIMH NIH HHS [K23 MH065281, MH65281] NR 50 TC 17 Z9 17 U1 3 U2 4 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD JAN PY 2005 VL 13 IS 1 BP 15 EP 22 DI 10.1176/appi.ajgp.13.1.15 PG 8 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA 886MO UT WOS:000226231700003 PM 15653936 ER PT J AU Uhlig, K Wang, SR Beck, GJ Kusek, JW Marcovina, SM Greene, T Levey, AS Sarnak, MJ AF Uhlig, K Wang, SR Beck, GJ Kusek, JW Marcovina, SM Greene, T Levey, AS Sarnak, MJ TI Factors associated with lipoprotein(a) in chronic kidney disease SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE lipoprotein(a) (Lp[a]); apoprotein(a) (apo[a]); chronic kidney disease (CKD); glomerular filtration rate (GFR) ID STAGE RENAL-DISEASE; APOLIPOPROTEIN(A) PHENOTYPES; CARDIOVASCULAR-DISEASE; PLASMA LIPOPROTEIN(A); HEMODIALYSIS-PATIENTS; NEPHROTIC SYNDROME; APO(A) FRAGMENTS; RISK-FACTORS; ISOFORMS; FAILURE AB Background. It is unclear whether lipoprotein(a) (Lp[a]) levels in patients with chronic kidney disease (CKD) are elevated as a result of reduced glomerular filtration rate (GFR) or other factors associated with CKD. The goal of this study is to describe the association of Lp(a) level with GFR in the context of apoprotein(a) (apo[a]) isoform size, race, and other kidney disease-related factors, such as proteinuria, serum albumin level, C-reactive protein (CRP) level, and serum lipid levels. Methods: Lp(a) and apo(a) isoforms were measured in serum samples obtained at baseline from 804 participants in the Modification of Diet in Renal Disease study (GFR range, 13 to 55 mL/min/1.73 m(2)). The cross-sectional association between Lp(a) level and GFR, apo(a) isoform size, race, and other variables was analyzed in univariate and multivariate linear regression. Results: Median Lp(a) level was greater in blacks than whites (97.5 versus 28.1 nmol/L; P < 0.001). Those with a low-molecular-weight apo(a) isoform size had greater Lp(a) levels than those with a high-molecular-weight apo(a) isoform size (57.5 versus 21.3 nmol/L; P < 0.001). Lp(a) level was not associated with GFR. Low-molecular-weight apo(a), black race, and greater levels of proteinuria, CRP, and triglycerides were independently associated with greater Lp(a) levels. Conclusion: In this population with CKD stages 3 to 4, GFR was not associated with Lp(a) level, whereas other factors related to CKD, such as proteinuria, CRP level, and triglyceride level, as well as genetic factors such as apo(a) isoform size and race, were associated with Lp(a) level. (C) 2004 by the National Kidney Foundation, Inc. C1 Tufts New England Med Ctr, Div Nephrol, Dept Med, Boston, MA 02111 USA. Cleveland Clin Fdn, Dept Biostat & Epidemiol, Cleveland, OH 44195 USA. NIH, Bethesda, MD 20892 USA. Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA. RP Uhlig, K (reprint author), Tufts New England Med Ctr, Div Nephrol, Dept Med, 750 Washington St,Box 391, Boston, MA 02111 USA. EM kuhlig@tufts-nemc.org FU NIDDK NIH HHS [UO1 DK 35073, 1 K23 DK02904] NR 38 TC 5 Z9 5 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 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JAN PY 2005 VL 45 IS 1 BP 28 EP 38 DI 10.1053/j.ajkd.2004.08.043 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA 890NE UT WOS:000226517300005 PM 15696441 ER PT J AU Wilson, J Axelsen, K Tang, S AF Wilson, J Axelsen, K Tang, S TI Medicaid prescription drug access restrictions: Exploring the effect on patient persistence with hypertension medications SO AMERICAN JOURNAL OF MANAGED CARE LA English DT Article ID THERAPY; POPULATION AB Objective: To compare rates of discontinuation of prescription therapy for hypertension in Medicaid patients with and without medication access restrictions. Study Design: Retrospective cohort study. Methods: Prescription data were extracted from a pharmacy claims database in a large state that implemented a Medicaid preferred drug list (PDL), both before and after the PDL was implemented. Prescriptions filled between June 2000 and May 2003 were included. Results: Medicaid patients taking prescription medications commonly used to treat hypertension were 39% (odds ratio = 1.39; 95% confidence interval, 1.21, 1.6) more likely to discontinue hypertension therapy after the restriction was implemented compared with Medicaid patients 1 year earlier when there were no restrictions. Patients were classified as "discontinued" if they had therapy available less than 50% of the time during the 12 months after implementation of the PDL. Before the PDL, 17% of patients receiving treatment with hypertension medication discontinued therapy. After the PDL, 21% of Medicaid patients taking hypertension medication discontinued therapy. After the PDL, Medicaid patients were significantly more likely to switch medications from a restricted to an unrestricted drug. Those patients also were less likely to have a restricted drug added to their therapy regimen. Conclusions: After implementation of the PDL, Medicaid patients were more likely to discontinue filling prescriptions for anti hypertensive medication. Because hypertension management is an important challenge within the Medicaid community, the potential connection between access restrictions and patient adherence to medication therapy is a worthy topic for further exploratory studies and quantitative outcomes research. C1 Morehouse Sch Med, Atlanta, GA 30310 USA. Pfizer Inc, Market Analyt Dept, New York, NY USA. Pfizer Inc, Outcomes Res, New York, NY USA. RP Wilson, J (reprint author), NIH, Natl Ctr Minor Hlth & Hlth Disparities, 6707 Damocracy Blvd,Suite 800, Bethesda, MD 20892 USA. EM wilsonjer@mail.nih.gov NR 17 TC 26 Z9 27 U1 0 U2 1 PU AMER MED PUBLISHING, M W C COMPANY PI JAMESBURG PA 241 FORSGATE DR, STE 102, JAMESBURG, NJ 08831 USA SN 1088-0224 J9 AM J MANAG CARE JI Am. J. Manag. Care PD JAN PY 2005 VL 11 SI SI BP SP27 EP SP34 PG 8 WC Health Care Sciences & Services; Health Policy & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 887GW UT WOS:000226294900005 PM 15700907 ER PT J AU Wang, Z Li, Q Huang, GS Guo, HZ Zhang, J Cheng, H Liu, SJ Xu, J Barenhoim-Stapleton, L Ried, T AF Wang, Z Li, Q Huang, GS Guo, HZ Zhang, J Cheng, H Liu, SJ Xu, J Barenhoim-Stapleton, L Ried, T TI Clinical report of congenital lymphatic malformations and partial gigantism of the hands associated with a heterogeneous karyotype SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Letter ID KLIPPEL-TRENAUNAY-SYNDROME; PROTEUS SYNDROME C1 Fourth Mil Med Univ, Xijing Hosp, Dept Pathol, Xian 710032, Peoples R China. Fourth Mil Med Univ, Xijing Hosp, Dept Obstet & Gynecol, Xian 710032, Peoples R China. Fourth Mil Med Univ, Xijing Hosp, Dept Radiol, Xian 710032, Peoples R China. NCI, NIH, Sect Canc Genom, Genet Branch,Ctr Canc Res, Bethesda, MD USA. RP Wang, Z (reprint author), Fourth Mil Med Univ, Xijing Hosp, Dept Pathol, Xian 710032, Peoples R China. EM path1018@fmmu.edu.cn NR 8 TC 0 Z9 0 U1 1 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD JAN 1 PY 2005 VL 132A IS 1 BP 106 EP 107 DI 10.1002/ajmg.a.30347 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 888NI UT WOS:000226381100021 PM 15472995 ER PT J AU Dezfulian, C Shojania, K Collard, HR Kim, HM Matthay, MA Saint, S AF Dezfulian, C Shojania, K Collard, HR Kim, HM Matthay, MA Saint, S TI Subglottic secretion drainage for preventing ventilator-associated pneumonia: a meta-analysis SO AMERICAN JOURNAL OF MEDICINE LA English DT Review DE ventilators; mechanical; pneumonia; infection control; respiratory tract infections; meta-analysis ID RANDOMIZED CONTROLLED-TRIALS; NOSOCOMIAL PNEUMONIA; MECHANICAL VENTILATION; CONTINUOUS ASPIRATION; ACQUIRED PNEUMONIA; INTUBATED PATIENTS; CLINICAL-TRIAL; STRESS-ULCER; MORTALITY; QUALITY AB Purpose: To assess the efficacy of subglottic secretion drainage in preventing ventilator-associated pneumonia. Methods: We performed a comprehensive, systematic meta-analysis of randomized trials that have, compared subglottic secretion drainage with standard endotracheal tube care in mechanically ventilated patients. Studies were identified by a computerized database search. review of bibliographies. and expert consultation. Summary fisk ratios or weighted mean differences with 95% confidence intervals were calculated for each outcome using a fixed-effects model. Results: Of 110 studies retrieved, five met the inclusion criteria and enrolled 896 patients. Subglottic secretion drainage reduced the incidence of ventilator-associated pneumonia by nearly half (risk ratio [RR] = 0.51; 95% confidence interval [CI]: 0.37 to 0.71). primarily by reducing early-onset pneumonia (pneumonia occurring within 5 to 7 days after intubation). Although significant heterogeneity was found for several endpoints, this was largely resolved by excluding a single outlying, study. In the remaining four studies, which recruited patients expected to require >72 hours of mechanical ventilation, secretion drainage shortened the duration of mechanical ventilation by 2 days (95% CI: 1.77 to 2.3 days) and the length of stay in the intensive care unit by 3 days (95% CI: 2.1 to 3.9 days), and delayed the onset of pneumonia by 6.8 days (95% CI: 5.5 to 8.1 days). Conclusion: Subglottic secretion drainage appears effective in preventing early-onset ventilator-associated pneumonia among patients expected to require >72 hours of mechanical ventilation. (C) 2005 Elsevier Inc. All rights reserved. C1 Natl Inst Hlth, Dept Crit Care Med, Bethesda, MD USA. Johns Hopkins Univ, Div Pediat Anesthesia & Crit Care Med, Dept Anesthesia & Crit Care Med, Baltimore, MD USA. Vet Adm Med Ctr, Ann Arbor, MI 48105 USA. Univ Michigan, Sch Med & Hlth Syst, Dept Med, Ann Arbor, MI USA. Univ Michigan, Sch Med & Hlth Syst, Patient Safety Enhancement Program, Ann Arbor, MI USA. Univ Michigan, Ctr Statist Consultat & Res, Ann Arbor, MI 48109 USA. Univ Calif San Francisco, Div Pulm & Crit Care Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA. Univ Colorado, Hlth Sci Ctr, Dept Med, Div Pulm Sci & Crit Care Med, Denver, CO 80262 USA. RP Dezfulian, C (reprint author), 10 Ctr Dr,Bldg 10,Room 7D43, Bethesda, MD 20892 USA. EM cdezfulian@cc.nih.gov OI Dezfulian, Cameron/0000-0002-4486-0446 FU AHRQ HHS [P20-HS11540]; NCHHSTP CDC HHS [PSOHL74005]; NHLBI NIH HHS [HL51854, HL51856] NR 37 TC 125 Z9 141 U1 1 U2 7 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9343 J9 AM J MED JI Am. J. Med. PD JAN PY 2005 VL 118 IS 1 BP 11 EP 18 DI 10.1016/j.amjmed.2004.07.051 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 888FN UT WOS:000226359700003 PM 15639202 ER PT J AU Vu, HV Ianosi-Irmie, MR Pridjian, CA Whitbred, JM Durst, JM Bagrov, AY Fedorova, OV Pridjian, G Puschett, JB AF Vu, HV Ianosi-Irmie, MR Pridjian, CA Whitbred, JM Durst, JM Bagrov, AY Fedorova, OV Pridjian, G Puschett, JB TI Involvement of marinobufagenin in a rat model of human preeclampsia SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Article DE preeclampsia; marinobufagenin; hypertension; Na+/K+ ATPase inhibition; deoxycorticosterone acetate ID UTERINE PERFUSION-PRESSURE; ESSENTIAL-HYPERTENSION; SODIUM-PUMP; EXPERIMENTAL TOXEMIA; VOLUME EXPANSION; PREGNANT RATS; OUABAIN; PLASMA; INHIBITOR; CONSTRICTION AB Background: Preeclampsia is a potentially devastating disorder of hypertension in pregnancy for which there is currently no definitive treatment short of delivery. The bufadienolide, marinobufagenin ( MBG), an inhibitor of Na+ / K+ ATPase, has been found to be elevated in extracellular fluid volume- expanded hypertensive patients, a condition similar to preeclampsia. Thus, these studies sought to examine the role of MBG in our rat model of preeclampsia. Methods and Results: Pregnant female rats were injected intraperitoneally with deoxycorticosterone acetate ( DOCA) and given 0.9% saline as drinking water for the duration of their pregnancy. Urinary MBG was measured using a DELFIA immunoassay. Blood pressure was measured via the tail- cuff method. Injections of anti- MBG antibody were given intraperitoneally or intravenously to hypertensive pregnant rats. MBG was given intraperitoneally to pregnant rats. Uterine arterioles were dissected free and their diameters were measured before and after perfusion of MBG, ouabain, or digoxin. MBG was found to be elevated in the pregnant + DOCA + saline ( PDS) rats compared to normal pregnant animals. In addition, when PDS rats were injected with anti- MBG antibody, there was a subsequent reduction in blood pressure. Administration of MBG in normal pregnant rats caused an elevation in blood pressure equivalent to the PDS model. Also, uterine vessel measurements showed an increased vasoconstrictive reactivity to MBG in the PDS animals vs. the normal pregnant controls; while no changes were observed with perfusion of digoxin or ouabain at the same concentration. Conclusion: These results suggest a relationship between MBG and a syndrome in rats resembling preeclampsia. Armed with these promising results, it would seem logical to further examine the role of MBG in human preeclampsia. Copyright (C) 2005 S. Karger AG, Basel. C1 Tulane Univ, Sch Med, Dept Med, New Orleans, LA 70112 USA. Tulane Univ, Sch Med, Dept Obstet & Gynecol, New Orleans, LA 70112 USA. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. RP Puschett, JB (reprint author), Tulane Univ, Sch Med, Dept Med, SL12,1430 Tulane Ave, New Orleans, LA 70112 USA. EM jpusche@tulane.edu NR 40 TC 52 Z9 52 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PY 2005 VL 25 IS 5 BP 520 EP 528 DI 10.1159/000088461 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA 972YP UT WOS:000232490000015 PM 16179779 ER PT J AU Boissy, RE Richmond, B Huizing, M Helip-Wooley, A Zhao, Y Koshoffer, A Gahl, WA AF Boissy, RE Richmond, B Huizing, M Helip-Wooley, A Zhao, Y Koshoffer, A Gahl, WA TI Melanocyte-specific proteins are aberrantly trafficked in melanocytes of Hermansky-Pudlak Syndrome-type 3 SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HERMANSKY-PUDLAK-SYNDROME; LYSOSOME-RELATED ORGANELLES; STORAGE-POOL DEFICIENCY; BETA-3A SUBUNIT; AP-3 ADAPTER; GENE; BIOGENESIS; COMPLEX; MUTATION; HPS4 AB Hermansky-Pudlak Syndrome-type 3 (HPS-3) is a relatively mild subtype of HPS with minimal cutaneous and ocular depigmentation. The HPS-3 gene encodes a novel protein of unknown function with a predicted molecular weight of 114 kd. To assess the role of the HPS3 protein in melanization, cultured melanocytes developed from HPS-3 patients were evaluated biochemically and histologically for activity and localization of melanocyte-specific proteins. Endogenous tyrosinase activity of HPS-3 melanocytes was substantial, but tyrosinase activity and melanin synthesis was suppressed in intact melanocytes. However, the level of suppression, as well as extent to which up-regulation by isobutylinethybcanthine and cholera toxin was muted, was less that in HPS-1 melanocytes. Ultrastructutally, HPS-3 melanocytes contained morphologically normal melanosomes, predominantly of stage I and II with minimal stage III and few stage IV melanosomes. Dihydroxyphenylalanine (DOPA) histochemistry demonstrated an increase in melanization of melanosoines. Unique to HPS-3 melanocytes; were numerous DOPA-positive 50-nm vesicles and tubular elements present throughout the cell body and dendrites. Tyrosinase, tyrosinase-related protein-1 (Tyrp1), dopachrome tautomerase (Dct), and LAMP1 and 3 localization in HPS-3 melanocytes, as evaluated by immunocytochemistry and confocal microscopy, demonstrated a fine, floccular distribution in contrast to the coarse, granular distribution characteristic of control melanocytes. The localization profile of other proteins expressed by melanocytes (ie, Silver/Pmel17, Melan-A/MART-1, LAMP2, Rab 27, transferrin, c-kit, adaptin-3, and the HPS1 protein) appeared normal These results suggest that a specific subset of melanocyte proteins are aberrantly trafficked throughout the HPS-3 melanocyte and may be responsible for the reduction in melanin synthesis. C1 Univ Cincinnati, Coll Med, Dept Dermatol, Cincinnati, OH 45267 USA. NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, Bethesda, MD 20892 USA. RP Boissy, RE (reprint author), Univ Cincinnati, Coll Med, Dept Dermatol, 231 Albert Sabin Way,ML-0592, Cincinnati, OH 45267 USA. EM boissyre@ucmail.uc.edu RI Koshoffer, Amy/N-2278-2014; 何, 敏仪/E-6352-2015 OI Koshoffer, Amy/0000-0001-8130-103X; FU NIAMS NIH HHS [R01 AR045429-04, 5 R01 AR45429, R01 AR045429] NR 49 TC 29 Z9 30 U1 2 U2 9 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JAN PY 2005 VL 166 IS 1 BP 231 EP 240 DI 10.1016/S0002-9440(10)62247-X PG 10 WC Pathology SC Pathology GA 883IN UT WOS:000226004900021 PM 15632015 ER PT J AU Tchabo, NE Liel, MS Kohn, EC AF Tchabo, NE Liel, MS Kohn, EC TI Applying proteomics in clinical trials - Assessing the potential and practical limitations in ovarian cancer SO AMERICAN JOURNAL OF PHARMACOGENOMICS LA English DT Editorial Material ID IMAGING MASS-SPECTROMETRY; TYROSINE KINASE INHIBITOR; CHRONIC MYELOID-LEUKEMIA; PHASE-I SAFETY; GROWTH-FACTOR; PROTEIN MICROARRAYS; TISSUE-SECTIONS; SERUM; DIAGNOSIS; EXPRESSION AB Ovarian cancer is the leading cause of death from gynecologic malignancies among American women and the fourth most frequent cause of death from cancer in women in Europe and the US. Despite appropriate surgical and chemotherapeutic intervention, the 5-year survival in patients with metastatic cancer remains poor. Currently available screening methods, including CA125, additional biomarkers, and transvaginal ultrasound lack the necessary sensitivity and specificity to provide accurate and cost-efficient screening for the general population or the ability to assess who will benefit most from each treatment. These limitations have prompted the study of proteomic technology and its application in ovarian cancer diagnostics. Proteomics is the study of molecules in the functional protein pathways of normal or diseased states. Clinical trials are currently being conducted to assess the sensitivity and specificity of serum proteomic patterns and additional clinical trials are designed to evaluate the effects of molecularly targeted agents on protein signaling pathways in human subjects. Overcoming both scientific and practical limitations will lead to increased knowledge of deranged protein networks in cancer cells. Clinical trials in proteomics may result in improved early detection, better monitoring, new drugs and molecularly targeted therapeutics, and individualized therapies. C1 NCI, Pathol Lab, Canc Res Ctr, Mol Signaling Sect Ctr, Bethesda, MD 20892 USA. RP Kohn, EC (reprint author), NCI, Pathol Lab, Canc Res Ctr, Mol Signaling Sect Ctr, Bldg 10,Rm 12N226,10 Ctr Dr, Bethesda, MD 20892 USA. EM kohne@mail.nih.gov NR 58 TC 13 Z9 14 U1 0 U2 1 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1175-2203 J9 AM J PHARMACOGENOMIC JI Am. J. Pharmacogenomics PY 2005 VL 5 IS 3 BP 141 EP 148 DI 10.2165/00129785-200505030-00001 PG 8 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 961XX UT WOS:000231696200001 PM 15952868 ER PT J AU Johnson, MD Yu, LR Conrads, TP Kinoshita, Y Uo, T McBee, JK Veenstra, TD Morrison, RS AF Johnson, MD Yu, LR Conrads, TP Kinoshita, Y Uo, T McBee, JK Veenstra, TD Morrison, RS TI The proteomics of neurodegeneration SO AMERICAN JOURNAL OF PHARMACOGENOMICS LA English DT Article ID CARBOXY-TERMINAL HYDROLASE; ALZHEIMERS-DISEASE BRAIN; OXIDATIVELY MODIFIED PROTEINS; PARKINSONS-DISEASE; MASS-SPECTROMETRY; TRANSGENIC MICE; NEURONAL CELLS; DIFFERENTIAL EXPRESSION; MULTIPROTEIN COMPLEXES; MITOCHONDRIAL PROTEINS AB The continuing improvement and refinement of proteomic and bioinformatic tools has made it possible to obtain increasing amounts of structural and functional information about proteins on a global scale. The emerging field of neuroproteomics promises to provide powerful strategies for further charactenzing neuronal dysfunction and cell loss associated with neurodegenerative diseases. Neuroproteomic studies have thus far revealed relatively comprehensive quantitative changes and post-translational modifications (mostly oxidative damage) of high abundance proteins, confirming deficits in energy production, protein degradation, antioxidant protein function, and cytoskeletal regulation associated with neurodegenerative diseases such as Alzheimer and Parkinson disease. The identification of changes in low-abundance proteins and characterization of their functions based on protein-protein interactions still await further development of proteomic methodologies and more dedicated application of these technologies by neuroscientists. Once accomplished, however, the resulting information will certainly provide a truly comprehensive view of neurodegeneration-associated changes in protein expression, facilitating the identification of novel biomarkers for the early detection of neurodegenerative diseases and new targets for therapeutic intervention. C1 Univ Washington, Sch Med, Dept Neurol Surg, Seattle, WA 98195 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. NCI, SAIC Frederick Inc, Lab Proteom & Analyt Technol, Frederick, MD USA. RP Morrison, RS (reprint author), Univ Washington, Sch Med, Dept Neurol Surg, 1959 NE Pacific St,Box 356470, Seattle, WA 98195 USA. EM yael@u.washington.edu FU NINDS NIH HHS [NS04767, NS35533, NS42699] NR 86 TC 20 Z9 21 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1175-2203 J9 AM J PHARMACOGENOMIC JI Am. J. Pharmacogenomics PY 2005 VL 5 IS 4 BP 259 EP 270 DI 10.2165/00129785-200505040-00006 PG 12 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 963YH UT WOS:000231842000006 PM 16078862 ER PT J AU Taube, SE Jacobson, JW Lively, TG AF Taube, SE Jacobson, JW Lively, TG TI Cancer diagnostics - Decision criteria for marker utilization in the clinic SO AMERICAN JOURNAL OF PHARMACOGENOMICS LA English DT Article ID NEGATIVE BREAST-CANCER; ACTIVATOR INHIBITOR TYPE-1; CELL LUNG-CANCER; SURGICAL ADJUVANT BREAST; FACTOR RECEPTOR GENE; BONE-MARROW; PLASMINOGEN-ACTIVATOR; IMMUNOHISTOCHEMICAL DETECTION; PRIMARY SURGERY; TUMOR-CELLS AB A new diagnostic tool must pass three major tests before it is adopted for routine clinical use. First, the tool must be robust and reproducible; second, the clinical value of the tool must be proven, i.e. the tool should reliably trigger a clinical decision that results in patient benefit; and, third, the clinical community has to be convinced of the need for this tool and the benefits it affords. Another factor that can influence the adoption of new tools relates to the cost and the vagaries of insurance reimbursement. The Cancer Diagnosis Program (CDP) of the US National Cancer Institute (NCI) launched the Program for the Assessment of Clinical Cancer Tests (PACCT) in 2000 to develop a process for moving the results of new technologies and new understanding of cancer biology more efficiently and effectively into clinical practice. PACCT has developed an algorithm that incorporates the iterative nature of assay development into an evaluation process that includes developers and end users. The effective introduction of new tests into clinical practice has been hampered by a series of common problems that are best described using examples of successes and failures. The successful application of the PACCT algorithm is described in the discussion of the recent development of the OncotypeDX(TM) assay and plan for a prospective trial of this assay by the NCI-supported Clinical Trials Cooperative Groups. The assay uses reverse transcription (RT)-PCR evaluation of a set of 16 genes that were shown to strongly associate with the risk of recurrence of breast cancer in women who presented with early stage disease (hormone responsive, and no involvement of the auxiliary lymph nodes). The test is highly reproducible. It provides information to aid the physician and patient in making important clinical decisions, including the aggressiveness of the therapy that should be recommended. A trial is planned to test whether OncotypeDXTM can be used as a standalone trigger for specific treatment decisions. The problems that have been encountered and have delayed the development of other diagnostic tools are exemplified in the development of tests for human epidermal growth factor receptor (HER2) overexpression, for predictors of response to epidermal growth factor receptor inhibitors, and for the detection of residual disease following chemotherapy. C1 Natl Canc Inst, Div Canc Treatment & Diagnosis, Canc Diagnost Program, Rockville, MD 20952 USA. RP Taube, SE (reprint author), Natl Canc Inst, Div Canc Treatment & Diagnosis, Canc Diagnost Program, EPN 6035A,6130 Execut Blvd, Rockville, MD 20952 USA. EM taubes@mail.nih.gov NR 46 TC 18 Z9 18 U1 0 U2 5 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1175-2203 J9 AM J PHARMACOGENOMIC JI Am. J. Pharmacogenomics PY 2005 VL 5 IS 6 BP 357 EP 364 DI 10.2165/00129785-200505060-00003 PG 8 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 001TZ UT WOS:000234562100002 PM 16336001 ER PT J AU Babb, PL Sithaldeen, R Ackermann, RR Newman, TK AF Babb, PL Sithaldeen, R Ackermann, RR Newman, TK TI Mitochondrial DNA sequence evidence for a deep phylogenetic split in chacma baboons (Papio hamadryas ursinus) and the phylogeographic implications for Papio systematics. SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Meeting Abstract C1 NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. Univ Cape Town, Dept Archaeol, ZA-7925 Cape Town, South Africa. NR 0 TC 1 Z9 1 U1 1 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. PY 2005 SU 40 BP 67 EP 68 PG 2 WC Anthropology; Evolutionary Biology SC Anthropology; Evolutionary Biology GA 900KX UT WOS:000227214900025 ER PT J AU Newman, TK Howell, S Barr, CS Babb, PL Westergaard, GC Higley, JD AF Newman, TK Howell, S Barr, CS Babb, PL Westergaard, GC Higley, JD TI Genetic and environmental influences on acquired dominance status in free ranging male rhesus macaques (Macaca mulatta). SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Meeting Abstract C1 NIAAA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. NIAAA, Clin Sci Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. PY 2005 SU 40 BP 157 EP 157 PG 1 WC Anthropology; Evolutionary Biology SC Anthropology; Evolutionary Biology GA 900KX UT WOS:000227214900369 ER PT J AU Schwandt, ML Shannon, C Lindell, SG Suomi, SJ Higley, JD AF Schwandt, ML Shannon, C Lindell, SG Suomi, SJ Higley, JD TI Low birth weight and hypothalamic-pituitary-adrenal (HPA) axis function in infant rhesus macaques. SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Meeting Abstract C1 NIAAA, Clin Studies Lab, NIH, Bethesda, MD USA. NICHD, Comparat Ethol Lab, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. PY 2005 SU 40 BP 185 EP 185 PG 1 WC Anthropology; Evolutionary Biology SC Anthropology; Evolutionary Biology GA 900KX UT WOS:000227214900479 ER PT J AU Sithaldeen, R Babb, PL Ackermann, RR Newman, TK AF Sithaldeen, R Babb, PL Ackermann, RR Newman, TK TI Assessing gene flow and population subdivision in chacma baboons (Papio hamadryas ursinus) using mitochondrial and nuclear DNA markers. SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Meeting Abstract C1 Univ Cape Town, Dept Archaeol, ZA-7700 Rondebosch, South Africa. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. PY 2005 SU 40 BP 191 EP 191 PG 1 WC Anthropology; Evolutionary Biology SC Anthropology; Evolutionary Biology GA 900KX UT WOS:000227214900504 ER PT J AU Kunos, G Batkai, S Pacher, P Wagner, JA Jarai, Z AF Kunos, G Batkai, S Pacher, P Wagner, JA Jarai, Z TI Cannabinoids and endotoxemia - Reply SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Letter ID ANANDAMIDE; HYPOTENSION; RECEPTORS; RATS C1 NIAAA, NIH, Bethesda, MD 20892 USA. Univ Wurzburg, Dept Med, D-97070 Wurzburg, Germany. Semmelweis Univ, Dept Med 1, H-1085 Budapest, Hungary. RP Kunos, G (reprint author), NIAAA, NIH, Bethesda, MD 20892 USA. RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014 NR 8 TC 0 Z9 0 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD JAN PY 2005 VL 288 IS 1 BP H451 EP H452 PG 2 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 879QT UT WOS:000225733000063 ER PT J AU Yang, ZW Asico, LD Yu, PY Wang, Z Jones, JE Bai, RK Sibley, DR Felder, RA Jose, PA AF Yang, ZW Asico, LD Yu, PY Wang, Z Jones, JE Bai, RK Sibley, DR Felder, RA Jose, PA TI D-5 dopamine receptor regulation of phospholipase D SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article; Proceedings Paper CT Cardiovascular Kidney Investigators Meeting CY MAY 28-31, 2004 CL Amelia Isl, FL DE hypertension ID SMOOTH-MUSCLE-CELLS; KINASE-C-ALPHA; SPONTANEOUSLY HYPERTENSIVE-RATS; ADP-RIBOSYLATION FACTOR; PROTEIN-KINASE; ANGIOTENSIN-II; DIRECTLY INTERACTS; BLOOD-PRESSURE; GROWTH-FACTOR; D ACTIVATION AB D-1-like receptors have been reported to decrease oxidative stress in vascular smooth muscle cells by decreasing phospholipase D (PLD) activity. However, the PLD isoform regulated by D-1-like receptors (D-1 or D-5) and whether abnormal regulation of PLD by D-1-like receptors plays a role in the pathogenesis of hypertension are unknown. The hypothesis that the D5 receptor is the D-1-like receptor that inhibits PLD activity and serves to regulate blood pressure was tested using D-5 receptor mutant mice (D-5(-/-)). We found that in the mouse kidney, PLD2, like the D-5 receptor, is mainly expressed in renal brush-border membranes, whereas PLD1 is mainly expressed in renal vessels with faint staining in brush-border membranes and collecting ducts. Total renal PLD activity is increased in D-5(-/-) mice relative to congenic D-5 wild-type (D-5(+/+)) mice. PLD2, but not PLD1, expression is greater in D-5(-/-) than in D-5(+/+) mice. The D-5 receptor agonist fenoldopam decreases PLD2, but not PLD1, expression and activity in human embryonic kidney-293 cells heterologously expressing the human D5 receptor, effects that are blocked by the D-5 receptor antagonist SCH-23390. These studies show that the D-5 receptor regulates PLD2 activity and expression. The hypertension in the D-5(-/-) mice is associated with increased PLD expression and activity. Impaired D-5 receptor regulation of PLD2 may play a role in the pathogenesis of hypertension. C1 Georgetown Univ, Med Ctr, Dept Physiol & Biophys, Washington, DC 20057 USA. Georgetown Univ, Med Ctr, Dept Pediat, Washington, DC 20057 USA. Georgetown Univ, Med Ctr, Inst Mol & Human Genet, Washington, DC 20057 USA. NINDS, Bethesda, MD 20892 USA. Univ Virginia, Ctr Hlth Sci, Dept Pathol, Charlottesville, VA USA. RP Jose, PA (reprint author), Georgetown Univ, Med Ctr, Dept Physiol & Biophys, 3800 Reservoir Rd NW, Washington, DC 20057 USA. EM pjose01@georgetown.edu FU NHLBI NIH HHS [HL-68686]; NIDDK NIH HHS [DK-39308] NR 48 TC 23 Z9 29 U1 1 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD JAN PY 2005 VL 288 IS 1 BP H55 EP H61 DI 10.1152/ajpheart.00627.2004 PG 7 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 879QT UT WOS:000225733000010 PM 15598876 ER PT J AU Hofman, K Primack, A Keusch, G Hrynkow, S AF Hofman, K Primack, A Keusch, G Hrynkow, S TI Addressing the growing burden of trauma and injury in low- and middle-income countries SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID MEDICAL-SERVICES; CARE SYSTEMS; IMPROVEMENTS; AFRICA; UGANDA AB Low- and middle-income countries suffer disproportionately from reduced life expectancy and quality of life. Injuries are overlooked as contributors to global inequities in health, yet the long-term disabilities they frequently produce represent a significant burden. The Fogarty International Center of the National Institutes of Health convened a panel of experts in trauma and injury from the United States and low- and middle income nations to identify research gaps in this area and opportunities to create new knowledge. Panel members identified sustainable programs of research established through stable linkages between institutions in high-income nations and those in low- and middle income nations as a priority. The resulting benefits of addressing the growing burden of trauma and injury to communities in resource-constrained settings around the world would be substantial. C1 NIH, Div Adv Studies & Policy Anal, Fogarty Int Ctr, Bethesda, MD 20892 USA. Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. RP Hofman, K (reprint author), NIH, Div Adv Studies & Policy Anal, Fogarty Int Ctr, 16 Ctr Dr,Room 202, Bethesda, MD 20892 USA. EM hofmank@mail.nih.gov OI Keusch, Gerald/0000-0001-5724-2965 NR 37 TC 101 Z9 107 U1 0 U2 6 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 2005 VL 95 IS 1 BP 13 EP 17 DI 10.2105/AJPH.2004.039354 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 884SW UT WOS:000226107500005 PM 15623852 ER PT J AU Gollust, SE Apse, K Fuller, BP Miller, PS Biesecker, BB AF Gollust, SE Apse, K Fuller, BP Miller, PS Biesecker, BB TI Community involvement in developing policies for genetic testing: Assessing the interests and experiences of individuals affected by genetic conditions SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID CARE DECISION-MAKING; QUALITY-OF-LIFE; PUBLIC-PARTICIPATION; PRENATAL-DIAGNOSIS; CYSTIC-FIBROSIS; PROTECTING COMMUNITIES; SELECTIVE ABORTION; LAY EXPERTISE; HEALTH; ATTITUDES AB Because the introduction of genetic testing into clinical medicine and public health creates concerns for the welfare of individuals affected with genetic conditions, those individuals should have a role in policy decisions about testing. Mechanisms for promoting participation range from membership on advisory committees to community dialogues to surveys that provide evidence for supporting practice guidelines. Surveys can assess the attitudes and the experiences of members of an affected group and thus inform discussions about that community's concerns regarding the appropriate use of a genetic test. Results of a survey of individuals affected with inherited dwarfism show how data can be used in policy and clinical-practice contexts. Future research of affected communities' interests should be pursued so that under-represented voices can be heard. C1 NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. Beth Israel Deaconess Med Ctr, Div Neurogenet, Boston, MA 02215 USA. NHGRI, Policy & Program Anal Branch, Bethesda, MD 20892 USA. US Equal Employment Opportunity Commiss, Washington, DC USA. RP Biesecker, BB (reprint author), NHGRI, Social & Behav Res Branch, NIH, 10 Ctr Dr Bldg 10,Rm 10C101, Bethesda, MD 20892 USA. EM barbarab@nhgri.nih.gov FU NHGRI NIH HHS [Z01 HG000123] NR 96 TC 25 Z9 25 U1 3 U2 6 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 2005 VL 95 IS 1 BP 35 EP 41 DI 10.2105/AJPH.2003.025734 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 884SW UT WOS:000226107500008 PM 15623855 ER PT J AU Fee, E Brown, TM AF Fee, E Brown, TM TI Florence Kelley: A factory inspector campaigns against sweatshop labor SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Editorial Material C1 Natl Lib Med, Hist Med Div, NIH, Bethesda, MD USA. Univ Rochester, Dept Hist, Rochester, NY USA. Univ Rochester, Dept Community & Prevent Med, Rochester, NY USA. RP Fee, E (reprint author), Bldg 38,Room 1E21,8600 Rockville Pike, Bethesda, MD 20894 USA. EM elizabeth_fee@nlm.nih.gov NR 5 TC 1 Z9 1 U1 1 U2 5 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 2005 VL 95 IS 1 BP 50 EP 50 DI 10.2105/AJPH.2004.052977 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 884SW UT WOS:000226107500011 PM 15623858 ER PT J AU Fee, E Brown, TM AF Fee, E Brown, TM TI "A doctors' war": Expert witnesses in late 19th-century America SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Editorial Material C1 Natl Lib Med, Hist Med Div, NIH, Bethesda, MD USA. Univ Rochester, Dept Hist, Rochester, NY 14627 USA. Univ Rochester, Dept Community & Prevent Med, Rochester, NY 14627 USA. RP Fee, E (reprint author), Bldg 38,Room 1E21,8600 Rockville Pike, Bethesda, MD 20894 USA. EM elizabeth_fee@nlm.nih.gov NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PY 2005 VL 95 SU 1 BP S28 EP S29 DI 10.2105/AJPH.2005.063594 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 950ZO UT WOS:000230898200007 PM 16030334 ER PT J AU Melnick, RL AF Melnick, RL TI A Daubert motion: A legal strategy to exclude essential scientific evidence in toxic tort litigation SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID EXPOSURE; ATRAZINE; CARCINOGENICITY; CHEMICALS; CANCER; 1,3-BUTADIENE; CAUSATION; INDUSTRY; RISKS; FROGS AB In the US Supreme Court's Daubert v Merrell Dow Pharmaceuticals, Inc decision, federal judges were directed to examine the scientific method underlying expert evidence and admit that which is scientifically reliable and relevant. However, if a judge does not have adequate training or experience in dealing with scientific uncertainty, understand the full value or limit of currently used methodologies, or recognize hidden assumptions, misrepresentations of scientific data, or the strengths of scientific inferences, he or she may reach an incorrect decision on the reliability and relevance of evidence linking environmental factors to human disease. This could lead to the unfair exclusion of valid scientific evidence, particularly that which is essential to a plaintiff's case in toxic tort litigation. C1 NIEHS, Environm Toxicol Program, NIH, Bethesda, MD USA. RP Melnick, RL (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. EM melnickr@niehs.nih.gov NR 31 TC 11 Z9 11 U1 0 U2 1 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PY 2005 VL 95 SU 1 BP S30 EP S34 DI 10.2105/AJPH.2004.046250 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 950ZO UT WOS:000230898200008 PM 16030335 ER PT J AU Taveira-DaSilva, AM Stylianou, MP Hedin, CJ Hathaway, O Moss, J AF Taveira-DaSilva, AM Stylianou, MP Hedin, CJ Hathaway, O Moss, J TI Bone mineral density in lymphangioleiomyomatosis SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article DE bisphosphonates; bone mineral density; interstitial lung disease; lung function; progesterone ID DEPOT-MEDROXYPROGESTERONE ACETATE; OBSTRUCTIVE PULMONARY-DISEASE; SMOOTH-MUSCLE-CELLS; CYSTIC-FIBROSIS; LUNG TRANSPLANTATION; PROGESTERONE-RECEPTORS; STEROID-RECEPTORS; NHANES-III; OSTEOPOROSIS; WOMEN AB Estrogen deficiency and pulmonary diseases are associated with bone mineral density (BMD) loss. Lymphangioleiomyomatosis (LAM), a disorder affecting women that is characterized by cystic lung lesions, is frequently treated with antiestrogen therapy, i.e., progesterone and/or oophorectomy. Therefore, we evaluated BIVID yearly in 211 LAM patients to determine the prevalence of BMD abnormalities, whether antiestrogen therapy decreased BMD, and if treatment with bisphosphonates prevented bone loss. Abnormal BMID was found in 70% of the patients and correlated with severity of lung disease and age. Greater severity of lung disease, menopause, and oophorectomy were associated with greater decline in BMD. After adjusting for differences in initial lung function and BMD, we found similar rates of BMD decline in progesterone-treated (n = 122) and untreated patients (n = 89). After similar adjustments, we found that bisphosphonate-treated patients (n = 98) had lower rates of decline in lumbar spine BMD (-0.004 +/- 0.003 vs. -0.015 +/- 0.003 gm/cm(2), p = 0.036) and T-scores (-0.050 +/- 0.041 vs. -0.191 +/- 0.041, P < 0.001) than untreated patients (n = 113). We conclude that abnormal BMD was frequent in LAM. Progesterone therapy was not associated with changes in BIVID; bisphosphonate therapy was associated with lower rates of bone loss. We recommend systematic evaluation of BMD and early treatment with bisphosphonates for patients with LAM. C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA. RP Taveira-DaSilva, AM (reprint author), NHLBI, Pulm Crit Care Med Branch, NIH, Bldg 10,Room 6D05,MSC 1590, Bethesda, MD 20892 USA. EM dasilvaa@nhlbi.nih.gov NR 62 TC 15 Z9 15 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN 1 PY 2005 VL 171 IS 1 BP 61 EP 67 DI 10.1164/rccm.200406-701OC PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 883BJ UT WOS:000225984800011 PM 15466255 ER PT J AU Yao, L Rider, L Plotz, P AF Yao, L Rider, L Plotz, P TI Increased muscle signal on STIR: Relationship to T2 relaxation and magnetization transfer contrast in muscle disease SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Meeting Abstract CT 105th Annual Meeting of the American-Roentgen-Ray-Society CY MAY 15-20, 2005 CL New Orleans, LA SP Amer Roentgen Ray Soc C1 NIH, Ctr Clin, Bethesda, MD USA. NIAMSD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PY 2005 VL 184 IS 4 SU S BP 32 EP 32 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 920VH UT WOS:000228717800124 ER PT J AU Summers, RM Franaszek, M Miller, MT Pickhardt, PJ Choi, JR Schindler, WR AF Summers, RM Franaszek, M Miller, MT Pickhardt, PJ Choi, JR Schindler, WR TI Computer-aided detection of polyps on oral contrast-enhanced CT colonography SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID VIRTUAL COLONOSCOPY; FEASIBILITY C1 Natl Inst Hlth, Dept Radiol, Bethesda, MD 20892 USA. Natl Naval Med Ctr, Bethesda, MD 20889 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. Walter Reed Army Med Ctr, Washington, DC 20307 USA. Natl Naval Med Ctr, San Diego, CA 92134 USA. RP Summers, RM (reprint author), Natl Inst Hlth, Dept Radiol, 10 Ctr Dr,Bldg 10,Rm 1C660,MSC 1182, Bethesda, MD 20892 USA. EM rms@nih.gov NR 8 TC 44 Z9 46 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JAN PY 2005 VL 184 IS 1 BP 105 EP 108 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 890JQ UT WOS:000226507900020 PM 15615958 ER PT J AU Avila, NA Chen, CC Reynolds, J Neumann, R Carrasquillo, JA AF Avila, NA Chen, CC Reynolds, J Neumann, R Carrasquillo, JA TI PET/CT to the rescue! FDG-PET enhances the diagnostic power of CT SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Meeting Abstract CT 105th Annual Meeting of the American-Roentgen-Ray-Society CY MAY 15-20, 2005 CL New Orleans, LA SP Amer Roentgen Ray Soc C1 NIH, Dept Diagnost Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. NIH, Dept Nucl Med, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PY 2005 VL 184 IS 4 SU S BP 125 EP 125 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 920VH UT WOS:000228717800523 ER PT J AU Harmon, WE McDonald, RA Reyes, JD Bridges, ND Sweet, SC Sommers, CM Guidinger, MK AF Harmon, WE McDonald, RA Reyes, JD Bridges, ND Sweet, SC Sommers, CM Guidinger, MK TI Pediatric transplantation, 1994-2003 SO AMERICAN JOURNAL OF TRANSPLANTATION LA English DT Article DE deceased donors; graft survival; immunosuppression; living donors; organ donation; patient survival; pediatric transplantation; SRTR; waiting list ID INTERSTITIAL LUNG-DISEASE; UNITED-STATES; KIDNEY-TRANSPLANTATION; LIVER-TRANSPLANTATION; RENAL-TRANSPLANTATION; INTERNATIONAL-SOCIETY; GRAFT-SURVIVAL; SINGLE-CENTER; RECIPIENTS; DONOR AB This article uses OPTN/SRTR data to review trends in pediatric transplantation over the last decade. In 2003, children younger than 18 made up 3% of the 82,885 candidates for organ transplantation and 7% of the 25,469 organ transplant recipients. Children accounted for 14% of the 6,455 deceased organ donors. Pediatric organ transplant recipients differ from their adult counterparts in several important aspects, including the underlying etiology of organ failure, the complexity of the surgical procedures, the pharmacokinetic properties of common immunosuppressants, the immune response following transplantation, the number and degree of comorbid conditions, and the susceptibility to post-transplant complications, especially infectious diseases. Specialized pediatric organ transplant programs have been developed to address these special problems, The transplant community has responded to the particular needs of children and has provided them special consideration in the allocation of deceased donor organs. As a result of these programs and protocols, children are now frequently the most successful recipients of organ transplantation; their outcomes following kidney, liver, and heart transplantation rank among the best. This article demonstrates that substantial improvement is needed in several areas: adolescent outcomes, outcomes following intestine transplants, and waiting list mortality among pediatric heart and lung candidates. C1 Childrens Hosp, Seattle, WA USA. Reg Med Ctr, Seattle, WA USA. Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA. NIAID, Bethesda, MD 20892 USA. Washington Univ, Sch Med, St Louis, MO USA. United Network Organ Sharing, Richmond, VA USA. Univ Renal Res & Educ Assoc, Sci Registry Transplant Recipients, Ann Arbor, MI USA. RP Harmon, WE (reprint author), Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA. EM william.harmon@TCH.Harvard.edu NR 32 TC 54 Z9 54 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1600-6135 J9 AM J TRANSPLANT JI Am. J. Transplant. PY 2005 VL 5 IS 4 BP 887 EP 903 DI 10.1111/j.1600-6135.2005.00834.x PN 2 PG 17 WC Surgery; Transplantation SC Surgery; Transplantation GA 904YQ UT WOS:000227534900006 PM 15760416 ER PT J AU Garcia, HH Del Brutto, OH Nash, TE White, AC Tsang, VCW Gilman, RH AF Garcia, HH Del Brutto, OH Nash, TE White, AC Tsang, VCW Gilman, RH TI New concepts in the diagnosis and management of neurocysticercosis (Taenia solium) SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID CEREBRAL CYSTICERCOSIS; FOLLOW-UP; SUBARACHNOID CYSTICERCI; ALBENDAZOLE THERAPY; CEREBROSPINAL-FLUID; ANTIGEN-DETECTION; SEIZURES; HYDROCEPHALUS; LESIONS; ASSAY AB Human neurocysticercosis, the infection of the nervous system by the larvae of Taenia solium, is a major cause of epileptic seizures and other neurologic morbidity worldwide. The diagnosis and treatment of neurocysticercosis have been considerably improved in recent years. This improvement includes identification and sequencing of specific antigens and development of new assays for laboratory diagnosis, recognition of the frequency and significance of edema around old, calcified cysts (associated to symptomatic episodes), results of a randomized blinded control treatment trial on treatment efficacy for intraparenchyrnal disease showing a clinical benefit of decreased seizures, and a much better assessment of the frequency and spectrum of cerebrovascular complications. These advances now permit a much better integration of clinical, serologic, and imaging data for diagnosis and therapeutic purposes. C1 Univ Peruana Cayetano Heredia, Dept Microbiol, Lima, Peru. Inst Nacl Ciencias Neurol, Cysticercosis Unit, Lima, Peru. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA. Hosp Clin Kennedy, Dept Neurol Sci, Guayaquil, Ecuador. NIAID, Parasit Dis Lab, Gastrointestinal Parasites Sect, NIH, Bethesda, MD USA. Baylor Coll Med, Dept Med, Infect Dis Sect, Houston, TX USA. Ben Taub Gen Hosp, Houston, TX 77030 USA. Natl Ctr Infect Dis, Div Parasit Dis, Immunol Branch, Ctr Dis Control, Atlanta, GA USA. RP Garcia, HH (reprint author), Univ Peruana Cayetano Heredia, Dept Microbiol, Lima, Peru. EM hgarcia@jshph.edu OI White, A Clinton/0000-0002-9668-4632 NR 54 TC 87 Z9 91 U1 0 U2 5 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD JAN PY 2005 VL 72 IS 1 BP 3 EP 9 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 900OM UT WOS:000227224200002 PM 15728858 ER PT J AU Boyd, SJ Tashkin, DP Huestis, MA Heishman, SJ Dermand, JC Simmons, MS Gorelick, DA AF Boyd, SJ Tashkin, DP Huestis, MA Heishman, SJ Dermand, JC Simmons, MS Gorelick, DA TI Strategies for quitting among non-treatment-seeking marijuana smokers SO AMERICAN JOURNAL ON ADDICTIONS LA English DT Article ID CANNABIS USE; DRUG-DEPENDENCE; ABUSE; CESSATION; ALCOHOL; OUTCOMES; YOUTH AB This study examines self-reported quitting strategies used by adult, non-treatment-seeking marijuana smokers. Sixty-five subjects rated the use and effectiveness of thirteen strategies on a self-developed instrument, the Marijuana Quit Questionnaire. The strategies clustered into three categories/factors, whether grouped by principal components analysis, mean helpfulness rating, or frequency of endorsement Change Environment, Seeking Organized/Professional Help, and Social Support Changing one's environment was rated as most helpful while seeking help from professionals was the least helpful. Clinicians are likely to see marijuana users in their practice and should be proactive in offering assistance, incorporating the strategies reported here into treatment plans for their marijuana-using patients. C1 NIDA, US Dept HHS, NIH, Intramural Res Program, Baltimore, MD 21224 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90024 USA. RP Gorelick, DA (reprint author), NIDA, US Dept HHS, NIH, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM dgorelic@intra.nida.nih.gov FU Intramural NIH HHS; NIDA NIH HHS [DA03018, DA04268] NR 16 TC 18 Z9 18 U1 3 U2 4 PU BRUNNER-ROUTLEDGE PI PHILADELPHIA PA 325 CHESTNUT ST, 8TH FL, PHILADELPHIA, PA 19106 USA SN 1055-0496 J9 AM J ADDICTION JI Am. J. Addict. PD JAN-FEB PY 2005 VL 14 IS 1 BP 35 EP 42 DI 10.1080/10550490590899835 PG 8 WC Substance Abuse SC Substance Abuse GA 897CO UT WOS:000226981800004 PM 15804875 ER PT J AU Bonham, VL Warshauer-Baker, E Collins, FS AF Bonham, VL Warshauer-Baker, E Collins, FS TI Race and ethnicity in the genome era - The complexity of the constructs SO AMERICAN PSYCHOLOGIST LA English DT Article ID SINGLE-NUCLEOTIDE POLYMORPHISMS; GENETIC-VARIATION; CANDIDATE GENES; NOVELTY SEEKING; HUMAN-EVOLUTION; ASSOCIATION; POPULATION; DIVERSITY; ANCESTRY; PATTERNS AB The vast amount of biological information that is now available through the completion of the Human Genome Project presents opportunities and challenges. The genomic era has the potential to advance an understanding of human genetic variation and its role in human health and disease. A challenge for genomics research is to understand the relationships between genomics, race, and ethnicity and the implications of uncovering these relationships. Robust and scholarly discourse on. the concept of race and ethnicity in genomic research should be expanded to include social and behavioral scientists. Interdisciplinary research teams are needed in. which psychologists, as well as other social and behavioral scientists, work collaboratively with geneticists and other natural scientists. C1 NHGRI, NIH, Bethesda, MD 20892 USA. RP Bonham, VL (reprint author), NHGRI, NIH, 31-4B09, Bethesda, MD 20892 USA. EM bonhamv@mail.nih.gov NR 67 TC 63 Z9 65 U1 0 U2 6 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0003-066X J9 AM PSYCHOL JI Am. Psychol. PD JAN PY 2005 VL 60 IS 1 BP 9 EP 15 DI 10.1037/0003-066X.60.1.9 PG 7 WC Psychology, Multidisciplinary SC Psychology GA 888PV UT WOS:000226387600002 PM 15641917 ER PT J AU Wang, VO Sue, S AF Wang, VO Sue, S TI In the eye of the storm - Race and genomics in research and practice SO AMERICAN PSYCHOLOGIST LA English DT Article ID PSYCHOLOGICAL-RESEARCH; PROSPECTIVE COHORT; GENETIC-STRUCTURE; PUBLIC-HEALTH; DRUG RESPONSE; ETHNICITY; METAANALYSIS; BEHAVIOR; RISK; DISCRIMINATION AB The difficulties of operationalizing race in research and practice for social, behavioral, and genetic researchers and practitioners are neither new, nor related to recent genetic knowledge. For geneticists, the bases for understanding groups are clines, observed traits that gradually change in frequency between geographic regions without distinct identifiable population boundaries and population histories that carry information about the distribution of genetic variants. For psychologists, race may not exist or be a social and cultural construct associated with fluid social inferences. Because definitions of populations and race can be socially and biologically incongruent, the authors suggest that geneticists and social and behavioral scientists and clinicians attend to external validity issues by operationalizing population and racial categories and avoiding race. proxies for other biological, social, and. cultural constructs in research designs, data analyses, and clinical practice. C1 NHGRI, Eth Legal & Social Implicat Program, NIH, US Dept HHS, Bethesda, MD 20893 USA. Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA. RP Wang, VO (reprint author), NHGRI, Eth Legal & Social Implicat Program, NIH, US Dept HHS, 5635 Fishers Lane,Suite 4076,MSC 9305, Bethesda, MD 20893 USA. EM otawangy@mail.nih.gov NR 77 TC 34 Z9 34 U1 0 U2 2 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0003-066X J9 AM PSYCHOL JI Am. Psychol. PD JAN PY 2005 VL 60 IS 1 BP 37 EP 45 DI 10.1037/0003-066X.60.1.37 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 888PV UT WOS:000226387600005 PM 15641920 ER PT J AU Haspel, N Zanuy, D Tsai, HH Ma, BY Wolfson, H Nussinov, R AF Haspel, Nurit Zanuy, David Tsai, Hui-Hsu (Gavin) Ma, Buyong Wolfson, Haim Nussinov, Ruth BE Sipe, JD TI Computational Approaches and Tools for Establishing Structural Models for Short Amyloid-forming Peptides SO AMYLOID PROTEINS: THE BETA SHEET CONFORMATION AND DISEASE, VOLS 1 AND 2 LA English DT Article; Book Chapter ID HUMAN CALCITONIN; MOLECULAR-DYNAMICS; FIBRIL FORMATION; BETA-SHEETS; SEQUENCE; DISEASE; SIMULATIONS; OLIGOMERS; FRAGMENT; STATE C1 [Nussinov, Ruth] SAIC Frederick Inc, Natl Canc Inst, Lab Expt & Computat Biol, Frederick, MD 21702 USA. RI Haspel, Nurit/D-1961-2017 NR 30 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-3-52761-934-4 PY 2005 BP 301 EP 315 DI 10.1002/9783527619344.ch13 D2 10.1002/9783527619344 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BXZ58 UT WOS:000297701200014 ER PT J AU Benyamini, H Gunasekaran, K Wolfson, H Nussinov, R AF Benyamini, Hadar Gunasekaran, Kannan Wolfson, Haim Nussinov, Ruth BE Sipe, JD TI Gelsolin SO AMYLOID PROTEINS: THE BETA SHEET CONFORMATION AND DISEASE, VOLS 1 AND 2 LA English DT Article; Book Chapter ID AMYLOIDOSIS-FINNISH TYPE; BETA-SHEET PROTEINS; FAMILIAL AMYLOIDOSIS; PLASMA GELSOLIN; ACTIN; DOMAIN; FRAGMENT; MUTATION; IDENTIFICATION; LOCALIZATION C1 [Nussinov, Ruth] SAIC Frederick Inc, Natl Canc Inst, Lab Expt & Computat Biol, Frederick, MD 21702 USA. NR 42 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-3-52761-934-4 PY 2005 BP 625 EP 634 DI 10.1002/9783527619344.ch23 D2 10.1002/9783527619344 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BXZ58 UT WOS:000297701200024 ER PT J AU Scott, DJ Schuck, P AF Scott, David J. Schuck, Peter BE Scott, D TI A Brief Introduction to the Analytical Ultracentrifugation of Proteins for Beginners SO ANALYTICAL ULTRACENTRIFUGATION: TECHNIQUES AND METHODS LA English DT Editorial Material; Book Chapter ID SEDIMENTATION COEFFICIENT DISTRIBUTIONS; VELOCITY ANALYTICAL ULTRACENTRIFUGATION; SIZE-DISTRIBUTION ANALYSIS; LAMM EQUATION; DENSITY GRADIENTS; BOUNDARY ANALYSIS; MOLECULAR-WEIGHT; EQUILIBRIUM-ANALYSIS; INHOMOGENEOUS-MEDIA; INTERFERENCE OPTICS C1 [Scott, David J.] Univ Nottingham, Sch Biosci, Natl Ctr Macromol Hydrodynam, Loughborough LE12 5RD, Leics, England. [Schuck, Peter] NIH, Div Bioengn & Phys Sci, ORS, OD, Bethesda, MD 20892 USA. RP Scott, DJ (reprint author), Univ Nottingham, Sch Biosci, Natl Ctr Macromol Hydrodynam, Loughborough LE12 5RD, Leics, England. EM dj.scott@nottingham.ac.uk; pschuck@helix.nih.gov NR 81 TC 40 Z9 41 U1 0 U2 3 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, CAMBRIDGE CB4 4WF, CAMBS, ENGLAND BN 978-1-84755-261-7 PY 2005 BP 1 EP 25 DI 10.1039/9781847552617-00001 D2 10.1039/9781847552617 PG 25 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Analytical; Polymer Science SC Biochemistry & Molecular Biology; Chemistry; Polymer Science GA BKZ71 UT WOS:000269698200001 ER PT J AU Schuck, P AF Schuck, Peter BE Scott, D TI Diffusion-Deconvoluted Sedimentation Coefficient Distributions for the Analysis of Interacting and Non-Interacting Protein Mixtures SO ANALYTICAL ULTRACENTRIFUGATION: TECHNIQUES AND METHODS LA English DT Article; Book Chapter ID VELOCITY ANALYTICAL ULTRACENTRIFUGATION; SIZE-DISTRIBUTION ANALYSIS; LAMM EQUATION; INHOMOGENEOUS-MEDIA; SELF-ASSOCIATION; SOLUTES; SYSTEMS; MACROMOLECULES; MODEL; EQUILIBRIUM AB By modeling the evolution of concentration profiles measured in a sedimentation velocity experiment with a distribution of Lamm equation solutions it is possible to calculate diffusion-free sedimentation coefficient distributions, c(s). For non-interacting or slowly interacting mixtures of sedimenting macromolecules, these report on the number and s value of the species present in solution. For rapidly interacting mixtures, the sedimentation boundaries and peaks in c(s) can be viewed as approximations of the asymptotic reaction boundary from Gilbert-Jenkins theory, which describe characteristic features of the reacting system, and provide a rigorous approach to the weight-average sedimentation coefficient. The extension to sedimentation coefficient distributions of the individual components in a mixture, c(k)(s), calculated by global modeling of multiple signals from the sedimentation process, can reveal the stoichiometry of protein complexes. This chapter reviews the theory, describes some aspects related to the experimental setup, and illustrates the practical use of c(s) and c(k)(s) in several examples. C1 NIH, Div Bioengn & Phys Sci, ORS, OD, Bethesda, MD 20892 USA. RP Schuck, P (reprint author), NIH, Div Bioengn & Phys Sci, ORS, OD, Bethesda, MD 20892 USA. EM pschuck@helix.nih.gov NR 40 TC 24 Z9 24 U1 0 U2 1 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, CAMBRIDGE CB4 4WF, CAMBS, ENGLAND BN 978-1-84755-261-7 PY 2005 BP 26 EP 50 D2 10.1039/9781847552617 PG 25 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Analytical; Polymer Science SC Biochemistry & Molecular Biology; Chemistry; Polymer Science GA BKZ71 UT WOS:000269698200002 ER PT J AU Lewis, MS Reily, MM AF Lewis, Marc S. Reily, Michael M. BE Scott, D TI Application of Weighted Robust Regression to Equilibrium Ultracentrifugation SO ANALYTICAL ULTRACENTRIFUGATION: TECHNIQUES AND METHODS LA English DT Article; Book Chapter C1 [Lewis, Marc S.; Reily, Michael M.] NIH, Div Bioengn & Phys Sci, Off Res Serv, Bethesda, MD 20892 USA. RP Lewis, MS (reprint author), NIH, Div Bioengn & Phys Sci, Off Res Serv, Bethesda, MD 20892 USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, CAMBRIDGE CB4 4WF, CAMBS, ENGLAND BN 978-1-84755-261-7 PY 2005 BP 152 EP 161 D2 10.1039/9781847552617 PG 10 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Analytical; Polymer Science SC Biochemistry & Molecular Biology; Chemistry; Polymer Science GA BKZ71 UT WOS:000269698200008 ER PT J AU Lewis, MS Reily, MM Holladay, LA AF Lewis, Marc S. Reily, Michael M. Holladay, Leslie A. BE Scott, D TI Fitting of Thermodynamic Data from Equilibrium Ultracentrifugation by Robust Least-Squares with Reduced Parameter Cross-Correlation Coefficients SO ANALYTICAL ULTRACENTRIFUGATION: TECHNIQUES AND METHODS LA English DT Article; Book Chapter ID PROTEIN; NONPOLAR; SURFACE; WATER C1 [Lewis, Marc S.; Reily, Michael M.; Holladay, Leslie A.] NIH, Div Bioengn & Phys Sci, Off Res Serv, Bethesda, MD 20892 USA. RP Lewis, MS (reprint author), NIH, Div Bioengn & Phys Sci, Off Res Serv, Bethesda, MD 20892 USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, CAMBRIDGE CB4 4WF, CAMBS, ENGLAND BN 978-1-84755-261-7 PY 2005 BP 372 EP 388 D2 10.1039/9781847552617 PG 17 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Analytical; Polymer Science SC Biochemistry & Molecular Biology; Chemistry; Polymer Science GA BKZ71 UT WOS:000269698200017 ER PT J AU Hackett, CJ Rotrosen, D Plaut, M AF Hackett, CJ Rotrosen, D Plaut, M TI Addressing challenges for allergists in vaccination to protect against smallpox SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Editorial Material C1 NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA. RP Hackett, CJ (reprint author), NIAID, Div Allergy Immunol & Transplantat, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. OI Hackett, Charles/0000-0003-4586-9669 NR 11 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 USA SN 1081-1206 J9 ANN ALLERG ASTHMA IM JI Ann. Allergy Asthma Immunol. PD JAN PY 2005 VL 94 IS 1 BP 1 EP 3 PG 3 WC Allergy; Immunology SC Allergy; Immunology GA 894EN UT WOS:000226773500002 PM 15702805 ER PT J AU Solomon, SD AF Solomon, SD TI A new wave of behavior change intervention research SO ANNALS OF BEHAVIORAL MEDICINE LA English DT Editorial Material C1 Off Behav & Social Sci, NIH, Bethesda, MD 20897 USA. RP Solomon, SD (reprint author), Off Behav & Social Sci, NIH, 1 Ctr Dr,Room 256, Bethesda, MD 20897 USA. EM ssolomon@nih.gov NR 9 TC 3 Z9 3 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0883-6612 J9 ANN BEHAV MED JI Ann. Behav. Med. PY 2005 VL 29 SU S BP 1 EP 3 DI 10.1207/s15324796abm2902s_1 PG 3 WC Psychology, Multidisciplinary SC Psychology GA 919WQ UT WOS:000228648700001 PM 15921482 ER PT J AU Resnick, B Bellg, AJ Borrelli, B DeFrancesco, C Breger, R Hecht, J Sharp, DL Levesque, C Orwig, D Ernst, D Ogedegbe, G Czajkowski, S AF Resnick, B Bellg, AJ Borrelli, B DeFrancesco, C Breger, R Hecht, J Sharp, DL Levesque, C Orwig, D Ernst, D Ogedegbe, G Czajkowski, S TI Examples of implementation and evaluation of treatment fidelity in the BCC studies: Where we are and where we need to go SO ANNALS OF BEHAVIORAL MEDICINE LA English DT Article ID LIFE; INTERVENTION; EFFICACY; PROGRAM; HEALTH; MODEL AB Treatment fidelity plays an important role in the research team's ability to ensure that a treatment has been implemented as intended and that the treatment has been accurately tested. Developing, implementing, and evaluating a treatment fidelity plan can be challenging. The treatment fidelity workgroup within the Behavior Change Consortium (BCC) developed guidelines to comprehensively evaluate treatment fidelity in behavior change research. The guidelines include evaluation of treatment fidelity with regard to study design, training of interventionists, delivery and receipt of the intervention, and enactment of the intervention in real-life settings. This article describes these guidelines and provides examples from four BCC studies as to how these recommended guidelines for fidelity were considered. Future work needs to focus not only on implementing treatment fidelity plans but also on quantifying the evaluations performed, developing specific criteria for interpretation of the findings, and establishing best practices of treatment fidelity. C1 Univ Maryland, Sch Nursing, Baltimore, MD 21201 USA. Brown Med Sch, Ctr Behav & Prevent Med, Providence, RI USA. Univ Rochester, Sch Nursing, Rochester, NY USA. SW Missouri State Univ, Springfield, MO 65802 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Univ New Mexico, Albuquerque, NM 87131 USA. Cornell Univ, Weill Med Coll, Ithaca, NY 14853 USA. NHLBI, NIH, Bethesda, MD USA. RP Resnick, B (reprint author), Univ Maryland, Sch Nursing, 655 W Lombard St, Baltimore, MD 21201 USA. EM barbresnick@aol.com NR 19 TC 57 Z9 57 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0883-6612 EI 1532-4796 J9 ANN BEHAV MED JI Ann. Behav. Med. PY 2005 VL 29 SU S BP 46 EP 54 DI 10.1207/s15324796abm2902s_8 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 919WQ UT WOS:000228648700008 PM 15921489 ER PT J AU Shrestha, S Smith, MW Beaty, TH Strathdee, SA AF Shrestha, S Smith, MW Beaty, TH Strathdee, SA TI Theory and methodology for utilizing genes as biomarkers to determine potential biological mixtures SO ANNALS OF EPIDEMIOLOGY LA English DT Review DE probability of mixture determination; short tandem repeats; biological mixtures; genetic biomarkers ID SINGLE-NUCLEOTIDE POLYMORPHISMS; FRAGMENT LENGTH POLYMORPHISMS; POLYMERASE CHAIN-REACTION; FORENSIC-SCIENCE-SERVICE; STR MULTIPLEX SYSTEM; TANDEM-REPEAT LOCI; HUMAN-GENOME; MOLECULAR EPIDEMIOLOGY; DRUG-USERS; Y-CHROMOSOME AB PURPOSE: Genetically determined Mixture information can be used as a surrogate for physical or behavioral characteristics in epidemiological studies examining research questions related to socially stigmatized behaviors and horizontally transmitted infections. A new measure, the probability of mixture discrimination (P(MD)), was developed to aid mixture analysis that estimates the ability to differentiate single from multiple genomes in biological mixtures. METHODS: Four autosomal short tandem repeats (STRs) were identified, genotyped and evaluated in African American, European American, Hispanic, and Chinese individuals to estimate PMD. Theoretical P(MD) frameworks were also developed for autosomal and sex-linked (X and Y) STR markers in potential male/male, male/female and female/female Mixtures. RESULTS: Autosomal STRs genetically determine the presence of multiple genomes in mixture samples Of unknown genders with more power than the apparently simpler X and Y chromosome STRs. Evaluation of four autosomal STR loci enables the detection of mixtures of DNA from multiple sources with above 99% probability in 211 four racial/ethnic populations. CONCLUSIONS: The genetic-based approach has applications in epidemiology that provide viable alternatives to survey-based study designs. The analysis of genes as biomarkers can be used as a gold standard for validating measurements front self-reported behaviors that tend to be sensitive or socially stigmatizing, such as those involving sex and drugs. C1 NCI, Lab Genomic Divers, SAIC Frederick, Frederick, MD 21702 USA. NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Univ Calif San Diego, Div Int Hlth & Cross Cultural Med, La Jolla, CA 92093 USA. RP Smith, MW (reprint author), NCI, Lab Genomic Divers, SAIC Frederick, Bldg 560,Rm 21-74, Frederick, MD 21702 USA. EM smithm@ncifcrf.gov RI Strathdee, Steffanie/B-9042-2009; Smith, Michael/B-5341-2012 FU NCI NIH HHS [N01-CO-12400]; NIDA NIH HHS [DA09225, DA8009] NR 107 TC 3 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1047-2797 J9 ANN EPIDEMIOL JI Ann. Epidemiol. PD JAN PY 2005 VL 15 IS 1 BP 29 EP 38 DI 10.1016/j.annepidem.2004.05.006 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 880OC UT WOS:000225798100005 PM 15571991 ER PT J AU Fessler, DMT Haley, KJ Lal, RD AF Fessler, DMT Haley, KJ Lal, RD TI Sexual dimorphism in foot length proportionate to stature SO ANNALS OF HUMAN BIOLOGY LA English DT Article DE foot length; stature; sexual dimorphism ID BLUNT ABDOMINAL-TRAUMA; PHYSICAL ATTRACTIVENESS; SHOE DESIGN; PREGNANCY; DIMENSIONS; EVOLUTION; SELECTION; HEIGHT; WOMEN; FOOTPRINTS AB Background: The preponderance of existing results suggests that, relative to stature, women have smaller feet than men. However, several investigations indicate that the relationship between foot length and stature may be curvilinear, a pattern that, due to the dimorphic nature of stature, would mask the true direction of pedal sexual dimorphism in published results. Aim: The study aimed to determine whether proportionate foot length is sexually dimorphic and, if so, the nature of that dimorphism. Materials and methods: Surveying genetically disparate populations ( USA, Turkey, and Native North and Central American), we examined data from three previous anthropometric studies ( Davis 1990, Parham et al. 1992, Ozaslan et al. 2003) and foot tracings from the Steggerda Collection at the US National Museum of Health and Medicine. Analyses explored sex differences in the ratio between foot length and stature, and tested for nonlinearity. Results: Although varying in degree across populations, proportionate to stature, female foot length is consistently smaller than male foot length. Conclusion: Given the biomechanical challenges posed by pregnancy, smaller female proportionate foot length is somewhat surprising, as foot length affects dorsoventral stability. It is possible that the observed pattern reflects intersexual selection for small female foot size, a cue of youth and nulliparity. C1 Univ Calif Los Angeles, Dept Anthropol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Ctr Behav Evolut & Culture, Los Angeles, CA 90095 USA. NIH, Dewitt Stetten Jr Museum Med Res, Bethesda, MD 20892 USA. Smithsonian Ctr Educ & Museum Studies, Washington, DC 20013 USA. RP Fessler, DMT (reprint author), Univ Calif Los Angeles, Dept Anthropol, 341 haines hall, Los Angeles, CA 90095 USA. EM dfessler@anthro.ucla.edu RI Fessler, Daniel/G-8485-2012 NR 55 TC 48 Z9 48 U1 1 U2 6 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0301-4460 J9 ANN HUM BIOL JI Ann. Hum. Biol. PD JAN-FEB PY 2005 VL 32 IS 1 BP 44 EP 59 DI 10.1080/03014460400027581 PG 16 WC Anthropology; Biology; Public, Environmental & Occupational Health SC Anthropology; Life Sciences & Biomedicine - Other Topics; Public, Environmental & Occupational Health GA 906WK UT WOS:000227675100005 PM 15788354 ER PT J AU Catani, M Jones, DK Ffytche, DH AF Catani, M Jones, DK Ffytche, DH TI Perisylvian language networks of the human brain SO ANNALS OF NEUROLOGY LA English DT Article ID DIFFUSION-TENSOR MRI; CONDUCTION APHASIA; WATER DIFFUSION; FRONTAL-CORTEX; FIBER PATHWAYS; LESION SITES; TRACKING; CONNECTIONS; MONKEY; ORIENTATION AB Early anatomically based models of language consisted of an arcuate tract connecting Broca's speech and Wernicke's comprehension centers; a lesion of the tract resulted in conduction aphasia. However, the heterogeneous clinical presentations of conduction aphasia suggest a greater complexity of perisylvian anatomical connections than allowed for in the classical anatomical model. This article re-explores perisylvian language connectivity using in vivo diffusion tensor magnetic resonance imaging tractography. Diffusion tensor magnetic resonance imaging data from 11 right-handed healthy male subjects were averaged, and the arcuate fasciculus of the left hemisphere reconstructed from this data using an interactive dissection technique. Beyond the classical arcuate pathway connecting Broca's and Wernicke's areas directly, we show a previously undescribed, indirect pathway passing through inferior parietal cortex. The indirect pathway runs parallel and lateral to the classical arcuate fasciculus and is composed of an anterior segment connecting Broca's territory with the inferior parietal lobe and a posterior segment connecting the inferior parietal lobe to Wernicke's territory. This model of two parallel pathways helps explain the diverse clinical presentations of conduction aphasia. The anatomical findings are also relevant to the evolution of language, provide a framework for Lichtheim's symptom-based neurological model of aphasia, and constrain, anatomically, contemporary connectionist accounts of language. C1 Kings Coll London, Inst Psychiat, Ctr Neuroimaging Sci, London SE5 8AZ, England. NICHHD, Sect Tissue Biophys & Biomimet, Lab Integrat Med & Biophys, NIH, Bethesda, MD 20892 USA. RP Catani, M (reprint author), Kings Coll London, Inst Psychiat, Ctr Neuroimaging Sci, PO 89,DeCrespigny Pk, London SE5 8AZ, England. EM m.catani@iop.kcl.ac.uk RI Jones, Derek/D-1460-2009; Catani, Marco/H-7801-2012; OI Catani, Marco/0000-0002-5488-6463; ffytche, Dominic/0000-0002-4214-9642; Jones, Derek/0000-0003-4409-8049 NR 51 TC 731 Z9 750 U1 6 U2 381 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JAN PY 2005 VL 57 IS 1 BP 8 EP 16 DI 10.1002/ana.20319 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 884SM UT WOS:000226106500003 PM 15597383 ER PT J AU Petrovitch, H Ross, GW Steinhorn, SC Abbott, RD Markesbery, W Davis, D Nelson, J Hardman, J Masaki, K Vogt, MR Launer, L White, LR AF Petrovitch, H Ross, GW Steinhorn, SC Abbott, RD Markesbery, W Davis, D Nelson, J Hardman, J Masaki, K Vogt, MR Launer, L White, LR TI AD lesions and infarcts in demented and non-demented Japanese-American men SO ANNALS OF NEUROLOGY LA English DT Article ID TANGLE PREDOMINANT FORM; ALZHEIMERS-DISEASE; SENILE-DEMENTIA; NEUROFIBRILLARY TANGLES; AUTOPSY POPULATION; VASCULAR DEMENTIA; CRITERIA; PLAQUES; PREVALENCE; PATHOLOGY AB Neocortical neuritic plaques and nettrofibrillary tangles are hallmark neuropathological lesions of dementia. Concomitant cerebrovascular lesions increase dementia severity in patients meeting neuropathological criteria for Alzheimer's disease and contribute to cognitive impairment in persons with mild entorhinal Alzheimer lesions. This study investigates whether individuals with sparse neocortical neuritic plaques experience increased odds of crossing the threshold to clinical dementia when they have coexistent cerebrovascular lesions. Dementia examinations were given to 3,734 men during the 1991-1993 Honolulu-Asia Aging Study examination and to 2,603 men during the 1994-1996 examination. Lesion quantification was done without clinical data. Among 333 autopsied men, 120 had dementia, 115 had marginal results, and 98 had normal cognition. In men with neurofibrillary tangles, dementia frequency increased with increasing neuritic plaque density, and increased further in the presence of cerebrovascular lesions. The association was strongest in men with sparse neuritic plaques (1-3/mm(2)) where dementia frequency more than doubled with coexistent cerebrovascular lesions (45 vs 20%). Among all dementia cases, 24% were linked to cerebrovascular lesions. Findings suggest cerebrovascular lesions are associated with a marked excess of dementia in cases with low neuritic plaque frequency. Prevention of cerebrovascular lesions may be critically important in preserving late-life cognitive function. C1 Univ Hawaii, John A Burns Sch Med, Pacific Hlth Res Inst, Honolulu, HI 96822 USA. Univ Hawaii, John A Burns Sch Med, Honolulu Dept Vet Affairs, Honolulu, HI 96822 USA. Univ Hawaii, John A Burns Sch Med, Honolulu Asia Aging Study, Kaukini Med Ctr, Honolulu, HI 96822 USA. Univ Hawaii, John A Burns Sch Med, Dept Med, Honolulu, HI 96822 USA. Univ Hawaii, John A Burns Sch Med, Dept Geriatr, Honolulu, HI 96822 USA. Univ Virginia, Sch Med, Div Biostat & Epidemiol, Charlottesville, VA 22908 USA. Univ Kentucky, Med Ctr, Sanders Brown Ctr Aging, Dept Pathol, Lexington, KY USA. Univ Kentucky, Med Ctr, Sanders Brown Ctr Aging, Dept Neurol, Lexington, KY USA. Univ Hawaii, John A Burns Sch Med, Dept Pathol, Honolulu, HI 96822 USA. NIA, Div Epidemiol Demog & Biostat, NIH, Bethesda, MD 20892 USA. RP Petrovitch, H (reprint author), 846 S Hotel St,Suite 307, Honolulu, HI 96813 USA. EM hpetrovitch@phrihawaii.org FU NIA NIH HHS [5R01 AG 017155-01, 1U01 AG 19349-01] NR 34 TC 147 Z9 150 U1 2 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JAN PY 2005 VL 57 IS 1 BP 98 EP 103 DI 10.1002/ana.20318 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 884SM UT WOS:000226106500013 PM 15562458 ER PT J AU Dennis, PA AF Dennis, PA TI Lipid based inhibitors of the serine/threonine kinase Akt SO ANNALS OF ONCOLOGY LA English DT Meeting Abstract CT 3rd International Symposium on Targeted Anticancer Therapies CY MAR 03-05, 2005 CL Amsterdam, NETHERLANDS SP AstraZeneca Oncol, Novartis Oncol, Pfizer Oncol, Bayer Healthcare Pharmaceut, Bristol-Mayers Squibb Co, Lilly, GlaxoSmithKline, ORTHO BIOTECH, MERCK, MDS Oncol, Roche Oncol, SCHERING C1 NCI, Bethesda, MD USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 2005 VL 16 SU 3 BP 16 EP 16 PG 1 WC Oncology SC Oncology GA 937RB UT WOS:000229942100007 ER PT J AU Posadas, EM Simpkins, F Liotta, LA MacDonald, C Kohn, EC AF Posadas, EM Simpkins, F Liotta, LA MacDonald, C Kohn, EC TI Proteomic analysis for the early detection and rational treatment of cancer - realistic hope? SO ANNALS OF ONCOLOGY LA English DT Review DE cancer; early detection; laser capture microdissection; proteomics; surface-enhanced laser desorption ionization; tissue lysate arrays ID LASER CAPTURE MICRODISSECTION; PROTEIN BIOCHIP TECHNOLOGY; PROSTATE-SPECIFIC ANTIGEN; IMMOBILIZED PH GRADIENTS; OVARIAN-CANCER; MASS-SPECTROMETRY; 2-DIMENSIONAL ELECTROPHORESIS; BREAST-CANCER; IDENTIFICATION; SERUM AB Proteomics is an emerging field in medical science focused on the library of proteins specific to a given biosystem, the proteome, and understanding relationships therein. This field incorporates technologies that can be applied to serum and tissue in order to extract important biological information to aid clinicians and scientists in understanding the dynamic biology of their system of interest, such as a patient with cancer. These tools include laser capture microdissection, tissue lysate arrays and mass spectrometry approaches. These new technologies are more potent coupled with advanced bioinformatics analysis. They are used to characterize the content of, and changes in, the proteome induced by physiological changes, benign and pathologic. The application of these tools has assisted in the discovery of new biomarkers and may lead to new diagnostic tests and improvements in therapeutics. These tools additionally can provide a molecular characterization of cancers, which may allow for individualized molecular therapy. Understanding the basic concepts and tools used will illustrate how best to apply these technologies for patient benefit for the early detection of cancer and improved patient care. C1 NCI, Pathol Lab, Bethesda, MD 20892 USA. NCI, FDA, Clin Proteom Program, Bethesda, MD USA. RP Posadas, EM (reprint author), Bldg 10,Room 12N226,10 Ctr Dr MSC 1906, Bethesda, MD 20892 USA. EM posadase@mail.nih.gov NR 41 TC 72 Z9 88 U1 1 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD JAN PY 2005 VL 16 IS 1 BP 16 EP 22 DI 10.1093/annonc/mdi004 PG 7 WC Oncology SC Oncology GA 885JR UT WOS:000226153400005 PM 15598930 ER PT J AU Wright, JJ AF Wright, JJ TI New therapies for an old oncogene: Src/Abl inhibitors in the treatment of hematologic malignancies and solid tumors SO ANNALS OF ONCOLOGY LA English DT Meeting Abstract CT 3rd International Symposium on Targeted Anticancer Therapies CY MAR 03-05, 2005 CL Amsterdam, NETHERLANDS SP AstraZeneca Oncol, Novartis Oncol, Pfizer Oncol, Bayer Healthcare Pharmaceut, Bristol-Mayers Squibb Co, Lilly, GlaxoSmithKline, ORTHO BIOTECH, MERCK, MDS Oncol, Roche Oncol, SCHERING C1 NCI, Invest Drug Branch, CTEP, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 2005 VL 16 SU 3 BP 29 EP 29 PG 1 WC Oncology SC Oncology GA 937RB UT WOS:000229942100039 ER PT J AU Crowell, JA Kopelovich, L AF Crowell, JA Kopelovich, L TI Molecular target identification using phenotypically normal cells from subjects with dominantly inherited predispositions to cancer SO ANNALS OF ONCOLOGY LA English DT Meeting Abstract CT 3rd International Symposium on Targeted Anticancer Therapies CY MAR 03-05, 2005 CL Amsterdam, NETHERLANDS SP AstraZeneca Oncol, Novartis Oncol, Pfizer Oncol, Bayer Healthcare Pharmaceut, Bristol-Mayers Squibb Co, Lilly, GlaxoSmithKline, ORTHO BIOTECH, MERCK, MDS Oncol, Roche Oncol, SCHERING C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 2005 VL 16 SU 3 BP 35 EP 35 PG 1 WC Oncology SC Oncology GA 937RB UT WOS:000229942100054 ER PT J AU Hiatt, R Wardle, J Vernon, S Austoker, J Bistanti, L Fox, S Gnauck, R Iverson, D Mandelson, M Reading, D Smith, R AF Hiatt, R Wardle, J Vernon, S Austoker, J Bistanti, L Fox, S Gnauck, R Iverson, D Mandelson, M Reading, D Smith, R TI Workgroup IV: public education. UICC International Workshop on Facilitating Screening for Colorectal Cancer, oslo, Norway (29 and 30 June 2002) SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT UICC International Workshop on Facilitating Screening for Colorectal Cancer CY JUN 29-SEP 30, 2002 CL Oslo, NORWAY SP Int Union Against Canc, Amer Canc Soc, Norwegian Canc Soc C1 Amer Canc Soc, Atlanta, GA 30329 USA. NCI, Rockville, MD USA. UCL, London, England. Univ Texas, Sch Publ Hlth, Houston, TX USA. Univ Oxford, Oxford, England. Local Hlth Author Milan, Milan, Italy. Univ Calif Los Angeles, Los Angeles, CA USA. Deutsch Klin Diagnost, D-6200 Wiesbaden, Germany. Univ Wollongong, Wollongong, NSW 2500, Australia. Grp Hlth Cooperat Puget Sound, Seattle, WA USA. Canc Council Victoria, Carlton, Vic, Australia. RP Smith, R (reprint author), Amer Canc Soc, 1599 Clifton Rd NE, Atlanta, GA 30329 USA. EM Robert.Smith@cancer.org NR 7 TC 6 Z9 6 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD JAN PY 2005 VL 16 IS 1 BP 38 EP 41 DI 10.1093/annonc/mdi033 PG 4 WC Oncology SC Oncology GA 885JR UT WOS:000226153400010 PM 15598935 ER PT J AU Ganti, AK Mulshine, JL AF Ganti, AK Mulshine, JL TI Lung cancer screening: panacea or pipe dream? SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT ESMO Scientific and Educational Conference (ESEC) CY JUN 02-05, 2005 CL Budapest, HUNGARY SP European Soc Med Oncol ID SPIRAL COMPUTED-TOMOGRAPHY; ACTION PROJECT; STAGE-I; CT; SURVIVAL; CZECHOSLOVAKIA; POPULATION; STATISTICS; MORTALITY; CARCINOMA C1 Univ Nebraska, Med Ctr, Dept Internal Med, Div Hematol Oncol, Omaha, NE USA. NIH, Intervent Sect,Aerodigest Chemoprevent Fac, Ctr Canc Res,CLin Ctr,NCI, US Dept HHS, Bethesda, MD 20892 USA. RP Univ Nebraska, Med Ctr, Dept Internal Med, Div Hematol Oncol, Omaha, NE USA. RI Ganti, Apar Kishor/D-5498-2015 OI Ganti, Apar Kishor/0000-0003-3724-2671 NR 45 TC 10 Z9 10 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0923-7534 EI 1569-8041 J9 ANN ONCOL JI Ann. Oncol. PY 2005 VL 16 SU 2 BP 215 EP 219 DI 10.1093/annonc/mdi723 PG 5 WC Oncology SC Oncology GA 938CL UT WOS:000229977400029 ER PT J AU Daly, KA Hoffman, HJ Casselbrant, ML Kvaerner, KJ Rovers, MM Uhari, M Zielhuis, G AF Daly, KA Hoffman, HJ Casselbrant, ML Kvaerner, KJ Rovers, MM Uhari, M Zielhuis, G TI Epidemiology, natural history, and risk factors SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article; Proceedings Paper CT 8th Post Symposium Research Conference CY JUN 07-08, 2003 CL Ft Lauderdale, FL ID ACUTE OTITIS-MEDIA; RESPIRATORY-TRACT INFECTIONS; TYMPANOSTOMY TUBE INSERTION; SYNCYTIAL VIRUS-INFECTION; ATTENDING DAY-CARE; A GENE LOCUS; PRESCHOOL-CHILDREN; EAR INFECTIONS; EFFUSION; CHILDHOOD C1 Univ Oulu, Dept Pediat & Adolescence, Oulu, Finland. Univ Minnesota, Dept Otolaryngol, Minneapolis, MN USA. NIDCD, NIH, Bethesda, MD USA. Univ Pittsburgh, Sch Med, Childrens Hosp Pittsburgh, Dept Otolaryngol, Pittsburgh, PA USA. Ullevaal Univ Hosp, Dept Otorhinolaryngol, Oslo, Norway. Univ Utrecht, Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands. Univ Nijmegen, Med Ctr, Dept Epidemiol & Biostat, Nijmegen, Netherlands. RP Daly, KA (reprint author), Univ Oulu, Dept Pediat & Adolescence, Oulu, Finland. RI Zielhuis, Gerhard/D-4229-2009; Zielhuis, Gerhard/H-8123-2014; Rovers, Maroeska/F-2969-2014 OI Rovers, Maroeska/0000-0002-3095-170X NR 60 TC 3 Z9 3 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 USA SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD JAN PY 2005 VL 114 IS 1 SU 194 BP 8 EP 15 PN 2 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA 888UJ UT WOS:000226399400003 ER PT J AU Giebink, GS Bakaletz, LO Barenkamp, SJ Green, B Gu, XX Heikkinen, T Hotomi, M Karma, P Kurono, Y Kyd, JM Murphy, TF Ogra, PL Patel, JA Pelton, SI AF Giebink, GS Bakaletz, LO Barenkamp, SJ Green, B Gu, XX Heikkinen, T Hotomi, M Karma, P Kurono, Y Kyd, JM Murphy, TF Ogra, PL Patel, JA Pelton, SI TI Vaccine SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article; Proceedings Paper CT 8th Post Symposium Research Conference CY JUN 07-08, 2003 CL Ft Lauderdale, FL ID NONTYPABLE HAEMOPHILUS-INFLUENZAE; ACUTE OTITIS-MEDIA; OUTER-MEMBRANE PROTEIN; MORAXELLA BRANHAMELLA CATARRHALIS; PNEUMOCOCCAL VIRULENCE PROTEINS; STREPTOCOCCUS-PNEUMONIAE; INTRANASAL IMMUNIZATION; CONJUGATE VACCINE; MIDDLE-EAR; NASOPHARYNGEAL CARRIAGE C1 Univ Minnesota, Sch Med, Dept Pediat, Minneapolis, MN 55455 USA. Wexner Inst Pediat Res, Childrens Res Inst, Dept Pediat, Columbus, OH USA. St Louis Univ, Sch Med, Dept Pediat, St Louis, MO USA. Wyeth Lederle Vaccines, W Henrietta, NY USA. NIDCD, NIH, Rockville, MD USA. Turku Univ Hosp, Dept Pediat, FIN-20520 Turku, Finland. Wakayama Med Univ, Dept Otolaryngol Head & Neck Surg, Wakayama, Japan. Univ Helsinki, Cent Hosp, Dept Otolaryngol, Helsinki, Finland. Univ Canberra, Div Sci & Design, Canberra, ACT, Australia. Kagoshima Univ, Dept Otolaryngol, Kagoshima 890, Japan. SUNY Buffalo, Sch Med, Childrens Hosp, Dept Pediat, Buffalo, NY USA. SUNY Buffalo, Div Infect Dis, Buffalo, NY USA. Univ Texas, Med Branch, Childrens Hosp, Dept Pediat, Galveston, TX 77550 USA. Boston Univ, Sch Med, Dept Pediat, Boston, MA 02215 USA. RP Giebink, GS (reprint author), Univ Minnesota, Sch Med, Dept Pediat, Minneapolis, MN 55455 USA. OI Kyd, Jennelle/0000-0002-3331-3658 NR 122 TC 3 Z9 3 U1 1 U2 1 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 USA SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD JAN PY 2005 VL 114 IS 1 SU 194 BP 86 EP 103 PN 2 PG 18 WC Otorhinolaryngology SC Otorhinolaryngology GA 888UJ UT WOS:000226399400010 ER PT J AU Mocellin, S Provenzano, M Rossi, CR Pilati, P Nitti, D Lise, M AF Mocellin, S Provenzano, M Rossi, CR Pilati, P Nitti, D Lise, M TI DNA array-based gene profiling - From surgical specimen to the molecular portrait of cancer SO ANNALS OF SURGERY LA English DT Review ID B-CELL LYMPHOMA; DIFFERENTIALLY EXPRESSED GENES; ARTIFICIAL NEURAL NETWORKS; SELF-ORGANIZING MAPS; CLASS-I EXPRESSION; BREAST-CANCER; OLIGONUCLEOTIDE ARRAYS; CDNA MICROARRAYS; PROSTATE-CANCER; TRANSCRIPTIONAL PROGRAM AB Cancer is a heterogeneous disease in most respects, including its cellularity, different genetic alterations, and diverse clinical behaviors. Traditional molecular analyses are reductionist, assessing only 1 or a few genes at a time, thus working with a biologic model too specific and limited to confront a process whose clinical outcome is likely to be governed by the combined influence of many genes. The potential of functional genomics is enormous, because for each experiment, thousands of relevant observations can be made simultaneously. Accordingly, DNA array, like other high-throughput technologies, might catalyze and ultimately accelerate the development of knowledge in tumor cell biology. Although in its infancy, the implementation of DNA array technology in cancer research has already provided investigators with novel data and intriguing new hypotheses on the molecular cascade leading to carcinogenesis, tumor aggressiveness, and sensitivity to antiblastic agents. Given the revolutionary implications that the use of this technology might have in the clinical management of patients with cancer, principles of DNA array-based tumor gene profiling need to be clearly understood for the data to be correctly interpreted and appreciated. In the present work, we discuss the technical features characterizing this powerful laboratory tool and review the applications so far described in the field of oncology. C1 Univ Padua, Dept Oncol & Surg Sci, Surg Branch, Padua, Italy. NIH, Dept Transfus Med, Immunogenet Sect, Ctr Clin, Bethesda, MD 20892 USA. RP Mocellin, S (reprint author), Univ Padua, Dipartimento Sci Oncol & Chirurg, Clin Chirurg Gen 2, Via Giustiniani,2, I-35128 Padua, Italy. EM mocellins@hotmail.com RI Rossi, Carlo Riccardo/A-7685-2010 OI Rossi, Carlo Riccardo/0000-0001-7875-5655 NR 115 TC 26 Z9 28 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD JAN PY 2005 VL 241 IS 1 BP 16 EP 26 DI 10.1097/01.sla.0000150157.83537.53 PG 11 WC Surgery SC Surgery GA 884KC UT WOS:000226082600004 PM 15621987 ER PT J AU Breedveld, FC Han, C Bala, M van der Heijde, D Baker, D Kavanaugh, AF Maini, RN Lipsky, PE AF Breedveld, FC Han, C Bala, M van der Heijde, D Baker, D Kavanaugh, AF Maini, RN Lipsky, PE TI Association between baseline radiographic damage and improvement in physical function after treatment of patients with rheumatoid arthritis SO ANNALS OF THE RHEUMATIC DISEASES LA English DT Article ID RADIOLOGIC DAMAGE; DISEASE-ACTIVITY; WORK DISABILITY; PROGRESSION; METHOTREXATE; INFLIXIMAB; COUNTS AB Objectives: To identify factors associated with poor physical function in rheumatoid arthritis and to assess whether baseline joint damage has an impact on improvement in physical function during infliximab treatment. Methods: 428 patients with active rheumatoid arthritis despite methotrexate treatment received methotrexate alone or with infliximab ( 3 mg/kg or 10 mg/kg every four or eight weeks) for 54 weeks ( the ATTRACT trial). Data on clinical outcomes and physical function ( assessed by the health assessment questionnaire (HAQ)) were collected. Structural damage was assessed using the van der Heijde modification of the Sharp score. Odds ratios ( OR) for factors associated with severe functional disability (HAQ greater than or equal to 2.0) at baseline were estimated using multiple logistic regression analyses, and baseline factors related to the change in physical function after treatment at week 54 were determined. Results: Baseline radiographic scores were correlated with baseline HAQ scores. After adjustment for demographic characteristics in the logistic regression model, baseline disease activity scores, radiological joint damage, fatigue, and morning stiffness were found to be associated with severe functional disability (HAQgreater than or equal to2.0), with OR values of 2.00 (1.53 to 2.63), 1.82 (1.15 to 2.87), 1.19 (1.05 to 1.34), and 1.07 (1.01 to 1.13), respectively. In multiple linear regression analysis, physical disability, joint damage, and fatigue at baseline were correlated with less improvement in physical function after treatment. Infliximab treatment was associated with greater improvement in physical function. Conclusions: Greater joint damage at baseline was associated with poorer physical function at baseline and less improvement in physical function after treatment, underlining the importance of early intervention to slow the progression of joint destruction. C1 Leiden Univ, Med Ctr, Dept Rheumatol, Leiden, Netherlands. Centocor Inc, Outcomes Res, Malvern, PA 19355 USA. Univ Hosp Maastricht, Dept Internal Med Rheumatol, Maastricht, Netherlands. Centocor Inc, Clin Res & Dev, Malvern, PA USA. Univ Calif San Diego, Div Rheumatol Allergy & Immunol, La Jolla, CA 92093 USA. Univ London Imperial Coll Sci Technol & Med, Kennedy Inst Rheumatol, London, England. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Breedveld, FC (reprint author), Leiden Univ, Med Ctr, Dept Rheumatol, Leiden, Netherlands. EM f.c.breedveld@lumc.nl NR 23 TC 48 Z9 50 U1 0 U2 1 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-4967 J9 ANN RHEUM DIS JI Ann. Rheum. Dis. PD JAN PY 2005 VL 64 IS 1 BP 52 EP 55 DI 10.1136/ard.2003.017160 PG 4 WC Rheumatology SC Rheumatology GA 880OW UT WOS:000225800100011 PM 15286005 ER PT S AU Cookson, MR AF Cookson, MR TI The biochemistry of Parkinson's disease SO ANNUAL REVIEW OF BIOCHEMISTRY SE Annual Review of Biochemistry LA English DT Review; Book Chapter DE lewy body; mitochondria; parkinsonism; proteasome; protein aggregation ID HUMAN ALPHA-SYNUCLEIN; AUTOSOMAL-DOMINANT PARKINSONISM; VECTOR-MEDIATED OVEREXPRESSION; UBIQUITIN LIGASE ACTIVITY; MULTIPLE SYSTEM ATROPHY; A-BETA COMPONENT; IN-VITRO; LEWY BODIES; CELL-DEATH; PROTEASOME INHIBITION AB Several genes have been identified for monogenic disorders that variably resemble Parkinson's disease. Dominant mutations in the gene encoding alpha-synuclein enhance the propensity of this protein to aggregate. As a consequence, these patients have a widespread disease with protein inclusion bodies in several brain areas. In contrast, mutations in several recessive genes (parkin, DJ-1, and PINK1) produce neuronal cell loss but generally without protein aggregation pathology. Progress has been made in understanding some of the mechanisms of toxicity: Parkin is an E3 ubiquitin ligase and DJ-1 and PINK1 appear to protect against mitochondrial damage. However, we have not yet fully resolved how the recessive genes relate to a-synuclein, or whether they represent different ways to induce a similar phenotype. C1 NIA, Neurogenet Lab, Cell Biol Sect, Bethesda, MD 20892 USA. RP Cookson, MR (reprint author), NIA, Neurogenet Lab, Cell Biol Sect, Bethesda, MD 20892 USA. EM cookson@mail.nih.gov NR 151 TC 403 Z9 418 U1 2 U2 58 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4154 BN 978-0-8243-0874-2 J9 ANNU REV BIOCHEM JI Annu. Rev. Biochem. PY 2005 VL 74 BP 29 EP 52 DI 10.1146/annurev.biochem.74.082803.133400 PG 24 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 955OH UT WOS:000231235100002 PM 15952880 ER PT S AU Storz, G Altuvia, S Wassarman, KM AF Storz, G Altuvia, S Wassarman, KM TI An abundance of RNA regulators SO ANNUAL REVIEW OF BIOCHEMISTRY SE Annual Review of Biochemistry LA English DT Review; Book Chapter DE noncoding RNA; antisense RNA; small RNA; microRNA ID NON-MESSENGER RNAS; SMALL NUCLEOLAR RNA; POLYMERASE-II TRANSCRIPTION; SM-LIKE PROTEIN; ESCHERICHIA-COLI; ANTISENSE RNA; NONCODING RNAS; POSTTRANSCRIPTIONAL REGULATION; COMPUTATIONAL IDENTIFICATION; CAENORHABDITIS-ELEGANS AB The importance of small, noncoding RNAs that act as regulators of transcription, of RNA modification or stability, and of mRNA translation is becoming increasingly apparent. Here we discuss current knowledge of regulatory RNA function and review how the RNAs have been identified in a variety of organisms. Many of the regulatory RNAs act through base-pairing interactions with target RNAs. The base-pairing RNAs can be grouped into two general classes: those that are encoded on the opposite strand of their target RNAs such that they contain perfect complementarity with their targets, and those that are encoded at separate locations on the chromosome and have imperfect base-pairing potential with their targets. Other regulatory RNAs act by modifying protein activity, in some cases by mimicking the structures of other RNA or DNA molecules. C1 NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. Hebrew Univ Jerusalem, Fac Med, Dept Mol Genet & Biotechnol, IL-91120 Jerusalem, Israel. Univ Wisconsin, Dept Bacteriol, Madison, WI 53706 USA. RP Storz, G (reprint author), NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. EM storz@helix.nih.gov; shoshy@cc.huji.ac.il; wassarman@bact.wisc.edu OI Storz, Gisela/0000-0001-6698-1241 NR 119 TC 249 Z9 267 U1 3 U2 33 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4154 BN 978-0-8243-0874-2 J9 ANNU REV BIOCHEM JI Annu. Rev. Biochem. PY 2005 VL 74 BP 199 EP 217 DI 10.1146/annurev.biochem.74.082803.133136 PG 19 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 955OH UT WOS:000231235100008 PM 15952886 ER PT S AU Kunkel, TA Erie, DA AF Kunkel, TA Erie, DA TI DNA mismatch repair SO ANNUAL REVIEW OF BIOCHEMISTRY SE Annual Review of Biochemistry LA English DT Review; Book Chapter DE DNA replication fidelity; mutagenesis; mutator; genome instability; error correction ID CELL NUCLEAR ANTIGEN; NONPOLYPOSIS COLORECTAL-CANCER; CLASS-SWITCH RECOMBINATION; ESCHERICHIA-COLI MUTS; REPLICATION PROTEIN-A; HUMAN EXONUCLEASE-I; CEREVISIAE MSH2-MSH6 COMPLEX; NUCLEOTIDE EXCISION-REPAIR; CENTER-DOT-C; SACCHAROMYCES-CEREVISIAE AB DNA mismatch repair (MMR) is an evolutionarily conserved process that corrects mismatches generated during DNA replication and escape proofreading. MMR proteins also participate in many other DNA transactions, such that inactivation of MMR can have wide-ranging biological consequences, which can be either beneficial or detrimental. We begin this review by briefly considering the multiple functions of MMR proteins and the consequences of impaired function. We then focus on the biochemical mechanism of MMR replication errors. Emphasis is on structure-function studies of MMR proteins, on how mismatches are recognized, on the process by which the newly replicated strand is identified, and on excision of the replication error. C1 Natl Inst Environm Hlth Sci, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA. Univ N Carolina, Venable & Kenal Labs, Curriculum Mat Sci, Chapel Hill, NC 27599 USA. RP Kunkel, TA (reprint author), Natl Inst Environm Hlth Sci, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. EM kunkel@niehs.nih.gov; derie@unc.edu FU NIGMS NIH HHS [GM-54316] NR 182 TC 719 Z9 741 U1 17 U2 179 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4154 BN 978-0-8243-0874-2 J9 ANNU REV BIOCHEM JI Annu. Rev. Biochem. PY 2005 VL 74 BP 681 EP 710 DI 10.1146/annurev.biochem.74.082803.133243 PG 30 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 955OH UT WOS:000231235100023 PM 15952900 ER PT S AU Davies, D AF Davies, D TI A quiet life with proteins SO ANNUAL REVIEW OF BIOPHYSICS AND BIOMOLECULAR STRUCTURE SE Annual Review of Biophysics LA English DT Review; Book Chapter DE crystallography; polynucleotides; structure; function ID ANTIBODY-ANTIGEN COMPLEX; CRYSTAL-STRUCTURE; 3-DIMENSIONAL STRUCTURE; RHIZOPUS-CHINENSIS; CATALYTIC DOMAIN; HIV-1 INTEGRASE; ACTIVE-SITE; DEOXYHYPUSINE SYNTHASE; ASPARTIC PROTEINASE; BINDING-SITE C1 NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA. RP Davies, D (reprint author), NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA. EM david.davies@nih.gov NR 42 TC 4 Z9 4 U1 2 U2 3 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1056-8700 BN 978-0-8243-1834-5 J9 ANNU REV BIOPH BIOM JI Annu. Rev. Biophys. Biomolec. Struct. PY 2005 VL 34 BP 1 EP 20 DI 10.1146/annurev.biophys.34.040204.144531 PG 22 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 939VD UT WOS:000230099600001 PM 15869381 ER PT S AU Southwick, SM Vythilingam, M Charney, DS AF Southwick, Steven M. Vythilingam, Meena Charney, Dennis S. TI The psychobiology of depression and resilience to stress: Implications for prevention and treatment SO ANNUAL REVIEW OF CLINICAL PSYCHOLOGY SE Annual Review of Clinical Psychology LA English DT Review; Book Chapter DE neurobiology; psychosocial; posttraumatic stress disorder ID ANXIETY-LIKE BEHAVIOR; STAGE BREAST-CANCER; NEUROPEPTIDE-Y NPY; SOCIAL SUPPORT; MAJOR DEPRESSION; TRYPTOPHAN-DEPLETION; MATERNAL-BEHAVIOR; LIFE EVENTS; UNIPOLAR DEPRESSION; OLDER PATIENTS AB This review discusses neurobiological and psychosocial factors associated with stress-induced depression and compares these factors with those believed to characterize stress resilience. Neurobiological factors that are discussed and contrasted include serotonin, the 5-HT1A receptor, polymorphisms of the 5-HT transporter gene, norepinephrine, alpha-2 adrenergic receptors, neuropeptide Y, polymorphisms of the alpha-2 adrenergic gene, dopamine, corticotropin-releasing hormone (CRH), dehydroepiandrosterone (DHEA), cortisol, and CRH receptors. These factors are described in the context of brain regions believed to be involved in stress, depression, and resilience to stress. Psychosocial factors associated with depression and/or stress resilience include positive emotions and optimism, humor, cognitive flexibility, cognitive explanatory style and reappraisal, acceptance, religion/spirituality, altruism, social support, role models, coping style, exercise, capacity to recover from negative events, and stress inoculation. The review concludes with potential psychological, social, spiritual, and neurobiological approaches to enhancing stress resilience, decreasing the likelihood of developing stress-induced depression/anxiety, and treating stress-induced psychopathology. C1 [Southwick, Steven M.] Yale Univ, Sch Med, Natl Ctr Post Traumat Stress Disorder, VA Connecticut Healthcare Syst, West Haven, CT 06516 USA. [Vythilingam, Meena] NIMH, Anxiety Disorders Clin, Washington, DC 20032 USA. [Charney, Dennis S.] Mt Sinai Hosp, Mt Sinai Sch Med, New York, NY 10029 USA. RP Southwick, SM (reprint author), Yale Univ, Sch Med, Natl Ctr Post Traumat Stress Disorder, VA Connecticut Healthcare Syst, West Haven, CT 06516 USA. EM Steven.southwick@med.va.gov; meena.vythi@nih.gov; dennis.charney@mssm.edu NR 196 TC 350 Z9 360 U1 36 U2 172 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1548-5943 BN 978-0-8243-3901-2 J9 ANNU REV CLIN PSYCHO JI Annu. Rev. Clin. Psychol. PY 2005 VL 1 BP 255 EP 291 DI 10.1146/annurev.clinpsy.1.102803.143948 PG 37 WC Psychology, Clinical; Psychology SC Psychology GA 295QA UT WOS:000255487800010 PM 17716089 ER PT S AU Koonin, EV AF Koonin, EV TI Orthologs, paralogs, and evolutionary genomics SO ANNUAL REVIEW OF GENETICS SE Annual Review of Genetics LA English DT Review; Book Chapter DE homolog; ortholog; paralog; pseudoortholog; pseudoparalog; xenolog ID HORIZONTAL GENE-TRANSFER; AUTHENTIC ORPHAN GENES; MOLECULAR CLOCK; PHYLOGENETIC CLASSIFICATION; HYPOTHETICAL PROTEINS; TERMINOLOGY MUDDLE; BACTERIAL GENOMES; DUPLICATE GENES; DOSAGE BALANCE; COG DATABASE AB Orthologs and paralogs are two fundamentally different types of homologous genes that evolved, respectively, by vertical descent from a single ancestral gene and by duplication. Orthology and paralogy are key concepts of evolutionary genomics. A clear distinction between orthologs and paralogs is critical for the construction of a robust evolutionary classification of genes and reliable functional annotation of newly sequenced genomes. Genome comparisons show that orthologous relationships with genes from taxonomically distant species can be established for the majority of the genes from each sequenced genome. This review examines in depth the definitions and subtypes of orthologs and paralogs, outlines the principal methodological approaches employed for identification of orthology and paralogy, and considers evolutionary and functional implications of these concepts. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. EM koonin@ncbi.nlm.nih.gov NR 104 TC 474 Z9 486 U1 9 U2 99 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4197 BN 978-0-8243-1239-8 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 2005 VL 39 BP 309 EP 338 DI 10.1146/annurev.genet.39.073003.114725 PG 30 WC Genetics & Heredity SC Genetics & Heredity GA 003MB UT WOS:000234685200015 PM 16285863 ER PT S AU Oppenheim, AB Kobiler, O Stavans, J Court, DL Adhya, S AF Oppenheim, AB Kobiler, O Stavans, J Court, DL Adhya, S TI Switches in bacteriophage lambda development SO ANNUAL REVIEW OF GENETICS SE Annual Review of Genetics LA English DT Review; Book Chapter DE genetic circuits; gene modules; developmental pathways; developmental decisions; threshold effects; host factors ID SITE-SPECIFIC RECOMBINATION; ESCHERICHIA-COLI MUTANT; LYSIS-LYSOGENY DECISION; DNA REPLICATION INVITRO; OOP ANTISENSE RNA; C-TERMINAL DOMAIN; PHAGE-LAMBDA; TRANSCRIPTION ANTITERMINATION; CIII-GENE; MESSENGER-RNA AB The lysis-lysogeny decision of bacteriophage lambda (lambda) is a paradigm for developmental genetic networks. There are three key features, which characterize the network. First, after infection of the host bacterium, a decision between lytic or lysogenic development is made that is dependent upon environmental signals and the number of infecting phages per cell. Second, the lysogenic prophage state is very stable. Third, the prophage enters lytic development in response to DNA-damaging agents. The CI and Cro regulators define the lysogenic and lytic states, respectively, as a bistable genetic switch. Whereas CI maintains a stable lysogenic state, recent studies indicate that Cro sets the lytic course not by directly blocking CI expression but indirectly by lowering levels of CII which activates d transcription. We discuss how a relatively, simple phage like lambda employs a complex genetic network in decision-making processes, providing a challenge for theoretical modeling. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Mol Genet & Biotechnol, IL-91120 Jerusalem, Israel. Weizmann Inst Sci, Dept Phys Complex Syst, IL-76100 Rehovot, Israel. NCI, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. NCI, Mol Biol Lab, Bethesda, MD 20892 USA. RP Oppenheim, AB (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Mol Genet & Biotechnol, IL-91120 Jerusalem, Israel. EM oppenhea@mail.nih.gov RI Kobiler, Oren/J-2268-2012 OI Kobiler, Oren/0000-0001-9914-3770 NR 112 TC 180 Z9 181 U1 4 U2 59 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4197 BN 978-0-8243-1239-8 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 2005 VL 39 BP 409 EP 429 DI 10.1146/annurev.genet.39.073003.113656 PG 21 WC Genetics & Heredity SC Genetics & Heredity GA 003MB UT WOS:000234685200018 PM 16285866 ER PT S AU Dean, M Annilo, T AF Dean, M Annilo, T TI Evolution of the ATP-binding cassette (ABC) transporter superfamily in vertebrates SO ANNUAL REVIEW OF GENOMICS AND HUMAN GENETICS SE Annual Review of Genomics and Human Genetics LA English DT Review; Book Chapter DE ATP-binding cassette (ABC) genes; human disease; pseudogene; gene conversion ID DISEASE GENE ABCR; MULTIDRUG-RESISTANCE; STARGARDT-DISEASE; MACULAR DEGENERATION; CYSTIC-FIBROSIS; P-GLYCOPROTEIN; LIPOFUSCIN ACCUMULATION; CAENORHABDITIS-ELEGANS; RETINITIS-PIGMENTOSA; SEQUENCE-ANALYSIS AB The ATP-binding cassette (ABC) superfamily of genes encode membrane proteins that transport a diverse set of substrates across membranes. Mutations in ABC transporters cause or contribute to many different Mendelian and complex disorders including adrenoleukodystrophy, cystic fibrosis, retinal degeneration, hypercholesterolemia, and cholestasis. The genes play important roles in protecting organisms from xenobiotics and transport compounds across the intestine, blood-brain barrier, and the placenta. There are 48 ABC genes in the human genome divided into seven subfamilies based on amino acid sequence similarities and phylogeny. These seven subfamilies are represented in all eukaryotic genomes and are therefore of ancient origin. Sequencing the genomes of numerous vertebrate organisms has allowed the complement of ABC transporters to be characterized and the evolution of the genes to be assessed. Most ABC transporters are conserved in all vertebrates, but there are also several examples of recent duplication and gene loss. For genes with a conserved ortholog, animal models have been identified or developed that can be used to probe the function and regulation of selected genes. Genes that are restricted to a specific group of animals may represent specialized functions that could provide insight into unique biological properties of that organism. Further characterization of all ABC transporters from the human genome and from model organisms will lead to additional insights into normal physiology and human disease. C1 Natl Canc Inst, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA. Univ Tartu, Inst Mol & Cell Biol, Dept Biotechnol, EE-51010 Tartu, Estonia. RP Dean, M (reprint author), Natl Canc Inst, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA. EM dean@ncifcrf.gov; tannilo@ebc.ee RI Dean, Michael/G-8172-2012; Annilo, Tarmo/J-2900-2013 OI Dean, Michael/0000-0003-2234-0631; Annilo, Tarmo/0000-0002-9588-3058 NR 77 TC 291 Z9 308 U1 3 U2 23 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1527-8204 BN 978-0-8243-3706-3 J9 ANNU REV GENOM HUM G JI Annu. Rev. Genomics Hum. Genet. PY 2005 VL 6 BP 123 EP 142 DI 10.1146/annurev.genom.6.080604.162122 PG 22 WC Genetics & Heredity SC Genetics & Heredity GA 972GE UT WOS:000232441500007 PM 16124856 ER PT S AU Drayna, D AF Drayna, D TI Human taste genetics SO ANNUAL REVIEW OF GENOMICS AND HUMAN GENETICS SE Annual Review of Genomics and Human Genetics LA English DT Review; Book Chapter DE chemosensory mechanisms; candidate genes; phenylthiocarbamide; sensory variation ID RESIDUAL FAMILY RESEMBLANCE; BITTER RECEPTOR GENE; UMAMI TASTE; SWEET TASTE; CHORDA TYMPANI; TRANSDUCTION; PHENYLTHIOCARBAMIDE; SENSITIVITY; PTC; GUSTDUCIN AB Humans show substantial differences in taste sensitivity to many different substances. Some of this variation is known to be genetic in origin, and many other inter-individual differences are likely to be partially or wholly determined by genetic mechanisms. Recent advances in the understanding of taste at the molecular level have provided candidate genes that can be evaluated for contributions to phenotypic differences in taste abilities. This approach has provided an understanding of variation in the ability to taste phenylthiocarbamide (PTC), and has resolved long-standing controversies about the genetics of this classic human genetic trait. Significant coding sequence variation exists in taste receptor genes, which suggests that PTC tasting may indicate more general taste sensory variation. However, many aspects of taste perception remain poorly characterized. Better understanding of the molecular components of salty and sour tastes is still needed, as is a more complete picture of second messenger and downstream signaling mechanisms for all taste modalities. More general studies of linkage and association between genetic markers and taste phenotypes may reveal genes encoding proteins that were previously unsuspected to be involved in this sensory process. C1 Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD 20850 USA. RP Drayna, D (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD 20850 USA. EM drayna@nidcd.nih.gov RI Marion-Poll, Frederic/D-8882-2011 OI Marion-Poll, Frederic/0000-0001-6824-0180 FU PHS HHS [Z01-00,0046-05] NR 82 TC 84 Z9 88 U1 10 U2 136 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1527-8204 BN 978-0-8243-3706-3 J9 ANNU REV GENOM HUM G JI Annu. Rev. Genomics Hum. Genet. PY 2005 VL 6 BP 217 EP 235 DI 10.1146/annurev.genom.6.080604.162340 PG 21 WC Genetics & Heredity SC Genetics & Heredity GA 972GE UT WOS:000232441500011 PM 16124860 ER PT S AU O'Brien, SJ Johnson, WE AF O'Brien, SJ Johnson, WE TI Big cat genomics SO ANNUAL REVIEW OF GENOMICS AND HUMAN GENETICS SE Annual Review of Genomics and Human Genetics LA English DT Review; Book Chapter DE Felidae; conservation; genomic archaeology; genomic prospecting; coalescent dating methods ID MOLECULAR-GENETIC VARIATION; ACUTE RESPIRATORY SYNDROME; FREE-RANGING CHEETAHS; NORTH-AMERICAN ZOOS; CONSERVATION GENETICS; ACINONYX-JUBATUS; WHOLE-GENOME; BIOLOGICAL CONSERVATION; IMMUNODEFICIENCY VIRUS; AFRICAN CHEETAH AB Advances in population and quantitative genomics, aided by the computational algorithms that employ genetic theory and practice, are now being applied to biological questions that surround free-ranging species not traditionally suitable for genetic enquiry. Here we review how applications of molecular genetic tools have been used to describe the natural history, present status, and future disposition of wild cat species. Insight into phylogenetic hierarchy, demographic contractions, geographic population substructure, behavioral ecology, and infectious diseases have revealed strategies for survival and adaptation of these fascinating predators. Conservation, stabilization, and management of the big cats are important areas that derive benefit from the genome resources expanded and applied to highly successful species, imperiled by an expanding human population. C1 Natl Canc Inst, Lab Genom Divers, Ft Detrick, MD 21702 USA. RP O'Brien, SJ (reprint author), Natl Canc Inst, Lab Genom Divers, Ft Detrick, MD 21702 USA. EM obrien@ncifcrf.gov RI Johnson, Warren/D-4149-2016 OI Johnson, Warren/0000-0002-5954-186X NR 102 TC 29 Z9 31 U1 7 U2 63 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1527-8204 BN 978-0-8243-3706-3 J9 ANNU REV GENOM HUM G JI Annu. Rev. Genomics Hum. Genet. PY 2005 VL 6 BP 407 EP 429 DI 10.1146/annurev.genom.6.080604.162151 PG 27 WC Genetics & Heredity SC Genetics & Heredity GA 972GE UT WOS:000232441500019 PM 16124868 ER PT S AU Berg, LJ Finkelstein, LD Lucas, JA Schwartzberg, PL AF Berg, LJ Finkelstein, LD Lucas, JA Schwartzberg, PL TI Tec family kinases in T lymphocyte development and function SO ANNUAL REVIEW OF IMMUNOLOGY SE Annual Review of Immunology LA English DT Review; Book Chapter DE Itk/Emt/Tsk; Rlk/Txk; Tec; phospholipase C-gamma; actin ID BRUTONS-TYROSINE-KINASE; PLECKSTRIN HOMOLOGY DOMAIN; CELL ANTIGEN RECEPTOR; X-LINKED AGAMMAGLOBULINEMIA; ALDRICH-SYNDROME PROTEIN; FACTOR-INDUCED RECRUITMENT; PROLINE-RICH SEQUENCES; BETA-GAMMA-SUBUNITS; ITK SH2 DOMAIN; SRC-FAMILY AB The Tee family tyrosine kinases are now recognized as important mediators of antigen receptor signaling in lymphocytes. Three members of this family, Itk, Rlk, and Tee, are expressed in T cells and activated in response to T cell receptor (TCR) engagement. Although initial studies demonstrated a role for these proteins in TCR-mediated activation of phospholipase C-gamma, recent data indicate that Tee family kinases also regulate actin cytoskeletal reorganization and cellular adhesion following TCR stimulation. In addition, Tee family kinases are activated downstream of G protein-coupled chemokine receptors, where they play parallel roles in the regulation of Rho GTPases, cell polarization, adhesion, and migration. In all these systems, however, Tee family kinases are not essential signaling components, but instead function to modulate or amplify signaling pathways. Although they quantitatively reduce proximal signaling, mutations that eliminate Tee family kinases in T cells nonetheless qualitatively alter T cell development and differentiation. C1 Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01655 USA. NHGRI, NIH, Bethesda, MD 20892 USA. RP Berg, LJ (reprint author), Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01655 USA. EM Leslie.Berg@umassmed.edu; pams@nhgri.nih.gov FU NCPDCID CDC HHS [CI000101]; NIAID NIH HHS [AI37584] NR 216 TC 181 Z9 186 U1 0 U2 5 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0732-0582 BN 978-0-8243-3023-1 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 2005 VL 23 BP 549 EP 600 DI 10.1146/annurev.immunol.22.012703.104743 PG 52 WC Immunology SC Immunology GA 923ZB UT WOS:000228947000018 PM 15771581 ER PT S AU Yewdell, JW Haeryfar, SMM AF Yewdell, JW Haeryfar, SMM TI Understanding presentation of viral antigens to CD8(+) T cells in vivo: The key to rational vaccine design SO ANNUAL REVIEW OF IMMUNOLOGY SE Annual Review of Immunology LA English DT Review; Book Chapter DE antigen presentation; CTL; virus; MHC ID MHC CLASS-I; CD8-ALPHA(+) DENDRITIC CELLS; HERPES-SIMPLEX VIRUS-1; HEAT-SHOCK PROTEINS; DRAINING LYMPH-NODE; CROSS-PRESENTATION; PRESENTING CELLS; CUTTING EDGE; IMMUNODOMINANCE HIERARCHY; PROCESSING PATHWAY AB CD8(+) T cells play a critical role in antiviral immunity by exerting direct antiviral activity against infected cells. Because of their ability to recognize all types of viral proteins, they offer the promise of providing broad immunity to viruses that evade humoral immunity by varying their surface proteins. Consequently, there is considerable interest in developing vaccines that elicit effective antiviral TCD8+ responses. Generating optimal vaccines ultimately requires rational design based on detailed knowledge of how TCD8+ are activated in vivo under natural circumstances. Here we review recent progress obtained largely by in vivo studies in mice to understand the mechanistic basis for activation of naive TCD8+ in virus infections. These studies point the way to detailed understanding and provide some key information for vaccine development, although much remains to be learned to enable truly rational vaccine design. C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. RP Yewdell, JW (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. EM jyewdell@niaid.nih.gov RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 104 TC 140 Z9 142 U1 1 U2 9 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0732-0582 BN 978-0-8243-3023-1 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 2005 VL 23 BP 651 EP 682 DI 10.1146/annurev.immunol.23041704.115702 PG 32 WC Immunology SC Immunology GA 923ZB UT WOS:000228947000020 PM 15771583 ER PT S AU Sospedra, M Martin, R AF Sospedra, M Martin, R TI Immunology of multiple sclerosis SO ANNUAL REVIEW OF IMMUNOLOGY SE Annual Review of Immunology LA English DT Review; Book Chapter DE autoimmunity; autoimmune mechanisms; neuroimmunology; demyelinating dieseases; EAE ID MYELIN BASIC-PROTEIN; T-CELL-RECEPTOR; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; NECROSIS-FACTOR-ALPHA; MESSENGER-RNA EXPRESSION; NATURAL-KILLER-CELLS; 2',3'-CYCLIC NUCLEOTIDE 3'-PHOSPHODIESTERASE; HUMAN PROTEOLIPID PROTEIN AB Multiple sclerosis (MS) develops in young adults with a complex predisposing genetic trait and probably requires an inciting environmental insult such as a viral infection to trigger the disease. The activation of CD4(+) autoreactive T cells and their differentiation into a Th1 phenotype are crucial events in the initial steps, and these cells are probably also important players in the long-term evolution of the disease. Damage of the target tissue, the central nervous system, is, however, most likely mediated by other components of the immune system, such as antibodies, complement, CD8(+) T cells, and factors produced by innate immune cells. Perturbations in immunomodulatory networks that include Th2 cells, regulatory CD4(+) T cells, NK cells, and others may in part be responsible for the relapsing-remitting or chronic progressive nature of the disease. However, an important paradigmatic shift in the study of MS has occurred in the past decade. It is now clear that MS is not just a disease of the immune system, but that factors contributed by the central nervous system are equally important and must be considered in the future. C1 NINDS, NIH, Cellular Immunol Sect, Neuroimmunol Branch, Bethesda, MD 20892 USA. RP Sospedra, M (reprint author), NINDS, NIH, Cellular Immunol Sect, Neuroimmunol Branch, Bethesda, MD 20892 USA. EM sospedrm@ninds.nih.gov; martinr@ninds.nih.gov NR 359 TC 1223 Z9 1255 U1 22 U2 218 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0732-0582 BN 978-0-8243-3023-1 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 2005 VL 23 BP 683 EP 747 DI 10.1146/annurev.immunol.23.021704.115707 PG 65 WC Immunology SC Immunology GA 923ZB UT WOS:000228947000021 PM 15771584 ER PT S AU Khakoo, AY Finkel, T AF Khakoo, AY Finkel, T TI Endothelial progenitor cells SO ANNUAL REVIEW OF MEDICINE SE Annual Review of Medicine LA English DT Review; Book Chapter DE stem cells; angiogenesis; vascular biology; cell therapy; vasculogenesis ID CORONARY-ARTERY-DISEASE; ISCHEMIC-HEART-DISEASE; BONE-MARROW CELLS; ACUTE MYOCARDIAL-INFARCTION; COLONY-STIMULATING FACTOR; HEMATOPOIETIC STEM-CELLS; NITRIC-OXIDE SYNTHASE; TUMOR ANGIOGENESIS; PERIPHERAL-BLOOD; THERAPEUTIC NEOVASCULARIZATION AB Endothelial progenitor cells area circulating, bone marrow-derived cell population that appears to participate in both vasculogenesis and vascular homeostasis. Questions persist regarding their functional characteristics, as well as the precise panel of cell surface markers that uniquely define this newly described progenitor cell population. We review experimental results obtained from both animal studies and recent clinical trials that suggest this cell type may have tremendous therapeutic potential for a wide range of human diseases. C1 NHLBI, NIH, Cardiovasc Branch, Mol Virol Lab, Bethesda, MD 21284 USA. RP Khakoo, AY (reprint author), NHLBI, NIH, Cardiovasc Branch, Mol Virol Lab, Bethesda, MD 21284 USA. EM khakooa@nhlbi.nih.gov; finkelt@nhlbi.nih.gov NR 105 TC 219 Z9 249 U1 0 U2 10 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4219 BN 978-0-8243-0556-7 J9 ANNU REV MED JI Annu. Rev. Med. PY 2005 VL 56 BP 79 EP 101 DI 10.1146/annurev.med.56.090203.104149 PG 23 WC Medicine, General & Internal SC General & Internal Medicine GA 904ND UT WOS:000227504100006 PM 15660503 ER PT S AU Kleeberger, SR Peden, D AF Kleeberger, SR Peden, D TI Gene-environment interactions in asthma and other respiratory diseases SO ANNUAL REVIEW OF MEDICINE SE Annual Review of Medicine LA English DT Review; Book Chapter DE pollutant; allergen; polymorphism; linkage analysis ID OBSTRUCTIVE PULMONARY-DISEASE; NECROSIS-FACTOR-ALPHA; S-TRANSFERASE M1; CHRONIC BERYLLIUM DISEASE; DIESEL EXHAUST PARTICLES; CLASS-II ALLELES; CHILDHOOD LUNG-FUNCTION; HOUSE-DUST ENDOTOXIN; LINKAGE ANALYSIS; AIR-POLLUTION AB It is generally agreed that many lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) have polygenic inheritance, and that the association of a specific genotype or genotypes with the disease is likely to vary between populations. Furthermore, it is recognized that the etiology of many lung diseases involves a complex interplay between genetic background and exposure to multiple environmental stimuli, and understanding the mechanisms through which genes and environment interact represents a major challenge for pulmonary researchers. We discuss experimental approaches and challenges that must be overcome to identify disease genes for asthma, COPD and chronic bronchitis, and occupational lung diseases. In particular, common polymorphisms in CD14, glutathione S-transferase, and tumor necrosis factor alpha have been found to be important in gene-environment interaction and asthma pathogenesis. An understanding of gene-environment interactions in complex lung diseases is essential to the development of new strategies for lung disease prevention and treatment. C1 Natl Inst Environm Hlth Sci, Lab Resp Biol, Environm Genet Grp, NIH, Res Triangle Pk, NC 27709 USA. Ctr Environm Med Asthma & Lung Biol, Div Immunol & Infect Dis, Dept Pediat, Chapel Hill, NC 27599 USA. RP Kleeberger, SR (reprint author), Natl Inst Environm Hlth Sci, Lab Resp Biol, Environm Genet Grp, NIH, Res Triangle Pk, NC 27709 USA. EM kleeber1@niehs.nih.gov FU NHLBI NIH HHS [HL6262404, R01-HL66559] NR 107 TC 74 Z9 79 U1 0 U2 4 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4219 BN 978-0-8243-0556-7 J9 ANNU REV MED JI Annu. Rev. Med. PY 2005 VL 56 BP 383 EP 400 DI 10.1146/annurev/med.56.062904.144908 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA 904ND UT WOS:000227504100021 PM 15660518 ER PT S AU Majdalani, N Gottesman, S AF Majdalani, N Gottesman, S TI The Rcs phosphorelay: A complex signal transduction system SO ANNUAL REVIEW OF MICROBIOLOGY SE Annual Review of Microbiology LA English DT Review; Book Chapter DE biofilm; Lon protease; exopolysaccharide; LuxR family ID ESCHERICHIA-COLI K-12; CAPSULAR POLYSACCHARIDE SYNTHESIS; ENTERICA SEROVAR TYPHIMURIUM; HIS-ASP PHOSPHORELAY; COLANIC-ACID POLYSACCHARIDE; SMALL RNA REGULATORS; CELL-DIVISION GENES; KLEBSIELLA-PNEUMONIAE; SALMONELLA-ENTERICA; ERWINIA-AMYLOVORA AB RcsC, RcsB, and RcsA were first identified as a sensor kinase, a response regulator, and an auxiliary regulatory protein, respectively, regulating the genes of capsular polysaccharide synthesis. Recent advances have demonstrated that these proteins are part of a complex phosphorelay, in which phosphate travels from the histidine kinase domain in RcsC to a response regulator domain in the same protein; from there to a phosphotransfer protein, RcsD; and from there to RcsB. In addition to capsule synthesis, which requires the unstable regulatory protein RcsA, RcsB also stimulates transcription of a small RNA, RprA; the cell division gene ftsZ; and genes encoding membrane and periplasmic proteins, including the osmotically inducible genes osmB and osmC. The Res system appears to play an important role in the later stages of biofilm development; induction of Rcs signaling by surfaces is consistent with this role. C1 NCI, Mol Biol Lab, Bethesda, MD 20892 USA. RP Majdalani, N (reprint author), NCI, Mol Biol Lab, Bldg 37, Bethesda, MD 20892 USA. EM susang@helix.nih.gov NR 122 TC 294 Z9 300 U1 2 U2 40 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4227 BN 978-0-8243-1159-9 J9 ANNU REV MICROBIOL JI Annu. Rev. Microbiol. PY 2005 VL 59 BP 379 EP 405 DI 10.1146/annurev.micro.59.050405.101230 PG 27 WC Microbiology SC Microbiology GA 980YT UT WOS:000233054800018 PM 16153174 ER PT S AU Hinnebusch, AG AF Hinnebusch, AG TI Translational regulation of GCN4 and the general amino acid control of yeast SO ANNUAL REVIEW OF MICROBIOLOGY SE Annual Review of Microbiology LA English DT Review; Book Chapter DE protein synthesis; initiation factors; Gcn2; eIF2; eIF2B ID GUANINE-NUCLEOTIDE-EXCHANGE; INITIATION FACTOR-II; TRANSFER-RNA-SYNTHETASE; PROTEIN-KINASE GCN2; OPEN READING FRAMES; POLYPEPTIDE-CHAIN INITIATION; TRANSCRIPTION FACTOR GCN4; VANISHING WHITE-MATTER; BINDING CASSETTE PROTEIN; UNCHARGED TRANSFER-RNA AB Cells reprogram gene expression in response to environmental changes by mobilizing transcriptional activators. The activator protein Gcn4 of the yeast Saccharomyces cerevisiae is regulated by an intricate translational control mechanism, which is the primary focus of this review, and also by the modulation of its stability in response to nutrient availability. Translation of GCN4 mRNA is derepressed in amino acid-deprived cells, leading to transcriptional induction of nearly all genes encoding amino acid biosynthetic enzymes. The trans-acting proteins that control GCN4 translation have general functions in the initiation of protein synthesis, or regulate the activities of initiation factors, so that the molecular events that induce GCN4 translation also reduce the rate of general protein synthesis. This dual regulatory response enables cells to limit their consumption of amino acids while diverting resources into amino acid biosynthesis in nutrient-poor environments. Remarkably, mammalian cells use the same strategy to downregulate protein synthesis while inducing transcriptional activators of stress-response genes under various stressful conditions, including amino acid starvation. C1 NICHHD, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA. RP Hinnebusch, AG (reprint author), NICHHD, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA. EM ahinnebusch@nih.gov NR 205 TC 561 Z9 571 U1 7 U2 59 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4227 BN 978-0-8243-1159-9 J9 ANNU REV MICROBIOL JI Annu. Rev. Microbiol. PY 2005 VL 59 BP 407 EP 450 DI 10.1146/annurev.micro.59.031805.133833 PG 44 WC Microbiology SC Microbiology GA 980YT UT WOS:000233054800019 PM 16153175 ER PT S AU Mattson, MP AF Mattson, MP TI Energy intake, meal frequency, and health: A neurobiological perspective SO ANNUAL REVIEW OF NUTRITION SE Annual Review of Nutrition LA English DT Review; Book Chapter DE BDNF; caloric restriction; insulin resistance; obesity; serotonin ID INSULIN-RESISTANCE SYNDROME; HUNTINGTIN MUTANT MICE; CENTRAL-NERVOUS-SYSTEM; CALORIC RESTRICTION; DIETARY RESTRICTION; NEUROTROPHIC-FACTOR; LIFE-SPAN; GLUCOSE-METABOLISM; RAT-BRAIN; MITOCHONDRIAL-FUNCTION AB The size and frequency of meals are fundamental aspects of nutrition that can have profound effects on the health and longevity of laboratory animals. In humans, excessive energy intake is associated with increased incidence of cardiovascular disease, diabetes, and certain cancers and is a major cause of disability and death in industrialized countries. On the other hand, the influence of meal frequency on human health and longevity is unclear. Both caloric (energy) restriction (CR) and reduced meal frequency/intermittent fasting can suppress the development of various diseases and can increase life span in rodents by mechanisms involving reduced oxidative damage and increased stress resistance. Many of the beneficial effects of CR and fasting appear to be mediated by the nervous system. For example, intermittent fasting results in increased production of brain-derived neurotrophic factor (BDNF), which increases the resistance of neurons in the brain to dysfunction and degeneration in animal models of neurodegenerative disorders; BDNF signaling may also mediate beneficial effects of intermittent fasting on glucose regulation and cardiovascular function. A better understanding of the neurobiological mechanisms by which meal size and frequency affect human health may lead to novel approaches for disease prevention and treatment. C1 NIA, Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. RP Mattson, MP (reprint author), NIA, Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA. EM mattsonm@grc.nia.nih.gov RI Mattson, Mark/F-6038-2012 NR 144 TC 129 Z9 134 U1 5 U2 37 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0199-9885 BN 978-0-8243-2825-2 J9 ANNU REV NUTR JI Annu. Rev. Nutr. PY 2005 VL 25 BP 237 EP 260 DI 10.1146/annurev.nutr.25.050304.092526 PG 24 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 962DD UT WOS:000231710300013 PM 16011467 ER PT S AU Chuang, DM Hough, C Senatorov, VV AF Chuang, DM Hough, C Senatorov, VV TI Glyceraldehyde-3-phosphate dehydrogenase, apoptosis and neurodegenerative diseases SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY SE Annual Review of Pharmacology and Toxicology LA English DT Review; Book Chapter DE GAPDH; overexpression; nuclear accumulation; intracellular sensor; neurodegeneration ID AMYLOID PRECURSOR PROTEIN; AGE-INDUCED APOPTOSIS; POTENTIAL ANTIDEMENTIA DRUG; CEREBELLAR GRANULE CELLS; FOCAL CEREBRAL-ISCHEMIA; REDUCES BRAIN-DAMAGE; HUNTINGTONS-DISEASE; NUCLEAR TRANSLOCATION; ALZHEIMERS-DISEASE; NEURONAL APOPTOSIS AB Increasing evidence supports the notion that glyceraldehyde-3phosphate dehydrogenase (GAPDH) is a protein with multiple functions, including its surprising role in apoptosis. GAPDH is overexpressed and accumulates in the nucleus during apoptosis induced by a variety of insults in diverse cell types. Knockdown of GAPDH using an antisense strategy demonstrates its involvement in the apoptotic cascade in which GAPDH nuclear translocation appears essential. Knowledge concerning the mechanisms underlying GAPDH nuclear translocation and subsequent cell death is growing. Additional evidence suggests that GAPDH may be an intracellular sensor of oxidative stress during early apoptosis. Abnormal expression, nuclear accumulation, changes in physical properties, and loss of glycolytic activity of GAPDH have been found in cellular and transgenic models as well as postmortem tissues of several neurodegenerative diseases. The interaction of GAPDH with disease-related proteins as well as drugs used to treat these diseases suggests that it is a potential molecular target for drug development. C1 NIMH, Mol Neurobiol Sect, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RP Chuang, DM (reprint author), NIMH, Mol Neurobiol Sect, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA. EM chuang@mail.nih.gov; chough@usuhs.mil; Senatorovv@nei.nih.gov NR 128 TC 197 Z9 209 U1 2 U2 11 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0362-1642 BN 978-0-8243-0444-7 J9 ANNU REV PHARMACOL JI Annu. Rev. Pharmacol. Toxicol. PY 2005 VL 45 BP 269 EP + DI 10.1146/annurev.pharmtox.45.120403.095902 PG 23 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 904NC UT WOS:000227504000011 PM 15822178 ER PT S AU Fukuto, JM Switzer, CH Miranda, KM Wink, DA AF Fukuto, JM Switzer, CH Miranda, KM Wink, DA TI Nitroxyl (HNO): Chemistry, biochemistry, and pharmacology SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY SE Annual Review of Pharmacology and Toxicology LA English DT Review; Book Chapter DE nitric oxide; thiols; calcitonin gene-related peptide; ischerma-reperfusion ID NITRIC-OXIDE SYNTHASE; NO-CENTER-DOT; DETERRENT AGENT CYANAMIDE; NEUTRAL AQUEOUS-SOLUTION; DIELS-ALDER REACTION; HYDROXY-L-ARGININE; ALDEHYDE DEHYDROGENASE; SUPEROXIDE-DISMUTASE; NITROSYL HYDRIDE; ANGELIS SALT AB Recent discoveries of novel and potentially important biological activity have spurred interest in the chemistry and biochemistry of nitroxyl (HNO). It has become clear that, among all the nitrogen oxides, HNO is unique in its chemistry and biology. Currently, the intimate chemical details of the biological actions of HNO are not well understood. Moreover, many of the previously accepted chemical properties of HNO have been recently revised, thus requiring reevaluation of possible mechanisms of biological action. Herein, we review these developments in HNO chemistry and biology. C1 Univ Calif Los Angeles, Sch Publ Hlth, Interdepartmental Program Mol Toxicol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90095 USA. Univ Arizona, Dept Chem, Tucson, AZ 85721 USA. NCI, Tumor Biol Sect, Radiat Biol Branch, Bethesda, MD 20892 USA. RP Fukuto, JM (reprint author), Univ Calif Los Angeles, Sch Publ Hlth, Interdepartmental Program Mol Toxicol, Los Angeles, CA 90095 USA. EM jfukuto@mednet.ucla.edu; cswitzer@ucla.edu; miranda@email.arizona.edu; wink@box-w.nih.gov RI Miranda, Katrina/B-7823-2009; Switzer, Christopher/D-9203-2013 NR 119 TC 78 Z9 81 U1 0 U2 24 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0362-1642 BN 978-0-8243-0444-7 J9 ANNU REV PHARMACOL JI Annu. Rev. Pharmacol. Toxicol. PY 2005 VL 45 BP 335 EP 355 DI 10.1146/annurev.pharmtox.45.120403.095959 PG 21 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 904NC UT WOS:000227504000014 PM 15822180 ER PT S AU Levin, IW Bhargava, R AF Levin, IW Bhargava, R TI Fourier transform infrared vibrational spectroscopic imaging: Integrating microscopy and molecular recognition SO ANNUAL REVIEW OF PHYSICAL CHEMISTRY SE Annual Review of Physical Chemistry LA English DT Review; Book Chapter DE Fourier transform infrared spectroscopy; interferometry; histopathology; brain tissue; bone tissue; breast tissue; esophageal tissue; skin tissue; prostate tissue; pharmaceuticals; single cells; drug delivery ID PLANE ARRAY DETECTION; RESOLVED FT-IR; GRAM-SCHMIDT ORTHOGONALIZATION; INDUCED REORIENTATION DYNAMICS; DISPERSED LIQUID-CRYSTAL; BARRETTS-ESOPHAGUS; POLYMERIC SYSTEMS; RAMAN-SPECTROSCOPY; DELIVERY SYSTEMS; SINGLE CELLS AB The recent development of Fourier transform infrared (FTIR) spectroscopic imaging has enhanced our capability to examine, on a microscopic scale, the spatial distribution of vibrational spectroscopic signatures of materials spanning the physical and biomedical disciplines. Recent activity in this emerging area has concentrated on instrumentation development, theoretical analyses to provide guidelines for imaging practice, novel data processing algorithms, and the introduction of the technique to new fields. To illustrate the impact and promise of this spectroscopic imaging methodology, we present fundamental principles of the technique in the context of FTIR spectroscopy and review new applications in various venues ranging from the physical chemistry of macromolecular systems to the detection of human disease. C1 NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. RP Levin, IW (reprint author), NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. EM iwl@helix.nih.gov; rb3l9b@nih.gov OI Bhargava, Rohit/0000-0001-7360-994X NR 129 TC 172 Z9 174 U1 6 U2 80 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-426X BN 978-0-8243-1056-1 J9 ANNU REV PHYS CHEM JI Annu. Rev. Phys. Chem. PY 2005 VL 56 BP 429 EP 474 DI 10.1146/annurev.physchem.56.092503.141205 PG 52 WC Chemistry, Physical SC Chemistry GA 954VX UT WOS:000231184400016 PM 15796707 ER PT J AU Charmandari, E Tsigos, C Chrousos, G AF Charmandari, E Tsigos, C Chrousos, G TI Endocrinology of the stress response SO ANNUAL REVIEW OF PHYSIOLOGY SE Annual Review of Physiology LA English DT Review; Book Chapter DE stress system; endocrinology of stress; stress-related disorders ID CORTICOTROPIN-RELEASING HORMONE; PITUITARY-ADRENAL AXIS; CENTRAL-NERVOUS-SYSTEM; SEXUALLY-ABUSED GIRLS; GROWTH-HORMONE; NEUROPEPTIDE-Y; RECEPTOR ANTAGONIST; CUSHINGS-SYNDROME; GENE-EXPRESSION; BIOCHEMICAL MANIFESTATIONS AB The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRE); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoinmume, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors. C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Hellen Natl Diabet Ctr, Athens, Greece. RP Charmandari, E (reprint author), NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. EM charmane@mail.nih.gov; chrousosG@aol.com RI Charmandari, Evangelia/B-6701-2011 NR 115 TC 556 Z9 586 U1 15 U2 115 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4278 EI 1545-1585 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 2005 VL 67 BP 259 EP 284 DI 10.1146/annurev.physiol.67.040403.120816 PG 28 WC Physiology SC Physiology GA 916SR UT WOS:000228406800012 PM 15709959 ER PT S AU Hewitt, SC Harrell, JC Korach, KS AF Hewitt, SC Harrell, JC Korach, KS TI Lessons in estrogen biology from knockout and transgenic animals SO ANNUAL REVIEW OF PHYSIOLOGY SE Annual Review of Physiology LA English DT Review; Book Chapter DE estrogen receptor; mammary gland; uterus; estrogen mechanisms ID EPIDERMAL-GROWTH-FACTOR; MAMMARY-GLAND DEVELOPMENT; BREAST-CANCER RISK; STEROID-RECEPTOR COACTIVATOR-1; TRANSCRIPTIONAL ACTIVATION; CELL-PROLIFERATION; UTERINE RESPONSES; CROSS-TALK; REPRODUCTIVE PHENOTYPES; TARGETED DISRUPTION AB Tremendous progress has been made in elucidating numerous critical aspects of estrogen signaling. New tools and techniques have enabled detailed molecular analysis of components that direct estrogen responses. At the other end of the spectrum, generation of a multiplicity of transgenic animals has allowed analysis of the physiological roles of the estrogen-signaling components in biologically relevant models. Here, we review the ever-increasing body of knowledge in the field of estrogen biology, especially as applied to the female reproductive processes. C1 NIEHS, Receptor Biol Sect, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA. RP Hewitt, SC (reprint author), NIEHS, Receptor Biol Sect, Reprod & Dev Toxicol Lab, POB 12233, Res Triangle Pk, NC 27709 USA. EM curtiss@niehs.nih.gov; Joshua.Harrell@UCHSC.edu; korach@niehs.nih.gov OI Korach, Kenneth/0000-0002-7765-418X NR 94 TC 177 Z9 184 U1 0 U2 6 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4278 BN 978-0-8243-0367-9 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 2005 VL 67 BP 285 EP 308 DI 10.1146/annurev.physiol.67.040403.115914 PG 26 WC Physiology SC Physiology GA 916SR UT WOS:000228406800013 PM 15709960 ER PT S AU Praetorius, HA Spring, KR AF Praetorius, HA Spring, KR TI A physiological view of the primary cilium SO ANNUAL REVIEW OF PHYSIOLOGY SE Annual Review of Physiology LA English DT Review; Book Chapter DE function; Ca2+; mechano-sensation; chemo-sensation; signal transduction; flow; polycystin ID LEFT-RIGHT ASYMMETRY; INTRAFLAGELLAR TRANSPORT IFT; CORTICAL COLLECTING DUCT; DISEASE GENE TG737; INDUCED FLUID-FLOW; CAENORHABDITIS-ELEGANS; MDCK CELLS; KINESIN-II; CHLAMYDOMONAS FLAGELLA; SITUS-INVERSUS AB The primary cilium, an organelle largely ignored by physiologists, functions both as a mechano-sensor and a chemo-sensor in renal tubular epithelia. This forgotten structure is critically involved in the determination of left-right sidedness during development and is a key factor in the development of polycystic kidney disease, as well as a number of other abnormalities. This review provides an update of our current understanding about the function of primary cilia. Much new information obtained in the past five years has been stimulated, in part, by discoveries of the primary cilium's key role in the genesis of polycystic kidney disease as well as its involvement in determination of left-right axis asymmetry. Here we focus on the various functions of the primary cilium rather than on its role in Pathology. C1 Univ Aarhus, Inst Clin, Water & Salt Res Ctr, DK-8200 Aarhus, Denmark. NHLBI, LKEM, NIH, Bethesda, MD 20892 USA. RP Praetorius, HA (reprint author), Univ Aarhus, Inst Clin, Water & Salt Res Ctr, DK-8200 Aarhus, Denmark. EM helle.praetorius@ki.au; springk@direcway.com NR 66 TC 176 Z9 183 U1 0 U2 18 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4278 BN 978-0-8243-0367-9 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 2005 VL 67 BP 515 EP 529 DI 10.1146/annurev.physiol.67.040403.101353 PG 15 WC Physiology SC Physiology GA 916SR UT WOS:000228406800021 PM 15709968 ER PT J AU Breen, N Meissner, HI AF Breen, N Meissner, HI TI Toward a system of cancer screening in the United States: Trends and opportunities SO ANNUAL REVIEW OF PUBLIC HEALTH SE Annual Review of Public Health LA English DT Review; Book Chapter DE access; quality; cost-effectiveness ID HEALTH INTERVIEW SURVEY; INCREASE MAMMOGRAPHY USE; PRIMARY-CARE PHYSICIANS; BREAST-CANCER; COLORECTAL-CANCER; CERVICAL-CANCER; OLDER WOMEN; PROSTATE-CANCER; PREVENTIVE CARE; MANAGED CARE AB The hard work of public health officials, physicians, and disease advocacy groups to educate Americans about the importance of early detection has resulted in uptake of screening tests at levels equivalent to or higher than in countries with organized cancer screening programs. However, the societal costs of high screening rates are larger in the United States than in other countries, including higher prices for screening, more unnecessary testing, and inefficiencies in delivery, especially in small practices. Further, screening rates are not evenly distributed across population groups, and the national expenditure on clinical and community research to promote cancer screening among individuals has not been matched by research efforts that focus on policy or clinical systems to increase screening widely throughout the population. We identify opportunities for organizational change that improve access to use, improve quality, and promote cost effectiveness in cancer screening delivery. C1 NCI, Hlth Serv & Econ Branch, Appl Res Program, Rockville, MD 20852 USA. NCI, Div Canc Control & Populat Sci, Behav Res Program, Appl Canc Screening Res Branch, Rockville, MD 20852 USA. RP Breen, N (reprint author), NCI, Hlth Serv & Econ Branch, Appl Res Program, Rockville, MD 20852 USA. EM Breenn@mail.nih.gov; HM36D@NIH.GOV NR 125 TC 25 Z9 26 U1 2 U2 5 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0163-7525 EI 1545-2093 J9 ANNU REV PUBL HEALTH JI Annu. Rev. Public Health PY 2005 VL 26 BP 561 EP 582 DI 10.1146/annurev.publhealth.26.021304.144703 PG 22 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 924LY UT WOS:000228981500024 PM 15760301 ER PT J AU Conniff, KM Scarlett, JM Goodman, S Appel, LD AF Conniff, KM Scarlett, JM Goodman, S Appel, LD TI Effects of a pet visitation program on the behavior and emotional state of adjudicated female adolescents SO ANTHROZOOS LA English DT Article DE adjudicated adolescents; animal-assisted activities; randomized trial ID ANIMAL-ASSISTED THERAPY AB This study was designed to assess the impact of an ongoing pet visitation program on the behavior and emotional state of adjudicated female adolescents at a medium secure residential facility over an eight-week period. To our knowledge, this study is the first randomized trial with a pretest-posttest design aimed at determining whether unstructured animal-assisted activities (AAA) have a positive impact on this unique population of adolescents. Using a random number table, 23 residents were randomly assigned to participate either in the pet visitation program (n = 13) or the facility's usual activities (n = 10). The program entailed weekly one-hour sessions during which participants were involved in activities such as grooming the animals, giving commands, playing fetch, and talking to the animals' handlers. To assess the programs effects on participants' behavior and emotional state, two quantitative instruments, the Youth Self-Report for Ages 11-18 (YSR) and the Resident Behavior Assessment (RBA), and a qualitative survey (designed by the researchers) were administered to the participants both prior to the pet visitation program and following its completion. Results from the two quantitative measures suggested that the pet visitation program did not have a significant effect on the behavior or emotional state of the pet visitation participants. Qualitative results indicated that most of the participants enjoyed some aspect of the pet visitation program. In light of the small sample size and the unanticipated difficulties encountered in the conduct of the study, this research should be considered a pilot study. The limitations inherent to studying the effects of AAA programs in adjudicated adolescents are discussed. C1 Cornell Univ, Epidemiol Sect, Coll Vet Med, Ithaca, NY 14853 USA. NCI, Neurooncol Branch, NIH, Bethesda, MD USA. NY State Off Children & Family Serv, Lansing Residential Ctr, Lansing, NY USA. Shelter Outreach Serv, Ithaca, NY USA. RP Scarlett, JM (reprint author), Cornell Univ, Epidemiol Sect, Coll Vet Med, S1 066 Schuman Hall, Ithaca, NY 14853 USA. EM jms15@cornell.edu NR 14 TC 7 Z9 7 U1 1 U2 11 PU PURDUE UNIV PRESS PI W LAFAYETTE PA 1207 SOUTH CAMPUS COURTS-E, W LAFAYETTE, IN 47907-1207 USA SN 0892-7936 J9 ANTHROZOOS JI Anthrozoos PY 2005 VL 18 IS 4 BP 379 EP 395 DI 10.2752/089279305785593974 PG 17 WC Anthropology; Environmental Studies; Sociology; Veterinary Sciences SC Anthropology; Environmental Sciences & Ecology; Sociology; Veterinary Sciences GA 025EB UT WOS:000236247000003 ER PT J AU Kamangar, F Strickland, PT Pourshams, A Malekzadeh, R Boffetta, P Roth, MJ Abnet, CC Saadatian-Elahi, M Rakhshani, N Brennan, P Etemadi, A Dawsey, SM AF Kamangar, F Strickland, PT Pourshams, A Malekzadeh, R Boffetta, P Roth, MJ Abnet, CC Saadatian-Elahi, M Rakhshani, N Brennan, P Etemadi, A Dawsey, SM TI High exposure to polycyclic aromatic hydrocarbons may contribute to high risk of esophageal cancer in northeastern Iran SO ANTICANCER RESEARCH LA English DT Article DE esophageal cancer; polycyclic hydrocarbons; Iran ID 1-HYDROXYPYRENE GLUCURONIDE; DNA ADDUCTS; LINXIAN; URINE; CHINA AB Background: The northeastern region of Iran has some of the highest rates of esophageal squamous cell carcinoma (ESCC) in the world. Materials and Methods: To investigate the role of polycyclic aromatic hydrocarbons (PAHs) in the etiology of ESCC in northeastern Iran, we measured urine 1-hydroxypyrene glucuronide (1-OHPG), a stable PAH metabolite, in 99 inhabitants of this area. Results: The median urine 1-OHPG in participants of this study was 4.2 pmol/ml. Forty-two subjects (42%) had levels ranging from 1 to 5 pmol/ml, indicative of moderate PAH exposure, and 41 (41%) had levels above 5 pmol/ml, indicative of very high exposure. Further analysis showed that 1-OHPG levels were high in all subgroups of our study subjects, including both sexes, rural and urban dwellers, and smokers and non-smokers. Only 15% of the variance in 1-OHPG was explained by age, sex, residence, smoking, nass, or opium consumption. This pattern of PAH exposure parallels the ESCC incidence pattern seen in this area. Conclusion: We conclude that people in northeastern Iran are exposed to widespread and very high levels of PAH, largely from unknown sources, and this may contribute to the high rates of ESCC observed in this area. C1 NCI, Canc Res Ctr, Canc Prevent Studies Branch, Baltimore, MD 21218 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA. Univ Tehran, Med Sci Shariati Hosp, Digest Dis Res Ctr, Tehran 14114, Iran. Int Agcy Res Canc, F-69372 Lyon, France. RP Kamangar, F (reprint author), NCI, Canc Prevent Studies Branch, CCR, 6116 Execut Blvd,Rm 705, Bethesda, MD 20892 USA. EM kamangaf@mail.nih.gov RI Etemadi, Arash/C-1386-2016; OI Etemadi, Arash/0000-0002-3458-1072; Abnet, Christian/0000-0002-3008-7843; Malekzadeh, Reza/0000-0003-1043-3814 NR 18 TC 61 Z9 63 U1 1 U2 3 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD JAN-FEB PY 2005 VL 25 IS 1B BP 425 EP 428 PG 4 WC Oncology SC Oncology GA 913FW UT WOS:000228138000005 PM 15816606 ER PT J AU Shen, M Berndt, SI Rothman, N Mumford, JL He, XZ Yeager, M Welch, R Chanock, S Keohavong, P Donahue, M Zheng, TZ Caporaso, N Lan, Q AF Shen, M Berndt, SI Rothman, N Mumford, JL He, XZ Yeager, M Welch, R Chanock, S Keohavong, P Donahue, M Zheng, TZ Caporaso, N Lan, Q TI Polymorphisms in the DNA base excision repair genes APEX1 and XRCC1 and lung cancer risk in Xuan Wei, China SO ANTICANCER RESEARCH LA English DT Article DE lung cancer; DNA repair; single nucleotide polymorphism; APEX1; XRCC1; ADPRT; LIG3 ID COAL COMBUSTION EMISSIONS; HUMAN-LYMPHOCYTES; MUTATIONS; XPD; SUSCEPTIBILITY; POPULATION; MECHANISMS; FREQUENCY; VARIANTS; EXPOSURE AB The lung cancer mortality rate in Xuan Wei is among the highest in China and has been causally attributed to high exposure to indoor smoky coal emissions, which contain high levels of PAHs and can lead to modified bases. We studied genetic polymorphisms in four DNA base excision repair genes in a population-based case-control study in Xuan Wei with 122 lung cancer cases and 122 controls. Homozygous carriers of the APEX1 148Glu variant had an increased risk (OR, 2.13; 95% CI, 0.96-4.74), whereas persons with the XRCC1 399Gln allele had a decreased risk (OR, 0.60; 95% CI, 0.35-1.02) of lung cancer compared with wild-type carriers. Subjects with both at-risk genotypes (APEX1 Glu148Glu and XRCC1 Arg399Arg) had a higher risk of lung cancer (OR: 3.34; 95% CI: 1.16-9.67). We found genetic variants in APEX1 and XRCC1 may alter the risk of lung cancer in a special population in China. C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. US EPA, Natl Hlth & Environ Effects Res Lab, Res Triangle Pk, NC 27711 USA. Chinese Ctr Dis Control & Prevent, Beijing 100005, Peoples R China. Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA 15260 USA. Yale Univ, Yale Sch Publ Hlth, New Haven, CT 06520 USA. RP Shen, M (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, MSC 7240,6120 Execut Blvd,EPS 511, Bethesda, MD 20892 USA. EM shenmi@mail.nih.gov OI Keohavong, Phouthone/0000-0001-7812-4925 NR 32 TC 58 Z9 61 U1 0 U2 0 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD JAN-FEB PY 2005 VL 25 IS 1B BP 537 EP 542 PG 6 WC Oncology SC Oncology GA 913FW UT WOS:000228138000024 PM 15816625 ER PT J AU Sepehr, A Kamangar, F Fahimi, S Saidi, F Abnet, CC Dawsey, SM AF Sepehr, A Kamangar, F Fahimi, S Saidi, F Abnet, CC Dawsey, SM TI Poor oral health as a risk factor for esophageal squamous dysplasia in northeastern Iran SO ANTICANCER RESEARCH LA English DT Article DE esophageal cancer; oral health; Iran ID CANCER AB Background: Northeastern Iran has one of the highest rates of esophageal squamous cell carcinoma (ESCC) in the world. The reasons for observing such high rates of ESCC in this area are not fully clear. The current study evaluates the association between some potential risk factors and squamous dysplasia, a precursor lesion of ESCC, in northeastern Iran. Materials and Methods: Using logistic regression, we compared potential risk factors of ESCC in 124 individuals with dysplasia and 50 normal individuals from northeastern Iran. Case/control status was histologically proven in all 174 study participants. Results: Poor oral health showed a dose-response association with ESCC risk (p for trend < 0.01). Edentulous individuals had 5-fold higher risk of dysplasia compared to participants with good oral health (p-value < 0.01). Conclusion: Our results are consistent with two other published studies that have shown oral health as a risk factor for ESCC. The high incidence of ESCC in northeastern Iran may be partly attributable to poor oral health. C1 NCI, Canc Prevent Studies Branch, CCR, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Int Agcy Res Canc, F-69372 Lyon, France. Iran Mehr Hosp, Dept Surg, Tehran, Iran. RP Kamangar, F (reprint author), NCI, Canc Prevent Studies Branch, CCR, 6116 Execut Blvd,Rm 705,Suite 705, Bethesda, MD 20892 USA. EM kamangaf@mail.nih.gov OI Abnet, Christian/0000-0002-3008-7843 NR 15 TC 25 Z9 25 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD JAN-FEB PY 2005 VL 25 IS 1B BP 543 EP 546 PG 4 WC Oncology SC Oncology GA 913FW UT WOS:000228138000025 PM 15816626 ER PT J AU Dorner, T Lipsky, PE AF Doerner, Thomas Lipsky, Peter E. BE Kropshofer, H Vogt, AB TI Contribution of B Cells to Autoimmune Pathogenesis SO ANTIGEN PRESENTING CELLS: FROM MECHANISMS TO DRUG DEVELOPMENT LA English DT Article; Book Chapter ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTI-CD20 MONOCLONAL-ANTIBODY; PRIMARY SJOGRENS-SYNDROME; COLD AGGLUTININ DISEASE; RECEPTOR SIGNAL-TRANSDUCTION; ENHANCED MUTATIONAL ACTIVITY; KAPPA GENE REARRANGEMENTS; VARIABLE-REGION GENES; LIGHT-CHAIN PAIRINGS; J-LAMBDA REPERTOIRE C1 [Doerner, Thomas] Univ Med Berlin, Coagulat Unit, D-10098 Berlin, Germany. [Lipsky, Peter E.] NIAMS, NIH, Autoimmun Branch, Bethesda, MD 20892 USA. RP Dorner, T (reprint author), Univ Med Berlin, Coagulat Unit, Campus Mitte,Schumannstr 20-21, D-10098 Berlin, Germany. NR 207 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-3-52760-702-0 PY 2005 BP 461 EP 501 DI 10.1002/3527607021.ch13 PG 41 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA BYA65 UT WOS:000297763100014 ER PT J AU Bray, M AF Bray, Mike BE Torrence, PF TI Viral Bioterrorism and Antiviral Countermeasures SO ANTIVIRAL DRUG DISCOVERY FOR EMERGING DISEASES AND BIOTERRORISM THREATS LA English DT Article; Book Chapter ID EBOLA HEMORRHAGIC-FEVER; PUBLIC-HEALTH MANAGEMENT; COWPOX VIRUS CHALLENGE; AEROSOLIZED CIDOFOVIR; BIOLOGICAL TERRORISM; PROTECTS MICE; INFECTIONS; SMALLPOX; PATHOGENESIS; PROPHYLAXIS C1 NIAID, Biodef Clin Res Branch, OCR, OD,NIH, Bethesda, MD 20892 USA. RP Bray, M (reprint author), NIAID, Biodef Clin Res Branch, OCR, OD,NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 36 TC 8 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-0-47171-671-6 PY 2005 BP 17 EP 28 D2 10.1002/0471716715 PG 12 WC Medicine, Research & Experimental; Virology SC Research & Experimental Medicine; Virology GA BYE08 UT WOS:000298179900003 ER PT J AU Tseng, CK AF Tseng, Christopher K. BE Torrence, PF TI Overview of Antiviral Drug Discovery and Development SO ANTIVIRAL DRUG DISCOVERY FOR EMERGING DISEASES AND BIOTERRORISM THREATS LA English DT Editorial Material; Book Chapter ID ACUTE-RESPIRATORY-SYNDROME; WEST-NILE-VIRUS; CONGO HEMORRHAGIC-FEVER; JAPANESE ENCEPHALITIS-VIRUS; SARS-ASSOCIATED CORONAVIRUS; RIFT-VALLEY FEVER; S-ADENOSYLHOMOCYSTEINE HYDROLASE; SEMLIKI-FOREST-VIRUS; HEPATITIS-C VIRUS; L-HOMOCYSTEINE HYDROLASE C1 NIAID, DMID, NIH, Bethesda, MD 20892 USA. RP Tseng, CK (reprint author), NIAID, DMID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 319 TC 9 Z9 9 U1 0 U2 3 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-0-47171-671-6 PY 2005 BP 31 EP 82 D2 10.1002/0471716715 PG 52 WC Medicine, Research & Experimental; Virology SC Research & Experimental Medicine; Virology GA BYE08 UT WOS:000298179900004 ER PT J AU Dube, MP Wu, JW Aberg, JA Deeg, MA McGovern, ME Alston, BL Shriver, SL Greenwald, ML Lee, D Stein, JH AF Dube, MP Wu, JW Aberg, JA Deeg, MA McGovern, ME Alston, BL Shriver, SL Greenwald, ML Lee, D Stein, JH TI Safety and efficacy of extended-release niacin for the treatment of dyslipidaemia in patients with HIV infection: a prospective, multicentre study (ACTG 5148) SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 7th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV CY NOV 13-16, 2005 CL Dublin, IRELAND C1 Indiana Univ, Indianapolis, IN 46204 USA. Harvard Univ, Stat & Data Anal Ctr, Boston, MA 02115 USA. NYU, New York, NY USA. Kos Pharmaceut, Weston, FL USA. NIH, Bethesda, MD 20892 USA. Social & Sci Syst Inc, Silver Spring, MD USA. Univ Calif San Diego, San Diego, CA 92103 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 8 BP L9 EP L10 PG 2 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 009SN UT WOS:000235133100029 ER PT J AU Morse, CG Mican, JM Jones, EC Joe, GO Forwentini, E Kovacs, JA AF Morse, CG Mican, JM Jones, EC Joe, GO Forwentini, E Kovacs, JA TI Incidence and natural history of osteonecrosis in HIV-infected adults SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 7th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV CY NOV 13-16, 2005 CL Dublin, IRELAND C1 NIH, Ctr Clin, Bethesda, MD 20892 USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 8 BP L52 EP L52 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 009SN UT WOS:000235133100100 ER PT J AU Ambrose, Z Julias, JG Boyer, PL KewalRamani, VN Hughes, SH AF Ambrose, Z Julias, JG Boyer, PL KewalRamani, VN Hughes, SH TI The level of RT in HIV-1 particles affects susceptibility to NNRTIs but not to 3TC SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. SAIC Frederick, Basic Res Program, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S96 EP S96 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800089 ER PT J AU Ambrose, Z Julias, JG Boyer, PL KewalRamani, VN Hughes, SH AF Ambrose, Z Julias, JG Boyer, PL KewalRamani, VN Hughes, SH TI The level of RT in HIV-1 particles affects susceptibility to NNRTIs but not to 3TC SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. SAIC Frederick, Basic Res Program, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 086 BP S96 EP S96 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100102 ER PT J AU Ambrose, Z Wiegand, A Kimata, J Maldarelli, F Hughes, SH Palmer, S Mellors, JW Coffin, JM Lifson, JD Ramani, VNK AF Ambrose, Z Wiegand, A Kimata, J Maldarelli, F Hughes, SH Palmer, S Mellors, JW Coffin, JM Lifson, JD Ramani, VNK TI NNRTI-resistance detected in RT-SHIV-infected macaques treated with single dose nevirapine SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. NCI, AIDS Vaccine Program, Frederick, MD 21701 USA. Baylor Coll Med, Houston, TX 77030 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S172 EP S172 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800160 ER PT J AU Ambrose, Z Wiegand, A Kimata, J Maldarelli, F Hughes, SH Palmer, S Mellors, JW Coffin, JM Lifson, JD Ramani, VNK AF Ambrose, Z Wiegand, A Kimata, J Maldarelli, F Hughes, SH Palmer, S Mellors, JW Coffin, JM Lifson, JD Ramani, VNK TI NNRTI-resistance detected in RT-SHIV-infected macaques treated with single dose nevirapine SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. NCI, AIDS Vaccine Program, Frederick, MD 21701 USA. Baylor Coll Med, Houston, TX 77030 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 157 BP S172 EP S172 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100173 ER PT J AU Boyer, PL Sarafianos, SG Arnold, E Hughes, SH AF Boyer, PL Sarafianos, SG Arnold, E Hughes, SH TI AZT resistance: why do HIV-1 and HIV-2 choose different pathways? SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, Frederick Canc Res & Dev Ctr, HIV Drug Resistance Program, Frederick, MD 21702 USA. Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Chem & Biol Chem, Piscataway, NJ 08854 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S92 EP S92 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800085 ER PT J AU Boyer, PL Sarafianos, SG Arnold, E Hughes, SH AF Boyer, PL Sarafianos, SG Arnold, E Hughes, SH TI AZT resistance: why do HIV-1 and HIV-2 choose different pathways? SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. Rutgers State Univ, Dept Chem & Chem Biol, Piscataway, NJ USA. Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 082 BP S92 EP S92 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100098 ER PT J AU Chin, MPS Rhodes, TD Chen, J Fu, W Hu, WS AF Chin, MPS Rhodes, TD Chen, J Fu, W Hu, WS TI Identification of a major restriction in HIV-1 intersubtype recombination SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S164 EP S164 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800152 ER PT J AU Chin, MPS Rhodes, TD Chen, J Fu, W Hu, WS AF Chin, MPS Rhodes, TD Chen, J Fu, W Hu, WS TI Identification of a major restriction in HIV-1 intersubtype recombination SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 149 BP S164 EP S164 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100165 ER PT J AU Garcia-Lerma, J McNulty, A Jennings, C Bennett, D Fitzgibbon, J Morack, R Ussery, M Folks, TM Kalish, ML Heneine, W AF Garcia-Lerma, J McNulty, A Jennings, C Bennett, D Fitzgibbon, J Morack, R Ussery, M Folks, TM Kalish, ML Heneine, W TI Evaluation of dried blood spots for HIV-1 drug resistance testing SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 CDC, Div HIV AIDS Prevent, NCHSTP, Atlanta, GA USA. Rush Med Coll, Chicago, IL 60612 USA. NIAID, Div AIDS, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 044 BP S49 EP S49 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100060 ER PT J AU Garcia-Lerma, JG McNulty, A Jennings, C Bennett, D Fitzgibbon, J Morack, R Ussery, M Folks, TM Kalish, ML Heneine, W AF Garcia-Lerma, JG McNulty, A Jennings, C Bennett, D Fitzgibbon, J Morack, R Ussery, M Folks, TM Kalish, ML Heneine, W TI Evaluation of dried blood spots for HIV-1 drug resistance testing SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 CDC, NCHSTP, Div HIV AIDS Prevent, Atlanta, GA 30333 USA. Rush Med Coll, Chicago, IL 60612 USA. NIAID, Div Aids, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S49 EP S49 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800047 ER PT J AU Kearney, M Palmer, S Maldarelli, F Polis, M Mican, J Stephens, R Rock, D Margolick, J Mellors, J Coffin, J AF Kearney, M Palmer, S Maldarelli, F Polis, M Mican, J Stephens, R Rock, D Margolick, J Mellors, J Coffin, J TI Frequent polymorphisms at protease and RT sites associated with drug resistance are detected in treatment naive patients by single genome sequencing SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Bethesda, MD 20892 USA. NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. SAIC, Frederick, MD USA. NIAID, CCMD Clin, NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Dept Infect Dis, Pittsburgh, PA USA. Johns Hopkins Univ, Dept Mol Microbiol & Immunol, Bloomberg Sch Publ Hlth, Baltimore, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S158 EP S158 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800146 ER PT J AU Kearney, M Palmer, S Maldarelli, F Polis, M Mican, J Stephens, R Rock, D Margolick, J Mellors, J Coffin, J AF Kearney, M Palmer, S Maldarelli, F Polis, M Mican, J Stephens, R Rock, D Margolick, J Mellors, J Coffin, J TI Frequent polymorphisms at protease and RT sites associated with drug resistance are detected in treatment naive patients by single genome sequencing SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Bethesda, MD 20892 USA. NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. SAIC, Frederick, MD USA. NIAID, CCMD Clin, NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Dept Infect Dis, Pittsburgh, PA USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 143 BP S158 EP S158 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100159 ER PT J AU King, M Palmer, S Wiegand, A Maldarelli, F Brun, S Kempf, D Hanna, G Coffin, J Mellors, J AF King, M Palmer, S Wiegand, A Maldarelli, F Brun, S Kempf, D Hanna, G Coffin, J Mellors, J TI The level of persistent viraemia below 50 copies/ml is associated with subsequent rebound to above 50 HIV RNA copies/mL for nelfinavir-treated subjects but not lopinavir/ritonavir-treated subjects SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Abbott Labs, Abbott Pk, IL 60064 USA. NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S36 EP S36 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800037 ER PT J AU King, M Palmer, S Wiegand, A Maldarelli, F Brun, S Kempf, D Hanna, G Coffin, J Mellors, J AF King, M Palmer, S Wiegand, A Maldarelli, F Brun, S Kempf, D Hanna, G Coffin, J Mellors, J TI The level of persistent viraemia below 50 copies/ml is associated with subsequent rebound to above 50 HIV RNA copies/mL for nelfinavir-treated subjects but not lopinavir/ritonavir-treated subjects SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Abbott Labs, Abbott Pk, IL 60064 USA. NCI, NIH, HIV Drug Resistance Program, Frederick, MD 21701 USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 034 BP S36 EP S36 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100050 ER PT J AU Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Wegner, S Lane, C AF Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Wegner, S Lane, C TI Treatment history and adherence information significantly improves prediction of virological response by neural networks SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 HIV Resistance Response Database Initiat, RDI, London, England. BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada. US Mil HIV Res Program, Rockville, MD USA. NIAID, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 2 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S57 EP S57 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800055 ER PT J AU Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Wegner, S Lane, C AF Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Wegner, S Lane, C TI Treatment history and adherence information significantly improves prediction of virological response by neural networks SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 HIV Resistance Response Database Initiat, London, England. BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada. US Mil Acad, HIV Res Program, Rockville, MD USA. NIAID, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 2 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 052 BP S57 EP S57 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100068 ER PT J AU Maldarelli, F Kearney, M Palmer, S Mican, J Rock-Kress, D Rehm, C Mellors, J Coffin, J AF Maldarelli, F Kearney, M Palmer, S Mican, J Rock-Kress, D Rehm, C Mellors, J Coffin, J TI Change in pro-pol allele frequency in chronic HIV-1 infection is slow and position specific SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA. NIAID, Lab LIR, NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S162 EP S162 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800150 ER PT J AU Maldarelli, F Kearney, M Palmer, S Mican, J Rock-Kress, D Rehm, C Mellors, J Coffin, J AF Maldarelli, F Kearney, M Palmer, S Mican, J Rock-Kress, D Rehm, C Mellors, J Coffin, J TI Change in pro-pol allele frequency in chronic HIV-1 infection is slow and position specific SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA. NIAID, Lab LIR, NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 BP S162 EP S162 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100163 ER PT J AU McIntyre, J Martinson, N Gray, GE Hall, DB Boltz, V Palmer, S Coffin, J Mellors, J Hopley, M Kimura, T Robinson, P Mayers, DL AF McIntyre, J Martinson, N Gray, GE Hall, DB Boltz, V Palmer, S Coffin, J Mellors, J Hopley, M Kimura, T Robinson, P Mayers, DL CA Trial 1413 Investigator Team TI Single dose nevirapine combined with a short course of combivir for prevention of mother to child transmission of HIV-1 can significantly decrease the subsequent development of maternal and infant resistant virus SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Univ Witwatersrand, Perinatal HIV Res Unit, Johannesburg, South Africa. Boehringer Ingelheim Pharmaceut Inc, Ridgefield, CT 06877 USA. NCI, Drug Resistance Program, Frederick, MD USA. Univ Pittsburgh, Pittsburgh, PA USA. Boehringer Ingelheim KG, Johannesburg, South Africa. NR 0 TC 8 Z9 8 U1 2 U2 2 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 2 BP S4 EP S4 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100018 ER PT J AU McIntyre, JA Martinson, N Gray, GE Hall, DB Boltz, V Palmer, S Coffin, J Mellors, J Hopley, M Kimura, T Robinson, P Mayers, DL AF McIntyre, JA Martinson, N Gray, GE Hall, DB Boltz, V Palmer, S Coffin, J Mellors, J Hopley, M Kimura, T Robinson, P Mayers, DL CA Trial 1413 Investigator Team TI Single dose nevirapine combined with a short course of combivir for prevention of mother to child transmission of HIV-1 can significantly decrease the subsequent development of maternal and infant resistant virus SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Univ Witwatersrand, Perinatal HIV Res Unit, Johannesburg, South Africa. Boehringer Ingelheim Pharmaceut Inc, Ridgefield, CT 06877 USA. NCI, Drug Resistance Program, Frederick, MD 21701 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. Boehringer Ingelheim ZA, Johannesburg, South Africa. NR 0 TC 8 Z9 8 U1 2 U2 2 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S4 EP S4 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800005 ER PT J AU Nikolenko, GN Frankenberry, KA Palmer, S Maldarelli, F Mellors, JW Coffin, JM Pathak, VK AF Nikolenko, GN Frankenberry, KA Palmer, S Maldarelli, F Mellors, JW Coffin, JM Pathak, VK TI RNase H domains obtained from treatment-experienced patients increase resistance to AZT SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, Frederick Canc Res & Dev Ctr, HIV Drug Resistance Program, Frederick, MD 21702 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. RI Delviks-Frankenberry, Krista/M-4822-2013 NR 0 TC 3 Z9 3 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S89 EP S89 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800082 ER PT J AU Nikolenko, GN Frankenberry, KA Palmer, S Maldarelli, F Mellors, JW Coffin, JM Pathak, VK AF Nikolenko, GN Frankenberry, KA Palmer, S Maldarelli, F Mellors, JW Coffin, JM Pathak, VK TI RNase H domains obtained from treatment-experienced patients increase resistance to AZT SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. Univ Pittsburgh, Pittsburgh, PA USA. RI Delviks-Frankenberry, Krista/M-4822-2013 NR 0 TC 3 Z9 3 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 079 BP S89 EP S89 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100095 ER PT J AU Nissley, DV Julias, J Flys, T Hughes, S Mellors, J Jackson, JB Strathern, J Eshleman, SH AF Nissley, DV Julias, J Flys, T Hughes, S Mellors, J Jackson, JB Strathern, J Eshleman, SH TI A sensitive phenotypical assay uncovers low frequency NNRTI-resistant HIV-1 RT variants in subtypes A, B, C and D from clinical samples SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 SAIC Frederick, Frederick, MD USA. NCI, Frederick, MD 21701 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S149 EP S149 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800139 ER PT J AU Nissley, DV Julias, J Flys, T Hughes, S Mellors, J Jackson, JB Strathern, J Eshleman, SH AF Nissley, DV Julias, J Flys, T Hughes, S Mellors, J Jackson, JB Strathern, J Eshleman, SH TI A sensitive phenotypical assay uncovers low frequency NNRTI-resistant HIV-1 RT variants in subtypes A, B, C and D from clinical samples SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 SAIC Frederick, Frederick, MD USA. NCI, Frederick, MD 21701 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 136 BP S149 EP S149 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100152 ER PT J AU Palmer, S Boltz, V Maldarelli, F Martiuson, N McIntyre, J Gray, G Hopley, M Kimura, T Mayers, D Robinson, P Coffin, J Mellors, J AF Palmer, S Boltz, V Maldarelli, F Martiuson, N McIntyre, J Gray, G Hopley, M Kimura, T Mayers, D Robinson, P Coffin, J Mellors, J CA Investigators 1413 Trial TI Short-course combivir (CBV) single dose nevirapine reduces but does not eliminate the selection of nevirapine-resistant HIV-1: improved detection by allele-specific PCR SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA. Chris Hani Baragwanath Hosp, Perinatal HIV Res Unit, Johannesburg, South Africa. Univ Witwatersrand, Johannesburg, South Africa. Boehringer Ingelheim ZA, Johannesburg, South Africa. Boehringer Ingelheim Pharmaceut Inc, Ridgefield, CT 06877 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S5 EP S5 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800006 ER PT J AU Palmer, S Boltz, V Maldarelli, F Martinson, N McIntyre, J Gray, G Hopley, M Kimura, T Mayers, D Robinson, P Coffin, J Mellors, J AF Palmer, S Boltz, V Maldarelli, F Martinson, N McIntyre, J Gray, G Hopley, M Kimura, T Mayers, D Robinson, P Coffin, J Mellors, J CA Investigators Trial 1413 TI Short-course combivir (CBV) single dose nevirapine reduces but does not eliminate the selection of nevirapine-resistant HIV-1: improved detection by allele-specific PCR SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21701 USA. Chris Hani Baragwanath Hosp, Perinatal HIV Res Unit, Johannesburg, South Africa. Univ Witwatersrand, Johannesburg, South Africa. Boehringer Ingelheim KG, Johannesburg, South Africa. Boehringer Ingelheim KG, Ridgefield, CT USA. Univ Pittsburgh, Pittsburgh, PA USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 3 BP S5 EP S5 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100019 ER PT J AU Sluis-Cremer, N Radzio, J Camarasa, M Tachedjian, G Nissley, D AF Sluis-Cremer, N Radzio, J Camarasa, M Tachedjian, G Nissley, D TI Role of the beta 7-beta 8-loop in the 51kDa subunit of HIV-1 reverse transcriptase in protein stability and drug resistance SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Univ Pittsburgh, Sch Med, Div Infect Dis, Viral Dis Unit, Pittsburgh, PA 15260 USA. CSIC, Inst Quim Med, E-28006 Madrid, Spain. Macfarlane Burnet Inst Med Res & Publ Hlth, Melbourne, Vic, Australia. NCI, SAIC Frederick, Basic Res Program, Reverse Transcript & Mol Biol Sect, Frederick, MD 21701 USA. RI Camarasa, Maria-Jose/B-6340-2015 OI Camarasa, Maria-Jose/0000-0002-4978-6468 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S99 EP S99 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800092 ER PT J AU Sluis-Cremer, N Radzio, J Camarasa, MJ Tachedjian, G Nissley, D AF Sluis-Cremer, N Radzio, J Camarasa, MJ Tachedjian, G Nissley, D TI Role of the beta 7-beta 8-loop in the 51kDa subunit of HIV-1 reverse transcriptase in protein stability and drug resistance SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 Univ Pittsburgh, Div Infect Dis, Sch Med, Viral Dis Unit, Pittsburgh, PA USA. CSIC, Inst Quim Med, E-28006 Madrid, Spain. Macfarlane Burnet Inst Med Res & Publ Hlth, Melbourne, Vic, Australia. NCI, SAIC, Basic Res Program, Reverse Transcript & Mol Biol Sect, Frederick, MD 21701 USA. RI Camarasa, Maria-Jose/B-6340-2015 OI Camarasa, Maria-Jose/0000-0002-4978-6468 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 089 BP S99 EP S99 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100105 ER PT J AU Wegner, S Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Lane, C AF Wegner, S Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Lane, C TI Global neural network models are superior to single clinic models as general quantitative predictors of virological treatment response SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 US Mil HIV Res Program, Rockville, MD USA. RDI, London, England. BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada. NIAID, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 SU 1 BP S58 EP S58 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 972RL UT WOS:000232470800056 ER PT J AU Wegner, S Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Lane, C AF Wegner, S Larder, BA Wang, D Revell, A Harrigan, R Montaner, J Lane, C TI Global neural network models are superior to single clinic models as general quantitative predictors of virological treatment response SO ANTIVIRAL THERAPY LA English DT Meeting Abstract CT 14th International HIV Drug Resistance Workshop CY JUN 07-11, 2005 CL Quebec City, CANADA C1 US Mil Acad, HIV Res Program, Rockville, MD USA. RDI, London, England. BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada. NIAID, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INT MEDICAL PRESS LTD PI LONDON PA 2-4 IDOL LANE, LONDON EC3R 5DD, ENGLAND SN 1359-6535 J9 ANTIVIR THER JI Antivir. Ther. PY 2005 VL 10 IS 4 MA 053 BP S58 EP S58 PG 1 WC Infectious Diseases; Pharmacology & Pharmacy; Virology SC Infectious Diseases; Pharmacology & Pharmacy; Virology GA 965PQ UT WOS:000231963100069 ER PT J AU Bandettini, PA Petridou, N Bodurka, J AF Bandettini, PA Petridou, N Bodurka, J TI Direct detection of neuronal activity with MRI: Fantasy, possibility, or reality? SO APPLIED MAGNETIC RESONANCE LA English DT Article ID MAGNETIC-RESONANCE; VISUAL-STIMULATION; BRAIN ACTIVATION; FMRI; CURRENTS; FIELDS; STIMULUS; GANGLIA; CORTEX AB Hemodynamic-based functional magnetic resonance imaging (fMRI) techniques have proven to be extremely robust and sensitive methods for noninvasive detection and mapping of human brain activation. Nevertheless, limitations in temporal and spatial resolution as well as interpretation remain because hemodynamic changes accompanying brain activation are relatively sluggish and variable and therefore imprecise measures of neuronal activity. A hope among brain imagers would be to possess a technique that would allow direct mapping of brain activity with spatial resolution on the order of a cortical column and temporal resolution on the order of an action potential or at least a postsynaptic potential. Recent efforts in understanding the direct effects of neuronal activity on MRI signal have provided some degree of hope for those who want a more precise noninvasive brain activation mapping technique than fMRI as we know it now. While the manner in which electrical currents influence MRI signal is well understood, the manner in which neuronal firing spatially and temporally integrates on the spatial scale of an MRI voxel to pro duce a magnetic field shift and subsequently an NMR phase and/or magnitude change is not well understood. It is also not established that this field shift would be large or long enough in duration to be detected. The objective of this paper is to provide a perspective of the work that has been performed towards the direction of achieving direct neuronal current imaging with MRI. A specific goal is to further clarify what is understood about the theoretical and practical possibilities of neuronal current imaging. Specifically discussed are modeling efforts, phantom studies, in vitro studies, and human studies. C1 NIMH, Unit Funct Imaging Methods, Funct MRI Facil, NIH, Bethesda, MD 20892 USA. NIMH, Unit Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA. RP Bandettini, PA (reprint author), NIMH, Unit Funct Imaging Methods, Funct MRI Facil, NIH, Bldg 10,Room 1D80,10 Ctr Dr,MSC 1148, Bethesda, MD 20892 USA. EM bandettini@nih.gov NR 38 TC 49 Z9 52 U1 2 U2 4 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0937-9347 EI 1613-7507 J9 APPL MAGN RESON JI Appl. Magn. Reson. PY 2005 VL 29 IS 1 BP 65 EP 88 DI 10.1007/BF03166956 PG 24 WC Physics, Atomic, Molecular & Chemical; Spectroscopy SC Physics; Spectroscopy GA 970QB UT WOS:000232323600005 ER PT J AU McCardle, P Cooper, J Freund, L AF McCardle, P Cooper, J Freund, L TI Language and genetics: Needs and opportunities SO APPLIED PSYCHOLINGUISTICS LA English DT Article AB This paper describes the next steps for establishing detailed, useful behavioral phenotypes and for moving forward in the study of the relationships among genes. the environment. and language disorders. Key issues are recognizing the continuum of language behaviors to accurately describe disorders and the spectrum of typical development. A coordinated plan with foundational studies that address definition. measurement, design, and analytical methods is needed. Researcher capacity must be increased, and a greater focus on communication across disciplines to successfully accomplish interdisciplinary. research is required. Language is not static, even in disorders: thus, we must study change over time. It is necessary to think about behavioral phenotypes in terms of developmental trajectories. Finally, data sharing and ethical and legal issues must be addressed. C1 NICHHD, NIH, Bethesda, MD 20892 USA. RP McCardle, P (reprint author), NICHHD, NIH, 6100 Execut Blvd,Room 4B05,MSC 7510, Bethesda, MD 20892 USA. EM mccardlp@mail.nih.gov NR 1 TC 7 Z9 7 U1 1 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD JAN PY 2005 VL 26 IS 1 BP 129 EP 135 DI 10.1017/S0142716405050101 PG 7 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 892ED UT WOS:000226631800010 ER PT J AU Hunt, CE AF Hunt, CE TI Gene-environment interactions: implications for sudden unexpected deaths in infancy SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review ID SEROTONIN TRANSPORTER GENE; BRAIN-STEM; SLEEP; ASSOCIATION; EXPRESSION; DISORDERS; VICTIMS; PROJECT; EVENTS; MODELS AB From the perspective of systems biology, genes and proteins interact to produce complex networks, which in turn interact with the environment to influence every aspect of our biological lives. Recent advances in molecular genetics and the identification of gene polymorphisms in victims of sudden infant death syndrome ( SIDS) are helping us better to understand that SIDS, like all other human conditions in health and disease, represents the confluence of specific environmental risk factors interacting in complex ways with specific polymorphisms to yield phenotypes susceptible to sudden and unexpected death in infancy. Failure to consider both genetic and environmental risk factors will impede research progress. C1 NHLBI, Natl Ctr Sleep Disorders Res, NIH, Bethesda, MD 20892 USA. RP Hunt, CE (reprint author), NHLBI, Natl Ctr Sleep Disorders Res, NIH, 1 Rockledge Ctr,Room 6022,6705 Rockledge Dr,7993, Bethesda, MD 20892 USA. EM huntc@nhlbi.nih.gov NR 39 TC 35 Z9 38 U1 0 U2 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD JAN PY 2005 VL 90 IS 1 BP 48 EP 53 DI 10.1136/adc.2004.051458 PG 6 WC Pediatrics SC Pediatrics GA 881KH UT WOS:000225865900013 PM 15613511 ER PT J AU Weissman, MM Wickramaratne, P Nomura, Y Warner, V Verdeli, H Pilowsky, DJ Grillon, C Bruder, G AF Weissman, MM Wickramaratne, P Nomura, Y Warner, V Verdeli, H Pilowsky, DJ Grillon, C Bruder, G TI Families at high and low risk for depression - A 3-generation study SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PROSPECTIVE-LONGITUDINAL COMMUNITY; GLOBAL ASSESSMENT SCALE; MAJOR DEPRESSION; PARENTAL DEPRESSION; AFFECTIVE-DISORDERS; ANXIETY DISORDERS; PSYCHIATRIC-DIAGNOSIS; EARLY-ADULTHOOD; CHILDREN; PSYCHOPATHOLOGY AB Background: The familial nature of early-onset major depressive disorder (MDD) has been documented in numerous family studies of adults and is supported by studies of offspring of parents with MDD, for whom the risk is more than 3-fold. None of the published high-risk studies have gone beyond 2 generations, and few have a longitudinal design. We report results of an approximately 20-year follow-up of families at high and low risk for depression. The first 2 generations were interviewed 4 times during this period. The offspring from the second generation are now adults and have children of their own, the third generation of the original cohort. Objective: To examine the familial aggregation of psychiatric disorders and functioning in grandchildren by their parents' and grandparents' depression status. Design: Longitudinal, retrospective cohort, family study. Participants: One hundred sixty-one grandchildren and their parents and grandparents. Main Outcome Measures: Lifetime rate of psychiatric disorder and functioning in grandchildren, stratified by parental and by grandparental depression Status, collected by clinicians blind to diagnoses of previous generations and to previous interviews. Results: There were high rates of psychiatric disorders, particularly anxiety disorders, in the grandchildren with 2 generations of major depression, with 59.2% of these grandchildren (mean age, 12 years) already having a psychiatric disorder. The effect of parental depression on grandchildren's outcomes differed significantly with grandparental depression status. Among families with a depressed grandparent, increased risk of anxiety (relative risk, 5.17; 95% confidence interval, 1.4-18.7; P=.01) and increased risk of any disorder (relative risk, 5.52; 95% confidence interval, 2.0-15.4; P=.002) were observed in grandchildren with a depressed parent as compared with those with nondepressed parents. The severity of parental depression, as measured by impairment, significantly increased the rate of a mood disorder in these grandchildren (relative risk, 2.44; 95% confidence interval, 1.1-5.5; P=.03). In contrast, among grandchildren with non-familial depression, ie, depressed parents with no depressed grandparents, there was no significant effect of parental MDD on grandchildren diagnoses. However, parental MDD, regardless of whether families had a depressed grandparent, had a significant impact on the grandchildren's overall functioning. Potential confounding variables did not affect the strength of the association with parental and grandparental depression. Conclusions: The association between parental MDD and child diagnosis is moderated by grandparental MDD status. The rates of psychopathology are highest in grandchildren of parents and grandparents with a moderately to severely impairing depression. Anxiety disorders are the early sign of psychopathology in the young grandchildren. Early interventions in the offspring of 2 generations affected with moderately to severely impairing MDD seem warranted. This familial group may be the target for neuroimaging, genetic, and other biological studies. C1 Columbia Univ, Dept Psychiat, U24, New York State Psychiat Inst, New York, NY 10032 USA. Columbia Univ, Dept Psychiat, Coll Phys & Surg, New York, NY 10032 USA. Columbia Univ, Mailman Sch Publ Hlth, New York, NY 10027 USA. Natl Inst Mental Hlth, Bethesda, MD USA. RP Weissman, MM (reprint author), Columbia Univ, Dept Psychiat, U24, New York State Psychiat Inst, 1051 Riverside Dr, New York, NY 10032 USA. EM mmw3@columbia.edu OI Weissman, Myrna/0000-0003-3490-3075 FU NIMH NIH HHS [R01 MH036197] NR 54 TC 231 Z9 233 U1 9 U2 35 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 2005 VL 62 IS 1 BP 29 EP 36 DI 10.1001/archpsyc.62.1.29 PG 8 WC Psychiatry SC Psychiatry GA 886TA UT WOS:000226250300004 PM 15630070 ER PT J AU Radel, M Vallejo, RL Iwata, N Aragon, R Long, JC Virkkunen, M Goldman, D AF Radel, M Vallejo, RL Iwata, N Aragon, R Long, JC Virkkunen, M Goldman, D TI Haplotype-based localization of an alcohol dependence gene to the 5q34 gamma-aminobutyric acid type a gene cluster SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CROSS-FOSTERING ANALYSIS; QUANTITATIVE TRAIT LOCI; GABA(A) RECEPTOR; LINKAGE DISEQUILIBRIUM; ASSOCIATION ANALYSIS; PSYCHIATRIC-DISORDERS; SUBUNIT VARIANT; COMPLEX TRAITS; RAT-BRAIN; ETHANOL AB Context: Pharmacobehavioral and pharmacogenetic evidence links gamma-aminobutyric acid type A (GABA(A)) receptors and chromosomal regions containing GABA(A) receptor genes to ethanol-related responses. The GABA(A) gene cluster on chromosome 5q34 is of particular interest in the genetics of alcohol dependence because of the gamma2 subunit requirement for ethanol's modulatory action on GABA(A) receptors, previous linkage findings in mice and humans implicating both GABRA6 and GABRG2, and reported associations of GABRA6, GABRB2, and GABRG2 alleles with alcohol dependence. Objective: To determine whether variation at the 5q34 GABAA gene cluster is implicated in differential susceptibility to alcohol dependence. Methods: Two large psychiatrically interviewed samples, a Southwestern Native American population sample (N = 433) and a Finnish sample (N = 511) with alcohol-dependent subjects and unaffected individuals, were geno-typed for 6 single nucleotide polymorphisms at the 5q34 GABA(A) gene cluster. In addition to sib-pair linkage and case-control association analyses, linkage disequilibrium mapping with haplotypes was used. Results: Sib-pair linkage of GABRG2 to alcohol dependence was observed in Finns (P=.008). Association of the GABRB2 1412T allele with alcohol dependence was detected in both populations (Finns, P=.01; Southwestern Native Americans, P=.008), and the GABRA6 1519T allele was associated in both Finns (P=.01) and Southwestern Native Americans (P=.03). Linkage disequilibrium mapping with 3-locus haplotypes yielded evidence for an alcohol-dependence locus at the GABA(A) gene cluster region in both populations. The most highly significant signals were at 3-locus haplotypes that included 1 or more GABRA6 polymorphisms, with the peak signal at a GABRA6 3-locus haplotype (Finns, empirical P=.004; Southwestern Native Americans, empirical P=.02). Conclusions: We detected sib-pair linkage of 5q34 GABAA receptor genes to alcohol dependence in Finns and found association both in Finns and in Southwestern Native Americans. In both populations, the haplotype localization implicates the region containing the Pro385Ser GABRA6 polymorphism and 2 other polymorphisms at GABRA6. C1 Natl Inst Alcohol Abuse & Alcoholism, Lab Neurogenet, NIH, Rockville, MD USA. Fujita Hlth Univ, Dept Psychiat, Toyoake, Aichi 47011, Japan. Univ Helsinki, Dept Psychiat, Helsinki, Finland. RP Radel, M (reprint author), Bioconsult, 17702 Calabar Dr, Gaithersburg, MD 20877 USA. EM martaradel@verizon.net RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 72 TC 50 Z9 52 U1 3 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 2005 VL 62 IS 1 BP 47 EP 55 DI 10.1001/archpsyc.62.1.47 PG 9 WC Psychiatry SC Psychiatry GA 886TA UT WOS:000226250300006 PM 15630072 ER PT J AU Pine, DS Klein, RG Roberson-Nay, R Mannuzza, S Moulton, JL Woldehawariat, G Guardino, M AF Pine, DS Klein, RG Roberson-Nay, R Mannuzza, S Moulton, JL Woldehawariat, G Guardino, M TI Response to 5% carbon dioxide in children and adolescents - Relationship to panic disorder in parents and anxiety disorders in subjects SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PREMENSTRUAL DYSPHORIC DISORDER; TEST-RETEST RELIABILITY; 35-PERCENT CO2; RESPIRATORY PSYCHOPHYSIOLOGY; VENTILATORY PHYSIOLOGY; MAJOR DEPRESSION; INHALATION; RISK; SENSITIVITY; HYPERSENSITIVITY AB Background: Carbon dioxide (CO2) sensitivity is postulated to be a familial risk marker of panic disorder (PD). Exaggerated responses to CO2 inhalation have been reported in adults with PD and their unaffected adult relatives, as well as in clinic-referred children with anxiety disorders. Objective: To test in a family-based design whether CO2 hypersensitivity is a familial risk marker for PD and associated with current anxiety disorders in children and adolescents. Setting and Participants: One hundred forty-two offspring (aged 9-19 years) of parents with PD, major depressive disorder, or no disorder. Forty-five (32%) had a current anxiety disorder, excluding specific phobia. Design and Main Outcome Measures: Parents and offspring received diagnostic assessments. Offspring underwent 5% CO2 inhalation at home. Panic symptoms and panic attacks were rated with the Acute Panic Inventory at baseline, while anticipating CO2 delivery ("threat"), and during CO2 inhalation. Respiratory rate and volume were measured with spirometry. Results: No group differences were found in Acute Panic Inventory ratings at baseline or in respiratory measures during threat. Risk for PD was not associated with CO2 sensitivity (panic symptoms and respiratory physiologic response). During CO2 inhalation, offspring with anxiety disorders, relative to offspring without anxiety disorders, experienced significantly more panic symptoms and panic attacks, as well as elevated respiratory rates. During threat, panic symptoms were significantly and independently associated with both parental PD and offspring anxiety disorders. Conclusions: No support was obtained for CO2 hypersensitivity as a familial risk marker for PD in children and adolescents. Links between childhood anxiety disorders and CO2 sensitivity were replicated. Familial risk for PD in children and adolescents may be associated with vulnerability to anticipatory anxiety. C1 Natl Inst Mental Hlth, Intramural Res Program, Sect Dev & Affect Neurosci, Bethesda, MD 20817 USA. NYU, Child Study Ctr, Sch Med, New York, NY USA. Nathan S Kline Inst Psychiat Res, Orangeburg, NY USA. Freedom From Fear, Staten Isl, NY USA. RP Pine, DS (reprint author), Natl Inst Mental Hlth, Intramural Res Program, Sect Dev & Affect Neurosci, Bldg 15-K,Room 110,MSC-2670, Bethesda, MD 20817 USA. EM daniel.pine@nih.gov FU NIMH NIH HHS [R01 MH-59171] NR 36 TC 40 Z9 42 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 2005 VL 62 IS 1 BP 73 EP 80 DI 10.1001/archpsyc.62.1.73 PG 8 WC Psychiatry SC Psychiatry GA 886TA UT WOS:000226250300009 PM 15630075 ER PT J AU Stewart, R Masaki, K Xue, QL Peila, R Petrovitch, H White, LR Launer, LJ AF Stewart, R Masaki, K Xue, QL Peila, R Petrovitch, H White, LR Launer, LJ TI A 32-year prospective study of change in body weight and incident dementia - The Honolulu-Asia aging study SO ARCHIVES OF NEUROLOGY LA English DT Article ID JAPANESE-AMERICAN MEN; ALZHEIMERS-DISEASE; HUMAN HYPOTHALAMUS; MASS INDEX; FOLLOW-UP; MORTALITY; POPULATION; RISK; AGE; APOE-EPSILON-4 AB Background: The course of weight loss associated with dementia is unclear, particularly prior to and around the onset of,the clinical syndrome. Objective: To compare the natural history of weight change from mid to late life in men with and without dementia in late life. Design and Setting: The Honolulu-Asia Aging Study, a 32-year, prospective, population-based study of Japanese American men who had been weighed on 6 occasions between 1965 and 1999 and who had been screened for dementia 3 times between 1991 and 1999. Participants: Of 1890 men (aged 77-98 years), 112 with incident dementia were compared with 1778 without dementia at the sixth examination (1997-1999). Main Outcome Measure: Weight change up to and including the sixth examination was treated as the dependent variable and estimated using a repeated measures analysis. Results: Groups with and without dementia did not differ with respect to baseline weight or change in weight from mid to late life (first 26 years' follow-up). In the late-life examinations (final 6 years), mean age- and education-adjusted weight loss was -0.22 kg/y (95% confidence intervals, -0.26 to -0.18) in participants without dementia. Men with incident dementia at the same examination had an additional yearly weight loss of -0.36 kg (95% confidence interval. -0.53 to -0.19). This was not changed substantially with adjustment for risk factors for vascular disease or functional impairment and was significant for both Alzheimer disease and vascular dementia subtypes. Conclusions: Dementia-associated weight loss begins before the onset of the clinical syndrome and accelerates by the time of diagnosis. The potential impact on prognosis should be considered in the case of elderly persons at risk for dementia. C1 NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA. Inst Psychiat, London, England. Hlth Res Inst, Honolulu, HI USA. Johns Hopkins Ctr Aging & Hlth, Baltimore, MD USA. RP Launer, LJ (reprint author), NIA, Lab Epidemiol Demog & Biometry, NIH, 7201 Wisconsin Ave,3C-309, Bethesda, MD 20892 USA. EM launerl@nia.nih.gov OI Stewart, Robert/0000-0002-4435-6397 FU NHLBI NIH HHS [N01 HC 05102]; NIA NIH HHS [N01 AG 42149] NR 36 TC 241 Z9 243 U1 1 U2 8 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 2005 VL 62 IS 1 BP 55 EP 60 DI 10.1001/archneur.62.1.55 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 887FD UT WOS:000226290100006 PM 15642850 ER PT J AU Buervenich, S Carmine, A Galter, D Shahabi, HN Johnels, B Holmberg, B Ahlberg, J Nissbrandt, H Eerola, J Hellstrom, O Tienari, P Matsuura, T Ashizawa, T Wullner, U Klockgether, T Zimprich, A Gasser, T Hanson, M Waseem, S Singleton, A McMahon, FJ Anvret, M Sydow, O Olson, L AF Buervenich, S Carmine, A Galter, D Shahabi, HN Johnels, B Holmberg, B Ahlberg, J Nissbrandt, H Eerola, J Hellstrom, O Tienari, P Matsuura, T Ashizawa, T Wullner, U Klockgether, T Zimprich, A Gasser, T Hanson, M Waseem, S Singleton, A McMahon, FJ Anvret, M Sydow, O Olson, L TI A rare truncating mutation in ADH1C (G 78Stop) shows significant association with Parkinson disease in a large international sample SO ARCHIVES OF NEUROLOGY LA English DT Article ID ALCOHOL-DEHYDROGENASE; VITAMIN-A; LOCALIZATION; BRAIN; MOUSE; RISK AB Background: Alcohol dehydrogenases (ADHs) may be involved in the pathogenesis of neurodegenerative disorders because of their multiple roles in detoxification pathways and retinoic acid synthesis. In a previous study, significant association of an ADH class IV allele with Parkinson disease (PD) was found in a Swedish sample. Patients: The previously associated single-nucleotide polymorphism plus 12 further polymorphisms in the ADH cluster on human chromosome 4q23 were screened for association in an extension of the original sample that now included 123 Swedish PD patients and 127 geographically matched control subjects. A rare nonsense single-nucleotide polymorphism in ADH1C (G78stop, rs283413) was identified in 3 of these patients but in no controls. To obtain sufficient power to detect a possible association of this rare variant with disease, we screened a large international sample of 1076 PD patients of European ancestry and 940 matched controls. Results: The previously identified association with an ADH class IV allele remained significant (P<.02) in the extended Swedish study. Furthermore, in the international collaboration, the G78stop mutation in ADH1C was found in 22 (2.0%) of the PD patients but only in 6 controls (0.6%). This association was statistically significant (x(1)(2) = 7.5; 2-sided P=.007; odds ratio, 3.25 [95% confidence interval, 1.31-8.05]). In addition, the G78stop mutation was identified in 4 (10.0%) of 40 Caucasian index cases with PD with mainly hereditary forms of the disorder. Conclusion: Findings presented herein provide further evidence for mutations in genes encoding ADHs as genetic risk factors for PD. C1 NIMH, Mood & Anxiety Disorders Program, Genet Unit, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Karolinska Inst, Dept Neurosci, Stockholm, Sweden. Karolinska Inst, Dept Mol Med, Clin Neurogenet Unit, Stockholm, Sweden. Karolinska Inst, Dept Clin Neurosci, Neurol Sect, Stockholm, Sweden. Univ Gothenburg, Dept Pharmacol, Gothenburg, Sweden. Univ Gothenburg, Dept Clin Neurosci, Gothenburg, Sweden. Univ Helsinki, Dept Neurol, Helsinki, Finland. Seinajoki Cent Hosp, Seinajoki, Finland. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Univ Texas, Med Branch, Dept Neurol, Galveston, TX 77550 USA. Univ Bonn, Dept Neurol, D-5300 Bonn, Germany. Univ Tubingen, Dept Neurodegenerat Dis, Hertie Inst Clin Brain Res, Tubingen, Germany. NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. NIA, Mol Genet Sect, NIH, Bethesda, MD 20892 USA. Astra Zeneca R&D Sodertalje, Sodertalje, Sweden. RP Buervenich, S (reprint author), NIMH, Mood & Anxiety Disorders Program, Genet Unit, NIH,Dept Hlth & Human Serv, 35 Convent Dr,Room 1A-209, Bethesda, MD 20892 USA. EM buervens@intra.nimh.nih.gov RI Galter, Dagmar/C-4826-2011; Singleton, Andrew/C-3010-2009; Tienari, Pentti/A-4893-2012; Zimprich, Alexander/A-5232-2017; OI Galter, Dagmar/0000-0001-6485-6244; Zimprich, Alexander/0000-0002-1668-5177; McMahon, Francis/0000-0002-9469-305X FU NINDS NIH HHS [R01 NS 041547] NR 21 TC 23 Z9 24 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 2005 VL 62 IS 1 BP 74 EP 78 DI 10.1001/archneur.62.1.74 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 887FD UT WOS:000226290100008 PM 15642852 ER PT J AU Wu, RM Bounds, R Lincoln, S Hulihan, M Lin, CH Hwu, WL Chen, J Gwinn-Hardy, K Farrer, M AF Wu, RM Bounds, R Lincoln, S Hulihan, M Lin, CH Hwu, WL Chen, J Gwinn-Hardy, K Farrer, M TI Parkin mutations and early-onset parkinsonism in a Taiwanese cohort SO ARCHIVES OF NEUROLOGY LA English DT Article ID GENE-MUTATIONS; DISEASE; ASSOCIATION; MORTALITY; CHINESE; PROTEIN AB Background: Loss of function of the parkin gene (PRKN) is the predominant genetic cause of juvenile and early-onset parkinsonism in Japan, Europe, and the United States. Objectives: To evaluate the frequency of PRKN mutations in Taiwanese (ethnic Chinese) patients with early-onset parkinsonism and to explore genotype-phenotype correlations. Design: Clinical assessment included medical, neurologic, and psychiatric evaluation. Genomic DNA sequencing and quantitative polymerase chain reaction were expression was formed to identify PRKN mutations. Gene ex examined in patient lymphoblastoid cell lines, in which PRKN mutations were identified. Patients: Forty-one Taiwanese patients with earlyonset parkinsonism (aged <50 years at onset). Results: Four of 41 probands had PRKN mutations. One proband had compound heterozygous mutations, with a PRKN exon 2 deletion and an exon 7 G284R substitution. The phenotype resembled typical Parkinson disease. Three patients were mutation carriers. One proband had PRKN exon 2 and exon 3 deletions in the same allele. However, this patient's phenotype was that of classic "parkin-proven" autosomal recessive juvenile parkinsonism, characterized by symmetrical foot dystonia at onset, gait disturbance, diurnal change, and very slow progression. The 2 remaining carriers had novel heterozygous exon 11 R396G substitutions. Patients with PRKN mutations were younger at onset than those without mutations, and they required a lower dose of levodopa despite longer disease duration. Conclusions: Mutations in PRKN are a rare cause of early-onset parkinsonism in Taiwanese individuals. The overall mutation frequency, adjusted for age at onset, was comparable with that reported for white cohorts; however, the point mutations identified seem to be population specific. C1 Natl Taiwan Univ Hosp, Dept Neurol, Taipei 100, Taiwan. Natl Taiwan Univ Hosp, Dept Pediat, Taipei 100, Taiwan. Natl Taiwan Univ Hosp, Dept Med Genet, Taipei 100, Taiwan. Natl Taiwan Univ, Coll Med, Taipei 100, Taiwan. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA. NINDS, Div Neurogenrt, Bethesda, MD 20892 USA. Mayo Clin, Neurogenet Lab, Dept Neurosci, Jacksonville, FL 32224 USA. RP Wu, RM (reprint author), Natl Taiwan Univ Hosp, Dept Neurol, 7,Chung Shan S Rd, Taipei 100, Taiwan. EM rmwu@ha.mc.ntu.edu.tw RI Gwinn, Katrina/C-2508-2009; OI HWU, WUH-LIANG/0000-0001-6690-4879; Lin, Chin-Hsien/0000-0001-8566-7573; Wu, Ruey-Meei/0000-0002-4947-5467 NR 27 TC 38 Z9 39 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 2005 VL 62 IS 1 BP 82 EP 87 DI 10.1001/archneur.62.1.82 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 887FD UT WOS:000226290100009 PM 15642853 ER PT J AU Silvestri, JM Lister, G Corwin, M Smok-Pearsall, SM Baird, TM Crowell, DH Cantey-Kiser, J Hunt, CE Tinsley, L Palmer, PH Mendenhall, RS Hoppenbrouwers, TT Neuman, MR Weese-Mayer, DE Willinger, M AF Silvestri, JM Lister, G Corwin, M Smok-Pearsall, SM Baird, TM Crowell, DH Cantey-Kiser, J Hunt, CE Tinsley, L Palmer, PH Mendenhall, RS Hoppenbrouwers, TT Neuman, MR Weese-Mayer, DE Willinger, M CA Study Grp TI Factors that influence use of a home cardiorespiratory monitor for infants - The collaborative home infant monitoring evaluation SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID DEATH-SYNDROME; APNEA; EVENTS; ALARMS; RISK AB Background: As part of the Collaborative Home Infant Monitoring Evaluation, a home monitor was developed to record breathing, heart rate, other physiologic variables, and the time the monitor was used. Objective: To determine the frequency of monitor use, factors that influence use, and validity of a model developed to predict use. Design: We developed a model to predict monitor use using multiple linear regression analysis; we then tested the validity of this model to predict adherence for the first week of monitoring and for the subsequent 4-week period (weeks 2-5). Setting: Clinical research centers in Chicago, Ill; Cleveland, Ohio; Honolulu, Hawaii; Los Angeles, Calif; and Toledo, Ohio. Patients: Preterm infants, infants younger than 1 month with a history of autopsy-confirmed sudden infant death syndrome in a sibling, and infants with an idiopathic apparent life-threatening event were divided into 2 cohorts based on enrollment date. Main Outcome Measure: Mean hours of monitor use per week. Results: In cohort 1, the variables available before monitoring were only weakly associated with total hours of monitor use in weeks 2 to 5 (total model r(2) = 0.08). However, when hours of monitor use in week 1 were included as a variable to predict monitor use in weeks 2 to 5, the r(2) increased to 0.64 for hours of monitor use per week. Conclusions: Our data show that monitor use in the first week was the most important variable for predicting subsequent monitor use. The study suggests that a major focus of home monitoring should be adherence in the first week, although it remains to be tested whether this adherence can be altered. C1 Univ Texas, SW Med Sch, Dept Pediat, Dallas, TX 75390 USA. Rush Univ, Rush Childrens Hosp, Rush Med Coll, Dept Pediat, Chicago, IL 60612 USA. Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Epidemiol & Biostat, Boston, MA 02118 USA. Case Western Reserve Univ, Sch Med, MetroHlth Med Ctr, Dept Pediat, Cleveland, OH USA. Case Western Reserve Univ, Sch Med, MetroHlth Med Ctr, Dept Obstet & Gynecol, Cleveland, OH USA. Univ Hawaii Manoa, John A Burns Sch Med, Kapiolani Med Ctr Women & Children, Dept Pediat, Honolulu, HI 96822 USA. Med Coll Ohio, Dept Pediat, Toledo, OH 43699 USA. Univ So Calif, Sch Med, Dept Pediat & Neonatol, Los Angeles, CA USA. Los Angeles Cty & Univ So Calif Med Ctr, Womens & Childrens Hosp, Los Angeles, CA 90033 USA. NICHHD, Pregnancy & Perinatol Branch, Ctr Res Mothers & Children, NIH, Bethesda, MD 20892 USA. Boston Univ, Sch Publ Hlth, Dept Pediat, Boston, MA USA. Boston Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Boston, MA USA. RP Lister, G (reprint author), Univ Texas, SW Med Sch, Dept Pediat, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM george.lister@utsouthwestern.edu FU NICHD NIH HHS [HD 28971, HD 29056, HD 29060, HD 29067, HD 29071, HD 29073, HD 34625] NR 14 TC 3 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD JAN PY 2005 VL 159 IS 1 BP 18 EP 24 DI 10.1001/archpedi.159.1.18 PG 7 WC Pediatrics SC Pediatrics GA 885IE UT WOS:000226149500003 PM 15630053 ER PT J AU Moore, RA Vorberg, I Priola, SA AF Moore, RA Vorberg, I Priola, SA TI Species barriers in prion diseases - brief review SO ARCHIVES OF VIROLOGY LA English DT Article ID CREUTZFELDT-JAKOB-DISEASE; SPONGIFORM ENCEPHALOPATHY BSE; CHRONIC WASTING DISEASE; TRANSMISSIBLE MINK ENCEPHALOPATHY; PROTEASE-RESISTANT FORMS; SCRAPIE INCUBATION-TIME; TRANSGENIC MICE; AMINO-ACID; NEUROBLASTOMA-CELLS; NMR STRUCTURE AB Transmissible spongiform encephalopathies (TSEs or prion diseases) are neurological disorders associated with the aggregation of a pathologic isoform of a host-encoded protein, termed prion protein (PrP). The pathologic isoform of PrP, termed PrPSc, is a major constituent of the infectious agent. TSE diseases are characterized by neurodegenerative failure and inevitable morbidity. Bovine spongiform encephalopathy (BSE) has been transmitted from cattle to humans to cause a new variant of Creutzfeldt-Jakob syndrome. The potential for chronic wasting disease to similarly cross the species barrier from cervids to humans is considered unlikely but possible. Thus, understanding how TSE agents overcome resistance to transmission between species is crucial if we are to prevent future epidemics. The species barrier usually can be abrogated to varying degrees in laboratory animals. Studies done with transgenic animals, tissue culture, and cell-free assays established PrP as being necessary for TSE pathogenesis and illustrated that certain amino acid residues are more influential than others for conferring resistance to TSE agent transmission. The essence of what constitutes a TSE agent's species compatibility is thought to be orchestrated by a complex interplay of contributions from its primary amino acid sequence, its glycoform patterns, and its three-dimensional structure. C1 NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. Tech Univ Munich, Inst Virol, D-8000 Munich, Germany. RP Moore, RA (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, 903 S 4th Str, Hamilton, MT 59840 USA. EM spriola@niaid.nih.gov NR 83 TC 43 Z9 43 U1 0 U2 12 PU SPRINGER WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 2005 SU 19 BP 187 EP 202 PG 16 WC Virology SC Virology GA 984RI UT WOS:000233321600016 PM 16355873 ER PT B AU Pearson, G Gill, M AF Pearson, G Gill, M GP SOC IMAGING SCI & TECHNOL TI An evaluation of motion JPEG 2000 for video archiving SO Archiving 2005, Final Program and Proceedings LA English DT Proceedings Paper CT 2nd IS&T Archiving Conference CY APR 26-29, 2005 CL Washington, DC SP IS&T, Amer Inst Conservat, Assoc Lib Collect & Tech Serv, Coalit Networked Informat, Digital Lib Federat, Digital Preservat Coalit, ECPA, Inter Soc Color Council, Museum Comp Network, Online Comp Lib Ctr, Res Lib Grp, SPIE AB Motion JPEG 2000 (MJ2) is one potential format for long-term video preservation. The format is attractive as an open standard with a truly lossless compression mode. Currently, three software-only MJ2 implementations are readily available, from the Open JPEG 2000 project, from the Kakadu project, and (incorporating Kakadu) from vendor Morgan Multimedia. These are given a snapshot evaluation here. Among the findings: on a modem desktop machine, the Kakadu-based implementations can decode and deliver quarter-screen or smaller lossless-MJ2-encoded videos without frame drops. The newer Open JPEG 2000, while improving, is not yet competitive. All the implementations have practical limitations on acceptable input formats, and inadequate or missing audio support. At higher image resolutions, playback without frame drops or reversion to lossy mode currently suggests hardware-based implementations. A practical impediment is limited availability of off-the-shelf board-level products. Competing candidate file formats for video-editing, archiving, and delivery currently offer better-defined storage of metadata. Some formats, such as MPEG4/AVC, achieve better compression at the expense of some lossiness. C1 Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, NIH, HHS, Bethesda, MD USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU SOC IMAGING SCIENCE & TECHNOLOGY PI SPRINGFIELD PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 USA BN 0-89208-255-0 PY 2005 BP 237 EP 243 PG 7 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA BCZ85 UT WOS:000232157800050 ER PT B AU Walker, FL Thoma, GR AF Walker, FL Thoma, GR GP SOC IMAGING SCI & TECHNOL TI Image preservation through PDF/A SO Archiving 2005, Final Program and Proceedings LA English DT Proceedings Paper CT 2nd IS&T Archiving Conference CY APR 26-29, 2005 CL Washington, DC SP IS&T, Amer Inst Conservat, Assoc Lib Collect & Tech Serv, Coalit Networked Informat, Digital Lib Federat, Digital Preservat Coalit, ECPA, Inter Soc Color Council, Museum Comp Network, Online Comp Lib Ctr, Res Lib Grp, SPIE AB The preservation of image collections is a goal of many libraries and organizations. Among the considerations for long-term preservation is the choice of file format. An emerging file format for preservation is PDF/A, which is a proposed international standard for long-term electronic document preservation. Since this file format can be used for image preservation, there are a number of considerations to be followed for converting image files to PDF/A, and also for ultimately migrating from PDF/A to successor file formats. As a result of research and development in electronic document delivery and file conversion, an Internet-based file migration system called MyMorph has been created at the National Library of Medicine. MyMorph was developed as a file migration service that allows the bulk conversion of electronic documents to PDF in a manner that minimizes certain aspects of the migration cost. The user interface permits file migration to proceed in batch mode, requiring minimal user interaction regardless of the number of files converted. After more than two years of use, the system is being modified to facilitate the creation of PDF/A files from source files consisting of scanned images. This paper details the design decisions for extending MyMorph to create image-based PDF/A files. C1 Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU SOC IMAGING SCIENCE & TECHNOLOGY PI SPRINGFIELD PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 USA BN 0-89208-255-0 PY 2005 BP 259 EP 263 PG 5 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA BCZ85 UT WOS:000232157800054 ER PT J AU Iribarren, C Gross, MD Darbinian, JA Jacobs, DR Sidney, S Loria, CM AF Iribarren, C Gross, MD Darbinian, JA Jacobs, DR Sidney, S Loria, CM TI Association of lipoprotein-associated phospholipase A(2) mass and activity with calcified coronary plaque in young adults - The CARDIA study SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE phospholipases; coronary calcification; young adults; atherosclerosis; risk factors ID PLATELET-ACTIVATING-FACTOR; C-REACTIVE PROTEIN; FACTOR ACETYLHYDROLASE ACTIVITY; AMERICAN-HEART-ASSOCIATION; LOW-DENSITY-LIPOPROTEIN; ARTERY-DISEASE; COMPUTED-TOMOGRAPHY; RISK-FACTORS; CALCIUM; PLASMA AB Objective - To examine the association of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) mass and activity with calcified coronary plaque in young adults. Methods and Results - Nested case-control study among CARDIA participants at the year 15 examination (2000 to 2001, 33 to 45 years old). Cases (n=266) were those with and controls (n=266) those without evidence of calcified coronary plaque by computed tomography matched 1:1 on sex and race. Lp-PLA(2) mass and activity were significantly higher in cases (296+/-101 ng/mL and 36.4+/-12.3 nmol/mL per minute) than in controls (267+/-80 ng/mL and 32.9+/-11.8 nmol/mL per minute). In age-adjusted conditional logistic regression, the odds ratio (OR) of calcified coronary plaque per 1 standard deviation (SD) increment was 1.40 (95% CI, 1.17 to 1.67) and 1.39 (95% CI, 1.14 to 1.70) for Lp-PLA(2) mass and activity, respectively. After adjusting for multiple covariates including low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, and C-reactive protein, a statistically significant association remained for Lp-PLA(2) mass (OR, 1.28; 95% CI, 1.03 to 1.60) but not for activity (OR, 1.09; 95% CI, 0.84 to 1.42). No evidence was found for interaction between Lp-PLA(2) mass or activity with LDL-C as predictors of calcified coronary plaque. Conclusion - An independent association of Lp-PLA(2) mass with calcified coronary plaque existed in young adults. Therefore, Lp-PLA(2) mass may be a useful marker of subclinical cardiovascular risk. C1 Kaiser Permanente, Div Res, Oakland, CA 94612 USA. Univ Minnesota, Sch Med, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Univ Oslo, Inst Nutr Res, Oslo, Norway. NHLBI, NIH, Div Epidemiol & Clin Applicat, Epidemiol & Biometry Program, Bethesda, MD 20892 USA. RP Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA. EM cgi@dor.kaiser.org FU NHLBI NIH HHS [1R01-HL53560-01A1, N01-HC-48050, N01-HC-48048, N01-HC-48047, N01-HC-48049] NR 44 TC 78 Z9 85 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 1079-5642 EI 1524-4636 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD JAN PY 2005 VL 25 IS 1 BP 216 EP 221 DI 10.1161/01.ATV.0000148322.89911.44 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 884DX UT WOS:000226065900036 PM 15499045 ER PT J AU Sneller, MC AF Sneller, MC TI Rituximab and Wegener's granulomatosis: Are B cells a target in vasculitis treatment? SO ARTHRITIS AND RHEUMATISM LA English DT Editorial Material ID ANCA-ASSOCIATED VASCULITIS; LIVED PLASMA-CELLS; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; THERAPY; AUTOANTIBODIES; DEPLETION; METHYLPREDNISOLONE; CORTICOSTEROIDS; AUTOIMMUNITY C1 NIAID, NIH, Bethesda, MD 20892 USA. RP Sneller, MC (reprint author), NIAID, NIH, Bldg 10,Room 11B-13, Bethesda, MD 20892 USA. EM MSNELLER@niaid.nih.gov NR 34 TC 37 Z9 40 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JAN PY 2005 VL 52 IS 1 BP 1 EP 5 DI 10.1002/art.20717 PG 5 WC Rheumatology SC Rheumatology GA 890JO UT WOS:000226507700001 PM 15641069 ER PT J AU Brenner, M Meng, HC Yarlett, NC Griffiths, MM Remmers, EF Wilder, RL Gulko, NS AF Brenner, M Meng, HC Yarlett, NC Griffiths, MM Remmers, EF Wilder, RL Gulko, NS TI The non-major histocompatibility complex quantitative trait locus Cia10 contains a major arthritis gene and regulates disease severity, pannus formation, and joint damage SO ARTHRITIS AND RHEUMATISM LA English DT Article ID COLLAGEN-INDUCED ARTHRITIS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; SINGLE-NUCLEOTIDE POLYMORPHISM; TYROSINE-PHOSPHATASE PTPN22; ADJUVANT-INDUCED ARTHRITIS; PRISTANE-INDUCED ARTHRITIS; RHEUMATOID-ARTHRITIS; LINKAGE ANALYSIS; SUSCEPTIBILITY LOCUS; CHROMOSOME 2 AB Objective. To construct rats congenic for the chromosome 2 arthritis-regulatory quantitative trait locus Cia10, originally identified in a (DA x ACI)F-2 intercross rat strain that had been assessed for collagen-induced arthritis (CIA), and to determine the effect of this congenic interval on arthritis severity, joint histologic structure, and cytokine transcription in rats with pristane-induced arthritis (PIA). Methods. A 52.6-MB interval derived from the ACI (CIA- and PIA-resistant) strain and containing the Cia10 interval was introgressed into the DA (arthritis-susceptible) background through genotype-guided congenic breeding. Homozygous male and female DA.ACI(Cia10) congenic rats were studied for their susceptibility to and severity of PIA, and were compared with same-sex DA rats. Histologic analyses were done on hind paws collected on day 32 following the pristane injection. Levels of interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha) messenger RNA (mRNA) were measured with real-time polymerase chain reaction on synovial tissues from day-32 ankles. Results. Both male and female DA.ACI(Cia10) congenic rats developed a significantly milder form of arthritis, with a 95% and 92% reduction in the arthritis severity index compared with DA male and female controls, respectively (males P less than or equal to 0.001 and females P = 0.003). DA.ACI(Cia10) congenic rat synovial tissue was more likely to preserve its normal histologic architecture, including minimal to no cartilage and bone erosions, synovial hyperplasia, and pannus formation, and reduced numbers of vessels (angiogenesis), when compared with DA synovial tissue. There was a 2.7- and 2.4-fold reduction in the amount of IL-1beta and TNFalpha mRNA, respectively, in the synovial tissue of DA.ACI(Cia10) congenic rats compared with DA rats. Sequencing analyses of complementary DNA for the Cia10-predicted candidate gene Ptpn8, the rat homolog of the rheumatoid arthritis (RA)-susceptibility gene PTPN22, revealed no polymorphisms between the DA and ACI strains. Conclusion. This study determined that Cia10 harbors a major autoimmune arthritis-regulatory gene. This gene regulates clinical disease severity, histologic damage, and the levels of at least two central proinflammatory cytokines. We are in the process of narrowing down the critical region for positional cloning of the Cia10 gene. The identification of this gene will provide novel targets or pathways for focused candidate-gene studies in RA. C1 N Shore Long Isl Jewish Res Inst, Lab Expt Rheumatol, Robert S Boas Ctr Genom & Human Genet, Manhasset, NY 11030 USA. VAMC, Salt Lake City, UT USA. Univ Utah, Salt Lake City, UT USA. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Gulko, NS (reprint author), N Shore Long Isl Jewish Res Inst, Lab Expt Rheumatol, Robert S Boas Ctr Genom & Human Genet, 350 Community Dr,Room 139, Manhasset, NY 11030 USA. EM pgulko@nshs.edu OI Brenner, Max/0000-0002-8010-148X FU NIAID NIH HHS [R01 AI 54348]; NIAMS NIH HHS [R01 AR046213, R01 AR 46213] NR 64 TC 36 Z9 37 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JAN PY 2005 VL 52 IS 1 BP 322 EP 332 DI 10.1002/art.20782 PG 11 WC Rheumatology SC Rheumatology GA 890JO UT WOS:000226507700041 PM 15641042 ER PT J AU Huber, AM Miller, FW Rider, LG AF Huber, AM Miller, FW Rider, LG TI Childhood Myositis Assessment Scale and muscle strength testing in patients with juvenile dermatomyositis: comment on the article by Huber et al - Reply SO ARTHRITIS AND RHEUMATISM LA English DT Letter C1 IWK Hlth Ctr, Halifax, NS, Canada. Dalhousie Univ, Halifax, NS, Canada. NIH, Bethesda, MD 20892 USA. RP Huber, AM (reprint author), IWK Hlth Ctr, Halifax, NS, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JAN PY 2005 VL 52 IS 1 BP 368 EP 369 DI 10.1002/art.20891 PG 2 WC Rheumatology SC Rheumatology GA 890JO UT WOS:000226507700057 ER PT J AU Leonard, WJ AF Leonard, WJ TI Interleukin-7 deficiency in rheumatoid arthritis SO ARTHRITIS RESEARCH & THERAPY LA English DT Article ID THYMIC STROMAL LYMPHOPOIETIN; T-CELL DEVELOPMENT; RECEPTOR; EXPRESSION; CYTOKINES; IMMUNODEFICIENCY; SURVIVAL; CLONING; IL-7 AB Interleukin-7 (IL-7) is a stromal factor that is crucial for the development of T lymphocytes in humans and mice, and also B lymphocytes in mice. IL-7 can act as a T cell growth factor as well as a critical anti-apoptotic survival factor. The essential non-redundant role of this cytokine for T cell development in vivo is indicated by the phenotype of murine knockout models as well as by humans with a T-B+NK+ form of severe combined immunodeficiency (SCID) resulting from mutations in IL-7 receptor a chain. IL-7 deficiency has now been found in patients with rheumatoid arthritis, a finding that relates not only to the T-lymphocyte status in this disease but also to the ability of patients with rheumatoid arthritis to recover from therapy-induced lymphopenia. C1 NIH, NHLBI, Lab Mol Immunol, Bethesda, MD USA. RP Leonard, WJ (reprint author), NIH, NHLBI, Lab Mol Immunol, Bethesda, MD USA. EM wjl@helix.nih.gov NR 19 TC 3 Z9 5 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PY 2005 VL 7 IS 1 BP 42 EP 43 DI 10.1186/ar1492 PG 2 WC Rheumatology SC Rheumatology GA 878DM UT WOS:000225626700027 PM 15642153 ER PT J AU Wahl, SM Chen, WJ AF Wahl, SM Chen, WJ TI Transforming growth factor-beta-induced regulatory T cells referee inflammatory and autoimmune diseases SO ARTHRITIS RESEARCH & THERAPY LA English DT Review ID IMMUNOLOGICAL SELF-TOLERANCE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; TRANSCRIPTION FACTOR FOXP3; LATENT TGF-BETA; IN-VIVO; PERIPHERAL-BLOOD; CD4(+) CD25(+); IMMUNE DEVIATION; DENDRITIC CELLS; ANTIGEN 4 AB Naturally occurring CD4(+) CD25(+) regulatory T cells mediate immune suppression to limit immunopathogenesis associated with chronic inflammation, persistent infections and autoimmune diseases. Their mode of suppression is contact-dependent, antigen-nonspecific and involves a nonredundant contribution from the cytokine transforming growth factor (TGF)-beta. Not only can TGF-beta mediate cell - cell suppression between the regulatory T cells and CD4(+)CD25(-) or CD8(+) T cells, but new evidence also reveals its role in the conversion of CD4(+)CD25(-) T cells, together with TCR antigen stimulation, into the regulatory phenotype. Elemental to this conversion process is induction of expression of the forkhead transcription factor, Foxp3. This context-dependent coercion of naive CD4(+) T cells into a powerful subset of regulatory cells provides a window into potential manipulation of these cells to orchestrate therapeutic intervention in diseases characterized by inadequate suppression, as well as a promising means of controlling pathologic situations in which excessive suppression dominates. C1 NIDCD, Cellular Immunol Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. NIDCD, Mucosal Immunol Unit, Oral Infect & Immun Branch, NIH, Bethesda, MD USA. RP Wahl, SM (reprint author), NIDCD, Cellular Immunol Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. EM smwahl@dir.nidcr.nih.gov NR 71 TC 47 Z9 61 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PY 2005 VL 7 IS 2 BP 62 EP 68 DI 10.1186/ar1504 PG 7 WC Rheumatology SC Rheumatology GA 905OY UT WOS:000227579900003 PM 15743491 ER PT J AU Leipe, J Skapenko, A Lipsky, PE Schulze-Koops, H AF Leipe, J Skapenko, A Lipsky, PE Schulze-Koops, H TI Regulatory T cells in rheumatoid arthritis SO ARTHRITIS RESEARCH & THERAPY LA English DT Review ID IMMUNOLOGICAL SELF-TOLERANCE; JUVENILE IDIOPATHIC ARTHRITIS; MYELIN BASIC-PROTEIN; CUTTING EDGE; IN-VITRO; FUNCTIONAL-CHARACTERIZATION; IMMUNE DYSREGULATION; MULTIPLE-SCLEROSIS; PERIPHERAL-BLOOD; DENDRITIC CELLS AB Apart from the deletion of autoreactive T cells in the thymus, various methods exist in the peripheral immune system to control specific human immune responses to self-antigens. One of these mechanisms involves regulatory T cells, of which CD(4+)CD(25+) T cells are a major subset. Recent evidence suggests that CD(4+)CD(25+) T cells have a role in controlling the development of autoimmune diseases in animals and in humans. The precise delineation of the function of CD(4+)CD(25+) T cells in autoimmune inflammation is therefore of great importance for the understanding of the pathogenesis of autoimmune diseases. Moreover, the ability to control such regulatory mechanisms might provide novel therapeutic opportunities in autoimmune disorders such as rheumatoid arthritis. Here we review existing knowledge of CD(4+)CD(25+) T cells and discuss their role in the pathogenesis of rheumatic diseases. C1 Univ Erlangen Nuremberg, Nikolaus Fiebiger Ctr Mol Med, Erlangen, Germany. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Schulze-Koops, H (reprint author), Univ Erlangen Nuremberg, Nikolaus Fiebiger Ctr Mol Med, Erlangen, Germany. EM schulze-koops@med3.imed.uni-erlangen.de NR 61 TC 49 Z9 63 U1 1 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PY 2005 VL 7 IS 3 BP 93 EP 99 DI 10.1186/ar1718 PG 7 WC Rheumatology SC Rheumatology GA 943EW UT WOS:000230336300001 PM 15899057 ER PT J AU Aletaha, D Nell, VP Stamm, T Uffmann, M Pflugbeil, S Machold, K Smolen, JS AF Aletaha, D Nell, VP Stamm, T Uffmann, M Pflugbeil, S Machold, K Smolen, JS TI Acute phase reactants add little to composite disease activity indices for rheumatoid arthritis: validation of a clinical activity score SO ARTHRITIS RESEARCH & THERAPY LA English DT Article ID C-REACTIVE PROTEIN; MODIFYING ANTIRHEUMATIC DRUGS; RANDOMIZED CONTROLLED-TRIAL; RADIOGRAPHIC DAMAGE; JOINT COUNTS; DISABILITY; METHOTREXATE; CARE; RHEUMATOLOGISTS; PROGRESSION AB Introduction Frequent assessments of rheumatoid arthritis ( RA) disease activity allow timely adaptation of therapy, which is essential in preventing disease progression. However, values of acute phase reactants (APRs) are needed to calculate current composite activity indices, such as the Disease Activity Score (DAS) 28, the DAS28-CRP (i.e. the DAS28 using C-reactive protein instead of erythrocyte sedimentation rate) and the Simplified Disease Activity Index (SDAI). We hypothesized that APRs make limited contribution to the SDAI, and that an SDAI-modification eliminating APRs-termed the Clinical Disease Activity Index (CDAI; i.e. the sum of tender and swollen joint counts [28 joints] and patient and physician global assessments [in cm]) - would have comparable validity in clinical cohorts. Method Data sources comprised an observational cohort of 767 RA patients ( average disease duration 8.1 +/- 10.6 years), and an independent inception cohort of 106 patients ( disease duration 11.5 +/- 12.5 weeks) who were followed prospectively. Results Our clinically based hypothesis was statistically supported: APRs accounted only for 15% of the DAS28, and for 5% of the SDAI and the DAS28-CRP. In both cohorts the CDAI correlated strongly with DAS28 (R = 0.89-0.90) and comparably to the correlation of SDAI with DAS28 ( R = 0.90-0.91). In additional analyses, the CDAI when compared to the SDAI and the DAS28 agreed with a weighted kappa of 0.70 and 0.79, respectively, and comparably to the agreement between DAS28 and DAS28-CRP. All three scores correlated similarly with Health Assessment Questionnaire (HAQ) scores ( R = 0.45-0.47). The average changes in all scores were greater in patients with better American College of Rheumatology response (P < 0.0001, analysis of variance; discriminant validity). All scores exhibited similar correlations with radiological progression ( construct validity) over 3 years ( R = 0.54 - 0.58; P < 0.0001). Conclusion APRs add little information on top ( and independent) of the combination of clinical variables included in the SDAI. A purely clinical score is a valid measure of disease activity and will have its greatest merits in clinical practice rather than research, where APRs are usually always available. The CDAI may facilitate immediate and consistent treatment decisions and help to improve patient outcomes in the longer term. C1 Med Univ Vienna, Dept Rheumatol, Vienna, Austria. NIH, NIAMSD, Bethesda, MD 20892 USA. Med Univ Vienna, Dept Radiol, Vienna, Austria. Lainz Hosp, Dept Med 2, A-1130 Vienna, Austria. RP Aletaha, D (reprint author), Med Univ Vienna, Dept Rheumatol, Vienna, Austria. EM aletahad@mail.nih.gov NR 46 TC 357 Z9 372 U1 0 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PY 2005 VL 7 IS 4 BP R796 EP R806 DI 10.1186/ar1740 PG 11 WC Rheumatology SC Rheumatology GA 952QH UT WOS:000231020100017 PM 15987481 ER PT J AU van Lent, PLEM Nabbe, KCAM Blom, AB Sloetjes, A Holthuysen, AEM Kolls, J Van de Loo, FAJ Holland, SM Van den Berg, WB AF van Lent, PLEM Nabbe, KCAM Blom, AB Sloetjes, A Holthuysen, AEM Kolls, J Van de Loo, FAJ Holland, SM Van den Berg, WB TI NADPH-oxidase-driven oxygen radical production determines chondrocyte death and partly regulates metalloproteinase-mediated cartilage matrix degradation during interferon-gamma-stimulated immune complex arthritis SO ARTHRITIS RESEARCH & THERAPY LA English DT Article ID ANTIGEN-INDUCED ARTHRITIS; CHRONIC GRANULOMATOUS-DISEASE; ARTICULAR-CARTILAGE; RHEUMATOID-ARTHRITIS; HYDROGEN-PEROXIDE; JOINT INFLAMMATION; SYNOVIAL-FLUID; UP-REGULATION; FC-RECEPTORS; LINING CELLS AB In previous studies we have found that Fc gamma RI determines chondrocyte death and matrix metalloproteinase (MMP)mediated cartilage destruction during IFN-gamma-regulated immune complex arthritis (ICA). Binding of immune complexes (ICs) to Fc gamma RI leads to the prominent production of oxygen radicals. In the present study we investigated the contribution of NADPH-oxidase-driven oxygen radicals to cartilage destruction by using p47phox(-/-) mice lacking a functional NADPH oxidase complex. Induction of a passive ICA in the knee joints of p47phox(-/-) mice resulted in a significant elevation of joint inflammation at day 3 when compared with wild-type (WT) controls as studied by histology. However, when IFN-gamma. was overexpressed by injection of adenoviral IFN-gamma. in the knee joint before ICA induction, a similar influx of inflammatory cells was found at days 3 and 7, comprising mainly macrophages in both mouse strains. Proteoglycan depletion from the cartilage layers of the knee joints in both groups was similar at days 3 and 7. Aggrecan breakdown in cartilage caused by MMPs was further studied by immunolocalisation of MMP-mediated neoepitopes (VDIPEN). VDIPEN expression in the cartilage layers of arthritic knee joints was markedly lower ( between 30 and 60%) in IFN-gamma-stimulated arthritic p47phox(-/-) mice at day 7 than in WT controls, despite significant upregulation of mRNA levels of various MMPs such as MMP-3, MMP-9, MMP-12 and MMP-13 in synovia and MMP-13 in cartilage layers as measured with quantitative RT-PCR. The latter observation suggests that oxygen radicals are involved in the activation of latent MMPs. Chondrocyte death, determined as the percentage of empty lacunae in articular cartilage, ranged between 20 and 60% at day 3 and between 30 and 80% at day 7 in WT mice, and was completely blocked in p47phox(-/-) mice at both time points. Fc gamma RI mRNA expression was significantly lower, and Fc gamma RII and Fc gamma RIII were higher, in p47phox(-/-) mice than in controls. NADPH-oxidase-driven oxygen radical production determines chondrocyte death and aggravates MMP-mediated cartilage destruction during IFN-gamma-stimulated IC-mediated arthritis. Upregulation of Fc gamma RI by oxygen radicals may contribute to cartilage destruction. C1 Univ Nijmegen, Med Ctr, St Radboud, Dept Rheumatol, Nijmegen, Netherlands. Univ Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA 15261 USA. NIAID, Dept Host Def, Bethesda, MD 20892 USA. RP van Lent, PLEM (reprint author), Univ Nijmegen, Med Ctr, St Radboud, Dept Rheumatol, Nijmegen, Netherlands. EM P.vanlent@reuma.umcn.nl RI van Lent, Peter/A-4269-2014; van de Loo, Fons/A-3425-2014; van Lent, Peter/A-4047-2014; Berg, W.B./H-8010-2014; Blom, A.B./L-4206-2015 OI van de Loo, Fons/0000-0002-5851-099X; NR 45 TC 16 Z9 16 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PY 2005 VL 7 IS 4 BP R885 EP R895 DI 10.1186/ar1760 PG 11 WC Rheumatology SC Rheumatology GA 952QH UT WOS:000231020100027 PM 15987491 ER PT J AU Phillips, SJ AF Phillips, SJ TI Untitled SO ARTIFICIAL ORGANS LA English DT Letter C1 NIH, Urbandale, IA 50322 USA. Natl Lib Med, Bethesda, MD 20894 USA. RP Phillips, SJ (reprint author), NIH, 8081 Cobblestone Rd, Urbandale, IA 50322 USA. EM SP226@aol.com NR 0 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0160-564X J9 ARTIF ORGANS JI Artif. Organs PD JAN PY 2005 VL 29 IS 1 BP 90 EP 90 DI 10.1111/j.1525-1594.2004.29019.x PG 1 WC Engineering, Biomedical; Transplantation SC Engineering; Transplantation GA 882GR UT WOS:000225927900017 ER PT B AU Memarzadeh, F Manning, A AF Memarzadeh, F Manning, A BE Geshwiler, M TI Control of ammonia production in animal research facilities through ventilation system design SO ASHRAE Transactions 2005, Vol 111, Pt 2 SE ASHRAE TRANSACTIONS LA English DT Proceedings Paper CT Annual Meeting of the American-Society-of-Heating-Refrigerating-and-Air-Conditioning-Engineers (ASHRAE) CY 2005 CL Denver, CO SP Amer Soc Heating Refrigerating & Air Conditioning Engineers AB This paper considers the effect of air properties on ammonia levels in the cages and main room space of an animal research facility containing mouse static micro-isolators. The ammonia production from mice is affected by the level of relative humidity (RH) of the air with higher production rates at elevated RH values. The manipulation of the room supply discharge air therefore, offers a means of reducing ammonia levels in both the cage and room. This paper outlines a study in which the air properties are considered with regard to ammonia production both experimentally and numerically, in the latter case using the technique of airflow modeling. The paper demonstrates that even relatively modest increases in supply temperature can have major implications with regards to ammonia production, leading to the possibility that it may be possible to increase the time between cage bedding changes. C1 NIH, Div Policy & Program Assessment, Bethesda, MD 20892 USA. RP Memarzadeh, F (reprint author), NIH, Div Policy & Program Assessment, Bldg 10, Bethesda, MD 20892 USA. NR 6 TC 3 Z9 3 U1 0 U2 3 PU AMER SOC HEATING, REFRIGERATING AND AIR-CONDITIONING ENGS PI ATLANTA PA 1791 TULLIE CIRCLE NE, ATLANTA, GA 30329 USA J9 ASHRAE TRAN PY 2005 VL 111 BP 203 EP 212 PN 2 PG 10 WC Construction & Building Technology; Engineering, Mechanical SC Construction & Building Technology; Engineering GA BDP17 UT WOS:000234678400018 ER PT S AU Walters, JR Hu, D Itoga, CA Parr-Brownlie, LC Bergstrom, DA AF Walters, JR Hu, D Itoga, CA Parr-Brownlie, LC Bergstrom, DA BE Bolam, JP Ingham, CA Magill, PJ TI Do local field potentials reflect synchronized spiking activity of neuronal populations in the basal ganglia? Studies in a rodent model of Parkinson's disease SO Basal Ganglia VIII SE ADVANCES IN BEHAVIORAL BIOLOGY LA English DT Proceedings Paper CT 8th Triennial Meeting of the International-Basal-Ganglia-Society CY SEP 05-09, 2004 CL Crieff, SCOTLAND SP Int Basal Ganglia Soc ID SUBTHALAMIC NUCLEUS NEURONS; MULTIPLE UNIT-ACTIVITY; GLOBUS-PALLIDUS; DOPAMINERGIC LESION; CEREBRAL-CORTEX; OSCILLATIONS; RAT; STIMULATION; HIPPOCAMPUS; DEPENDENCY C1 NINDS, NIH, Porter Neurosci Ctr, Neurophysiol Pharmacol Sect, Bethesda, MD 20892 USA. RP Bergstrom, DA (reprint author), NINDS, NIH, Porter Neurosci Ctr, Neurophysiol Pharmacol Sect, Bethesda, MD 20892 USA. NR 35 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES SN 0099-9962 BN 0-387-28065-0 J9 ADV BEHAV BIOL PY 2005 VL 56 BP 37 EP 46 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA BDT82 UT WOS:000235292700003 ER PT S AU Gerfen, CR AF Gerfen, CR BE Bolam, JP Ingham, CA Magill, PJ TI D1-dopamine receptor supersensitivity in the dopamine-depleted striatum involves a novel activation of ERK1/2 SO Basal Ganglia VIII SE ADVANCES IN BEHAVIORAL BIOLOGY LA English DT Proceedings Paper CT 8th Triennial Meeting of the International-Basal-Ganglia-Society CY SEP 05-09, 2004 CL Crieff, SCOTLAND SP Int Basal Ganglia Soc ID EARLY GENE INDUCTION; C-FOS; NMDA RECEPTORS; KINASE CASCADE; MESSENGER-RNA; EXPRESSION; D1; NEURONS; STIMULATION; PLASTICITY AB A key feature of basal ganglia organization is the existence of the "direct" and "indirect" pathways, which arise from two distinct intermingled populations of medium spiny neurons within the striatum and connect either directly or indirectly with the output nuclei of the basal ganglia. Physiologically, these neuron populations are often indistinguishable as both respond similarly to excitatory inputs from the cortex. On the other hand, they display very distinct responses mediated by signal transduction systems, which are responsible for gene expression changes underlying long term neuronal plasticity. These differences are due to the clear segregation of D1 and D2 dopamine receptor (D1r and D2r) subtypes, respectively to direct and indirect striatal projection neurons. The opposing functional effects of dopamine on these striatal projection neurons is evident following lesions of the nigrostriatal dopamine system, which results In Increases in gene expression in the D2 receptor-expressing indirect projection neurons and suppression of gene expression in D1 receptor-expressing direct projection neurons. Treatments with D2 receptor agonists normalize gene expression in indirect projection neurons. However, D1 agonist treatment results in a supersensitive response in direct pathway neurons. This D1 receptor supersensitive response in the dopamine-depleted striatum is distinct from D1 receptor response in the dopamine-intact striatum suggesting that there is an irreversible reorganization of the linkage between the D1 receptor and signal transduction systems. Our studies demonstrate that in the dopamine-depleted striatum the D1 supersensitive response is a consequence of a novel linkage of D1 receptors to the extracellular receptor kinase (ERK1/2). C1 NIMH, LSN, Sect Neuroanat, Bethesda, MD 20892 USA. RP Gerfen, CR (reprint author), NIMH, LSN, Sect Neuroanat, 35 Convent Dr, Bethesda, MD 20892 USA. NR 26 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES SN 0099-9962 BN 0-387-28065-0 J9 ADV BEHAV BIOL PY 2005 VL 56 BP 275 EP 284 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA BDT82 UT WOS:000235292700025 ER PT J AU Londos, C Sztalryd, C Tansey, JT Kimmel, AR AF Londos, C Sztalryd, C Tansey, JT Kimmel, AR TI Role of PAT proteins in lipid metabolism SO BIOCHIMIE LA English DT Article ID HORMONE-SENSITIVE LIPASE; DIFFERENTIATION-RELATED PROTEIN; A-MEDIATED LIPOLYSIS; STORAGE DROPLET; PERILIPIN-A; ADIPOCYTES; TIP47; CELLS; TRANSLOCATION; STIMULATION AB One of the central reactions in bodily energy metabolism is lipolysis in adipocytes, the reaction that governs the release of stored fatty acids from the adipocyte triacylglycerol pool, which constitutes the major energy reserve in animals. These fatty acids are then transported by serum albumin to various tissues to supply their energy requirements. This reaction was previously thought to result from phosphorylation and activation of hormone-sensitive lipase by protein kinase A (PKA) but is now known to be governed by a translocation of the lipase from the cytosol to the surface of the intracellular lipid droplet that houses the reservoir of TAG. This droplet is coated with perilipin A, which is also phosphorylated by PKA in response to lipolytic stimuli, and phosphorylation of perilipin A is essential for HSL translocation and stimulated lipolysis. (c) 2005 Published by Elsevier SAS. C1 NIDDK, NIH, Bethesda, MD 20896 USA. RP Londos, C (reprint author), NIDDK, NIH, Bldg 50,Room 3140, Bethesda, MD 20896 USA. EM deanl@intra.niddk.nih.gov NR 29 TC 172 Z9 195 U1 1 U2 18 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PD JAN PY 2005 VL 87 IS 1 BP 45 EP 49 DI 10.1016/j.biochi.2004.12.010 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 905OJ UT WOS:000227577900009 PM 15733736 ER PT J AU Ferrari, M Downing, G AF Ferrari, M Downing, G TI Medical nanotechnology - Shortening clinical trials and regulatory pathways? SO BIODRUGS LA English DT Article ID CARBON NANOTUBES; CELLULAR TARGETS; PROSTATE-CANCER; ANNEXIN-V; IN-VIVO; EXPRESSION; RECEPTOR; CELLS; NANOPARTICLES; ANGIOGENESIS AB Nanotechnology, the science of creating structures, devices, and systems with a length scale of approximately 1-100 nanometers, is poised to have a revolutionary effect on biomedical research and clinical science. By operating at the same scale as most biomacromolecules, nanoscale devices can afford a detailed view of the molecules and events that drive cellular systems and that lie at the heart of disease, and thus, nanotechnology can impact the drug discovery, development, and clinical testing of novel pharmaceuticals. Already, nanoscale drug delivery vehicles are in clinical use, but those successes represent just one way in which nanotechnology will prove useful. One promising nanoscale technology under development may provide real-time, in vivo measurements of apoptosis, and thus may afford an early signal of therapeutic efficacy, both in human clinical trials and in preclinical screening. Microfluidic systems, built of nanoscale components, can enable a host of rapid, massively parallel, high-throughput screening systems, while nanoscale sensors in a wide variety of formats are ready to provide multiplexed biochemical and genetic measurements in living systems. These advances could be utilized to shave time and expense from multiple stages of the drug discovery and development effort. C1 Ohio State Univ, Davis Heart & Lung Res Inst 110U, Columbus, OH 43210 USA. NCI, Bethesda, MD 20892 USA. RP Ferrari, M (reprint author), Ohio State Univ, Davis Heart & Lung Res Inst 110U, 473 W 12th Ave, Columbus, OH 43210 USA. EM ferrari.5@osu.edu NR 44 TC 18 Z9 18 U1 1 U2 7 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1173-8804 J9 BIODRUGS JI Biodrugs PY 2005 VL 19 IS 4 BP 203 EP 210 DI 10.2165/00063030-200519040-00001 PG 8 WC Oncology; Immunology; Pharmacology & Pharmacy SC Oncology; Immunology; Pharmacology & Pharmacy GA 960JG UT WOS:000231585900001 PM 16128604 ER PT J AU Karev, GP Berezovskaya, FS Koonin, EV AF Karev, GP Berezovskaya, FS Koonin, EV TI Modeling genome evolution with a diffusion approximation of a birth-and-death process SO BIOINFORMATICS LA English DT Article; Proceedings Paper CT 5th International Conference in Bioinformatics - In Silico Biology, Computational Genomics and Evolutionary Biology CY NOV 07-19, 2005 CL Atlanta, GA SP Georgia Tech - Oak Ridge Natl Lab ID GENE; BIOLOGY AB Motivation: In our previous studies, we developed discrete-space birth, death and innovation models (BDIMs) of genome evolution. These models explain the origin of the characteristic Pareto distribution of paralogous gene family sizes in genomes, and model parameters that provide for the evolution of these distributions within a realistic time frame have been identified. However, extracting the temporal dynamics of genome evolution from discrete-space BDIM was not technically feasible. We were interested in obtaining dynamic portraits of the genome evolution process by developing a diffusion approximation of BDIM. Results: The diffusion version of BDIM belongs to a class of continuous-state models whose dynamics is described by the Fokker-Plank equation and the stationary solution could be any specified Pareto function. The diffusion models have time-dependent solutions of a special kind, namely, generalized self-similar solutions, which describe the transition from one stationary distribution of the system to another; this provides for the possibility of examining the temporal dynamics of genome evolution. Analysis of the generalized self-similar solutions of the diffusion BDIM reveals a biphasic curve of genome growth in which the initial, relatively short, self-accelerating phase is followed by a prolonged phase of slow deceleration. This evolutionary dynamics was observed both when genome growth started from zero and proceeded via innovation (a potential model of primordial evolution), and when evolution proceeded from one stationary state to another. In biological terms, this regime of evolution can be tentatively interpreted as a punctuated-equilibrium-like phenomenon whereby evolutionary transitions are accompanied by rapid gene amplification and innovation, followed by slow relaxation to a new stationary state. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. Howard Univ, Dept Math, Washington, DC 20059 USA. RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. EM koonin@ncbi.nlm.nih.gov NR 24 TC 1 Z9 1 U1 1 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1367-4803 J9 BIOINFORMATICS JI Bioinformatics PY 2005 VL 21 SU 3 BP 11 EP 19 DI 10.1093/bioinformatics/bti1202 PG 8 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Computer Science, Interdisciplinary Applications; Mathematical & Computational Biology; Statistics & Probability SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Computer Science; Mathematical & Computational Biology; Mathematics GA 002XP UT WOS:000234645800003 ER PT S AU Zeng, Q Kim, E Crowell, J Tse, T AF Zeng, Q Kim, E Crowell, J Tse, T BE Oliveira, JL Maojo, V MartinSanchez, F Pereira, AS TI A text corpora-based estimation of the familiarity of health terminology SO BIOLOGICAL AND MEDICAL DATA ANALYSIS, PROCEEDINGS SE Lecture Notes in Computer Science LA English DT Article; Proceedings Paper CT 6th International Symposium on Biological and Medical Data Analysis CY NOV 10-11, 2005 CL Aveiro, PORTUGAL ID LITERACY AB In a pilot effort to improve health communication we created a method for measuring the familiarity of various medical terms. To obtain term familiarity data, we recruited 21 volunteers who agreed to take medical terminology quizzes containing 68 terms. We then created predictive models for familiarity based on term occurrence in text corpora and reader's demographics. Although the sample size was small, our preliminary results indicate that predicting the familiarity of medical terms based on an analysis of the frequency in text corpora is feasible. Further, individualized familiarity assessment is feasible when demographic features are included as predictors. C1 Harvard Univ, Sch Med, Decis Syst Grp, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA. RP Zeng, Q (reprint author), Harvard Univ, Sch Med, Decis Syst Grp, Boston, MA 02115 USA. EM qzeng@dsg.harvard.edu; ejkim@dsg.harvard.edu; jcrowell@dsg.harvard.edu; tse@nlm.nih.gov NR 11 TC 7 Z9 7 U1 0 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-29674-3 J9 LECT NOTES COMPUT SC PY 2005 VL 3745 BP 184 EP 192 PG 9 WC Biochemical Research Methods; Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Medical Informatics SC Biochemistry & Molecular Biology; Computer Science; Medical Informatics GA BDM89 UT WOS:000234378000019 ER PT J AU Deep-Soboslay, A Akil, M Martin, CE Bigelow, LB Herman, MM Hyde, TM Kleinman, JE AF Deep-Soboslay, A Akil, M Martin, CE Bigelow, LB Herman, MM Hyde, TM Kleinman, JE TI Reliability of psychiatric diagnosis in postmortem research SO BIOLOGICAL PSYCHIATRY LA English DT Article DE mood disorders; postmortem diagnosis; psychological autopsy; record review; schizophrenia ID PSYCHOLOGICAL AUTOPSY; ADOLESCENT SUICIDE; SCHIZOPHRENIA; DISORDERS; DEMENTIA; VALIDITY; BRAIN AB Background: Postmortem human brain research is an important approach for identifying the cellular, molecular, and genetic pathways involved in the pathophysiology of psychiatric disorders. One critical component in postmortem research is the reliability of psychiatric diagnoses used to define study cohorts. Finding reliable methods for assessing lifetime psychiatric diagnoses in subjects after death is extremely challenging. Methods: Two commonly used approaches were compared: psychiatric record reviews and Postmortem family interviews. We hypothesized that these two methods would lead to more diagnostic agreement for subjects with schizophrenia than those with mood disorders. For 37 cases, psychiatric records were reviewed retrospectively using the Diagnostic Evaluation After Death, and family members were interviewed using the Structured Clinical Interview for DSM-IV Results: Comparison of diagnoses derived from these two approaches generated an overall kappa coefficient of. 67. Kappa coefficients for the schizophrenia cohort were .94, .68 for the major depressive disorder cohort, and .58 for the bipolar disorder cohort. Conclusions. Thus, although it may be sufficient to establish the postmortem diagnosis of schizophrenia using one of the two methods, the best method for reaching an accurate postmortem diagnosis for mood disorders is more difficult to determine and requires further study. C1 NIMH, NIH, Clin Brain Disorders Branch, Sect Neuropathol, Bethesda, MD 20892 USA. RP Kleinman, JE (reprint author), NIMH, NIH, Clin Brain Disorders Branch, Sect Neuropathol, 10 Ctr Dr,Room 45235, Bethesda, MD 20892 USA. EM kleinmaj@intra.nimh.nih.gov NR 19 TC 36 Z9 36 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JAN 1 PY 2005 VL 57 IS 1 BP 96 EP 101 DI 10.1016/j.biopsych.2004.10.016 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 889CT UT WOS:000226421800014 PM 15607306 ER PT J AU Drevets, WC Price, JL AF Drevets, Wayne C. Price, Joseph L. BE Licinio, J Wong, ML TI Neuroimaging and Neuropathological Studies of Mood Disorders SO BIOLOGY OF DEPRESSION: FROM NOVEL INSIGHTS TO THERAPEUTIC STRATEGIES LA English DT Article; Book Chapter ID CEREBRAL-BLOOD-FLOW; POSITRON-EMISSION-TOMOGRAPHY; MAJOR DEPRESSIVE DISORDER; MEDIAL PREFRONTAL CORTEX; ANTERIOR CINGULATE CORTEX; STRUCTURAL BRAIN ABNORMALITIES; SEROTONIN TRANSPORTER BINDING; OBSESSIVE-COMPULSIVE DISORDER; EARLY-ONSET DEPRESSION; SEVERE MENTAL-ILLNESS AB Neuroimaging studies of major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of brain function, structure, and serotonin receptor pharmacology in areas of the prefrontal cortex, amygdala, striatum, and hippocampus that have been implicated by other types of evidence in the modulation of emotional behavior. The structural imaging abnormalities within these regions persist across episodes, but can be attenuated by some mood-stabilizing therapies. Some of the structural imaging abnormalities appear to exist prior to the onset of depressive episodes in subjects who are at high familial risk for developing mood disorders, while others appear to become more prominent with continuing illness. In many of these regions post mortem histopathological studies have shown abnormal reductions of synaptic markers and glial cells, with no corresponding loss of neurons in MDD and BD. Because these abnormalities appear relatively specific for brain regions that play major roles in modulating or inhibiting the endocrine, autonomic, behavioral, and emotional experiential responses to stressors or threats, they may be associated with impairments of emotion regulation that underlie the clinical manifestations of abnormal mood episodes. C1 [Drevets, Wayne C.; Price, Joseph L.] NIMH MIB, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA. RP Drevets, WC (reprint author), NIMH MIB, Mood & Anxiety Disorders Program, NIH, 15K North Dr,MSC 2670, Bethesda, MD 20892 USA. NR 188 TC 8 Z9 8 U1 5 U2 5 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-3-52761-967-2 PY 2005 BP 427 EP 465 DI 10.1002/9783527619672.ch17 D2 10.1002/9783527619672 PG 39 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BXY97 UT WOS:000297648100018 ER PT J AU Gold, PW AF Gold, P. W. BE Licinio, J Wong, ML TI Stress System Dysregulation in Depression: From Molecular Biology to New Treatment Opportunities SO BIOLOGY OF DEPRESSION: FROM NOVEL INSIGHTS TO THERAPEUTIC STRATEGIES LA English DT Article; Book Chapter ID CORTICOTROPIN-RELEASING HORMONE; SEASONAL AFFECTIVE-DISORDER; PITUITARY-ADRENAL AXIS; PLASMA NOREPINEPHRINE LEVELS; CHRONIC-FATIGUE-SYNDROME; CORONARY-HEART-DISEASE; BONE-MINERAL DENSITY; CEREBRAL-BLOOD-FLOW; MAJOR DEPRESSION; CEREBROSPINAL-FLUID C1 NIMH, NIH, Clin Neuroendocrinol Branch, Bethesda, MD 20892 USA. RP Gold, PW (reprint author), NIMH, NIH, Clin Neuroendocrinol Branch, Bldg 10,Rm 2D46,10 Ctr Dr,MSC 1284, Bethesda, MD 20892 USA. NR 115 TC 1 Z9 1 U1 1 U2 1 PU BLACKWELL SCIENCE PUBL PI OXFORD PA OSNEY MEAD, OXFORD OX2 0EL, ENGLAND BN 978-3-52761-967-2 PY 2005 BP 539 EP 555 DI 10.1002/9783527619672.ch21 D2 10.1002/9783527619672 PG 17 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BXY97 UT WOS:000297648100022 ER PT J AU Tanaka, M Kihara, M Hennebold, OD Eppig, JJ Viveiros, MM Emery, BR Carrell, DT Kirkman, NJ Meczekalski, B Zhou, J Bondy, CA Becker, M Schultz, RM Misteli, T De la Fuente, R King, GJ Adashi, EY AF Tanaka, M Kihara, M Hennebold, OD Eppig, JJ Viveiros, MM Emery, BR Carrell, DT Kirkman, NJ Meczekalski, B Zhou, J Bondy, CA Becker, M Schultz, RM Misteli, T De la Fuente, R King, GJ Adashi, EY TI H1FOO is coupled to the initiation of oocytic growth SO BIOLOGY OF REPRODUCTION LA English DT Article DE meiosis; oocyte development ID LINKER HISTONE FUNCTION; SOMATIC SUBTYPES; NUCLEAR TRANSFER; GENE-EXPRESSION; MOUSE OOCYTES; H1; CHROMATIN; CELLS; SUPPRESSION; ZEBRAFISH AB We previously reported the discovery of a novel mammalian Hi linker histone termed H1FOO (formerly H1OO), a replacement H1, the expression of which is restricted to the growing/ maturing oocyte and to the zygote. The significance of this pre-embryonic H1 draws on its substantial orthologous conservation, singular structural attributes, selectivity for the germ cell lineage, prolonged nucleosomal residence, and apparent predominance among germ cell His. Herein, we report that the intronic, single-copy, five-exon ( greater than or equal to5301 base pair) H1foo gene maps to chromosome 6 and that the corresponding primary H1foo transcript gives rise to two distinct, alternatively spliced mRNA species (H1foo(alpha) and H1foo(beta)). The expression of the oocytic H1FOO transcript and protein proved temporally coupled to the recruitment of resting primordial follicles into a developing primary follicular cohort and thus to the critical transition marking the onset of oocytic growth. The corresponding potential protein isoforms (H1FOO, and H1FOO,), both nuclear localization sequence-endowed but export consensus sequence-free and possessing a significant net positive charge, localized primarily to perinucleolar heterochromatin in the oocytic germinal vesicle. Further investigation will be required to define the functional role of the H1FOO protein in the ordering of the chromatin of early mammalian development as well as its potential role in defining the primordial-to-primary follicle transition. C1 Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Div Reprod Sci, Salt Lake City, UT 84112 USA. Keio Univ, Sch Med, Dept Obstet & Gynecol, Shinjuku Ku, Tokyo 1600082, Japan. Chiba Univ, Sch Med, Dept Obstet & Gynecol, Chuo Ku, Chiba 2608670, Japan. Oregon Hlth Sci Univ, Oregon Natl Primate Res Ctr, Div Reprod Sci, Beaverton, OR 97006 USA. Jackson Lab, Bar Harbor, ME 04609 USA. Univ Penn, Sch Vet Med, Ctr Anim Transgenesis & Germ Cell Res, Kennett Sq, PA 19348 USA. Univ Utah, Sch Med, Dept Surg, Div Urol, Salt Lake City, UT 84132 USA. Univ Med Sci, Dept Gynecol Endocrinol, PL-60535 Poznan, Poland. NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. Univ Penn, Dept Biol, Philadelphia, PA 19104 USA. RP Adashi, EY (reprint author), Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Div Reprod Sci, 2000 Circle Hope,Room 5221, Salt Lake City, UT 84112 USA. EM eadashi@hsc.utah.edu RI Viveiros, Maria/P-4120-2015 NR 26 TC 38 Z9 45 U1 0 U2 3 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD JAN PY 2005 VL 72 IS 1 BP 135 EP 142 DI 10.1095/biolreprod.104.032474 PG 8 WC Reproductive Biology SC Reproductive Biology GA 882TF UT WOS:000225960500016 PM 15371275 ER PT J AU Ghanayem, BI Witt, KL El-Hadri, L Hoffler, U Kissling, GE Shelby, MD Bishop, JB AF Ghanayem, BI Witt, KL El-Hadri, L Hoffler, U Kissling, GE Shelby, MD Bishop, JB TI Comparison of germ cell mutagenicity in male CYP2E1-null and wild-type mice treated with acrylamide: Evidence supporting a glycidamide-mediated effect SO BIOLOGY OF REPRODUCTION LA English DT Article DE acrylamide; CYP2E1-null mice; dominant lethals; environment; male reproductive tract; reproductive toxicant; sperm ID CYTOCHROME-P450 2E1 CYP2E1; UNSCHEDULED DNA-SYNTHESIS; HUMAN PERIPHERAL-BLOOD; HERITABLE TRANSLOCATIONS; GENETIC POLYMORPHISMS; LOCUS MUTATIONS; C-14 ACRYLAMIDE; DOSE-RESPONSE; MOUSE; METABOLISM AB Acrylamide is an animal carcinogen and probable human carcinogen present in appreciable amounts in heated carbohydrate-rich foodstuffs. It is also a germ cell mutagen, inducing dominant lethal mutations and heritable chromosomal translocations in postmeiotic sperm of treated mice. Acrylamide's affinity for male germ cells has sometimes been overlooked in assessing its toxicity and defining human health risks. Previous investigations of acrylamide's germ cell activity in mice showed stronger effects after repeated administration of low doses compared with a single high dose, suggesting the possible involvement of a stable metabolite. A key oxidative metabolite of acrylamide is the epoxide glycidamide, generated by cytochrome P4502E1 (CYP2E1). To explore the role of CYP2E1 metabolism in the germ cell mutagenicity of acrylamide, CYP2E1-null and wild-type male mice were treated by intraperitoneal injection with 0, 12.5, 25, or 50 mg acrylamide (5 ml saline)(-1) kg(-1) day(-1) for 5 consecutive days. At defined times after exposure, males were mated to untreated B6C3F(1) females. Females were killed in late gestation and uterine contents were examined. Dose-related increases in resorption moles (chromosomally aberrant embryos) and decreases in the numbers of pregnant females and the proportion of living fetuses were seen in females mated to acrylamide-treated wild-type mice. No changes in any fertility parameters were seen in females mated to acrylamide-treated CYP2E1-null mice. Our results constitute the first unequivocal demonstration that acrylamide-induced germ cell mutations in male mice require CYP2E1-mediated epoxidation of acrylamide. Thus, CYP2E1 polymorphisms in human populations, resulting in variable enzyme metabolic activities, may produce differential susceptibilities to acrylamide toxicities. C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NIEHS, Toxicol Operat Branch, Res Triangle Pk, NC 27709 USA. NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. NIEHS, Off Program Dev, Res Triangle Pk, NC 27709 USA. RP Ghanayem, BI (reprint author), NIEHS, Lab Pharmacol & Chem, POB 12233,MD B3-10,111 Alexander Dr, Res Triangle Pk, NC 27709 USA. EM ghanayem@niehs.nih.gov NR 48 TC 62 Z9 72 U1 1 U2 4 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD JAN PY 2005 VL 72 IS 1 BP 157 EP 163 DI 10.1095/biolreprod.104.033308 PG 7 WC Reproductive Biology SC Reproductive Biology GA 882TF UT WOS:000225960500019 PM 15355880 ER PT J AU Balaban, RS AF Balaban, RS TI Multi-photon excitation fluorescence microscopy, in vivo. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 70 EP 70 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556300012 ER PT J AU Armant, DR Leach, RE Romero, R Edwin, S Kilburn, BA Petkova, A Edwards, HJ AF Armant, DR Leach, RE Romero, R Edwin, S Kilburn, BA Petkova, A Edwards, HJ TI First trimester human cytotrophoblast cells survive low oxygen with help from HB-EGF. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Wayne State Univ, Detroit, MI USA. Univ Illinois, Chicago, IL USA. NIH, DHHS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 81 EP 81 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556300064 ER PT J AU Falco, G Hamatani, T Lee, SL Ko, MSH AF Falco, G Hamatani, T Lee, SL Ko, MSH TI Identification and characterization of zy-gotic genome activation gene 1 (Zga1) in mouse. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 NIA, NIH, Baltimore, MD 21224 USA. RI Ko, Minoru/B-7969-2009 OI Ko, Minoru/0000-0002-3530-3015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 102 EP 102 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556300157 ER PT J AU Wu, JM Takahashi, DL Lawson, MS Pau, F Mattison, JA Ingram, DK Roth, GS Lane, MA Ottinger, MA Zelinski, MB AF Wu, JM Takahashi, DL Lawson, MS Pau, F Mattison, JA Ingram, DK Roth, GS Lane, MA Ottinger, MA Zelinski, MB TI Benefits of calorie restriction (CR) on ovarian response to exogenous gonadotropins and preimplantation embryonic development in old rhesus monkeys. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Univ Maryland, College Pk, MD 20742 USA. Oregon Hlth Sci Univ, Beaverton, OR USA. NIA, Baltimore, MD 21224 USA. Merck & Co Inc, Rahway, NJ 07065 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 109 EP 109 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556300187 ER PT J AU Goto, M Goulding, EH Eddy, EM O'Brien, DA AF Goto, M Goulding, EH Eddy, EM O'Brien, DA TI Male mice lacking speriolin produce defective sperm and abnormal zygotes. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Univ N Carolina, Sch Med, Chapel Hill, NC USA. Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 152 EP 152 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556300378 ER PT J AU Nagashima, T Maruyama, T Uchida, H Masuda, H Masanori, O Arase, T Asada, H Ozato, K Yoshimura, Y AF Nagashima, T Maruyama, T Uchida, H Masuda, H Masanori, O Arase, T Asada, H Ozato, K Yoshimura, Y TI Expression and localization of bromodomain protein 4 (Brd4) during oocyte maturation and fertilization in mice. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Keio Univ, Sch Med, Tokyo, Japan. NICHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 177 EP 177 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556301019 ER PT J AU Hewitt, SC Korach, KS AF Hewitt, SC Korach, KS TI Estren behaves as a weak estrogen rather than a non-genomic selective activator in the uterus. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 179 EP 180 PG 2 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556301031 ER PT J AU Nowak, R Bunick, D Nakai, M Couse, J Korach, K Chen, L AF Nowak, R Bunick, D Nakai, M Couse, J Korach, K Chen, L TI Expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in reproductive tissues of estrogen receptor-alpha and -beta knockout mice. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Univ Illinois, Urbana, IL 61801 USA. Natl Inst Environm Sci, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 184 EP 185 PG 2 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556301053 ER PT J AU Vallee, M Aiba, K Piao, Y Palin, MF Ko, MSH Sirard, MA AF Vallee, M Aiba, K Piao, Y Palin, MF Ko, MSH Sirard, MA TI Cross-species comparison of gene expression profile in the oocyte using oligonucleotide arrays. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Univ Laval, CRBR, Quebec City, PQ, Canada. NIA, NIH, Baltimore, MD 21224 USA. AAFC, Dairy & Swine Res & Dev Ctr, Lennoxville, PQ, Canada. RI Sirard, Marc/A-9112-2011; Ko, Minoru/B-7969-2009 OI Ko, Minoru/0000-0002-3530-3015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 192 EP 192 PG 1 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556301086 ER PT J AU Jayes, FCL Couse, JF Emmen, JMA Korach, KS AF Jayes, FCL Couse, JF Emmen, JMA Korach, KS TI Serum inhibin-A levels in estrogen receptor-null mice are increased in females lacking trogen receptor-alpha but not estrogen receptor-beta. SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract CT 38th Annual Meeting of the Society-for-the-Study-of-Reproduction CY JUL 24-27, 2005 CL Ctr Rech Biol Reproduct, Quebec City, CANADA HO Ctr Rech Biol Reproduct C1 Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 USA SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 2005 SI SI BP 223 EP 224 PG 2 WC Reproductive Biology SC Reproductive Biology GA 946EX UT WOS:000230556301229 ER PT J AU Yogeeswari, P Sriram, D Veena, V Kavya, R Rakhra, K Ragavendran, JV Mehta, S Thirumurugan, R Stables, JP AF Yogeeswari, P Sriram, D Veena, V Kavya, R Rakhra, K Ragavendran, JV Mehta, S Thirumurugan, R Stables, JP TI Synthesis of aryl semicarbazones as potential anticonvulsant agents SO BIOMEDICINE & PHARMACOTHERAPY LA English DT Article DE anticonvulsant; aryl semicarbazones; neurotoxicity ID ANTIEPILEPTIC DRUG DEVELOPMENT; MAXIMAL ELECTROSHOCK SCREEN; PROGRAM; RATS AB A series of 4-ethoxyphenyl semicarbazones (1-10) have been synthesized using an appropriate synthetic route and characterized by elemental analyses and spectral data. The anticonvulsant activity of all the synthesized compounds was evaluated against maximal electroshock induced seizures (MES) and subcutaneous pentylenetetrazole (scPTZ) induced seizure models in mice. The neurotoxicity was assessed using the rotorod method. All the test compounds were administered at doses of 30, 100, and 300 mg/kg body weight and the anticonvulsant activity was noted at 0.5 and 4 h time intervals after the drug administration. Among the compounds tested, compounds except 3, 4 and 10 showed protection from seizures in both the animal models. Compounds 6 and 8 were found to increase gamma-aminobutyric acid (GABA) levels in the medulla oblongata region of the rat brain. (c) 2005 Elsevier SAS. All rights reserved. C1 Birla Inst Technol & Sci, Med Chem Res Lab, Pharm Grp, Pilani 333031, Rajasthan, India. NIH, Epilepsy Branch, Preclin Pharmacol Sect, Bethesda, MD 20892 USA. RP Yogeeswari, P (reprint author), Birla Inst Technol & Sci, Med Chem Res Lab, Pharm Grp, Pilani 333031, Rajasthan, India. EM pyogee@bits-pilani.ac.in OI Rathinasabapathy, Thirumurugan/0000-0002-7330-0552 NR 23 TC 33 Z9 37 U1 0 U2 0 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0753-3322 J9 BIOMED PHARMACOTHER JI Biomed. Pharmacother. PD JAN-FEB PY 2005 VL 59 IS 1-2 BP 51 EP 55 DI 10.1016/j.biopha.2004.04.013 PG 5 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 910VC UT WOS:000227959300009 PM 15740936 ER PT S AU Sollers, JJ Yonezawa, Y Silver, RA Merritt, MM Thayer, JF AF Sollers, JJ Yonezawa, Y Silver, RA Merritt, MM Thayer, JF BE Caldwell, JA Wesensten, NJ TI An ambulatory recording system for the assessment of autonomic changes across multiple days. SO Biomonitoring for Physiological and Cognitive Performance during Military Operations SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Biomonitoring for Physiological and Cognitive Performance during Military Operations CY MAR 31-APR 01, 2005 CL Orlando, FL SP SPIE, Ball Aerosp & Technol Corp, Univ Cent Florida, Coll Opt & Photon, Florida Space Inst, FOI, Swedish Defense Res Agcy, Univ Central Florida DE heart period variability; ambulatory monitoring; R-spike detection AB Recent evidence indicates that poor autonomic regulation, indexed by decreased heart period variability (HPV), is associated with decreased working memory. HPV analyses are computed on the interbeat interval time series derived from the electrocardiogram (EKG). Unfortunately, the duration of the data collection and the issue of the size of ambulatory monitors with sufficient storage capacity for multi-day records is somewhat problematic. In the present paper we describe a system that allows for the collection of large amounts of high quality data using a small data collection device. The recording system consists of a miniature, single-module electrocardiogram-recording device. This module consists of an integrated three-electrode device that is attached to the chest of the subject. A low power 8-bit micro-controller detects the R-spike and stores the time between R-spikes in milliseconds on a 512 KB EEPROM. This system can record continuously for over four days. This system will allow the recording of cardio-dynamics in the field and provide highly reliable data across multiple days. The use of this device to assess physiological function in military operations would allow researchers to examine longer data records across several contexts and to understand the role of changes in autonomic function as they relate to performance. C1 NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Sollers, JJ (reprint author), NIA, Intramural Res Program, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 0-8194-5782-5 J9 P SOC PHOTO-OPT INS PY 2005 VL 5797 BP 56 EP 62 DI 10.1117/12.604413 PG 7 WC Behavioral Sciences; Instruments & Instrumentation; Physiology SC Behavioral Sciences; Instruments & Instrumentation; Physiology GA BCR90 UT WOS:000230979900007 ER PT S AU Thayer, JF Hansen, AL Sollers, JJ Johnsen, BH AF Thayer, JF Hansen, AL Sollers, JJ Johnsen, BH BE Caldwell, JA Wesensten, NJ TI Heart rate variability as an index of prefrontal neural function in military settings SO Biomonitoring for Physiological and Cognitive Performance during Military Operations SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Biomonitoring for Physiological and Cognitive Performance during Military Operations CY MAR 31-APR 01, 2005 CL Orlando, FL SP SPIE, Ball Aerosp & Technol Corp, Univ Cent Florida, Coll Opt & Photon, Florida Space Inst, FOI, Swedish Defense Res Agcy, Univ Central Florida DE heart rate variability; neurovisceral integration; executive function; working memory ID WORKING-MEMORY; COGNITIVE FUNCTION; CORTEX; MECHANISMS; EMOTION; PERSPECTIVE; MODULATION; DEPRESSION; BEHAVIOR; NETWORK AB In the present paper we describe a model of neurovisceral integration in which a set of neural structures involved in cognitive, affective, and autonomic regulation are related to heart rate variability (HRV) and cognitive performance. We will provide pharmacological and neuroimaging data in support of the neural structures linking the central nervous system to HRV. Next, we will review a number of studies from our group using military cadets showing that individual differences in HRV are related to performance on tasks associated with executive function and prefrontal cortical activity. In the first study, individual differences in resting HRV we related to performance on executive and nonexecutive function tasks. The results showed that greater HRV was associated with better performance on executive function tasks. In the second study we add a stressor (shock avoidance) to the previous paradigm and show that those with greater HRV were more stress tolerant. Specifically, those with greater HRV were not adversely affected by the added stressor. In the last experiment, HRV was manipulated by physical detraining. Again, those that maintained their HRV at the post-test showed better performance on executive function tasks. We propose that these findings have important implications for the development of biomarkers related to performance in modem warfighters. C1 NIA, Baltimore, MD 21224 USA. RP Thayer, JF (reprint author), NIA, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 41 TC 2 Z9 2 U1 1 U2 9 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 0-8194-5782-5 J9 P SOC PHOTO-OPT INS PY 2005 VL 5797 BP 71 EP 77 DI 10.1117/12.604420 PG 7 WC Behavioral Sciences; Instruments & Instrumentation; Physiology SC Behavioral Sciences; Instruments & Instrumentation; Physiology GA BCR90 UT WOS:000230979900009 ER PT J AU Gunasekaran, K Nussinov, R AF Gunasekaran, K Nussinov, R TI Analysis of ordered and disordered protein complexes reveals structural features discriminating between stable and unstable monomers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, SAIC Frederick, Frederick, MD USA. Tel Aviv Univ, SAIC Frederick, NCI Frederick, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 3A EP 3A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500009 ER PT J AU Keskin, O Ma, BY Nussinov, R AF Keskin, O Ma, BY Nussinov, R TI Hot regions in protein-protein interactions: The organization and contribution of structurally conserved hot spot residues SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Koc Univ, Istanbul, Turkey. NCI, SAIC, Frederick, MD 21701 USA. Tel Aviv Univ, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 5A EP 5A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500016 ER PT J AU Tan, X Mizuuchi, K AF Tan, X Mizuuchi, K TI Single-molecule study of protein-DNA interactions in DNA recombination reaction: Is there a memory effect to MuB assembly target DNA? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIDDK, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 14A EP 15A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500061 ER PT J AU Milescu, M Vobecky, J Kim, JI Swartz, KJ AF Milescu, M Vobecky, J Kim, JI Swartz, KJ TI Interaction between gating modifier toxins and lipid membranes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NINDS, Mol Physiol & Biophys Sect, NIH, Bethesda, MD 20892 USA. Kwangju Inst Sci & Technol, Dept Life Sci, Kwangju, Saint Helena, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 20A EP 20A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500090 ER PT J AU Polozov, IV Zimmerberg, J Gawrisch, K AF Polozov, IV Zimmerberg, J Gawrisch, K TI Lipid domains and diffusion studied by pulsed field gradient H-1 MAS NMR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, NIH, Bethesda, MD USA. NIAAA, NIH, Rockville, MD 20852 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 26A EP 26A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500117 ER PT J AU Dustman, JM Casas, RS Scheidt, HA Eldho, NV Teague, WE Gawrisch, K AF Dustman, JM Casas, RS Scheidt, HA Eldho, NV Teague, WE Gawrisch, K TI Lipid hydrocarbon chain dynamics and lateral diffusion in a polyunsaturated lipid matrix SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, NIH, Rockville, MD 20852 USA. RI Scheidt, Holger A./C-1416-2014 NR 0 TC 3 Z9 3 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 27A EP 27A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500124 ER PT J AU Bell, SM Choi, S Curran, PK Mindell, JA AF Bell, SM Choi, S Curran, PK Mindell, JA TI Probing conformational changes in a prokaryotic CIC chloride transporter using site-directed fluorescence labeling SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Johns Hopkins Univ, Baltimore, MD USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 29A EP 30A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500136 ER PT J AU Pan, YP Ma, BY Keskin, O Nussinov, R AF Pan, YP Ma, BY Keskin, O Nussinov, R TI Characterization of the conformational state and flexibility of HIV-1 gp120 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Natl Canc Inst, Frederick, MD USA. Koc Univ, Istanbul, Turkey. Tel Aviv Univ, IL-69978 Tel Aviv, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 34A EP 34A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500163 ER PT J AU Kubelka, J Eaton, WA Hoftichter, J AF Kubelka, J Eaton, WA Hoftichter, J TI The kinetics of an ultrafast folding protein analyzed with a free energy surface model SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 42A EP 42A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500203 ER PT J AU Baxter, TK Gagnon, S Davis-Harrison, R Beck, J Binz, AK Turner, R Biddison, W Baker, B AF Baxter, TK Gagnon, S Davis-Harrison, R Beck, J Binz, AK Turner, R Biddison, W Baker, B TI Strategic mutations in the class I MHC HLA-A2 independently affect both peptide binding and T cell receptor recognition SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Notre Dame, Notre Dame, IN 46556 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 43A EP 43A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500208 ER PT J AU Clemens, JR Davis-Harrison, RL Gagnon, SJ Biddison, WE Baker, BM AF Clemens, JR Davis-Harrison, RL Gagnon, SJ Biddison, WE Baker, BM TI Testing "functional selection" in TCR recognition of ligand SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Notre Dame, Notre Dame, IN 46556 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 43A EP 44A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500209 ER PT J AU Zhurkin, VB Tolstorukov, MY Olson, WK AF Zhurkin, VB Tolstorukov, MY Olson, WK TI DNA bending induced by A-tracts: Comparison of X-ray and NMR structures with DNA cyclization and gel electrophoresis SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Rutgers State Univ, New Brunswick, NJ 08903 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 58A EP 58A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500281 ER PT J AU Sidorova, NY Muradymov, S Rau, DC AF Sidorova, NY Muradymov, S Rau, DC TI Water release accompanying DNA-BamHI binding as measured by novel self-cleavage assay SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 63A EP 63A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500311 ER PT J AU Leikina, E Delanoe, H Melikov, K Waring, AJ Lehrer, RI Chernomordik, LV AF Leikina, E Delanoe, H Melikov, K Waring, AJ Lehrer, RI Chernomordik, LV TI Retrocyclin-2 inhibits early stages of membrane fusion reactions mediated by envelope glycoproteins of diverse viruses. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, NIH, Bethesda, MD USA. Univ Calif Los Angeles, Dept Med, Los Angeles, CA USA. RI Melikov, Kamran/A-6604-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 66A EP 66A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500322 ER PT J AU Biswas, S Blank, PS Zimmerberg, J AF Biswas, S Blank, PS Zimmerberg, J TI Cholesterol expand fusion pore in influenza hemagglutinin mediated fusion SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 68A EP 68A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500335 ER PT J AU Zaitseva, EM Mittal, A Chernomordik, LV AF Zaitseva, EM Mittal, A Chernomordik, LV TI The role of envelope-capsid interaction in Sindbis virus mediated fusion SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, LCMB, NIH, Bethesda, MD USA. RI Mittal, Aditya/E-3087-2010 OI Mittal, Aditya/0000-0002-4030-0951 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 68A EP 69A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500336 ER PT J AU Santiago, DJ Shannon, TR Rios, E Stern, MD AF Santiago, DJ Shannon, TR Rios, E Stern, MD TI Skeletal and cardiac Ca2+ sparks "mano a mano". A comparison of source kinetics by morphometry and modeling. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Rush Univ, Chicago, IL 60612 USA. Natl Inst Hlth, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 86A EP 86A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500420 ER PT J AU Sirenko, S Maltseva, LA Crider, D Stern, MD Lakatta, EG Maltsev, VA AF Sirenko, S Maltseva, LA Crider, D Stern, MD Lakatta, EG Maltsev, VA TI Coordinated spontaneous local oscillatory Ca2+ release from separate sites in cardiac myocytes derived from mouse embryonic stem cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, Baltimore, MD 21224 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 88A EP 88A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500432 ER PT J AU Maltsev, VA Vinogradova, TM Stern, MD Lakatta, EG AF Maltsev, VA Vinogradova, TM Stern, MD Lakatta, EG TI Local subsarcolemmal Ca2+ releases within rabbit sinoatrial nodal cells not only regulate beating rate but also ensure normal rhythm during protein kinase A inhibition. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, Ctr Gerontol Res, NIH, Baltimore, MD 21224 USA. NR 0 TC 5 Z9 5 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 89A EP 90A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500437 ER PT J AU Lu, SJ Borst, DE Horowits, R AF Lu, SJ Borst, DE Horowits, R TI N-RAP expression during mouse heart development SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 118A EP 118A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500574 ER PT J AU Xu, SG Gu, J White, H Offer, G Yu, LP Bethesda, NIH AF Xu, SG Gu, J White, H Offer, G Yu, LP Bethesda, NIH TI Structural effects on myosin of three ATPase inhibitors SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Eastern Virginia Med Sch, Norfolk, VA 23501 USA. Univ Bristol, Bristol, Avon, England. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 124A EP 124A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500602 ER PT J AU Davis, JS Epstein, ND AF Davis, JS Epstein, ND TI Identification and quantitative characterization of the kinetic source of tension in skeletal muscle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 126A EP 126A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500611 ER PT J AU Song, LS Pi, YQ Guatimosim, S Kim, SJ Yatani, A Kudej, RK Zhang, QX Hittinger, L Ghaleh, B Cheng, HP Vatner, DE Lederer, WJ Vatner, SF AF Song, LS Pi, YQ Guatimosim, S Kim, SJ Yatani, A Kudej, RK Zhang, QX Hittinger, L Ghaleh, B Cheng, HP Vatner, DE Lederer, WJ Vatner, SF TI Impaired cellular Ca+2 handling in compensated canine left ventricular hypertrophy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 UMBI, MBC, Baltimore, MD USA. Univ Med & Dent New Jersey, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA. NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. RI Lederer, William/B-1285-2010; Song, Long-Sheng/D-5899-2012 NR 0 TC 1 Z9 2 U1 0 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 135A EP 136A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500655 ER PT J AU Zhang, PJ Subramaniam, S AF Zhang, PJ Subramaniam, S TI Imaging of chemotaxis receptor clusters in E-coli cells overproducing Tsr SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, NIH, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 144A EP 145A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500699 ER PT J AU Klauda, JB Brooks, BR MacKerell, AD Venable, RM Pastor, RW AF Klauda, JB Brooks, BR MacKerell, AD Venable, RM Pastor, RW TI Lipid bilayers: Structural and dynamical properties with an improved force field fit to ab initio quantum mechanics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, NIH, Bethesda, MD 20892 USA. Univ Maryland, Baltimore, MD 21201 USA. US FDA, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA. RI Klauda, Jeffery/A-4345-2008 NR 0 TC 1 Z9 1 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 148A EP 149A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500718 ER PT J AU Lefman, J Morrison, R Subramaniam, S AF Lefman, J Morrison, R Subramaniam, S TI Towards high-throughput transmission electron microscopy imaging using a multi-specimen, cartridge loading device and automated data acquisition SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, Cell Biol Lab, Bethesda, MD 20892 USA. Gatan UK, Abingdon, Oxon, England. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 148A EP 148A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500716 ER PT J AU Kim, J Batteas, JD Forbes, JG Wang, KA AF Kim, J Batteas, JD Forbes, JG Wang, KA TI Fabrication and characterization of patterned surfaces for single protein arrays by scanning probe techniques SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Natl Inst Stand & Technol, Gaithersburg, MD 20899 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 156A EP 156A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500754 ER PT J AU Toptygin, D Gronenborn, AM Brand, L AF Toptygin, D Gronenborn, AM Brand, L TI Spectrally- and time-resolved fluorescence of 5-fluorotryptophan and normal tryptophan in the B1 domain of streptococcal protein G. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA. NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 161A EP 161A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500782 ER PT J AU Ignatov, M Randolph, J Tsutsui, Y Dash, C LeGrice, SFJ Barkley, M AF Ignatov, M Randolph, J Tsutsui, Y Dash, C LeGrice, SFJ Barkley, M TI Photophysical characterization of a novel fluorescent nucleotide base analog: 6-methyl-pyrollo-[2,3-d]-pyrimidine-2(3H)-one SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Case Western Reserve Univ, Cleveland, OH 44106 USA. Glenn Res Corp, Sterling, VA USA. NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 163A EP 163A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500789 ER PT J AU Michelman-Ribeiro, A Nossal, R Horkay, F Boukari, H AF Michelman-Ribeiro, A Nossal, R Horkay, F Boukari, H TI Fluorescence correlation spectroscopy study of probe diffusion in Poly(vinyl alcohol) solutions and gels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 165A EP 165A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500802 ER PT J AU Chanturiya, AN Glushakova, S Yin, D Zimmerberg, J AF Chanturiya, AN Glushakova, S Yin, D Zimmerberg, J TI Is there any effect of magnetic field on malaria parasite replication in human red blood cells? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 171A EP 171A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500832 ER PT J AU Gaede, HC Luckett, KM Polozov, IV Yeliseev, AA Wong, KKY Gawrisch, K AF Gaede, HC Luckett, KM Polozov, IV Yeliseev, AA Wong, KKY Gawrisch, K TI NMR studies on single lipid bilayers supported in cylindrical aluminum oxide nanopores - Reconstitution of GPCR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, NIH, Rockville, MD 20852 USA. RI Yeliseev, Alexei/B-3143-2009; Gaede, Holly/B-7392-2015 OI Gaede, Holly/0000-0003-4444-4394 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 187A EP 187A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500910 ER PT J AU Xiao, BL Jiang, MT Zhao, MC Yang, DM Sutherland, C Lai, FA Walsh, MP Cheng, HP Chen, SRW AF Xiao, BL Jiang, MT Zhao, MC Yang, DM Sutherland, C Lai, FA Walsh, MP Cheng, HP Chen, SRW TI Characterization of a novel protein kinase a phosphorylation site, serine-2030, reveals no hyperphosphorylation of the cardiac ryanodine receptor in heart failure SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Calgary, Calgary, AB, Canada. Med Coll Wisconsin, Milwaukee, WI 53226 USA. NIH, Baltimore, MD USA. Univ Wales Coll Cardiff, Coll Med, Cardiff CF1 3NS, S Glam, Wales. NR 0 TC 1 Z9 1 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 188A EP 188A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500913 ER PT J AU Jiang, DW Xiao, BL Wang, RW Yang, DM Choi, P Zhang, L Cheng, HP Chen, SRW AF Jiang, DW Xiao, BL Wang, RW Yang, DM Choi, P Zhang, L Cheng, HP Chen, SRW TI RyR2 mutations linked to ventricular tachycardia increase store overload induced Ca2+ release (SOICR) activity and luminal Ca2+ activation without altering FKBP12.6-RyR2 interaction SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Calgary, Calgary, AB, Canada. NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 189A EP 189A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500919 ER PT J AU Brochet, DX Yang, DM Di Maio, A Lederer, WJ Franzini-Armstrong, C Cheng, HP AF Brochet, DX Yang, DM Di Maio, A Lederer, WJ Franzini-Armstrong, C Cheng, HP TI Sarcoplasmic reticulum nanostore depletion during a calcium spark in intact cardiac cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Univ Penn, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA. Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Baltimore, MD 21201 USA. RI Lederer, William/B-1285-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 190A EP 190A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500924 ER PT J AU Inbar, Y Nussinov, R Wolfson, H AF Inbar, Y Nussinov, R Wolfson, H TI Prediction of multi-molecular assemblies and protein structures by multiple combinatorial docking SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Tel Aviv Univ, IL-69978 Tel Aviv, Israel. NCI, SAIC, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 198A EP 198A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500959 ER PT J AU Oke, O Burgess, S Wang, F Sellers, JR White, HD Knight, PJ Trinick, J AF Oke, O Burgess, S Wang, F Sellers, JR White, HD Knight, PJ Trinick, J TI Post power stroke lead heads in myosin V SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Leeds, Leeds, W Yorkshire, England. NHLBI, NIH, Bethesda, MD 20892 USA. Eastern Virginia Med Sch, Norfolk, VA 23501 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 205A EP 205A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500991 ER PT J AU Kovacs, M Wang, F Sellers, JR AF Kovacs, M Wang, F Sellers, JR TI Mechanism of action of the membrane motor myosin X SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD 20892 USA. RI Kovacs, Mihaly/A-6841-2011 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 206A EP 206A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378500998 ER PT J AU Ma, BY Nussinov, R AF Ma, BY Nussinov, R TI Release factors eRF1 and RF2: A universal mechanism controls the large conformational changes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 SAIC Frederick, NCI, NIH, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 210A EP 210A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501016 ER PT J AU Cohen, JA Podgornik, R Hansen, PL Parsegian, VA AF Cohen, JA Podgornik, R Hansen, PL Parsegian, VA TI Connecting the dots: PEG osmotic pressures follow universal scaling laws SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, LPSB, NIH, Bethesda, MD USA. Univ Pacific, San Francisco, CA USA. Univ Ljubljana, Ljubljana, Slovenia. Univ So Denmark, Odense M, Denmark. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 NR 0 TC 0 Z9 0 U1 0 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 236A EP 236A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501151 ER PT J AU Petrache, HI Belloni, L Zemb, T Parsegian, VA AF Petrache, HI Belloni, L Zemb, T Parsegian, VA TI Specific ion adsorption on Zwitterionic bilayers: Charge regulation and ionic screening of dispersion forces SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD USA. CEA, Serv Chim Mol, Saclay, France. RI ZEMB, Thomas/E-5958-2010 NR 1 TC 1 Z9 1 U1 2 U2 4 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 236A EP 236A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501152 ER PT J AU Hess, ST Farrington, J Baumgart, T Zimmerberg, J AF Hess, ST Farrington, J Baumgart, T Zimmerberg, J TI Lateral organization and domain partitioning of influenza hemagglutinin in fibroblast cell plasma membranes and membrane blebs SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Maine, Orono, ME USA. NICHD, LCMB, NIH, Bethesda, MD USA. Cornell Univ, Ithaca, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 239A EP 239A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501169 ER PT J AU Scheidt, HA Muller, P Herrmann, A Arnold, K Gawrisch, K Huster, D AF Scheidt, HA Muller, P Herrmann, A Arnold, K Gawrisch, K Huster, D TI Comparing the biophysical properties of sterols in lipid membranes - what is special about cholesterol? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Leipzig, D-7010 Leipzig, Germany. NIAAA, NIH, Rockville, MD USA. Humboldt Univ, Berlin, Germany. RI Scheidt, Holger A./C-1416-2014 NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 240A EP 241A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501176 ER PT J AU Kucerka, N Liu, YF Chu, NJ Petrache, HI Tristram-Nagle, S Nagle, JF AF Kucerka, N Liu, YF Chu, NJ Petrache, HI Tristram-Nagle, S Nagle, JF TI Structure of fully hydrated fluid phase DMPC and DLPC lipid bilayers using X-ray scattering from oriented multilamellar arrays and from large unilamellar vesicles SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. NIH, Bethesda, MD 20892 USA. RI Tristram-Nagle, Prof. Stephanie/N-7811-2014; Nagle, John/B-1917-2015 OI Tristram-Nagle, Prof. Stephanie/0000-0003-2271-7056; Nagle, John/0000-0002-9844-5934 NR 0 TC 11 Z9 11 U1 0 U2 4 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 245A EP 245A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501196 ER PT J AU Petrache, HI Brown, MF AF Petrache, HI Brown, MF TI Correspondence of states and universal features of lipid acyl chain packing as determined by solid state H-2 NMR spectroscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Univ Arizona, Dept Phys, Tucson, AZ 85721 USA. Univ Arizona, Dept Chem, Tucson, AZ 85721 USA. NR 1 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 247A EP 247A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501210 ER PT J AU Schagina, LV Ostroumova, OS Gurnev, PA Takemoto, JY Malev, VV AF Schagina, LV Ostroumova, OS Gurnev, PA Takemoto, JY Malev, VV TI Voltage-dependent synchronization of gating of cyclic lipodepsipeptide ion channels in planar lipid bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 RAS, Inst Cytol, St Petersburg, Russia. NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. Utah State Univ, Logan, UT 84322 USA. RI Ostroumova, Olga/N-8636-2013; Takemoto, Jon/A-5309-2011 OI Takemoto, Jon/0000-0001-9919-9168 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 247A EP 247A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501212 ER PT J AU Ostroumova, OS Gurnev, PA Takemoto, JY Malev, VV Schagina, LV AF Ostroumova, OS Gurnev, PA Takemoto, JY Malev, VV Schagina, LV TI Kinetic parameters of cyclic lipodepsipeptide ion channels in planar lipid bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 RAS, Inst Cytol, St Petersburg, Russia. NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. Utah State Univ, Logan, UT 84322 USA. RI Ostroumova, Olga/N-8636-2013; Takemoto, Jon/A-5309-2011 OI Takemoto, Jon/0000-0001-9919-9168 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 248A EP 248A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501216 ER PT J AU Ramalingam, AB Swartz, KJ AF Ramalingam, AB Swartz, KJ TI Mutagenesis at the interface between gating modifier toxins and voltage sensors in Kv2.1 channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NINDS, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 249A EP 249A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501220 ER PT J AU Jin, AJ Choi, EJ Niu, SL Smith, PD Litman, BJ AF Jin, AJ Choi, EJ Niu, SL Smith, PD Litman, BJ TI Atomic force microscopy studies of rhodopsin (a G protein-coupled receptor) molecules in vision membranes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, OD, ORS, DBEPS, Bethesda, MD 20892 USA. NIAAA, NIH, LMBB, SFS, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 253A EP 253A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501238 ER PT J AU Xiong, W Zhang, C Zheng, H Zheng, LH Lu, B Zhou, Z AF Xiong, W Zhang, C Zheng, H Zheng, LH Lu, B Zhou, Z TI Calcium- and dynamin-independentendocytosis in dorsal root ganglion neurons SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Inst Neurosci, Shanghai, Peoples R China. Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China. NINDS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 259A EP 260A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501269 ER PT J AU Jin, AJ Prasad, K Smith, PD Lafer, EM Nossal, RJ AF Jin, AJ Prasad, K Smith, PD Lafer, EM Nossal, RJ TI Clathrin coated vesicle elasticity via atomic force microscopy and elastic thin shell analysis SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, OD, ORS, DBEPS, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Dept Biochem, San Antonio, TX 78285 USA. NICHD, NIH, Lab Integrat & Med Biophys, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 260A EP 261A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501274 ER PT J AU Ferguson, ML Prasad, K Sackett, DL Schuck, P Boukari, H Lafer, EM Nossal, RJ AF Ferguson, ML Prasad, K Sackett, DL Schuck, P Boukari, H Lafer, EM Nossal, RJ TI The effect of solution conditions on the conformation of clathrin triskelions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Maryland College Pk, NIH, Bethesda, MD USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX 78285 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 261A EP 262A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501279 ER PT J AU Josephson, IR Guia, A Lederer, WJ Lakatta, EG Stern, MD AF Josephson, IR Guia, A Lederer, WJ Lakatta, EG Stern, MD TI Calcium concentration-dependence of inactivation of unitary L-type Ca channels. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Maryland, Inst Biotechnol, Baltimore, MD 21201 USA. NIA, Baltimore, MD 21224 USA. RI Lederer, William/B-1285-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 274A EP 274A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501338 ER PT J AU Lin, SY Holt, JR Vollrath, MA Garcia-Anoveros, J Geleoc, G Kwan, K Hoffman, MP Zhang, DS Corey, DP AF Lin, SY Holt, JR Vollrath, MA Garcia-Anoveros, J Geleoc, G Kwan, K Hoffman, MP Zhang, DS Corey, DP TI TRPA1 is a candidate for the mechanosensitive transduction channel of vertebrate hair cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. MIT, Boston, MA USA. Univ Virginia, Charlottesville, VA 22903 USA. Northwestern Univ, Chicago, IL 60611 USA. NIDCR, Bethesda, MD USA. NR 0 TC 4 Z9 4 U1 1 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 287A EP 288A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501400 ER PT J AU Contreras, JE Holmgren, M AF Contreras, JE Holmgren, M TI Quaternary ammonium blockade of cyclic nucleotide-gated (CNG) channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 292A EP 292A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501423 ER PT J AU Lyashkov, A Vinogradova, T Yang, DM Zhu, WH Lakatta, E AF Lyashkov, A Vinogradova, T Yang, DM Zhu, WH Lakatta, E TI Crosstalk between muscarinic receptor stimulation and PKA signaling in modulation of local submembrane calcium releases and beating rate of rabbit sinoatrial nodal cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 298A EP 299A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501453 ER PT J AU Vinogradova, TM Lyashkov, AE Zhu, WZ Spurgeon, H Maltsev, VA Lakatta, EG AF Vinogradova, TM Lyashkov, AE Zhu, WZ Spurgeon, H Maltsev, VA Lakatta, EG TI Constitutive phosphodiesterase activity confers negative feedback on intrinsic cAMP-PKA regulation of local subsarcolemmal calcium releases and spontaneous beating in rabbit sinoatrial nodal cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 6 Z9 6 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 303A EP 303A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501471 ER PT J AU Horowits, R Dhume, A AF Horowits, R Dhume, A TI Targeted disruption of N-RAP gene function by RNA interference (RNAi): A role for N-RAP in myofibril organization SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 307A EP 307A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501492 ER PT J AU Yadavalli, VK Forbes, JG Wang, K AF Yadavalli, VK Forbes, JG Wang, K TI Elasticity of single native nebulin molecules. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 312A EP 312A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501515 ER PT J AU Smirnov, AV Combs, CA Blinova, K Knutson, JR Balaban, RS AF Smirnov, AV Combs, CA Blinova, K Knutson, JR Balaban, RS TI Two-photon fluorescence lifetime imaging of mitochondrial NADH in live cardiac myocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, LBC, NIH, Bethesda, MD 20892 USA. NHLBI, LCE, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 330A EP 330A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501601 ER PT J AU Lee, EH Gronenborn, AM Schulten, K AF Lee, EH Gronenborn, AM Schulten, K TI Molecular modeling and dynamics studies of GB1 F26A protein fibril SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Illinois, Urbana, IL 61801 USA. NIH, Chem Phys Lab, Bethesda, MD 20892 USA. RI Schulten, Klaus/D-5561-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 331A EP 331A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501603 ER PT J AU Kobrinsky, E Mager, DE Bentil, SA Murata, S Abernethy, DR Soldatov, NM AF Kobrinsky, E Mager, DE Bentil, SA Murata, S Abernethy, DR Soldatov, NM TI Identification of functional signaling plasma membrane macro- and micro-domains from wavelet analysis of FRET microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, NIH, Bethesda, MD 20892 USA. Univ Yamanashi, Dept Pathol, Yamanashi, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 337A EP 337A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501640 ER PT J AU Thaler, C Koushik, SV Blank, PS Vogel, SS AF Thaler, C Koushik, SV Blank, PS Vogel, SS TI Quantitative multiphoton spectral imaging and its use for measuring resonance energy transfer SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, NIH, Rockville, MD 20852 USA. NICHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 338A EP 338A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501642 ER PT J AU Jobsis, PD Combs, CA Balaban, RS AF Jobsis, PD Combs, CA Balaban, RS TI Emission ratiometric determination of cellular pH by 2-photon microscopy of 2,3-dicyanohydroquinone and 2-photon microscope emission spectral calibration SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 340A EP 340A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501651 ER PT J AU Cho, EH Costes, SV Lockett, SJ AF Cho, EH Costes, SV Lockett, SJ TI Simple protocols for quantitative characterization of optical microscopy performance. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, SAIC, Frederick, MD 21701 USA. Lawrence Berkeley Natl Lab, Berkeley, CA USA. RI Costes, Sylvain/D-2522-2013; Cho, Edward/B-3727-2012 OI Costes, Sylvain/0000-0002-8542-2389; Cho, Edward/0000-0002-0278-334X NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 344A EP 344A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501671 ER PT J AU Rothstein, EC Balaban, RS AF Rothstein, EC Balaban, RS TI Secondary optical inner filter effects on two-photon excitation microscopy of NAD(P)H in mouse skeletal muscle, in vivo SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 345A EP 345A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501676 ER PT J AU Cruceanu, M Stephen, AG Fisher, RJ Gorelick, RJ Williams, MC AF Cruceanu, M Stephen, AG Fisher, RJ Gorelick, RJ Williams, MC TI Screening chemical compounds for anti-IHV-1 NC activity by using single DNA molecule stretching experiments SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Northeastern Univ, CIRCS, Boston, MA 02115 USA. SAIC Frederick Inc, AIDS Vaccine Program, NCI, Frederick, MD USA. RI Fisher, Robert/B-1431-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 348A EP 348A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501696 ER PT J AU Harry, JB Kobrinsky, E Abernethy, DR Soldatov, NM AF Harry, JB Kobrinsky, E Abernethy, DR Soldatov, NM TI New short splice variants of the human cardiac Ca(v)Beta(2) subunit: Redefining the major functional motifs SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Natl Inst Aging, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 366A EP 366A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501786 ER PT J AU Xu, JH Graver, KJ Toptygin, D Savetchenko, RS Meadow, ND Roseman, S Brand, L Knutson, JR AF Xu, JH Graver, KJ Toptygin, D Savetchenko, RS Meadow, ND Roseman, S Brand, L Knutson, JR TI Femtosecond decay associated spectra of tryptophan in proteins: Solvent relaxation vs. heterogeneity SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 372A EP 372A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501813 ER PT J AU Shafrir, Y Shrivastava, IR Guy, HR AF Shafrir, Y Shrivastava, IR Guy, HR TI Models of the structure and gating mechanism of the NaChBac channel SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 379A EP 379A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501844 ER PT J AU Hirata, Y Collet, C Wang, X Weisleder, N Brotto, M Pan, Z Cheng, HP Ma, JJ AF Hirata, Y Collet, C Wang, X Weisleder, N Brotto, M Pan, Z Cheng, HP Ma, JJ TI Fluttered Ca2+ sparks and Ca2+ bursts in intact adult mammalian skeletal muscle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, Baltimore, MD 21224 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. RI Weisleder, Noah/A-7098-2013 OI Weisleder, Noah/0000-0002-2619-8022 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 383A EP 383A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501865 ER PT J AU Tocchetti, CG Wang, W Katori, T Aon, MA O'Rourke, B Miranda, KM Wink, DA Cheng, HP Kass, DA Paolocci, N AF Tocchetti, CG Wang, W Katori, T Aon, MA O'Rourke, B Miranda, KM Wink, DA Cheng, HP Kass, DA Paolocci, N TI Nitroxyl increases calcium release from ryanodine receptors in a thiolsensitive but cGMP-independent manner. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Univ Arizona, Tucson, AZ USA. NCI, NIH, Bethesda, MD 20892 USA. RI Miranda, Katrina/B-7823-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 384A EP 384A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501868 ER PT J AU Azarov, I Huang, KT Cass, M Basu, S Cho, M Nichols, JS Gladwin, MT Hogg, N Kim-Shapiro, DB AF Azarov, I Huang, KT Cass, M Basu, S Cho, M Nichols, JS Gladwin, MT Hogg, N Kim-Shapiro, DB TI NO uptake rates of normal and sickle red blood cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Wake Forest Univ, Winston Salem, NC 27109 USA. NIH, Bethesda, MD 20892 USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 391A EP 391A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501906 ER PT J AU Rifkind, JM Nagababu, E Ramasamy, S AF Rifkind, JM Nagababu, E Ramasamy, S TI S-nitrosohemoglobin Formation: a mechanism involving electron delocalization in the heme pocket SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, Baltimore, MD 21224 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 391A EP 391A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501907 ER PT J AU Tsai, HHG Nussinov, R AF Tsai, HHG Nussinov, R TI Simulations of amyloidogenic peptide self-assembly in atomistic detail using replica-exchange molecular dynamics algorithm SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, SAIC Frederick, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 401A EP 401A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501956 ER PT J AU Mishra, SH Germann, MW Darby, MK AF Mishra, SH Germann, MW Darby, MK TI Design and evaluation of HIV-RNA binding zinc finger proteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Georgia State Univ, Atlanta, GA 30303 USA. NIEHS, Chapel Hill, NC USA. RI German, Markus/L-1531-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 406A EP 406A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501985 ER PT J AU Voloshchuk, N Hawkins, ME Davenport, L AF Voloshchuk, N Hawkins, ME Davenport, L TI Mapping the DNA binding site of HIV-1 integrase using fluorescent oligonucleotides and fluorescence polarization SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 CUNY, Brooklyn Coll, Brooklyn, NY 11210 USA. NCI, Pediat Branch, NIH, Bethesda, MD 20892 USA. CUNY Grad Sch & Univ Ctr, New York, NY 10036 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 406A EP 407A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378501986 ER PT J AU Hayakawa, E Tokumasu, F Takeuchi, T Dvorak, JA AF Hayakawa, E Tokumasu, F Takeuchi, T Dvorak, JA TI The effect of lipoarabinomannan, Mycobacterium tuberculosis - derived lipids on lipid membrane domain structure SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAID, NIH, Rockville, MD USA. Japan Sci & Technol Agcy, PRESTO, Kawaguchi, Japan. Keio Univ, Sch Med, Tokyo, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 417A EP 418A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502041 ER PT J AU Pacifico, AM Mitchell, DC Hines, KG AF Pacifico, AM Mitchell, DC Hines, KG TI Comparison of membrane properties for 22 : 6N-3 coupled with PC vs. 22 : 6N-3 coupled with PE SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 417A EP 417A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502037 ER PT J AU Tekle, E Oubrahim, H Dzekunov, SM Kolb, J Schoenbach, KH Chock, BP AF Tekle, E Oubrahim, H Dzekunov, SM Kolb, J Schoenbach, KH Chock, BP TI Selective field effects on intracellular vacuoles and vesicle membranes with nano-second electric pulses SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, LB, NIH, Bethesda, MD 20892 USA. Maxcyte Inc, Gaithersburg, MD USA. Old Dominion Univ, Ctr Bioelect, Norfolk, VA USA. RI Kolb, Juergen/A-5515-2016 OI Kolb, Juergen/0000-0002-0434-5001 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 417A EP 417A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502039 ER PT J AU Niu, SL Mitchell, DC AF Niu, SL Mitchell, DC TI Membrane protein packing density modulates bilayer properties and receptor function SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 428A EP 429A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502095 ER PT J AU Bailey, BW Lewis, J Mitchell, DC AF Bailey, BW Lewis, J Mitchell, DC TI Synaptosomal GABA(A) receptor flumazenil binding varies with gender during chronic n-3 fatty acid deficiency SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, NIH, Bethesda, MD USA. RI Bailey, Brian/B-1732-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 429A EP 429A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502096 ER PT J AU Hopper, RK Carroll, S Aponte, A Balaban, RS AF Hopper, RK Carroll, S Aponte, A Balaban, RS TI Proteomic screen of calcium-induced mitochondrial protein phosphorylation: functional characterization of a novel phosphorylation of manganese superoxide dismutase SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 435A EP 435A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502124 ER PT J AU Kazemi, N Rostovtseva, TK AF Kazemi, N Rostovtseva, TK TI Effect of lipid composition on VDAC channel voltage-gating SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 444A EP 444A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502167 ER PT J AU Kobrinsky, E Tiwari, S Maltsev, VR Harry, B Soldatov, NM AF Kobrinsky, E Tiwari, S Maltsev, VR Harry, B Soldatov, NM TI Differential role of Ca(v)1.2 alpha 1 subunit tails in regulation of the L-type C2+ channel by membrane potential, beta Subunits and Ca2+ ions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIA, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 448A EP 448A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502183 ER PT J AU Guy, HR Shrivastava, IR Durell, SR AF Guy, HR Shrivastava, IR Durell, SR TI Modifications of models of the structure and gating mechanism of the KvAP channel to fit EM data SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 457A EP 457A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502228 ER PT J AU Phillips, LR Li-Smerin, Y Kim, JI Swartz, KJ AF Phillips, LR Li-Smerin, Y Kim, JI Swartz, KJ TI Protein-protein interactions between Hanatoxin and the voltage-sensors during gating of Kv channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. Kwangju Inst Sci & Technol, Dept Life Sci, Kwangju, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 459A EP 459A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502239 ER PT J AU Sukhareva, M Swartz, KJ AF Sukhareva, M Swartz, KJ TI The actions of Hanatoxin on single Kv2.1 channels. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 460A EP 460A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502240 ER PT J AU Halverson, KM Panchal, RG Nguyen, TL Gussio, R Little, SF Misakian, M Bavari, S Kasianowicz, JJ AF Halverson, KM Panchal, RG Nguyen, TL Gussio, R Little, SF Misakian, M Bavari, S Kasianowicz, JJ TI Electrophysiological analysis of anthrax toxin interactions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 USAMRIID, Ft Detrick, MD USA. NCI, SAIC, Frederick, MD 21701 USA. NIST, Gaithersburg, MD 20899 USA. NIST, ACSL, Gaithersburg, MD 20899 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 476A EP 477A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502319 ER PT J AU Kretschmannova, K Gonzalez-Iglesias, AE Tomic, M Stojilkovic, SS AF Kretschmannova, K Gonzalez-Iglesias, AE Tomic, M Stojilkovic, SS TI Expression and role of hyperpolarization activated channels in prolactin-secreting pituitary cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, ERRB, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 476A EP 476A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502315 ER PT J AU Zahanich, I Wiese, C Rolletschek, A Heubach, JF Kania, G Boheler, KR Ravens, U Wobus, AM AF Zahanich, I Wiese, C Rolletschek, A Heubach, JF Kania, G Boheler, KR Ravens, U Wobus, AM TI Electrophysiological characterization of intestinal epithelial-derived multipotent nestin-expressing progenitor cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Tech Univ Dresden, D-8027 Dresden, Germany. Inst Plant Genet & Crop Plant Res, Gatersleben, Germany. NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 477A EP 477A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502321 ER PT J AU Iwasa, KH Fang, J AF Iwasa, KH Fang, J TI Effects of tarantula toxin GsMTx4 and amphipathic ions that affect mechanosensitive channels on the membrane motor of outer hair cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 505A EP 506A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502465 ER PT J AU Weisleder, N Wang, X Collet, C Zhou, JS Chu, Y Hirata, Y Zhao, XL Pan, Z Brotto, M Cheng, HP Ma, JJ AF Weisleder, N Wang, X Collet, C Zhou, JS Chu, Y Hirata, Y Zhao, XL Pan, Z Brotto, M Cheng, HP Ma, JJ TI Stress-induced uncontrolled calcium sparks as dystrophic signals in mammalian skeletal muscle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. Rush Univ, Sch Med, Chicago, IL 60612 USA. NIA, Baltimore, MD 21224 USA. RI Zhao, Xiaoli/G-4106-2012; Weisleder, Noah/A-7098-2013 OI Weisleder, Noah/0000-0002-2619-8022 NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 534A EP 535A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502615 ER PT J AU Harries, D Gurnev, PA Parsegian, VA Bezrukov, SM AF Harries, D Gurnev, PA Parsegian, VA Bezrukov, SM TI Probing molecular hydration in binding of cyclodextrin to ion channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 545A EP 545A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502667 ER PT J AU Makareeva, E Leikin, S AF Makareeva, E Leikin, S TI Triple helix of type I procollagen is thermally unstable at body temperature SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Nice, NIH, Bethesda, MD USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 561A EP 561A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502743 ER PT J AU Piszczek, G Rozycki, J Singh, SK Maurizi, MR Ginsburg, A AF Piszczek, G Rozycki, J Singh, SK Maurizi, MR Ginsburg, A TI Interactions of ClpA hexamer with substrate peptides SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 563A EP 563A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502754 ER PT J AU Todd, BA Rau, DC Parsegian, A AF Todd, BA Rau, DC Parsegian, A TI Phase diagrams from single molecule DNA condensation SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 566A EP 566A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502771 ER PT J AU Choi, EJ Dimitriadis, EK AF Choi, EJ Dimitriadis, EK TI Atomic force microscopy investigation of cytochrome c interaction with anionic supported bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIH, DBEPS, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 582A EP 582A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502852 ER PT J AU Gurnev, PA Oppenheim, AB Winterhalter, M Bezrukov, SM AF Gurnev, PA Oppenheim, AB Winterhalter, M Bezrukov, SM TI Detecting lambda-phage binding to single LamB receptor in planar lipid bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. RAS, Inst Cytol, St Petersburg, Russia. Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Mol Genet, Jerusalem, Israel. Int Univ Bremen, Bremen, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 584A EP 585A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502864 ER PT J AU Nestorovich, EM Sugawara, E Nikaido, H Bezrukov, S AF Nestorovich, EM Sugawara, E Nikaido, H Bezrukov, S TI Pseudomonas aeruginosa porin OprF: Properties of the channel SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NICHD, NIH, Bethesda, MD USA. Univ Calif Berkeley, Berkeley, CA 94720 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 584A EP 584A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502859 ER PT J AU Sonawane, KD Shrivastava, IR Guy, R AF Sonawane, KD Shrivastava, IR Guy, R TI Models of the structure and gating mechanism of the hERG channel SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 605A EP 605A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378502960 ER PT J AU Kloda, JH Bailey, BW Swenby, NP Mitchell, DC AF Kloda, JH Bailey, BW Swenby, NP Mitchell, DC TI Expression of the GABA(A) receptor in Xenopus oocytes with altered levels of plasma membrane cholesterol SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAAA, NIH, Bethesda, MD USA. RI Bailey, Brian/B-1732-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 618A EP 618A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503022 ER PT J AU Silberberg, SD Chang, TH Swartz, KJ AF Silberberg, SD Chang, TH Swartz, KJ TI Rearrangements in rat P2X(4) receptor channels during gating SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 618A EP 619A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503025 ER PT J AU Silberberg, SD Swartz, KJ AF Silberberg, SD Swartz, KJ TI Regions of P2X(4) receptor channels essential for modulation by ivermectin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 619A EP 619A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503026 ER PT J AU Tasneem, A Iyer, LM Jakobsson, E Aravind, L AF Tasneem, A Iyer, LM Jakobsson, E Aravind, L TI Prokaryotic and eukaryotic homologues of ACh receptor channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ Illinois, Beckman Inst Adv Sci & Technol, Natl Ctr Supercomp Applicat, Urbana, IL 61801 USA. NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 620A EP 620A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503032 ER PT J AU Sakamoto, T Limouze, J Straight, AF Combs, CA Sellers, JR AF Sakamoto, T Limouze, J Straight, AF Combs, CA Sellers, JR TI Blebbistatin, a myosin II inhibitor, is rapidly photoinactivated by blue light SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD 20892 USA. Stanford Univ, Palo Alto, CA 94304 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 633A EP 633A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503096 ER PT J AU Root, DD Forbes, J Yadavalli, V Wang, K AF Root, DD Forbes, J Yadavalli, V Wang, K TI Nanomechanics of coiled-coil domains in myosin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 Univ N Texas, Denton, TX 76203 USA. NIAMS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 634A EP 634A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503102 ER PT J AU Toth, J Wang, F Sellers, JR AF Toth, J Wang, F Sellers, JR TI Drosophila Myosin V: Mechanism and in vivo motile properties SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 645A EP 646A PN 2 PG 2 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503159 ER PT J AU Sakamoto, T Yildiz, A Selvin, PR Sellers, JR AF Sakamoto, T Yildiz, A Selvin, PR Sellers, JR TI Use of neck length mutants to test the lever arm model for myosin V action SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD 20892 USA. Univ Illinois, Urbana, IL 61801 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 646A EP 646A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503160 ER PT J AU Robblee, JP Henn, A Hannemann, DE de la Cruz, EM AF Robblee, JP Henn, A Hannemann, DE de la Cruz, EM TI Thermodynamics of nucleotide binding to actomyosin VI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD 20892 USA. Univ Leeds, Leeds LS2 9JT, W Yorkshire, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 647A EP 647A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503166 ER PT J AU Yang, Y Sakamoto, T Xu, Q Thirumurugan, K Knight, PJ Sellers, JR AF Yang, Y Sakamoto, T Xu, Q Thirumurugan, K Knight, PJ Sellers, JR TI Characterization of Drosophila myosin VIIB SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NHLBI, Bethesda, MD USA. Univ Leeds, Leeds, W Yorkshire, England. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 647A EP 647A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503167 ER PT J AU Forbes, JG Wang, K AF Forbes, JG Wang, K TI Single-molecule dynamic stiffness SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 49th Annual Meeting of the Biopysical-Society CY FEB 12-16, 2005 CL Long Beach, CA SP Biopys Soc C1 NIAMS, DHHS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 2005 VL 88 IS 1 SU S BP 663A EP 663A PN 2 PG 1 WC Biophysics SC Biophysics GA 888MM UT WOS:000226378503250 ER PT S AU Stojilkovic, SS Zivadinovic, D Hegedis, A Marjanovic, M AF Stojilkovic, SS Zivadinovic, D Hegedis, A Marjanovic, M BE Vucinic, Z Djuricic, B Stojilkovic, SS Andjus, PR TI Radoslav K. Andjus (1926-2003) - A brief summary of his life and work SO BIOPHYSICS FROM MOLECULES TO BRAIN: IN MEMORY OF RADOSLAV K. ANDJUS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 22nd International Biophysics Symposium CY OCT 09-14, 2004 CL Belgrade, SERBIA MONTENEG SP Yugoslav Biophys Soc DE thermophysiology; suspended animation and resuscitation; brain metabolism; hibernation; biological rhythms; temperature adaptation and acclimation; cryoprotection; endocrinology; electroretinography; biophysical modeling ID GROWING MALE-RAT; DEVELOPMENTAL PATTERN; PROTEIN DENATURATION; JACULUS-ORIENTALIS; BIOPHYSICAL MODELS; BODY TEMPERATURES; APRES CONGELATION; LH LEVELS; ANDROGEN; REANIMATION AB Radoslav K. Andjus was a professor of physiology and biophysics at the University of Belgrade, Serbia, from 1953 to 1992. He was an elected member of the Serbian Academy of Sciences and Arts, the International Academy of Astronautics, and the Montenegrin Academy of Sciences and Arts. He published over 190 papers in domestic and international journals and three textbooks. The main field of his research was thermophysiology. He studied hypothermia, suspended animation and resuscitation, hibernation and biological rhythms, temperature adaptation and acclimation, and cryoprotection. Professor Andjus also contributed significantly to the fields of brain metabolism, endocrinology, electroretinography, as well as biophysical modeling and theoretical biology. C1 NICHD, ERRB, NIH, Bethesda, MD 20892 USA. Univ Texas, Med Branch, Galveston, TX 77555 USA. Univ Belgrade, Ctr Multidisciplinary Studies, Belgrade, Serbia Monteneg. Eastern Illinois Univ, Dept Biol Sci, Charleston, IL 61920 USA. RP Stojilkovic, SS (reprint author), NICHD, ERRB, NIH, Bldg 49,Room 6A-36,49 Convent Dr,MSC 4510, Bethesda, MD 20892 USA. EM stankos@helix.nih.gov; stankos@helix.nih.gov NR 60 TC 1 Z9 1 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-549-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2005 VL 1048 BP 1 EP 9 DI 10.1196/annals.1342.002 PG 9 WC Biophysics; Multidisciplinary Sciences SC Biophysics; Science & Technology - Other Topics GA BDJ14 UT WOS:000233712300001 PM 16154917 ER PT S AU Stojilkovic, SS Tomic, M Mu-Lan, HE Yan, ZH Koshimizu, TA Zemkova, H AF Stojilkovic, SS Tomic, M Mu-Lan, HE Yan, ZH Koshimizu, TA Zemkova, H BE Vucinic, Z Djuricic, B Stojilkovic, SS Andjus, PR TI Molecular dissection of purinergic P2X receptor channels SO BIOPHYSICS FROM MOLECULES TO BRAIN: IN MEMORY OF RADOSLAV K. ANDJUS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 22nd International Biophysics Symposium CY OCT 09-14, 2004 CL Belgrade, SERBIA MONTENEG SP Yugoslav Biophys Soc DE ATP; purinergic receptors; P2X; agonist binding domain; gating; deactivation; desensitization; resensitization; chimeras ID ATP-GATED CHANNELS; C-TERMINAL DOMAIN; ION-CHANNEL; PROTEIN-KINASE; BINDING-SITE; DESENSITIZATION; RESIDUES; SUBUNIT; IDENTIFICATION; AGONIST AB The P2X receptors (P2XRs) are a family of ATP-gated channels expressed in the plasma membrane of numerous excitable and nonexcitable cells and play important roles in control of cellular functions, such as neurotransmission, hormone secretion, transcriptional regulation, and protein synthesis. MRS are homomeric or heteromeric proteins, formed by assembly of at least three of seven subunits named P2X(1)-P2X(7). All subunits possess intracellular Nand C-termini, two transmembrane domains, and a relatively large extracellular ligand-binding loop. ATP binds to still an unidentified extracellular domain, leading to a sequence of conformational transitions between closed, open, and desensitized states. Removal of, extracellular ATP leads to deactivation and resensitization of receptors. Activated P2XRs generate inward currents caused by Na+ and Ca2+ influx through the pore of channels, and thus mediate membrane depolarization and facilitation of voltage-gated calcium entry in excitable cells. No crystal structures are available for MRS and these receptors have no obvious similarity to other ion channels or ATP binding proteins, which limits the progress in understanding the relationship between molecular structure and conformational transitions of receptor in the presence of agonist and after its washout. We summarize here the alternative approaches in studies on molecular properties of MRS, including heteromerization, chimerization, mutagenesis, and biochemical studies. C1 NICHD, ERRB, NIH, Sect Cellular Signaling,Endocrinol & Reprod Res B, Bethesda, MD 20892 USA. RP Stojilkovic, SS (reprint author), NICHD, ERRB, NIH, Sect Cellular Signaling,Endocrinol & Reprod Res B, Bldg 49,Room 6A-36,49 Convent Dr, Bethesda, MD 20892 USA. EM stankos@helix.nih.gov; stankos@helix.nih.gov RI Zemkova, Hana/C-1844-2012; Tomic, Melanija/C-3371-2016; OI Koshimizu, Taka-aki/0000-0001-5292-7535 NR 45 TC 24 Z9 24 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-549-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2005 VL 1048 BP 116 EP 130 DI 10.1196/annals.1342.011 PG 15 WC Biophysics; Multidisciplinary Sciences SC Biophysics; Science & Technology - Other Topics GA BDJ14 UT WOS:000233712300010 PM 16154926 ER PT S AU Lee, PR Cohen, JE Becker, KG Fields, RD AF Lee, PR Cohen, JE Becker, KG Fields, RD BE Vucinic, Z Djuricic, B Stojilkovic, SS Andjus, PR TI Gene expression in the conversion of early-phase to late-phase long-term potentiation SO BIOPHYSICS FROM MOLECULES TO BRAIN: IN MEMORY OF RADOSLAV K. ANDJUS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 22nd International Biophysics Symposium CY OCT 09-14, 2004 CL Belgrade, SERBIA MONTENEG SP Yugoslav Biophys Soc DE late-LTP; LTD; metaplasticity; BDNF; synaptic tag; activity-dependent plasticity; long-term memory; gene transcription; microarray; synaptic plasticity; hippocampus ID RAT HIPPOCAMPAL SLICES; NERVE GROWTH-FACTOR; ACTIVITY-DEPENDENT EXPRESSION; SYNAPTIC PLASTICITY; PROTEIN-SYNTHESIS; NEURONAL-ACTIVITY; MESSENGER-RNAS; BDNF-GENE; IN-VITRO; LTP AB Changes in gene expression associated with different forms of synaptic plasticity in rat hippocampus were investigated. Microarray analysis revealed differential expression of hundreds of genes 30 min after synaptic or antidromic stimulation in different patterns. Results of selected genes were verified by LightCycler RT-PCR. Synaptic activation in a theta burst protocol, which induced long-term potentiation (LTP), increased the mRNA abundance of BDNF-exon 1, but antidromic stimulation in the presence of CNQX, APV, and MCPG (to block glutamatergic synapses) decreased the level of mRNA of this transcript, as did 1 Hz synaptic stimulation. The opposite regulation of this BDNF transcript after firing of the postsynaptic neuron, coincidently or uncorrelated with synaptic firing, is consistent with the effects of BDNF on synaptic transmission, suggesting possible involvement in strengthening and weakening CA1 synapses after correlated versus uncorrelated firing of the postsynaptic neurons with its synaptic inputs. Possible involvement of transcriptional regulation of BDNF in the conversion of early-phase LTP to late-phase LTP are discussed in the context of previous studies by Dudek & Fields (Proc. Natl. Acad. Sci. USA 99: 3962-3967) showing that this conversion can be induced by antidromic stimulation of CA1 neurons in the absence of excitatory synaptic activity. C1 NICHD, Nervous Syst Dev & Plastic Sect, NIH, Bethesda, MD 20892 USA. NIA, DNA Array Unit, NIH, Baltimore, MD 21224 USA. RP Fields, RD (reprint author), NICHD, Nervous Syst Dev & Plastic Sect, NIH, Bldg 35,Room 2A211,MSC 3713,35 Lincoln Dr, Bethesda, MD 20892 USA. EM fieldsd@mail.nih.gov OI Becker, Kevin/0000-0002-6794-6656 NR 58 TC 29 Z9 31 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-549-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2005 VL 1048 BP 259 EP 271 DI 10.1196/annals.1342.023 PG 13 WC Biophysics; Multidisciplinary Sciences SC Biophysics; Science & Technology - Other Topics GA BDJ14 UT WOS:000233712300022 PM 16154938 ER PT J AU Venkatesh, B Venkatesh, S Jayadevan, S Rifkind, JM Manoharan, PT AF Venkatesh, B Venkatesh, S Jayadevan, S Rifkind, JM Manoharan, PT TI Studies on heme release from normal and metal ion reconstituted hemoglobin mediated through ionic surfactant SO BIOPOLYMERS LA English DT Article DE electron paramagnetic resonance; Fourier transform-Raman; surfactant; hemoglobin; reconstituted hemoglobin ID DERIVATIVES AB The interaction of metal-substituted hemoglobin (MHb), where M = Ni and Cu (T-state with no O-2 and CO binding capability) and Fe (R-state when CO is bound), with cationic cityl trimethyl ammonium bromide (CTAB) and anionic (sodium dodecyl sulfate-SDS) surfactants has been studied using spectroscopic techniques- UV-visible, electron paramagnetic resonance (EPR), and Fourier transform-Raman-with additional supportive evidence coming from conductivity measurements. We observed the loss of 5-coordination in all three hemoglobins below the critical micelle concentration (CMC) of surfactant, with noticeable differences, suggesting differing mechanisms involved in this process. In addition, above the CMC, Ni- and Cu-hemes were found to leave their proteins more easily than Fe-heme, presumably due to weaker or no bond with the proximal histidine in the former. The released heme is stabilized by micellar media through a hydrophobic interaction process. Of the two surfactants, CTAB seems to be capable of releasing the heme better than SDS and it is attributed to the greater hydrophobicity of CTAB though the charge of the surfactant plays an important role. (C) 2005 Wiley Periodicals, Inc. C1 Indian Inst Technol, Dept Chem, Madras 600036, Tamil Nadu, India. Indian Inst Technol, Reg Sophisticated Instrumentat Ctr, Madras 600036, Tamil Nadu, India. Univ Madras, Dept Chem Phys, Madras 600025, Tamil Nadu, India. NIA, Mol Dynam Sect, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA. RP Manoharan, PT (reprint author), Indian Inst Technol, Dept Chem, Madras 600036, Tamil Nadu, India. EM ptm@rsic.iitm.ernet.in NR 20 TC 6 Z9 6 U1 0 U2 4 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 1 BP 18 EP 25 DI 10.1002/bip.20194 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 896XS UT WOS:000226968400003 PM 15614803 ER PT J AU Pinilla, C Sospedra, M Zhao, YD Simon, R Martin, R AF Pinilla, C Sospedra, M Zhao, YD Simon, R Martin, R TI T cell specificity examined in a systematic and comprehensive manner using peptide positional scanning libraries SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 Torrey Pines Inst Mol Studies, San Diego, CA USA. NINDS, NIH, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 499 EP 499 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200076 ER PT J AU Lynch, MP Rawale, S Jacobson, S Kaumaya, PTP AF Lynch, MP Rawale, S Jacobson, S Kaumaya, PTP TI Novel retro-inverso envelope peptide mimetic fusion inhibitors as a potential therapy for HTLV-1 infected individuals SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NINDS, NIH, Dept Microbiol, Bethesda, MD 20892 USA. NINDS, NIH, Dept Obstet & Gynecol, Bethesda, MD 20892 USA. NINDS, NIH, Viral Immunol Sect, Bethesda, MD 20892 USA. Ohio State Univ, Arthur G James Comprehens Canc Ctr, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 508 EP 508 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200103 ER PT J AU Shi, ZD Peruzzi, B Dharmawardana, PG Leech, T Appella, E Worthy, KM Bindu, LK Fisher, RJ Bottaro, DP Burke, TR AF Shi, ZD Peruzzi, B Dharmawardana, PG Leech, T Appella, E Worthy, KM Bindu, LK Fisher, RJ Bottaro, DP Burke, TR TI Synthesis and use of C-terminally biotinylated peptidomimetics with high Grb2 SH2 domain-binding affinity SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, CCR, Med Chem Lab, Frederick, MD 21702 USA. SAIC Frederick, Prot Chem Lab, Frederick, MD 21702 USA. NCI, NIH, CCR, Cell Biol Lab, Bethesda, MD 20892 USA. NCI, NIH, CCR, Urol Oncol Branch, Bethesda, MD 20892 USA. RI Fisher, Robert/B-1431-2009; Bottaro, Donald/F-8550-2010; Burke, Terrence/N-2601-2014 OI Bottaro, Donald/0000-0002-5057-5334; NR 0 TC 0 Z9 0 U1 0 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 516 EP 516 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200142 ER PT J AU Burke, TR Kang, SU Choi, WJ Shi, ZD Karki, R Phan, J Worthy, KM Bindu, LK Nicklaus, M Waugh, DS Fisher, RJ AF Burke, TR Kang, SU Choi, WJ Shi, ZD Karki, R Phan, J Worthy, KM Bindu, LK Nicklaus, M Waugh, DS Fisher, RJ TI Application of phenylphosphate mimetics to the design and synthesis of olefin metathesisderived Grb2 SH2 domain-binding macrocycles SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, CCR, Med Chem Lab, Ft Detrick, MD 21702 USA. NCI, NIH, CCR, Macromol Crystallog Lab, Frederick, MD 21702 USA. SAIC Frederick, Prot Chem Lab, Frederick, MD USA. RI Fisher, Robert/B-1431-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 536 EP 536 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200242 ER PT J AU Krajewski, K Marchand, C Pommier, Y Roller, PP AF Krajewski, K Marchand, C Pommier, Y Roller, PP TI Effect of dimerization and tetramerization on the potency of HIV-1 integrase inhibitory peptides SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, Med Chem Lab, Frederick, MD 21702 USA. NCI, NIH, Mol Pharmacol Lab, Bethesda, MD 20892 USA. RI Marchand, Christophe/D-8559-2016 NR 2 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 557 EP 557 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200342 ER PT J AU Roller, PP Jiang, S Li, P Long, YQ Johnson, M Dickson, R AF Roller, PP Jiang, S Li, P Long, YQ Johnson, M Dickson, R TI Sunflower derived trypsin inhibitors as antimetastatics SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, Med Chem Lab, Frederick, MD 21702 USA. Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 568 EP 568 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200391 ER PT J AU Guiotto, A Calderan, A Ruzza, P Osler, A Rubini, C Jo, DG Tang, SC Arumgam, T Mattson, MP Borin, G AF Guiotto, A Calderan, A Ruzza, P Osler, A Rubini, C Jo, DG Tang, SC Arumgam, T Mattson, MP Borin, G TI Synthesis and evaluation of neuroprotective alpha,beta-unsaturated aldehyde scavenger histidyl-containing analogs of carnosine SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 CNR, Inst Biomol Chem, Padova Unit, I-35131 Padua, Italy. NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. RI Guiotto, Andrea/A-4720-2009; Mattson, Mark/F-6038-2012 NR 0 TC 0 Z9 0 U1 0 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 569 EP 569 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200395 ER PT J AU Jiang, S Wang, SM Roller, PP AF Jiang, S Wang, SM Roller, PP TI Synthesis of symmetrical dimeric dicarboxylic acid linked peptides on solid support SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, Med Chem Lab, Frederick, MD 21702 USA. Univ Michigan, Ctr Canc, Ann Arbor, MI 48109 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 570 EP 570 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200403 ER PT J AU Dyba, M Tarasova, NI Michejda, CJ AF Dyba, M Tarasova, NI Michejda, CJ TI Tetra and pentapeptide derivatives of hemiasterlin. Synthesis and activity studies. SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, Struct Biophys Lab, Mol Aspects Drug Design Sect, Frederick, MD 21702 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 571 EP 572 PG 2 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200408 ER PT J AU Pinilla, C Sospedra, M Zhao, YD Simon, R Martin, R AF Pinilla, C Sospedra, M Zhao, YD Simon, R Martin, R TI T cell specificity examined in a systematic and comprehensive manner using peptide positional scanning libraries SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 Torrey Pines Inst Mol Studies, La Jolla, CA USA. NINDS, NIH, Bethesda, MD USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 571 EP 571 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200406 ER PT J AU Shiotani, K Miyazaki, A Li, T Tsuda, Y Ambo, A Sasaki, Y Bryant, SD Jinsmaa, Y Lazarus, LH Okada, Y AF Shiotani, K Miyazaki, A Li, T Tsuda, Y Ambo, A Sasaki, Y Bryant, SD Jinsmaa, Y Lazarus, LH Okada, Y TI Systematic study on the structure-activity relationship of pyrazinone ring-containing bioactive opioid ligands SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 Kobe Gakuin Univ, Grad Sch Food & Med Sci, Kobe, Hyogo 6512180, Japan. Kobe Gakuin Univ, Fac Pharmaceut Sci, Kobe, Hyogo 6512180, Japan. Kobe Gakuin Univ, HRC, Kobe, Hyogo 6512180, Japan. Tohoku Pharmaceut Univ, Sendai, Miyagi 9818558, Japan. NIEHS, LCBRA, Med Chem Grp, Res Triangle Pk, NC 27709 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 571 EP 571 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200405 ER PT J AU Liu, F Oishi, S Karki, R Shi, ZD Worthy, KM Bindu, LK Maderia, M Nicklaus, M Barchi, JJ Fisher, RJ Burke, TR AF Liu, F Oishi, S Karki, R Shi, ZD Worthy, KM Bindu, LK Maderia, M Nicklaus, M Barchi, JJ Fisher, RJ Burke, TR TI High affinity Grb2 SH2 domain-binding macrocycles derived from ring-closing metathesis of alkenylglycine residues with beta-vinyl phosphotyrosyl mimetics SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 NCI, NIH, Med Chem Lab, CCR, Frederick, MD 21702 USA. SAIC Frederick, Prot Chem Lab, Frederick, MD 21702 USA. RI Fisher, Robert/B-1431-2009; Barchi Jr., Joseph/N-3784-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 574 EP 574 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200420 ER PT J AU Nikiforovich, GV Mihalik, B Catt, KJ Marshall, GR AF Nikiforovich, GV Mihalik, B Catt, KJ Marshall, GR TI Molecular mechanisms of constitutive activity in GPCRs: Mutations at position 111 of the angiotensin AT(1) receptor SO BIOPOLYMERS LA English DT Meeting Abstract CT 19th American Peptide Symposium CY JUN 18-23, 2005 CL San Diego, CA SP Amer Peptide Soc, AAPPTEC, Amer Peptide Co, Amer Hlth/GE Healthcare, Amgen Inc, BACHEM, BIOMOL Int, C S Bio Co, Cambridge Res Biochem, Chemico Int Inc, Chem Today, Eli Lilly & Co, ESCOM Sci Fdn, Genentech, Hofffman-La Roche Inc, Merck Res Lab, Midwest Bio-Tech Inc, NeoMPS Inc, New England BioLabs Inc, Novo Nordisk A/S, Peptides Int Inc, PharmaChem, PolyPeptide Lab Inc, RSP Amino Acide LLC, Senn Chem USA, Sinopep Pharmaceut Inc, SynPep Corp, Synthetech Inc, UCB Bioproducts Inc C1 Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO 63110 USA. NICHHD, Endocrinol & Reprod Res Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 4 BP 588 EP 589 PG 2 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 937CC UT WOS:000229901200488 ER PT J AU Lung, FDT Chang, CW Chong, MC Liou, CC Li, P Peach, ML Nicklaus, MC Lou, BS Roller, PP AF Lung, FDT Chang, CW Chong, MC Liou, CC Li, P Peach, ML Nicklaus, MC Lou, BS Roller, PP TI Small nonphosphorylated Grb2-SH2 domain antagonists evaluated by surface resonance plasmon technology SO BIOPOLYMERS LA English DT Article DE signal transduction pathway; Ras; Grb2; SH2 domain; BIACORE X; surface plasmon resonance; peptides ID PHOSPHATE-CONTAINING LIGANDS; CONFERRING HIGH-AFFINITY; STRUCTURE-BASED DESIGN; SH2 DOMAIN; STRUCTURAL BASIS; PEPTIDE BINDING; INHIBITOR; REQUIREMENTS AB The growth factor receptor-binding protein-Src homology 2 (Grb2-SH2) domain plays an important role in the oncogenic Ras signal transduction pathway, which involves cell proliferation and differentiation. Therefore, the Grb2-SH2 domain has been chosen as our target for development of potential antiproliferative agents. Herein, we report the study of the inhibitory effects of small nonphosphorylated peptide analogs interacting with the Grb2-SH2 domain protein by surface plasmon resonance (SPR) technology. A set of 8 related peptide analogs were synthesized, purified, and characterized. Their inhibitory effects on Grb2-SH2 were evaluated by the SPR technology developed with the BIACORE X instrument. The lead peptide, Fmoc-Glu-Tyr-Aib-Asn-NH2 (Fmoc-E-Y-Aib-N,- Fmoc: 9-fluorenylmethyoxycarbonyl; Aib = alpha-amino isobutyric acid) inhibited Grb2-SH2 domain function with an IC50 value of 8.7 mu M. A molecular modeling study of the lead peptide indicated that the glutamate in the Fmoc peptide is ideally positioned to form a strong salt bridge to Arg 67 in the Grb2-SH2 domain, using both its backbone carbonyl and its acidic group. Residue Glu 89 in Grb2-SH2 flips inward to fill the binding site and partially replace the phosphate group as a hydrogen-bond acceptor. Results of these studies provide important information for further development of potent nonphosphorylated peptide inhibitors of the Grb2-SH2 domain. (C) 2005 Wiley Periodicals, Inc. C1 Tunghai Univ, Dept Chem, Taichung 40704, Taiwan. China Med Univ, Inst Nutr, Taichung, Taiwan. NCI, Med Chem Lab, FCRDC, Ft Detrick, MD 21702 USA. Chang Gung Univ, Ctr Gen Educ, Div Chem, Tao Yuan, Taiwan. RP Lung, FDT (reprint author), Tunghai Univ, Dept Chem, Taichung 40704, Taiwan. EM fdlung@mail.thu.edu.tw RI Nicklaus, Marc/N-4183-2014 NR 31 TC 8 Z9 8 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PY 2005 VL 80 IS 5 BP 628 EP 635 DI 10.1002/bip.20209 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 970UF UT WOS:000232334800002 PM 15660381 ER PT J AU Dunson, DB Herring, AH AF Dunson, DB Herring, AH TI Bayesian latent variable models for mixed discrete outcomes SO BIOSTATISTICS LA English DT Article DE discrete time survival; joint model; latent variables; multiple binary outcomes; Poisson counts; proportional hazards; random effects; tumor multiplicity ID LONGITUDINAL COUNT DATA; GAMMA FRAILTY MODEL; CLUSTERED BINARY; TRAIT MODELS AB In studies of complex health conditions, mixtures of discrete outcomes (event Lime. count. binary, ordered categorical) are commonly collected. For example, studies of skin tumorigenesis record latency time prior to the first tumor, increases in the number of tumors at each week. and the occurrence of internal tumors at the time of death. Motivated by this application, we propose a general underlying Poisson variable framework for mixed discrete outcomes, accommodating dependency through an additive gamma frailty model for the Poisson means. The model has log-linear. complementary log-log. and proportional hazards forms for count, binary and discrete event time outcomes, respectively. Simple closed form expressions can be derived for the marginal expectations, variances. and correlations. Following a Bayesian approach to inference, conditionally-conjugate prior distributions are chosen that facilitate posterior computation via an MCMC algorithm. The methods are illustrated using data from a Tg.AC mouse bioassay study. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Dept Biostat, Chapel Hill, NC 27515 USA. RP Dunson, DB (reprint author), NIEHS, Biostat Branch, POB 12233,MD A3-03, Res Triangle Pk, NC 27709 USA. EM dunson1@niehs.nih.gov NR 31 TC 26 Z9 27 U1 0 U2 8 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1465-4644 J9 BIOSTATISTICS JI Biostatistics PD JAN PY 2005 VL 6 IS 1 BP 11 EP 25 DI 10.1093/biostatistics/kxh025 PG 15 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA 888AJ UT WOS:000226346300002 PM 15618524 ER PT J AU Dobbin, K Simon, R AF Dobbin, K Simon, R TI Sample size determination in microarray experiments for class comparison and prognostic classification SO BIOSTATISTICS LA English DT Article DE experimental design; gene expression; microarrays; sample size ID DIFFERENTIALLY EXPRESSED GENES; FALSE DISCOVERY RATE; CDNA MICROARRAY; DESIGN; NORMALIZATION; VARIANCE; MODEL AB Determining sample sizes for microarray experiments is important but the complexity of these experiments, and the large amounts of data they produce, can make the sample size issue seem daunting. and tempt researchers to use rules of thumb in place of formal calculations based on the goals of the experiment. Here we present formulae for determining sample sizes to achieve a variety of experimental goals, including class comparison and the development of prognostic markers. Results are derived which describe the impact of pooling, technical replicates and dye-swap arrays on sample size requirements. These results are shown to depend on the relative sizes of different sources of variability. A variety of common types of experimental situations and designs used with single-label and dual-label microarrays are considered. We discuss procedures for controlling the false discovery rate. Our calculations are based on relatively simple yet realistic statistical models for the data, and provide straightforward sample size calculation formulae. C1 NCI, Biometr Res Branch, Bethesda, MD 20892 USA. RP Dobbin, K (reprint author), NCI, Biometr Res Branch, 6130 Execut Blvd, Bethesda, MD 20892 USA. EM dobbinke@mail.nih.gov NR 21 TC 91 Z9 99 U1 0 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1465-4644 J9 BIOSTATISTICS JI Biostatistics PD JAN PY 2005 VL 6 IS 1 BP 27 EP 38 DI 10.1093/biostatistics/kxh015 PG 12 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA 888AJ UT WOS:000226346300003 PM 15618525 ER PT J AU Fay, MP AF Fay, MP TI Random marginal agreement coefficients: rethinking the adjustment for chance when measuring agreement SO BIOSTATISTICS LA English DT Article DE concordance correlation coefficient; kappa; random maraginal agreement coefficient; reliability; weighted kappa ID CONCORDANCE CORRELATION-COEFFICIENT; INTERRATER AGREEMENT; KAPPA-COEFFICIENTS AB Agreement coefficients quantify how well a set of instruments agree in measuring some response on a population of interest. Many standard agreement coefficients (e.g. kappa for nominal, weighted kappa for ordinal, and the concordance correlation coefficient (CCC) for continuous responses) may indicate increasing agreement as the marginal distributions of the two instruments become more different even as the true cost of disagreement stays the same or increases. This problem has been described for the kappa coefficients; here we describe it for the CCC. We propose a solution for all types of responses in the form of random marginal agreement coefficients (RMACs), which use a different adjustment for chance than the standard agreement coefficients. Standard agreement coefficients model chance agreement using expected agreement between two independent random variables each distributed according to the marginal distribution of one of the instruments. RMACs adjust for chance by modeling two independent readings both from the mixture distribution that averages the two marginal distributions. In other words. both independent readings represent first a random choice of instrument, then a random draw from the marginal distribution of the chosen instrument. The advantage of the resulting RMAC is that differences between the two marginal distributions will not induce greater apparent agreement. As with the standard agreement coefficients, the RMACs do not require any assumptions about the bivariate distribution of the random variables associated with the two instruments. We describe the RMAC for nominal. ordinal and continuous data, and show through the delta method how to approximate the variances of sonic important special cases. C1 Natl Inst Allergy & Infect Dis, Bethesda, MD 20892 USA. RP Fay, MP (reprint author), Natl Inst Allergy & Infect Dis, 6700B Rockledge Dr MSC 7609, Bethesda, MD 20892 USA. EM mfay@niaid.nih.gov RI Fay, Michael/A-2974-2008; OI Fay, Michael P./0000-0002-8643-9625 NR 19 TC 22 Z9 22 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1465-4644 J9 BIOSTATISTICS JI Biostatistics PD JAN PY 2005 VL 6 IS 1 BP 171 EP 180 DI 10.1093/biostatistics/kxh027 PG 10 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA 888AJ UT WOS:000226346300013 PM 15618535 ER PT J AU Schaupp, CJ Jiang, GJ Myers, TG Wilson, MA AF Schaupp, CJ Jiang, GJ Myers, TG Wilson, MA TI Active mixing during hybridization improves the accuracy and reproducibility of microarray results SO BIOTECHNIQUES LA English DT Article ID GENE-EXPRESSION; OLIGONUCLEOTIDE C1 NIAID, Bethesda, MD 20892 USA. RP Wilson, MA (reprint author), Ambion Inc, 2130 Woodward St, Austin, TX 78744 USA. EM mwilson@ambion.com NR 11 TC 24 Z9 25 U1 0 U2 1 PU EATON PUBLISHING CO PI WESTBOROUGH PA ONE RESEARCH DRIVE, SUITE 400A, PO BOX 1070, WESTBOROUGH, MA 01581-6070 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 2005 VL 38 IS 1 BP 117 EP 119 DI 10.2144/05381MT01 PG 3 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 889CU UT WOS:000226421900022 PM 15679093 ER PT J AU Bleckwenn, NA Bentley, WE Shiloach, J AF Bleckwenn, NA Bentley, WE Shiloach, J TI Vaccinia virus-based expression of gp120 and EGFP: Survey of mammalian host cell lines SO BIOTECHNOLOGY PROGRESS LA English DT Article; Proceedings Paper CT Conference on Cell Culture Engineering IX CY MAR 07-12, 2004 CL Cancun, MEXICO ID RECOMBINANT PROTEIN-PRODUCTION; SYSTEM; PURIFICATION; CULTURES; VECTORS; BATCH; DNA AB Production of recombinant proteins with the vaccinia virus expression system in five mammalian cell lines (HeLa, BS-C-1, Vero, MRC-5, and 293) was investigated for protein yield and proper posttranslational modifications. Regulatory acceptance of the host cell line was taken into consideration, where Vero, MRC-5, and 293 were considered more acceptable to the regulatory authorities. Relevant process knowledge for ease of scale-up with the particular cell type was also considered. Two proteins were expressed, enhanced green fluorescent protein (EGFP) in the cytoplasm and gp120, an HIV envelope coat protein that is secreted into the culture medium. HeLa cells produced the most EGFP at 17.2mug/well with BS-C-1 and 293 following. BS-C-1 produced the most gp120 at 28.2mug/mL with 293 and Vero following. Therefore, of the three most appropriate cell lines (Vero, MRC-5, and 293) for production processes, the best results were obtained with 293 cells. Although MRC-5 had a very high productivity on a per cell basis, the low cell density and slow growth rate made the overall production insufficient. Because gp120 contained a significant amount of posttranslational modification, this protein, produced by the different cell lines, was further analyzed by PNGase digestion suggesting N-linked glycosylation modifications in all cell lines tested. On the basis of these results and overall process considerations, 293 cells are recommended for further production process optimization in a serum-free suspension system. C1 NIDDK, Biotechnol Unit, NIH, DHHS, Bethesda, MD 20892 USA. Univ Maryland, Dept Chem Engn, College Pk, MD 20742 USA. Univ Maryland, Inst Biotechnol, Ctr Biosyst Res, College Pk, MD 20742 USA. RP Shiloach, J (reprint author), NIDDK, Biotechnol Unit, NIH, DHHS, Bldg 14A Rm 173,9000 Rockville Pike, Bethesda, MD 20892 USA. EM yossi@nih.gov NR 31 TC 2 Z9 3 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD JAN-FEB PY 2005 VL 21 IS 1 BP 186 EP 191 DI 10.1021/bp0498185 PG 6 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 896LE UT WOS:000226934800025 PM 15903257 ER PT J AU Nellis, DF Ekstrom, DL Kirpotin, DB Zhu, JW Andersson, R Broadt, TL Ouellette, TF Perkins, SC Roach, JM Drummond, DC Hong, KL Marks, JD Park, JW Giardina, SL AF Nellis, DF Ekstrom, DL Kirpotin, DB Zhu, JW Andersson, R Broadt, TL Ouellette, TF Perkins, SC Roach, JM Drummond, DC Hong, KL Marks, JD Park, JW Giardina, SL TI Preclinical manufacture of an anti-HER2 scFv-PEG-DSPE, liposome-inserting conjugate. 1. Gram-scale production and purification SO BIOTECHNOLOGY PROGRESS LA English DT Article ID SINGLE-CHAIN ANTIBODIES; TARGETED DELIVERY; ENHANCED EFFICACY; ESCHERICHIA-COLI; PHAGE LIBRARIES; IN-VITRO; IMMUNOLIPOSOMES; SELECTION AB A GMP-compliant process is described for producing F5cys-PEG-lipid conjugate. This material fuses with preformed, drug-loaded liposomes, to form "immunoliposomes" that bind to HER2/neu overexpressing carcinomas, stimulates drug internalization, and ideally improves the encapsulated drug's therapeutic index. The soluble, single-chain, variable region antibody fragment, designated F5cys, was produced in E. coli strain RV308 using high-density cultures. Affinity adsorption onto horizontally tumbled Streamline rProtein-A resin robustly recovered F5cys from high-pressure-disrupted, whole-cell homogenates. Two product-related impurity classes were identified: F5cys with mid-sequence discontinuities and F5cys with remnants of a pelB leader peptide. Low-pressure cation exchange chromatography, conducted at elevated pH under reducing conditions, enriched target F5cys relative to these impurities and prepared a C-terrainal cysteine for conjugation. Site-directed conjugation, conducted at pH 5.9 +/- 0.1 with reaction monitoring and cysteine quenching, yielded F5cys-MP-PEG(2000)DSPE. Low-pressure size exclusion chromatography separated spontaneously formed, high-molecular-weight conjugate micelles from low-molecular-weight impurities. When formulated at 1-2 mg/mL in 10 mM trisodium citrate, 10% sucrose (w/v), at pH 6.4 (110), the conjugate was stable when stored below -70 degreesC. Six scale-up lots were compared. The largest 40-L culture produced enough F5cys to manufacture 2,085 mg of conjugate, enough to support planned preclinical and future clinical trials. The conjugate was 93% pure, as measured by polyacrylamide gel electrophoresis. Impurities were primarily identified as product-related. Residual endotoxin, rProtein A, and genomic DNA, were at acceptable levels. This study successfully addressed a necessary step in the scale-up of immunoliposome-encapsulated therapeutics. C1 SAIC Frederick Inc, Natl Canc Inst Frederick, Frederick, MD 21702 USA. Calif Pacific Med Ctr, Res Inst, Liposome Res Lab, San Francisco, CA 94115 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA. Hermes Biosci Inc, San Francisco, CA 94080 USA. RP Giardina, SL (reprint author), SAIC Frederick Inc, Natl Canc Inst Frederick, POB B, Frederick, MD 21702 USA. EM giardina@mail.ncifcrf.gov FU NCI NIH HHS [N01-CO-12400, P50-CA 58207-01] NR 23 TC 62 Z9 65 U1 1 U2 23 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD JAN-FEB PY 2005 VL 21 IS 1 BP 205 EP 220 DI 10.1021/bp049840y PG 16 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 896LE UT WOS:000226934800028 PM 15903260 ER PT J AU Nellis, DF Giardina, SL Janini, GM Shenoy, SR Marks, JD Tsai, R Drummond, DC Hong, K Park, JW Ouellette, TF Perkins, SC Kirpotin, DB AF Nellis, DF Giardina, SL Janini, GM Shenoy, SR Marks, JD Tsai, R Drummond, DC Hong, K Park, JW Ouellette, TF Perkins, SC Kirpotin, DB TI Preclinical manufacture of anti-HER2 liposome-inserting, scFv-PEG-Lipid conjugate. 2. Conjugate micelle identity, purity, stability, and potency analysis SO BIOTECHNOLOGY PROGRESS LA English DT Article ID CHROMATOGRAPHY AB Analytical methods optimized for micellar F5cYs-MP-PEG(2000)-DPSE protein-lipopolymer conjugate are presented. The apparent micelle molecular weight, determined by size exclusion chromatography, ranged from 330 to 960 kDa. The F5cys antibody and conjugate melting points, determined by differential scanning calorimetry, were near 82 degreesC. Traditional methods for characterizing monodisperse protein species were inapplicable to conjugate analysis. The isoelectric point of F5cys (9.2) and the conjugate (8.9) were determined by capillary isoelectric focusing (cIEF) after addition of the zwitterionic detergent CHAPS to the buffer. Conjugate incubation with phospholipase B selectively removed DSPE lipid groups and dispersed the conjugate prior to separation by chromatographic methods. Alternatively, adding 2-propanol (29.4 vol %) and n-butanol (4.5 vol %) to buffers for salt-gradient cation exchange chromatography provided gentler, nonenzymatic dispersion, resulting in well-resolved peaks. This method was used to assess stability, identify contaminants, establish lotto-lot comparability, and determine the average chromatographic purity (93%) for conjugate lots, described previously. The F5cys amino acid content was confirmed after conjugation. The expected conjugate avidity for immobilized HER-2/neu was measured by bimolecular interaction analysis (BIAcore). Mock therapeutic assemblies were made by conjugate insertion into preformed doxorubicin-encapsulating liposomes for antibody-directed uptake of doxorubicin by HER2-overexpressing cancer cells in vitro. Together these developed assays established that the manufacturing method as described in the first part of this study consistently produced F5cys-MP-PEG(2000)-DSPE having sufficient purity, stability, and functionality for use in preclinical toxicology investigations. C1 SAIC Frederick Inc, Natl Canc Inst Frederick, Frederick, MD 21702 USA. Calif Pacific Med Ctr, Res Inst, Liposome Res Lab, San Francisco, CA 94115 USA. NCI, Ctr Canc Res, Molecular Targets Dev Program, Frederick, MD 21702 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA. Hermes Biosci Inc, San Francisco, CA 94080 USA. RP Kirpotin, DB (reprint author), SAIC Frederick Inc, Natl Canc Inst Frederick, POB B, Frederick, MD 21702 USA. EM giardina@mail.nciferf.gov; dkirpo@hermesbio.com FU NCI NIH HHS [N01-CO-12400] NR 7 TC 56 Z9 60 U1 0 U2 18 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD JAN-FEB PY 2005 VL 21 IS 1 BP 221 EP 232 DI 10.1021/bp049839z PG 12 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 896LE UT WOS:000226934800029 PM 15903261 ER PT J AU Gao, KM Calabrese, JR AF Gao, KM Calabrese, JR TI Newer treatment studies for bipolar depression SO BIPOLAR DISORDERS LA English DT Review DE antipsychotics; bipolar depression; mood stabilizer; novel agents; rTMS ID PLACEBO-CONTROLLED TRIAL; LITHIUM MAINTENANCE TREATMENT; CONTROLLED 18-MONTH TRIAL; WEEKLY SYMPTOMATIC STATUS; DOUBLE-BLIND; I DISORDER; NATURAL-HISTORY; MOOD DISORDERS; LAMOTRIGINE; INOSITOL AB Objective: Depressive symptoms of bipolar disorder have more negative impact on a patient's life than manic symptoms. This review focused on the emerging efficacy data for treatments in bipolar depression. Methods: English-language literature cited in Medline was searched with terms bipolar depression, clinical trial, and trial. Randomized, placebo-controlled trials of newer studies with older agents and all studies with newer or novel agents were prioritized. Open-label studies of novel agents presented at major scientific meetings were also included. Results: Olanzapine, olanzapine-fluoxetine combination (OFC), and quetiapine were superior to placebo in the acute treatment of bipolar depression. Lamotrigine only significantly reduced core symptoms of depression compared with placebo. Pramipexole, a dopamine D2/D3 receptor agonist and omega-3 fatty acids, a polyunsaturated fatty acid, augmentation to mood stabilizer (MS) had superiority to placebo in reducing depressive symptoms. Topiramate augmentation of an MS was equally as effective as Bupropion-SR. Patients treated with an MS responded well to the addition of agomelatine, a melatonin receptor agonist with 5-HT2C antagonist properties. However, inositol and repetitive transcranial magnetic stimulation did not separate from placebo. Lamotrigine and olanzapine, and to a lesser extent, divalproex, are superior to placebo in preventing depressive relapses. All agents were relatively well tolerated. Conclusions: Olanzapine, OFC, and quetiapine are effective in the acute treatment of bipolar depression. Compared with lithium and divalproex, lamotrigine is more effective in preventing bipolar depression. Larger controlled studies of the other agents in the acute and maintenance treatment of bipolar depression are warranted. C1 Case Western Reserve Univ, Sch Med, Univ Hosp Cleveland, Mood Disorders Program,NIMH,Bipolar Res Ctr, Cleveland, OH 44106 USA. RP Gao, KM (reprint author), 11400 Euclid Ave,Suite 200, Cleveland, OH 44106 USA. EM keming.gao@uhhs.com NR 39 TC 34 Z9 34 U1 1 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1398-5647 J9 BIPOLAR DISORD JI Bipolar Disord. PY 2005 VL 7 SU 5 BP 13 EP 23 DI 10.1111/j.1399-5618.2005.00250.x PG 11 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 999FU UT WOS:000234375100003 PM 16225556 ER PT J AU Byrd, JC Rai, K Peterson, BL Appelbaum, FR Morrison, VA Kolitz, JE Shepherd, L Hines, JD Schiffer, CA Larson, RA AF Byrd, JC Rai, K Peterson, BL Appelbaum, FR Morrison, VA Kolitz, JE Shepherd, L Hines, JD Schiffer, CA Larson, RA TI Addition of rituximab to fludarabine may prolong progression-free survival and overall survival in patients with previously untreated chronic lymphocytic leukemia: an updated retrospective comparative analysis of CALGB 9712 and CALGB 9011 SO BLOOD LA English DT Article ID THERAPY; TRIAL; EXPRESSION; LYMPHOMA; MUTATION; PHASE-2; GENES; CD38; CAP AB Fludarabine and rituximab combination therapies in chronic lymphocytic leukemia (CLL) have yielded promising early results, but no comparative efficacy data relative to standard fludarabine treatment regimens have been reported. To assess the effect of the addition of rituximab to fludarabine therapy, we retrospectively compared the treatment outcome of patients with similar clinical characteristics enrolled on 2 multicenter clinical trials performed by the Cancer and Leukemia Group B and the US Intergroup that used fludarabine and rituximab (CALGB 9712, n = 104) or fludarabine (CALGB 9011, n = 178). In multivariate analyses controlling for pretreatment characteristics, the patients receiving fludarabine and rituximab had a significantly better progression-free survival (PFS; P < .0001) and overall survival (OS; P = .0006) than patients receiving fludarabine therapy. Two-year PFS probabilities were 0.67 versus 0.45, and 2-year OS probabilities were 0.93 versus 0.81. Infectious toxicity was similar between the 2 treatment approaches. These comparative data are retrospective and could be confounded by differences in supportive care or dissimilar enrollment of genetic subsets on each trial. Confirmation of these findings will require a prospective randomized trial comparing fludarabine and rituximab to fludarabine. C1 Ohio State Univ, Div Hematol Oncol, Dept Med, Columbus, OH 43210 USA. Long Isl Jewish Med Ctr, Div Hematol, New Hyde Pk, NY 11042 USA. Long Isl Jewish Med Ctr, Div Oncol, New Hyde Pk, NY 11042 USA. Ctr Stat, CALGB, Durham, NC USA. Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA. Univ Minnesota, Hematol Oncol Sect, Vet Affairs Med Ctr, Minneapolis, MN USA. Cornell Univ, Coll Med, Dept Med, N Shore Univ Hosp, Manhasset, NY 11030 USA. Kingston Gen Hosp, Dept Pathol, NCI, Canada Clin Trials Grp, Kingston, ON K7L 2V7, Canada. Case Western Reserve Univ, Sch Med, Dept Med, Cleveland, OH 44106 USA. Wayne State Univ, Dept Med, Sch Med, Detroit, MI 48202 USA. Univ Chicago, Dept Med, Chicago, IL 60637 USA. RP Byrd, JC (reprint author), Ohio State Univ, Div Hematol Oncol, Dept Med, Starling Loving Hall,Rm 302, Columbus, OH 43210 USA. EM byrd-3@medctr.osu.edu OI Larson, Richard/0000-0001-9168-3203 FU NCI NIH HHS [CA47642, CA02599, CA03927, CA04326, CA04457, CA07190, CA07968, CA08025, CA11083, CA11789, CA12046, CA12449, CA13650, CA14548, CA15488, CA16116, CA16450, CA21060, CA21076, CA21115, CA26806, CA27525, CA31809, CA31946, CA31983, CA32102, CA32291, CA33601, CA35279, CA35421, CA37135, CA39229, CA41287, CA45374, CA45389, CA45400, CA45418, CA45564, CA45808, CA47555, CA47559, CA47577, CA49883, CA52784, CA54697, CA59307, CA60247, CA74811, CA77298, CA77440, CA77597, CA77651, CA77658] NR 22 TC 293 Z9 304 U1 0 U2 4 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 2005 VL 105 IS 1 BP 49 EP 53 DI 10.1128/blood-2004-03-0796 PG 5 WC Hematology SC Hematology GA 883FV UT WOS:000225997100016 PM 15138165 ER PT J AU Rosenberg, PS Socie, G Alter, BP Gluckman, E AF Rosenberg, PS Socie, G Alter, BP Gluckman, E TI Risk of head and neck squamous cell cancer and death in patients with Fanconi anemia who did and did not receive transplants SO BLOOD LA English DT Article ID BONE-MARROW-TRANSPLANTATION; LOW-DOSE CYCLOPHOSPHAMIDE; SOLID MALIGNANT-TUMORS; SEVERE APLASTIC-ANEMIA; FALSE DISCOVERY RATE; VERSUS-HOST-DISEASE; THORACOABDOMINAL IRRADIATION; CONDITIONING REGIMEN; HUMAN-PAPILLOMAVIRUS; DONORS AB Hematopoietic stem cell transplant (SCT) is currently the only therapy that can restore normal hematopoiesis in patients with Fanconi anemia (FA). Patients with FA have a high baseline risk of squamous cell cancers (SCCs) of the head, neck, and esophagus, and SCT conditioning may increase SCC incidence. We evaluated the risks of SCC and death in 145 patients with FA in the North American Survey (NAS) cohort who did not receive transplants, and 117 patients with FA in the Hopital Saint Louis (SLH) cohort who did receive transplants. The age-specific hazard of SCC was 4.4-fold higher in patients who received transplants than in those who did not (P = .003), and SCCs occurred at significantly younger ages in the former (respective medians, 18 and 33 years, P = .004). Survival after SCC was similarly poor in both cohorts (P = .135, median, 13 months). The hazard of SCC increased at a greater than linear rate, to 4.4% per year by age 40 in NAS and 4.7% per year by 10 years after transplant in SLH. In SLH, the hazard of non-SCC death was biphasic, declining significantly (P = .004) from 7.1% per month during the first 6 months after transplant to 0.13% per month (1.6% per year) after the first year. Acute and chronic graft-versus-host diseases were significant SCC risk factors. Adverse event rates in these cohorts provide historical control rates to assess emerging therapies for FA. C1 NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA. NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD USA. Hop St Louis, Serv Hematol Greffe Moelle, Paris, France. RP Rosenberg, PS (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,Execut Plaza S,Rm 7006, Rockville, MD 20852 USA. EM rosenbep@mail.nih.gov NR 46 TC 117 Z9 121 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 JAN 1 PY 2005 VL 105 IS 1 BP 67 EP 73 DI 10.1182/blood-2004-04-1652 PG 7 WC Hematology SC Hematology GA 883FV UT WOS:000225997100019 PM 15331448 ER PT J AU Zeng, S Xu, ZH Lipkowitz, S Longley, JB AF Zeng, S Xu, ZH Lipkowitz, S Longley, JB TI Regulation of stem cell factor receptor signaling by Cbl family proteins (Cbl-b/c-Cbl) SO BLOOD LA English DT Article ID C-KIT; UBIQUITIN LIGASE; DOWN-MODULATION; JNK ACTIVATION; RING-TYPE; PHOSPHORYLATION; APOPTOSIS; KINASES; COMPLEX; INTERNALIZATION AB Activation of the KIT receptor tyrosine kinase contributes to the pathogenesis of several human diseases, but the mechanisms regulating KIT signaling have not been fully characterized. Here, we show that stem cell factor (SCF), the ligand for KIT, induces the interaction between KIT and Cbl proteins and their mutual degradation. Upon SCF stimulation, KIT binds to and induces the phosphorylation of Cbl proteins, which in turn act as E3 ligases, mediating the ubiquitination and degradation of KIT and themselves. Tyrosine kinase binding and RING finger domains of Cbl are essential for Cbl-mediated ubiquitination and degradation of KIT. We propose a negative feedback loop controlling the SCF-KIT signaling pathway, in which SCF activates KIT. The activated KIT in turn induces phosphorylation and activation of Cbl proteins. The Cbl proteins then bind and direct the degradation of activated KIT, leading to down-regulation of KIT signaling. (C) 2005 by The American Society of Hematology. C1 Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Dermatol, New York, NY 10032 USA. NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA. RP Xu, ZH (reprint author), Columbia Univ, Coll Phys & Surg, Dept Pathol, 630 W 168th St, New York, NY 10032 USA. EM zx18@columbia.edu NR 30 TC 73 Z9 74 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 JAN 1 PY 2005 VL 105 IS 1 BP 226 EP 232 DI 10.1182/blood-2004-05-1768 PG 7 WC Hematology SC Hematology GA 883FV UT WOS:000225997100041 PM 15315962 ER PT J AU Powell, DJ Dudley, ME Robbins, PF Rosenberg, SA AF Powell, DJ Dudley, ME Robbins, PF Rosenberg, SA TI Transition of late-stage effector T cells to CD27(+) CD28(+) tumor-reactive effector memory T cells in humans after adoptive cell transfer therapy SO BLOOD LA English DT Article ID INTERLEUKIN-7 RECEPTOR; FUNCTIONAL-PROPERTIES; VIRUS-INFECTIONS; IN-VIVO; LYMPHOCYTES; EXPRESSION; SUBSETS; IL-7; GENERATION; DIFFERENTIATION AB In humans, the pathways of memory T-cell differentiation remain poorly defined. Recently, adoptive cell transfer (ACT) of tumor-reactive T lymphocytes to metastatic melanoma patients after nonmyeloablative chemotherapy has resulted in persistence of functional, tumor-reactive lymphocytes, regression of disease, and induction of melanocyte-directed autoimmunity in some responding patients. In the current study, longitudinal phenotypic analysis was performed on melanoma antigen-specific CD8(+) T cells during their transition from in vitro cultured effector cells to long-term persistent memory cells following ACT to 6 responding patients. Tumor-reactive T cells used for therapy were generally late-stage effector cells with a CD27(Lo) CD28(Lo) CD45RA(-) CD62 ligand(-) (CD62L(-)) CC chemokine receptor 7(-) (CCR7(-)) interieukin-7 receptor alpha(Lo) (IL-7Ralpha(Lo)) phenotype. After transfer, rapid up-regulation and continued expression of IL-7Ralpha in vivo suggested an important role for IL-7R in immediate and long-term T-cell survival. Although the tumor antigen-specific T-cell population contracted between 1 and 4 weeks after transfer, stable numbers of CD27(+) CD28(+) tumor-reactive T cells were maintained, demonstrating their contribution to the development of long-term, melanoma-reactive memory CD8+ T cells in vivo. At 2 months after transfer, melanoma-reactive T cells persisted at high levels and displayed an effector memory phenotype, including a CD27(+) CD28(+) CD62L(-) CCR7(-) profile, which may explain in part their ability to mediate tumor destruction. (C) 2005 by The American Society of Hematology. C1 NCI, Surg Branch, Bethesda, MD 20892 USA. RP Powell, DJ (reprint author), NCI, Surg Branch, Bldg 10,Rm 3W-3940,10 Ctr Dr,MSC 1201, Bethesda, MD 20892 USA. EM sar@nih.gov FU Intramural NIH HHS [Z01 SC003811-32] NR 55 TC 171 Z9 175 U1 1 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 2005 VL 105 IS 1 BP 241 EP 250 DI 10.1182/blood-2004-06-2482 PG 10 WC Hematology SC Hematology GA 883FV UT WOS:000225997100043 PM 15345595 ER PT J AU Rasmussen, T Kuehl, M Lodahl, M Johnsen, HE Dahl, IMS AF Rasmussen, T Kuehl, M Lodahl, M Johnsen, HE Dahl, IMS TI Possible roles for activating RAS mutations in the MGUS to MM transition and in the intramedullary to extramedullary transition in some plasma cell tumors SO BLOOD LA English DT Article ID POLYMERASE-CHAIN-REACTION; MULTIPLE-MYELOMA; K-RAS; N-RAS; LINE ANBL6; EXPRESSION; ONCOGENES; PROGRESSION; CD56; TRANSFORMATION AB To assess a possible role in tumor progression, the occurrence and type of K- and N-RAS mutations were determined in purified tumor cells, including samples from patients with premalignant monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma (MM), and extramedullary, plasma cell (PC) tumors (ExPCTs). Immunophenotypic aberrant PCs were flow sorted from 20 MGUS, 58 MM, and 13 ExPCT patients. One RAS mutation was identified in 20 MGUS tumors (5%), in contrast to a much higher prevalence of RAS mutations in all stages of MM (about 31%). Further, oncogene analyses showed that RAS mutations are not evenly distributed among different molecular subclasses of MM, with the prevalence being increased in MM-expressing cyclin D1 (P =.015) and decreased in MM with t(4;14) (P = .055). We conclude that RAS mutations often provide a genetic marker if not a causal event in the evolution of MGUS to MM. Surprisingly, RAS mutations were absent in bone marrow tumor cells from all patients with ExPCT, a result significantly different from intramedullary MM (P = .001). From 3 of 6 patients with paired intramedullary and extramedullary PCs and identical immunoglobulin heavy chain gene (IgH) sequences, RAS mutations were identified only in extramedullary PCs, suggesting a role for RAS mutations in the transition from intramedullary to extramedullary tumor. (C) 2005 by The American Society of Hematology. C1 Univ Copenhagen, Herlev Hosp, Dept Hematol, DK-2730 Herlev, Denmark. NCI, Genet Branch, Canc Res Ctr, Naval Hosp, Bethesda, MD 20892 USA. Univ Tromso Hosp, Sect Hematol, N-9012 Tromso, Norway. RP Rasmussen, T (reprint author), Univ Copenhagen, Herlev Hosp, Dept Hematol, L54P4, DK-2730 Herlev, Denmark. EM thra@herlevhosp.kbhamt.dk NR 32 TC 87 Z9 90 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 JAN 1 PY 2005 VL 105 IS 1 BP 317 EP 323 DI 10.1182/blood-2004-03-0833 PG 7 WC Hematology SC Hematology GA 883FV UT WOS:000225997100053 PM 15339850 ER PT J AU Bhanu, NV Trice, TA Lee, YT Gantt, NM Oneal, P Schwartz, JD Noel, P Miller, JL AF Bhanu, NV Trice, TA Lee, YT Gantt, NM Oneal, P Schwartz, JD Noel, P Miller, JL TI A sustained and pancellular reversal of gamma-globin gene silencing in adult human erythroid precursor cells SO BLOOD LA English DT Article ID GROWTH-FACTOR-BETA; FETAL-HEMOGLOBIN; HEREDITARY PERSISTENCE; ERYTHROPOIESIS; EXPRESSION; PROLIFERATION; DIFFERENTIATION; PROGENITORS; ANEMIA; ACTIVATION AB We systematically compared cytokine-mediated increases or decreases in proliferation with globin gene and protein expression in adult human erythroblasts. Despite their opposite effects on growth, stem cell factor (SCF) and transforming growth factor-beta (TGF-B) had synergistic effects with respect to fetal hemoglobin (HbF): average HbF/HbF + adult hemoglobin (HbA) ratio in erythropoietin (EPO) = 1.4 +/- 1.0%; EPO + TGF-B = 10.8 +/- 1.9%; EPO + SCF = 19.1 +/- 6.2%; and EPO + SCF + TGF-B (EST) = 39.3 +/- 6.3%. Polymerase chain reaction (PCR) revealed significant increases in gamma-globin transcripts that were balanced by reduced beta-globin transcripts. Single-cell quantitative PCR demonstrated a complete reversal of gamma-globin gene silencing with detectable gamma-globin mRNA in more than 95% of the cells. Immunostaining with HbF antibodies also showed a pancellular distribution in EST (96.2 +/- 0.01% HbF positive) compared with a heterocellular distribution in EPO (42.9 +/- 0.01% HbF positive). As shown here for the first time, a robust and pancellular reversal of gamma-globin gene silencing among hemoglobinized erythroblasts from adult humans may be achieved in the absence of hereditary mutation or direct genomic manipulation. (C) 2005 by The American Society of Hematology. C1 NIH, Mol Med Branch, Dept Lab Med, Hematol Serv, Bethesda, MD 20892 USA. NIDDK, Mol Med Branch, Bethesda, MD USA. RP Miller, JL (reprint author), NIH, Mol Med Branch, Dept Lab Med, Hematol Serv, Bldg 10,Room 9B17,10 Ctr Dr, Bethesda, MD 20892 USA. EM jm7f@nih.gov NR 32 TC 29 Z9 30 U1 1 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 2005 VL 105 IS 1 BP 387 EP 393 DI 10.1182/blood-2004-04-1599 PG 7 WC Hematology SC Hematology GA 883FV UT WOS:000225997100063 PM 15367428 ER PT J AU Anderson, SA Glod, J Arbab, AS Noel, M Ashari, P Fine, HA Frank, JA AF Anderson, SA Glod, J Arbab, AS Noel, M Ashari, P Fine, HA Frank, JA TI Noninvasive MR imaging of magnetically labeled stem cells to directly identify neovasculature in a glioma model SO BLOOD LA English DT Article ID TUMOR ANGIOGENESIS; TRANSFECTION AGENT; TRANSPLANTATION; NEOVASCULARIZATION; FERUMOXIDES; TRACKING; GROWTH AB Bone marrow-derived endothelial precursor cells incorporate into neovasculature and have been successfully used as vehicles for gene delivery to brain tumors. To determine whether systemically administered Sca1(+) bone marrow cells labeled with superparamagnetic iron oxide nanoparticles can be detected by in vivo magnetic resonance imaging in a mouse brain tumor model, mouse Sca1(+) cells were labeled in vitro with ferumoxides-poly-L-lysine complexes. Labeled or control cells were administered intravenously to glioma-bearing severe combined immunodeficient (SCID) mice. Magnetic resonance imaging (MRI) was performed during tumor growth. Mice that received labeled cells demonstrated hypointense regions within the tumor that evolved over time and developed a continuous dark hypointense ring at a consistent time point. This effect was not cleared by administration of a gadolinium contrast agent. Histology showed iron-labeled cells around the tumor rim in labeled mice, which expressed CD31 and von Willebrand factor, indicating the transplanted cells detected in the tumor have differentiated into endothelial-like cells. These results demonstrate that MRI can detect the incorporation of magnetically labeled bone marrow-derived precursor cells into tumor vasculature as part of ongoing angiogenesis and neovascularization. This technique can be used to directly identify neovasculature in vivo and to facilitate gene therapy by noninvasively monitoring these cells as gene delivery vectors. (C) 2005 by The American Society of Hematology. C1 NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. NCI, Neurooncol Branch, Bethesda, MD 20892 USA. NIH, Expt Neuroimaging Sect, Lab Diagnost Radiol Res, Bethesda, MD 20892 USA. RP Anderson, SA (reprint author), NINDS, Neuroimmunol Branch, NIH, Bldg 10 Rm B1N256,10 Ctr Dr MSC 1074, Bethesda, MD 20892 USA. EM sanderso@helix.nih.gov NR 23 TC 181 Z9 197 U1 5 U2 11 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 2005 VL 105 IS 1 BP 420 EP 425 DI 10.1182/blood-2004-06-2222 PG 6 WC Hematology SC Hematology GA 883FV UT WOS:000225997100068 PM 15331444 ER PT J AU Ronckers, CM Erdmann, CA Land, CE AF Ronckers, CM Erdmann, CA Land, CE TI Radiation and breast cancer: a review of current evidence SO BREAST CANCER RESEARCH LA English DT Review DE breast cancer; genetics; interaction; radiation ID ATOMIC-BOMB SURVIVORS; LONG-TERM SURVIVORS; CHILDHOOD HODGKINS-DISEASE; NIJMEGEN BREAKAGE SYNDROME; 2ND MALIGNANT NEOPLASMS; MAMMARY CARCINOGENESIS; RISK-FACTORS; FOLLOW-UP; COLLABORATIVE REANALYSIS; CONTRALATERAL BREAST AB This paper summarizes current knowledge on ionizing radiation-associated breast cancer in the context of established breast cancer risk factors, the radiation dose-response relationship, and modifiers of dose response, taking into account epidemiological studies and animal experiments. Available epidemiological data support a linear dose-response relationship down to doses as low as about 100 mSv. However, the magnitude of risk per unit dose depends strongly on when radiation exposure occurs: exposure before the age of 20 years carries the greatest risk. Other characteristics that may influence the magnitude of dose-specific risk include attained age ( that is, age at observation for risk), age at first full-term birth, parity, and possibly a history of benign breast disease, exposure to radiation while pregnant, and genetic factors. C1 NCI, Div Canc Epidemiol & Genet, NIH, HHS, Bethesda, MD 20892 USA. Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA. RP Ronckers, CM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, HHS, Bethesda, MD 20892 USA. EM ronckerc@mail.nih.gov NR 111 TC 135 Z9 138 U1 0 U2 7 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1465-542X J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 1 BP 21 EP 32 DI 10.1186/bcr970 PG 12 WC Oncology SC Oncology GA 886RV UT WOS:000226247000005 PM 15642178 ER PT J AU Brinton, LA AF Brinton, LA TI Do breast implants after a mastectomy affect subsequent prognosis and survival? SO BREAST CANCER RESEARCH LA English DT Review ID AUGMENTATION MAMMAPLASTY; WOMEN; RECONSTRUCTION; CANCER; SURGERY; POPULATION; POSTMASTECTOMY; IMMEDIATE; MORTALITY AB In a large study, published in this issue of Breast Cancer Research, Le and colleagues report that women receiving implants after mastectomies for early-stage breast cancer experience lower breast cancer mortality than women not receiving implants. Assessment of survival patterns among women receiving reconstructive implants is complex given unique patient characteristics, disease attributes, and treatment patterns. The interpretation of reduced mortality from breast cancer must be assessed in light of significantly reduced risks of death from most other causes. In contrast, patients receiving post-mastectomy implants had elevated rates of suicide, consistent with findings among women with cosmetic implants. Additional well-designed investigations are needed to clarify survival patterns among women receiving reconstructive implants. C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Brinton, LA (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. EM Brinton@nih.gov RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 22 TC 1 Z9 1 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 2 BP 61 EP 63 DI 10.1186/bcr1003 PG 3 WC Oncology SC Oncology GA 905QC UT WOS:000227583300004 PM 15743512 ER PT J AU Lamb, CA Helguero, LA Giulianelli, S Soldati, R Vanzulli, SI Molinolo, A Lanari, C AF Lamb, CA Helguero, LA Giulianelli, S Soldati, R Vanzulli, SI Molinolo, A Lanari, C TI Antisense oligonucleotides targeting the progesterone receptor inhibit hormone-independent breast cancer growth in mice SO BREAST CANCER RESEARCH LA English DT Article ID MEDROXYPROGESTERONE ACETATE MPA; MOUSE MAMMARY-TUMORS; ESTROGEN PLUS PROGESTIN; BALB/C FEMALE MICE; N-NITROSOUREA MNU; REPLACEMENT THERAPY; ANTIPROGESTIN ONAPRISTONE; CELL-PROLIFERATION; ANTITUMOR-ACTIVITY; DUCTAL CARCINOMAS AB Introduction Previous data from our laboratory suggested that progesterone receptors (PRs) are involved in progestin-independent growth of mammary carcinomas. To investigate this possibility further, we studied the effects of PR antisense oligodeoxynucleotides (asPR) on in vivo tumor growth. Method BALB/c mice with subcutaneous 25 mm(2) mammary carcinomas expressing estrogen receptor-alpha and PR were either injected intraperitoneally with 1 mg asPR every 24 or 12 hours for 5 - 10 days, or subcutaneously with RU 486 (6.5 mg/kg body weight) every 24 hours. Control mice received vehicle or scPR. Results Significant inhibition of tumor growth as well as a significant decrease in bromodeoxyuridine uptake was observed in asPR-treated mice, which correlated with histological signs of regression and increased apoptosis. Mice treated with RU 486 experienced almost complete tumor regression. No differences were detected between vehicle-treated and scPR-treated mice. Anti-progestin-treated and asPR-treated mice were in a continuous estrous/meta-estrous state. Decreased phosphorylated extracellular signal-regulated kinase (ERK) 1 and ERK2 levels and estrogen receptor-alpha expression were observed as late events in RU 486-treated and asPR-treated mice with regressing tumors. Conclusion We demonstrate, for the first time, inhibition of tumor growth in vivo using asPR. Our results provide further evidence for a critical and hierarchical role of the PR pathway in mammary carcinomas. C1 Consejo Nacl Invest Cient & Tecn, Inst Biol & Med Expt, RA-1033 Buenos Aires, DF, Argentina. Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA. RP Consejo Nacl Invest Cient & Tecn, Inst Biol & Med Expt, RA-1033 Buenos Aires, DF, Argentina. EM clanari@dna.uba.ar RI Helguero, Luisa/B-1221-2013 OI Helguero, Luisa/0000-0001-8237-2390 NR 45 TC 17 Z9 17 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1465-542X EI 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 6 BP R1111 EP R1121 DI 10.1186/bcr1345 PG 11 WC Oncology SC Oncology GA 993LZ UT WOS:000233956900037 PM 16457691 ER PT J AU Li, Y Millikan, RC Bell, DA Cui, L Tse, CKJ Newman, B Conway, K AF Li, Y Millikan, RC Bell, DA Cui, L Tse, CKJ Newman, B Conway, K TI Polychlorinated biphenyls, cytochrome P450 1A1 (CYP1A1) polymorphisms, and breast cancer risk among African American women and white women in North Carolina: a population-based case-control study SO BREAST CANCER RESEARCH LA English DT Review DE breast cancer; CYP1A1; polychlorinated biphenyls ID CHLORINATED-HYDROCARBON LEVELS; ORGANOCHLORINE COMPOUNDS; BLOOD-LEVELS; SERUM; PCBS; PESTICIDES; GENOTYPE; RESIDUES; TISSUE; GENE AB Introduction Epidemiologic studies have not shown a strong relationship between blood levels of polychlorinated biphenyls (PCBs) and breast cancer risk. However, two recent studies showed a stronger association among postmenopausal white women with the inducible M2 polymorphism in the cytochrome P450 1A1 (CYP1A1) gene. Methods In a population-based case-control study, we evaluated breast cancer risk in relation to PCBs and the CYP1A1 polymorphisms M1 (also known as CYP1A1*2A), M2 (CYP1A1*2C), M3 (CYP1A1*3), and M4 (CYP1A1*4). The study population consisted of 612 patients (242 African American, 370 white) and 599 controls (242 African American, 357 white). Results There was no evidence of strong joint effects between CYP1A1 M1-containing genotypes and total PCBs in African American or white women. Statistically significant multiplicative interactions were observed between CYP1A1 M2-containing genotypes and elevated plasma total PCBs among white women (P value for likelihood ratio test = 0.02). Multiplicative interactions were also observed between CYP1A1 M3-containing genotypes and elevated total PCBs among African American women (P value for likelihood ratio test = 0.10). Conclusions Our results confirm previous reports that CYP1A1 M2-containing genotypes modify the association between PCB exposure and risk of breast cancer. We present additional evidence suggesting that CYP1A1 M3-containing genotypes modify the effects of PCB exposure among African American women. Additional studies are warranted, and meta-analyses combining results across studies will be needed to generate more precise estimates of the joint effects of PCBs and CYP1A1 genotypes. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. Queensland Univ Technol, Sch Publ Hlth, Kelvin Grove, Qld, Australia. RP Millikan, RC (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA. EM millikan@email.unc.edu FU NCI NIH HHS [P50-CA58223, P30 CA016086, P30-CA16086, P50 CA058223]; NIEHS NIH HHS [R01-ES07128, P42-ES05948, P30 ES010126, P42 ES005948] NR 39 TC 49 Z9 52 U1 0 U2 9 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 1 BP R12 EP R18 DI 10.1186/bcr941 PG 7 WC Oncology SC Oncology GA 886RV UT WOS:000226247000013 PM 15642161 ER PT J AU Rehman, A Chahal, MS Tang, XT Bruce, JE Pommier, Y Daoud, SS AF Rehman, A Chahal, MS Tang, XT Bruce, JE Pommier, Y Daoud, SS TI Proteomic identification of heat shock protein 90 as a candidate target for p53 mutation reactivation by PRIMA-1 in breast cancer cells SO BREAST CANCER RESEARCH LA English DT Article ID TUMOR-SUPPRESSOR PROTEIN; COLON-CARCINOMA CELLS; HEAT-SHOCK-PROTEIN; NUCLEAR TRANSLOCATION; MUTANT P53; MOLECULAR CHAPERONE; GENE MUTATION; WILD-TYPE; EXPRESSION; HSP90 AB Introduction A loss of p53 function resulting from mutation is prevalent in human cancers. Thus, restoration of p53 function to mutant p53 using small compounds has been extensively studied for cancer therapy. We previously reported that PRIMA-1 ( for 'p53 reactivation and induction of massive apoptosis') restored the transcriptional activity of p53 target genes in breast cancer cells with a p53 mutation. By using functional proteomics approach, we sought to identify molecular targets that are involved in the restoration of normal function to mutant p53. Methods PRIMA-1 treated cell lysates were subjected to immunoprecipitation with DO-1 primary antibody against p53 protein, and proteins bound to p53 were separated on a denaturing gel. Bands expressed differentially between control and PRIMA-1-treated cells were then identified by matrix-assisted laser desorption ionization-time-of-flight spectrometry. Protein expression in whole cell lysates and nuclear extracts were confirmed by Western blotting. The effect of combined treatment of PRIMA-1 and adriamycin in breast cancer cells was determined with a cytotoxicity assay in vitro. Results PRIMA-1 treated cells distinctly expressed a protein band of 90 kDa that was identified as heat shock protein 90 (Hsp90) by the analysis of the 90 kDa band tryptic digest. Immunoblotting with isoform-specific antibodies against Hsp90 identified this band as the alpha isoform of Hsp90 (Hsp90 alpha). Coimmunoprecipitation with anti-Hsp90 alpha antibody followed by immunoblotting with DO-1 confirmed that p53 and Hsp90 alpha were interacting proteins. PRIMA-1 treatment also resulted in the translocation of Hsp90 alpha to the nucleus by 8 hours. Treatment of cells with PRIMA-1 alone or in combination with adriamycin, a DNA-targeted agent, resulted in increased sensitivity of tumor cells. Conclusion The studies demonstrate that PRIMA-1 restores the p53-Hsp90 alpha interaction, enhances the translocation of the p53-Hsp90 alpha complex and reactivates p53 transcriptional activity. Our preliminary evidence also suggests that PRIMA-1 could be considered in combination therapy with DNA-targeted agents for the treatment of breast cancer, especially for tumors with aberrant p53 function. C1 Washington State Univ, Dept Pharmaceut Sci, Pullman, WA 99164 USA. Washington State Univ, Pharmacol & Toxicol Grad Program, Pullman, WA 99164 USA. Washington State Univ, Dept Chem, Pullman, WA 99164 USA. NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Daoud, SS (reprint author), Washington State Univ, Dept Pharmaceut Sci, Pullman, WA 99164 USA. EM daoud@mail.wsu.edu NR 38 TC 34 Z9 37 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 5 BP R765 EP R774 DI 10.1186/bcr1290 PG 10 WC Oncology SC Oncology GA 970TJ UT WOS:000232332200035 PM 16168122 ER PT J AU Shilkaitis, A Green, A Punj, V Steele, V Lubet, R Christov, K AF Shilkaitis, A Green, A Punj, V Steele, V Lubet, R Christov, K TI Dehydroepiandrosterone inhibits the progression phase of mammary carcinogenesis by inducing cellular senescence via a p16-dependent but p53-independent mechanism SO BREAST CANCER RESEARCH LA English DT Article ID 7,12-DIMETHYLBENZ(A) ANTHRACENE DMBA; BREAST-CANCER; TUMOR-CELLS; RAT; GLAND; AGENTS; DHEA; PROLIFERATION; EXPRESSION; PHENOTYPE AB Introduction Dehydroepiandrosterone ( DHEA), an adrenal 17-ketosteroid, is a precursor of testosterone and 17 beta-estradiol. Studies have shown that DHEA inhibits carcinogenesis in mammary gland and prostate as well as other organs, a process that is not hormone dependent. Little is known about the molecular mechanisms of DHEA-mediated inhibition of the neoplastic process. Here we examine whether DHEA and its analog DHEA 8354 can suppress the progression of hyperplastic and premalignant ( carcinoma in situ) lesions in mammary gland toward malignant tumors and the cellular mechanisms involved. Methods Rats were treated with N-nitroso-N-methylurea and allowed to develop mammary hyperplastic and premalignant lesions with a maximum frequency 6 weeks after carcinogen administration. The animals were then given DHEA or DHEA 8354 in the diet at 125 or 1,000 mg/kg diet for 6 weeks. The effect of these agents on induction of apoptosis, senescence, cell proliferation, tumor burden and various effectors of cellular signaling were determined. Results Both agents induced a dose-dependent decrease in tumor multiplicity and in tumor burden. In addition they induced a senescent phenotype in tumor cells, inhibited cell proliferation and increased the number of apoptotic cells. The DHEA-induced cellular effects were associated with increased expression of p16 and p21, but not p53 expression, implicating a p53-independent mechanism in their action. Conclusion We provide evidence that DHEA and DHEA 8354 can suppress mammary carcinogenesis by altering various cellular functions, inducing cellular senescence, in tumor cells with the potential involvement of p16 and p21 in mediating these effects. C1 Univ Illinois, Dept Surg Oncol, Chicago, IL 60612 USA. NCI, Div Canc Prevent, Bethesda, MD 20892 USA. RP Christov, K (reprint author), Univ Illinois, Dept Surg Oncol, 840 S Wood St, Chicago, IL 60612 USA. EM Christov@UIC.edu FU NCI NIH HHS [N01-CN-55179-MAO] NR 28 TC 15 Z9 18 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 IS 6 BP R1132 EP R1140 DI 10.1186/bcr1350 PG 9 WC Oncology SC Oncology GA 993LZ UT WOS:000233956900039 PM 16457693 ER PT J AU Barrett, MT Sampas, N Ben-Dor, A Scheffer, A Anderson, P Tsang, P Gooden, C Walker, R Curry, B Kincaid, R Lipson, D Bittner, M Yakhini, Z Meltzer, PS Bruhn, L Laderman, S AF Barrett, MT Sampas, N Ben-Dor, A Scheffer, A Anderson, P Tsang, P Gooden, C Walker, R Curry, B Kincaid, R Lipson, D Bittner, M Yakhini, Z Meltzer, PS Bruhn, L Laderman, S TI Comparative genomic hybridization using oligonucleotide arrays and total genomic DNA SO BREAST CANCER RESEARCH LA English DT Meeting Abstract CT 3rd International Symposium on the Molecular Biology of Breast Cancer CY JUN 22-26, 2005 CL Molde, NORWAY C1 Agilent Technol, Palo Alto, CA USA. Translat Genom Inst, Phoenix, AZ USA. NHGRI, Bethesda, MD 20892 USA. RI Kincaid, Robert/B-6683-2009 OI Kincaid, Robert/0000-0002-4344-0853 NR 1 TC 0 Z9 0 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 SU 2 BP S51 EP S51 DI 10.1186/bcr1170 PG 1 WC Oncology SC Oncology GA 970SS UT WOS:000232330500123 ER PT J AU Damalas, A Weis, L Nordgard, SH Kristensen, VN Gardner, K Cheng, G Gelinas, C Levrero, M Strano, S Borresen-Dale, AL Rotter, V Oren, M Blandino, G AF Damalas, A Weis, L Nordgard, SH Kristensen, VN Gardner, K Cheng, G Gelinas, C Levrero, M Strano, S Borresen-Dale, AL Rotter, V Oren, M Blandino, G TI Mutant p53 exerts its gain of function through activation of the NF-kappa B pathway SO BREAST CANCER RESEARCH LA English DT Meeting Abstract CT 3rd International Symposium on the Molecular Biology of Breast Cancer CY JUN 22-26, 2005 CL Molde, NORWAY C1 Regina Elena Inst Canc Res, Dept Expt Oncol, Rome, Italy. Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. Norwegian Radium Hosp, Inst Canc Res, Dept Genet, Oslo, Norway. NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. NCI, DHHS, NIH, CCR, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA. Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA. Univ Roma La Sapienza, Fdn Andrea Cesalpino, Rome, Italy. Univ Oslo, Norwegian Radium Hosp, Fac Div, Oslo, Norway. RI Blandino, Giovanni/B-1137-2013; strano, sabrina/B-6743-2013; Nord, Silje/R-5212-2016 OI Blandino, Giovanni/0000-0002-6970-2241; strano, sabrina/0000-0002-6341-4230; Nord, Silje/0000-0002-3271-5356 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 SU 2 BP S53 EP S53 DI 10.1186/bcr1176 PG 1 WC Oncology SC Oncology GA 970SS UT WOS:000232330500129 ER PT J AU Johnson, KA Ford, LG AF Johnson, KA Ford, LG TI A critical need for molecular markers of breast cancer risk and risk reduction SO BREAST CANCER RESEARCH LA English DT Meeting Abstract CT 3rd International Symposium on the Molecular Biology of Breast Cancer CY JUN 22-26, 2005 CL Molde, NORWAY C1 NCI, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 SU 2 BP S26 EP S26 DI 10.1186/bcr1111 PG 1 WC Oncology SC Oncology GA 970SS UT WOS:000232330500064 ER PT J AU Nordgard, SH Sorlie, T Chanock, SJ Borresen-Dale, AL Gardner, K Kristensen, VN AF Nordgard, SH Sorlie, T Chanock, SJ Borresen-Dale, AL Gardner, K Kristensen, VN TI Promoter composition predicts gene classes in microarray expression analyses of breast cancer SO BREAST CANCER RESEARCH LA English DT Meeting Abstract CT 3rd International Symposium on the Molecular Biology of Breast Cancer CY JUN 22-26, 2005 CL Molde, NORWAY C1 Norwegian Radium Hosp, Dept Genet, Oslo, Norway. NCI, Sect Genom Variat, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. NCI, Lab Receptor Biol, Bethesda, MD 20892 USA. NCI, Ctr Adv Technol, Gene Express & Microarray Facil, Bethesda, MD 20892 USA. RI Nord, Silje/R-5212-2016 OI Nord, Silje/0000-0002-3271-5356 NR 3 TC 0 Z9 0 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 SU 2 BP S48 EP S49 DI 10.1186/bcr1164 PG 2 WC Oncology SC Oncology GA 970SS UT WOS:000232330500117 ER PT J AU Paik, S AF Paik, S TI Methods for gene expression profiling in clinical trials for breast cancer SO BREAST CANCER RESEARCH LA English DT Meeting Abstract CT 6th Madrid Breast Cancer Conference CY JUN 01-03, 2005 CL Madrid, SPAIN ID RNA; TUMOR C1 Natl Surg Adjuvant Breast & Bowel Project, Div Pathol, Pittsburgh, PA USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2005 VL 7 SU 1 BP S2 EP S2 DI 10.1186/bcr1207 PG 1 WC Oncology SC Oncology GA 970SB UT WOS:000232328800004 ER PT J AU Anderson, WF Jatoi, I AF Anderson, WF Jatoi, I TI Distinct breast cancer incidence and survival patterns according to histopathology: analysis of the NCI's SEER database. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NCI, Bethesda, MD 20892 USA. Natl Naval Med Res Inst, Bethesda, MD USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S147 EP S147 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100397 ER PT J AU Arun, B Valero, V Hornbeak, J Gong, Y Broglio, K Logan, C Browne, D Hortobagyi, G Sneige, N AF Arun, B Valero, V Hornbeak, J Gong, Y Broglio, K Logan, C Browne, D Hortobagyi, G Sneige, N TI Celecoxib downregulats estrogen receptor expression in breast tissue of women at increased risk for developing breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. BMO, Houston, TX USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S169 EP S169 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100457 ER PT J AU Brufsky, A Rugo, H Tripathy, D Kaufman, P Mayer, M Paik, S Ulcickas-Yood, M Yardley, D Tan-Chiu, E AF Brufsky, A Rugo, H Tripathy, D Kaufman, P Mayer, M Paik, S Ulcickas-Yood, M Yardley, D Tan-Chiu, E TI registHER: treatments and clinical outcomes from a prospective observational cohort study of patients with HER2-positive metastatic breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Univ Pittsburgh, Ctr Canc, Pittsburgh, PA USA. UCSF Comprehens Canc Ctr, San Francisco, CA USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA. Patient Advocate, New York, NY USA. Natl Surg Adjuvant Breast Bowel Project, Pittsburgh, PA USA. EpiSource LLC, New Haven, CT USA. Yale Univ, Sch Med, New Haven, CT USA. Sarah Cannon Canc Ctr, Nashville, TN USA. Canc Res Network, Plantation, FL USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S148 EP S148 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100400 ER PT J AU Buxton, MB Bondi, SM Au, A Crothers, J Carey, LA DeMichele, A Dorsey, KC Dressler, L Harden, AT Gray, JW Haqq, CM Madhavan, S Perou, C Petricoin, EF AF Buxton, MB Bondi, SM Au, A Crothers, J Carey, LA DeMichele, A Dorsey, KC Dressler, L Harden, AT Gray, JW Haqq, CM Madhavan, S Perou, C Petricoin, EF CA I-SPY Clin Investigators TI Methods to optimize tissue collection and assay performance from 16-gauge core biopsies in the I-SPY Trial. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ N Carolina, Chapel Hill, NC USA. Univ Penn, Philadelphia, PA 19104 USA. NCI, Rockville, MD USA. US FDA, Rockville, MD 20857 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S54 EP S55 PG 2 WC Oncology SC Oncology GA 985VP UT WOS:000233407100147 ER PT J AU Christov, K Muccio, D Brouillette, W Atigadda, R Desphande, A Bland, K Beenken, S Grubbs, C Lubet, R AF Christov, K Muccio, D Brouillette, W Atigadda, R Desphande, A Bland, K Beenken, S Grubbs, C Lubet, R TI Chemopreventive efficacy of new RXR specific retinoids against mammary cancers and correlations with short-term biomarkers. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Univ Illinois, Chicago, IL USA. Univ Alabama, Birmingham, AL USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S169 EP S169 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100458 ER PT J AU Davidson, B Vogel, V Wickerham, L AF Davidson, B Vogel, V Wickerham, L TI Oncologist-patient discussion of adjuvant hormonal therapy: results of a linguistic study focusing on patient adherence/persistence SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 MBS Vox, Wayne, NJ USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. NSABP, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S80 EP S81 PG 2 WC Oncology SC Oncology GA 985VP UT WOS:000233407100218 ER PT J AU Gergich, NL Pfalzer, LA McGarvey, CL Augustine, EA Springer, B Gerber, LH Soballe, PW AF Gergich, NL Pfalzer, LA McGarvey, CL Augustine, EA Springer, B Gerber, LH Soballe, PW TI One year outcomes of an early identification and intervention model to reduce upper extremity morbidity related to breast cancer treatment SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Natl Naval Med Res Inst, Bethesda, MD 20892 USA. NIH, Bethesda, MD 48503 USA. Univ Michigan, Flint, MI 20307 USA. Walter Reed Army Med Ctr, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S269 EP S269 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100729 ER PT J AU Grubbs, C Christov, K You, M Wang, Y Steele, V Juliana, M Lubet, R AF Grubbs, C Christov, K You, M Wang, Y Steele, V Juliana, M Lubet, R TI Chemopreventive effects of the EGFr inhibitor Iressa in the methylnitrosourea (MNU) - induced model of mammary carcinogenesis. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Univ Alabama, Birmingham, AL USA. Univ Illinois, Chicago, IL USA. Washington Univ, St Louis, MO USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S170 EP S170 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100461 ER PT J AU Hudis, C Citron, M Berry, D Cirrincione, C Gradishar, W Davidson, N Martino, S Livingston, R Ingle, J Perez, E Abrams, J Schilsky, R Ellis, M Muss, H Norton, L Winer, E AF Hudis, C Citron, M Berry, D Cirrincione, C Gradishar, W Davidson, N Martino, S Livingston, R Ingle, J Perez, E Abrams, J Schilsky, R Ellis, M Muss, H Norton, L Winer, E TI Five year follow-up of INT C9741: dose-dense (DD) chemotherapy (CRx) is safe and effective. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 MSKCC, New York, NY USA. ProHlth Care Assoc, Lake Success, NY USA. MD Anderson, Houston, TX USA. CALGB Stat Off & Data Ops, Durham, NC USA. Northwestern Univ, Chicago, IL 60611 USA. Johns Hopkins, Kimmel Comp Ca Ctr, Baltimore, MD USA. JWCI, Santa Monica, CA USA. Univ Washington, Seattle, WA 98195 USA. Mayo, Rochester, MN USA. Mayo Clin, Jacksonville, FL 32224 USA. NCI, Bethesda, MD 20892 USA. CALGB Cent Off, Chicago, IL USA. Washington Univ, St Louis, MO USA. Univ Vermont, Burlington, VT USA. DFCI, Boston, MA USA. NR 0 TC 40 Z9 41 U1 1 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S20 EP S21 PG 2 WC Oncology SC Oncology GA 985VP UT WOS:000233407100056 ER PT J AU Li, Y Kim, H Uray, I Bissonnette, R Lamph, W Johnson, K Brown, P AF Li, Y Kim, H Uray, I Bissonnette, R Lamph, W Johnson, K Brown, P TI Identification of genes modulated by LGD1069, a rexinoid that prevents mammary tumorigenesis. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Ligand Pharmaceut Inc, San Diego, CA USA. Baylor Coll Med, Houston, TX 77030 USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S173 EP S173 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100468 ER PT J AU Lubet, R Grubbs, C Steele, V Eto, I Juliana, M Kopelovich, L AF Lubet, R Grubbs, C Steele, V Eto, I Juliana, M Kopelovich, L TI Chemopreventive effects of the statins, lipitor (Atorvastatin) and lovastatin, in the methyinitrosourea (MNU) induced model of mammary carcinogenesis. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NCI, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S171 EP S171 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100463 ER PT J AU Mamounas, E Tang, G Bryant, J Paik, S Shak, S Costantino, J Watson, D Wickerham, DL Wolmark, N AF Mamounas, E Tang, G Bryant, J Paik, S Shak, S Costantino, J Watson, D Wickerham, DL Wolmark, N TI Association between the 21-gene recurrence score assay (RS) and risk of locoregional failure in node-negative, ER-positive breast cancer: results from NSABP B-14 and NSABP B-20. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NSABP, Pittsburgh, PA USA. Aultman Hlth Fdn, Canton, OH USA. Genom Hlth Inc, Redwood City, CA USA. Allegheny Gen Hosp, Pittsburgh, PA 15212 USA. NR 0 TC 12 Z9 13 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S16 EP S16 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100044 ER PT J AU Solit, DB Basso, A Smith-Jones, P Modi, S Norton, L Larson, S Neckers, L Scher, H Hudis, C Rosen, N AF Solit, DB Basso, A Smith-Jones, P Modi, S Norton, L Larson, S Neckers, L Scher, H Hudis, C Rosen, N TI Inhibitors of Hsp90 induce the degradation of HER2 and inhibit the growth of HER2-dependent breast tumors. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NCI, Rockville, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S28 EP S28 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100074 ER PT J AU Vargas, Y Parsons, A Heurtin-Roberts, S Verschraegen, C Moser, R McCaskill-Stevens, W AF Vargas, Y Parsons, A Heurtin-Roberts, S Verschraegen, C Moser, R McCaskill-Stevens, W TI Eligibility to the study of tamoxifen and raloxifene (STAR) by ethnicity in New Mexico (NM). SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NCI, NIH, Bethesda, MD 20892 USA. UNM, Albuquerque, NM USA. RI Heurtin-Roberts, Suzanne/D-7274-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S157 EP S158 PG 2 WC Oncology SC Oncology GA 985VP UT WOS:000233407100426 ER PT J AU Walshe, JM Vatas, U Berman, AW Steinberg, SM Llppman, ME Anderson, WF Swain, SM AF Walshe, JM Vatas, U Berman, AW Steinberg, SM Llppman, ME Anderson, WF Swain, SM TI Adjuvant chemotherapy in stage II node positive male breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S176 EP S177 PG 2 WC Oncology SC Oncology GA 985VP UT WOS:000233407100478 ER PT J AU Yang, SX Simon, RM Wedam, SB Modrusan, Z Smith, V de Sauvage, F Swain, M AF Yang, SX Simon, RM Wedam, SB Modrusan, Z Smith, V de Sauvage, F Swain, M TI Response in gene expression profile to bevacizumab treatment in patients with inflammatory and locally advanced breast cancer SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 28th Annual San Antonio Breast Cancer Symposium CY DEC 08-11, 2005 CL San Antonio, TX SP San Antonio Canc Inst, Baylor Coll Med, an NCI-Designated Clin Canc Ctr, Canc Therapy & Res Ctr, Univ Texas San Antonio, Hlth Sci Ctr C1 NCI, Bethesda, MD 20892 USA. Genentech Inc, San Francisco, CA 94080 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2005 VL 94 SU 1 BP S93 EP S93 PG 1 WC Oncology SC Oncology GA 985VP UT WOS:000233407100249 ER PT J AU Man, YG Zhang, Y Shen, T Zeng, X Tauler, J Mulshine, JL Strauss, BL AF Man, YG Zhang, Y Shen, T Zeng, X Tauler, J Mulshine, JL Strauss, BL TI cDNA expression profiling reveals elevated gene expression in cell clusters overlying focally disrupted myoepithelial cell layers: implications for breast tumor invasion SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE cDNA microarray; ductal carcinoma in situ; mRNA expression; myoepithelial cell layer; signature genes; tumor progression and invasion ID EPITHELIAL-CELLS; CANCER INVASION; PROGRESSION; CARCINOMA; CARCINOGENESIS; METASTASIS; MICRODISSECTION; MECHANISMS; INVITRO; GROWTH AB Background. Our previous studies revealed that a subset of mammary ductal carcinoma in situ ( DCIS) contained focally disrupted myoepithelial ( ME) cell layers that were predominantly overlain by estrogen receptor ( ER) negative cells, which showed a substantially higher rate of cell proliferation and genetic alterations than adjacent ER positive cells within the same duct. This study attempted to assess whether these cells also had a different expression pro. le on tumor progression related genes. Design. Consecutive sections were made from frozen tissues of 30 DCIS with focally disrupted ME cell layers and associated ER negative cell clusters. ER negative and adjacent ER positive cells within the same duct were microdissected for RNA extraction and amplication. Amplified RNA was converted to biotin-labeled cDNAs and interrogated with 'Cancer PathwayFinder' arrays. Results. Cells within each or among ER negative clusters were immunohistochemically and morphologically similar, whereas they differed substantially from adjacent cells within the same duct. Of 20-paired informative ER negative and positive cells, 15 genes were differentially expressed. Of which, 11( 73.3%) were higher in ER negative, 2 (13.3%) were higher in ER positive, and 2 ( 13.3%) were equal in these cells ( p < 0.01). Of 11 up-regulated genes in ER negative cells, 8 indirectly or directly promote proliferation and progression, and 3 promote apoptosis. Conclusion. ER negative cell clusters showed a significantly higher expressing frequency of multiple tumor progression related genes than their adjacent ER positive counterparts, suggesting that they are likely to be biologically more aggressive and have a greater potential for invasion. C1 Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, Washington, DC 20306 USA. Amer Registry Pathol, Washington, DC USA. SuperArray Biosci Corp, Frederick, MD USA. Quest Diagnost Inc, Teterboro, NJ USA. NCI, Intervent Sect, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. RP Man, YG (reprint author), Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, 6825 16th St NW, Washington, DC 20306 USA. EM man@afip.osd.mil NR 39 TC 32 Z9 33 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD JAN PY 2005 VL 89 IS 2 BP 199 EP 208 DI 10.1007/s10549-004-2049-6 PG 10 WC Oncology SC Oncology GA 896NE UT WOS:000226940000014 PM 15692763 ER PT J AU Jia, J Tomaszewski, JE Hanrahan, C Coward, L Noker, P Gorman, G Nikonenko, B Protopopova, M AF Jia, J Tomaszewski, JE Hanrahan, C Coward, L Noker, P Gorman, G Nikonenko, B Protopopova, M TI Pharmacodynamics and pharmacokinetics of SQ109, a new diamine-based antitubercular drug SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE antituberculosis; ethambutol; SQ109; pharmacodynamics; pharmacokinetics ID MYCOBACTERIUM-TUBERCULOSIS; MICE; IDENTIFICATION; AMANTADINE; TISSUE AB 1 SQ109 is a novel [1,2]-diamine-based ethambutol (EMB) analog developed from high-throughput combinatorial screening. The present study aimed at characterizing its pharmacodynamics and pharmacokinetics. 2 The antimicrobial activity of SQ109 was confirmed in vitro (Mycobacterium tuberculosis-infected murine macrophages) and in vivo (M. tuberculosis-infected C57BL/6 mice) and compared to isoniazid (INH) and EMB. SQ109 showed potency and efficacy in inhibiting intracellular M. tuberculosis that was similar to INH, but superior to EMB. In vivo oral administration of SQ109 (0.1-25 mgkg(-1)day(-1)) to the mice for 28 days resulted in dose-dependent reductions of mycobacterial load in both spleen and lung comparable to that of EMB administered at 100 mg kg(-1)day(-1), but was less potent than INH at 25 mg kg(-1)day(-1). Monitoring of SQ109 levels in mouse tissues on days 1, 14 and 28 following 28-day oral administration (10 mg kg(-1)day(-1)) revealed that lungs and spleen contained the highest concentration of SQ109, at least 10 times above its MIC. 3 Pharmacokinetic profiles of SQ109 in mice following a single administration showed its C-max as 1038 (intravenous (i.v.)) and 135 ng ml(-1) (p.o.), with an oral T-max of 0.31 h. The elimination t(1/2) of SQ109 was 3.5 (i.v.) and 5.2h (p.o.). The oral bioavailability was 4%. However, SQ109 displayed a large volume of distribution into various tissues. The highest concentration of SQ109 was present in lung (> MIC), which was at least 120-fold (p.o.) and 180-fold (i.v.) higher than that in plasma. The next ranked tissues were spleen and kidney. SQ109 levels in most tissues after a single administration were significantly higher than that in blood. High tissue concentrations of SQ109 persisted for the observation period (10 h). 4 This study demonstrated that SQ 109 displays promising in vitro and in vivo antitubercular activity with favorable targeted tissue distribution properties. C1 NCI, Dev Therapeut Program, EPN, NIH, Rockville, MD 20852 USA. So Res Inst, Birmingham, AL 35255 USA. Sequella Inc, Rockville, MD USA. RP Jia, J (reprint author), NCI, Dev Therapeut Program, EPN, NIH, Rm 8042,6130 Execut Blvd, Rockville, MD 20852 USA. EM jiale@mail.nih.gov NR 26 TC 7 Z9 8 U1 1 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0007-1188 EI 1476-5381 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD JAN PY 2005 VL 144 IS 1 BP 80 EP 87 DI 10.1038/sj.bjp.0705984 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 892JA UT WOS:000226645300010 ER PT J AU Prathikanti, S Weinberger, DR AF Prathikanti, S Weinberger, DR TI Psychiatric genetics - the new era: genetic research and some clinical implications SO BRITISH MEDICAL BULLETIN LA English DT Article ID VAL(108/158) MET GENOTYPE; BIPOLAR DISORDER; SCHIZOPHRENIA; RISK; SUSCEPTIBILITY; POLYMORPHISM; POOR; PHARMACOKINETICS; MEDICINE; SIBLINGS AB Impressive advances in the last decade have been made in the genetics and neuroscience of neuropsychiatric illness. Synergies between complex genetics, elaboration of intermediate phenotypes (Egan et al. ( 2004) Schizophrenia. London: Blackwell) and novel applications in neuroimaging (Bookheimer et al. ( 2000) N Engl J Med, 343, 450 - 456) are revealing the effects of positively associated disease alleles on aspects of neurological function. Genes such as NRG-1, DISC1, RGS4, COMT, PRODH, DTNBP1, G72, DAAO, GRM3 (Harrison and Weinberger ( 2005) Mol Psychiatry, 10, 40 - 68) and others have been implicated in schizophrenia along with 5-HTTPR ( Ogilvie et al. ( 1996) Lancet, 347, 731 - 733; Caspi et al. ( 2003) Science, 301, 386 - 389) and BDNF (Geller et al. ( 2004) Am J Psychiatry, 161, 1698 - 1700) in affective disorders. As the genetics and complex neurocircuits of these and disorders are being untangled, parallel applications in pharmacogenomics and gene-based drug metabolism are shaping a drive for personalized medicine. Genetic research and pharmacogenomics suggest that the subcategorization of individuals based on various sets of susceptibility alleles will make the treatment of neuropsychiatric and other illnesses more predictable and effective. C1 NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA. RP Weinberger, DR (reprint author), NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, NIH, Room 4S-235,10 Ctr Dr, Bethesda, MD 20892 USA. EM weinberd@mail.nih.gov NR 41 TC 24 Z9 26 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0007-1420 J9 BRIT MED BULL JI Br. Med. Bull. PY 2005 VL 73-74 BP 107 EP 122 DI 10.1093/bmb/ldh055 PG 16 WC Medicine, General & Internal SC General & Internal Medicine GA 997BK UT WOS:000234219800009 PM 16365481 ER PT J AU Kschischo, M Lassig, M Yu, YK AF Kschischo, M Lassig, M Yu, YK TI Toward an accurate statistics of gapped alignments SO BULLETIN OF MATHEMATICAL BIOLOGY LA English DT Article ID HIDDEN MARKOV-MODELS; SEQUENCE ALIGNMENT AB Sequence alignment has been an invaluable toot for finding homologous sequences. The significance of the homology found is often quantified statistically by p-values. Theory for computing p-values exists for gapless alignments [Karlin, S., Altschul, S.F., 1990. Methods for assessing the statistical significance of molecular sequence features by using general scoring schemes. Proc. Natl. Acad. Sci. USA 87, 2264-2268; Karlin, S., Dembo A., 1992. Limit distributions of maximal segmental score among Markov-dependent partial sums. Adv. Appl. Probab. 24, 13-140], but a full generalization to alignments with gaps is not yet complete. We present a unified statistical analysis of two common sequence comparison algorithms: maximum-score (Smith-Waterman) alignments and their generalized probabilistic counterparts, including maximum-likelihood alignments and hidden Markov models. The most important statistical characteristic of these algorithms is the distribution function of the maximum score S-max, resp. the maximum free energy F-max, for mutually uncorrelated random sequences. This distribution is known empirically to be of the Gumbel form with an exponential tail P(S-max > x) similar to exp(-lambdax) for maximum-score alignment and P(F-max > x) similar to exp(-lambdax) for some classes of probabilistic alignment. We derive an exact expression for; for particular probabilistic alignments. This result is then used to obtain accurate. values for generic probabilistic and maximum-score alignments. Although the result demonstrated uses a simple match-mismatch scoring system, it is expected to be a good starting point for more general scoring functions. (C) 2004 Society for Mathematical Biology. Published by Elsevier Ltd. All rights reserved. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. Univ Appl Sci Koblenz, D-53424 Remagen, Germany. Univ Cologne, Inst Theoret Phys, D-50937 Cologne, Germany. Florida Atlantic Univ, Dept Phys, Boca Raton, FL 33431 USA. RP Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. EM kschischo@rheinahrcampus.de; lassig@thp.Uni-Koeln.de; yyu@fau.edu NR 28 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0092-8240 EI 1522-9602 J9 B MATH BIOL JI Bull. Math. Biol. PD JAN PY 2005 VL 67 IS 1 BP 169 EP 191 DI 10.1016/j.bulm.2004.07.001 PG 23 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA 899KU UT WOS:000227144100009 PM 15691544 ER PT J AU Bertram, R Sherman, A AF Bertram, Richard Sherman, Arthur BE Coombes, S Bressloff, PC TI NEGATIVE CALCIUM FEEDBACK: THE ROAD FROM CHAY-KEIZER SO BURSTING: THE GENESIS OF RHYTHM IN THE NERVOUS SYSTEM LA English DT Article; Book Chapter ID PANCREATIC BETA-CELLS; BURSTING ELECTRICAL-ACTIVITY; ACTION-POTENTIALS; EXCITABLE CELL; ISLET CELLS; K+ CHANNELS; OSCILLATIONS; MODEL; CA2+; MEMBRANE AB We trace the development of negative feedback by Ca2+ as a driving mechanism for bursting in the Chay-Keizer model for insulin-secreting pancreatic beta-cells and successor models. We focus on the role of the endoplasmic reticulum in providing the slow kinetic components needed to obtain bursting that lasts more than a few seconds. The fast/slow analysis applied by Rinzel to Chay-Keizer is generalized to elucidate the properties of bursting when there are two slow, negative feedback variables. Citations are provided to the current literature on further ramifications to Chay-Keizer that can be dissected by similar techniques. C1 [Bertram, Richard] Florida State Univ, Dept Math, Tallahassee, FL 32306 USA. [Bertram, Richard] Florida State Univ, Inst Mol Biophys, Tallahassee, FL 32306 USA. [Sherman, Arthur] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA. RP Bertram, R (reprint author), Florida State Univ, Dept Math, Tallahassee, FL 32306 USA. EM bertram@math.fsu.edu; asherman@nih.gov NR 45 TC 11 Z9 11 U1 0 U2 0 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-9-81270-323-1 PY 2005 BP 19 EP 48 DI 10.1142/9789812703231_0002 D2 10.1142/9789812703231 PG 30 WC Mathematical & Computational Biology; Neurosciences SC Mathematical & Computational Biology; Neurosciences & Neurology GA BYR29 UT WOS:000299842100003 ER PT J AU Roper, P Brown, CH Bourque, CW Armstrong, WE AF Roper, Peter Brown, Colin H. Bourque, Charles W. Armstrong, William E. BE Coombes, S Bressloff, PC TI AUTOREGULATION OF BURSTING OF AVP NEURONS OF THE RAT HYPOTHALAMUS SO BURSTING: THE GENESIS OF RHYTHM IN THE NERVOUS SYSTEM LA English DT Article; Book Chapter ID MAGNOCELLULAR NEUROSECRETORY-CELLS; SUPRAOPTIC NUCLEUS NEURONS; KAPPA-OPIOID RECEPTOR; MAMMALIAN NEUROENDOCRINE CELLS; DEPOLARIZING AFTER-POTENTIALS; IN-VITRO; POTASSIUM CHANNELS; VASOPRESSIN CELLS; NERVE-TERMINALS; PHASIC BURSTS C1 [Roper, Peter] NIDDK, Lab Biol Modelling, NIH, Bethesda, MD 20892 USA. [Brown, Colin H.] Univ Otago, Ctr Neuroendocrinol, Sch Med Sci, Dunedin, New Zealand. [Brown, Colin H.] Univ Otago, Dept Physiol, Sch Med Sci, Dunedin, New Zealand. [Bourque, Charles W.] Montreal Gen Hosp, Ctr Res Neurosci, Montreal, PQ H3G 1A4, Canada. [Armstrong, William E.] Univ Tennessee, Dept Anat & Neurobiol, Coll Med, Memphis, TN USA. RP Roper, P (reprint author), NIDDK, Lab Biol Modelling, NIH, 12A South Dr, Bethesda, MD 20892 USA. EM proper@helix.nih.gov; colin.brown@stonebow.otago.ac.nz; charles.bourque@mcgill.ca; warmstrong@utmem.edu OI Brown, Colin/0000-0003-2305-846X NR 63 TC 1 Z9 1 U1 0 U2 1 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-9-81270-323-1 PY 2005 BP 49 EP 88 DI 10.1142/9789812703231_0003 D2 10.1142/9789812703231 PG 40 WC Mathematical & Computational Biology; Neurosciences SC Mathematical & Computational Biology; Neurosciences & Neurology GA BYR29 UT WOS:000299842100004 ER PT J AU de Vries, G Sherman, A AF de Vries, Gerda Sherman, Arthur BE Coombes, S Bressloff, PC TI BEYOND SYNCHRONIZATION: MODULATORY AND EMERGENT EFFECTS OF COUPLING IN SQUARE-WAVE BURSTING SO BURSTING: THE GENESIS OF RHYTHM IN THE NERVOUS SYSTEM LA English DT Article; Book Chapter ID PANCREATIC BETA-CELLS; ELECTRONIC NEURONS; MODEL; OSCILLATIONS; BURSTERS; HETEROGENEITY; ISLETS; BEHAVIOR; SPIKING; NOISE AB We show that diffusive coupling of square-wave bursters, beyond the expected effect of synchronization, can greatly influence the characteristics of the oscillations. For cells that are already bursters, coupling tends to increase burst period. Cells that are not bursters, but near a bursting regime, can be induced to burst by coupling; we call this emergent bursting. Both effects require that coupling be strong enough to synchronize the slow bursts but not the fast spikes. We therefore review in detail the transitions of the fast subsystem from out-of-phase spiking to in-phase spiking as coupling strength is increased and the consequences for the full fast-slow bursting system. The beginnings of an extension of the theory to synaptic coupling are indicated. C1 [de Vries, Gerda] Univ Alberta, Dept Math & Stat Sci, Edmonton, AB T6G 2G1, Canada. [Sherman, Arthur] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA. RP de Vries, G (reprint author), Univ Alberta, Dept Math & Stat Sci, Edmonton, AB T6G 2G1, Canada. EM devries@math.ualberta.ca; asherman@nih.gov NR 37 TC 5 Z9 5 U1 0 U2 0 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-9-81270-323-1 PY 2005 BP 243 EP 272 DI 10.1142/9789812703231_0010 D2 10.1142/9789812703231 PG 30 WC Mathematical & Computational Biology; Neurosciences SC Mathematical & Computational Biology; Neurosciences & Neurology GA BYR29 UT WOS:000299842100011 ER PT J AU Butera, R Rubin, J Terman, D Smith, J AF Butera, Robert Rubin, Jonathan Terman, David Smith, Jeffrey BE Coombes, S Bressloff, PC TI OSCILLATORY BURSTING MECHANISMS IN RESPIRATORY PACEMAKER NEURONS AND NETWORKS SO BURSTING: THE GENESIS OF RHYTHM IN THE NERVOUS SYSTEM LA English DT Article; Book Chapter ID PRE-BOTZINGER COMPLEX; PERSISTENT SODIUM CURRENT; RHYTHM GENERATION; IN-VITRO; PREBOTZINGER COMPLEX; EXCITABLE-MEMBRANES; MEDULLARY SLICES; MODELS; INACTIVATION; MODULATION AB An excitatory network of bursting neurons are postulated to be involved in generating the rhythm of breathing in the pre-Botzinger complex of the mammalian brainstem. A subpopulation of these neurons exhibit complex voltage-dependent properties with multi-state behavior consisting of silence, oscillatory bursting and tonic spiking activity modes. In this chapter we review the development of single cell models, followed by simulation-based studies of population dynamics of a network of such model cells. In particular, we find that excitatory synaptic coupling increases the range of parameter space where bursting occurs, and that parameter heterogeneity of intrinsic and synaptic properties further increases this range, as well as the range of frequencies where bursting occurs at a network level. The mechanisms underlying these findings have been elucidated by recent mathematical analyses. We start with a geometric fast/slow approach to analyze bursting dynamics, including transitions to tonic spiking states in single model neurons as well as synaptically coupled pairs of model cells. Certain aspects of the increased dynamic range due to synaptic coupling can be understood from the effects of coupling strength on the bifurcation structure of a single, self-coupled cell. Additional complexity emerges when neuron pairs exhibit synchrony of spikes within bursts. Here synaptic coupling changes the form of bursting from square-wave bursting to a bursting class known as fold/fold cycle or "top hat bursting". A two-variable slow averaged system analysis reveals the existence of, and transitions between, two subtypes of bursting. To conclude the chapter, we extend the fast/slow analysis to a larger cell population with heterogeneities, which further enhance the dynamic range of network bursting. We determine conditions for synchronized whole-population bursting, allowing for gradual jumps between the silent and active phases of each burst cycle. We conclude by highlighting unresolved problems in modeling and analyzing this system as well as considering limitations of our studies to date. C1 [Butera, Robert] Georgia Inst Technol, Lab Neuroengn, Sch Elect & Comp Engn, Atlanta, GA 30332 USA. [Rubin, Jonathan] Univ Pittsburgh, Dept Math, Pittsburgh, PA 15260 USA. [Terman, David] Ohio State Univ, Dept Math, Columbus, OH 43210 USA. [Smith, Jeffrey] NINDS, Cellular & Syst Neurobiol Sect, Neural Control Lab, NIH, Bethesda, MD 20892 USA. RP Butera, R (reprint author), Georgia Inst Technol, Lab Neuroengn, Sch Elect & Comp Engn, Atlanta, GA 30332 USA. EM rbutera@ece.gatech.edu; rubin@math.pitt.edu; terman@math.ohio-state.edu; jsmith@helix.nih.gov OI Butera, Robert/0000-0002-1806-0621 NR 45 TC 7 Z9 7 U1 0 U2 3 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-9-81270-323-1 PY 2005 BP 303 EP 346 DI 10.1142/9789812703231_0012 D2 10.1142/9789812703231 PG 44 WC Mathematical & Computational Biology; Neurosciences SC Mathematical & Computational Biology; Neurosciences & Neurology GA BYR29 UT WOS:000299842100013 ER PT J AU Jemal, A Murray, T Ward, E Samuels, A Tiwari, RC Ghafoor, A Feuer, EJ Thun, MJ AF Jemal, A Murray, T Ward, E Samuels, A Tiwari, RC Ghafoor, A Feuer, EJ Thun, MJ TI Cancer statistics, 2005 SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Article ID SURVIVAL; TRENDS; WHITES AB Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute and mortality data from the National Center for Health Statistics. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,372,910 new cancer cases and 570,280 deaths are expected in the United States in 2005. When deaths are aggregated by age, cancer has surpassed heart disease as the leading cause of death for persons younger than 85 since 1999. When adjusted to delayed reporting, cancer incidence rates stabilized in men from 1995 through 2001 but continued to increase by 0.3% per year from 1987 through 2001 in women. The death rate from all cancers combined has decreased by 1.5% per year since 1993 among men and by 0.8% per year since 1992 among women. The mortality rate has also continued to decrease from the three most common cancer sites in men (lung and bronchus, colon and rectum, and prostate) and from breast and colorectal cancers in women. Lung cancer mortality among women has leveled off after increasing for many decades. In analyses by race and ethnicity, African American men and women have 40% and 20% higher death rates from all cancers combined than White men and women, respectively. Cancer incidence and death rates are lower in other racial and ethnic groups than in Whites and African Americans for all sites combined and for the four major cancer sites. However, these groups generally have higher rates for stomach, liver, and cervical cancers than Whites. Furthermore, minority populations are more likely to be diagnosed with advanced stage disease than are Whites. Progress in reducing the burden of suffering and death from cancer can be accelerated by applying existing cancer control knowledge across all segments of the population. C1 Amer Canc Soc, Dept Epidemiol & Surveillance Res, Surveillance Data Syst, Atlanta, GA 30329 USA. Amer Canc Soc, Dept Epidemiol & Surveillance Res, Surveillance Informat Serv, Atlanta, GA 30329 USA. Natl Canc Inst, Div Canc Control & Populat Sci, Stat Res & Applicat Branch, Rockville, MD USA. RP Jemal, A (reprint author), Amer Canc Soc, Dept Epidemiol & Surveillance Res, Surveillance Data Syst, Atlanta, GA 30329 USA. NR 14 TC 3193 Z9 3437 U1 3 U2 77 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD JAN-FEB PY 2005 VL 55 IS 1 BP 10 EP 30 PG 21 WC Oncology SC Oncology GA 958YK UT WOS:000231483900007 PM 15661684 ER PT J AU Jin, AY Kohn, H Beguin, C Andurkar, SV Stables, JP Weaver, DF AF Jin, AY Kohn, H Beguin, C Andurkar, SV Stables, JP Weaver, DF TI A quantitative structure-activity relationship study for alpha-substituted acetamido-N-benzylacetamide derivatives - A novel anticonvulsant drug class SO CANADIAN JOURNAL OF CHEMISTRY-REVUE CANADIENNE DE CHIMIE LA English DT Article DE QSAR; anticonvulsant; benzylacetamide; functionalized amino acid; amido ketones ID LEAST-SQUARES REGRESSION; MOLECULAR-FIELD ANALYSIS; AMINO-ACID-DERIVATIVES; RECEPTOR ANTAGONISTS; EPILEPSY; SERIES; AGENTS; QSAR; PARTITION; ENERGY AB A library of 35 benzylacetamide derivatives was evaluated for anticonvulsant activity as reflected in the ED50 (mg/kg) required to suppress seizure activity in the maximal electroshock seizure (MES) test. Using the method of partial least-squares regression in conjunction with cross-validation, the influence of 31 topological, electronic, physicochemical, and structural properties on anticonvulsant activity was investigated. A QSAR model of the logED(50) in the MES test was established (R-adj(2) = 0.77) as a function of the following seven properties: the Wiener index on distance code (Wmean), the mean information index on atomic composition (rIac), the partial charge at the C-terminal carbonyl carbon (qCC), the sum of partial charges in the a substituent (qalphatotal), the number of hydrogen bond donors and acceptors in the a substituent (Hdalpha and Haalpha), and the calculated value of the squared n-octanol/water partition coefficient. Based on this model, two new amido ketone compounds - (R,S)-2-acetamido-5-phenyl-3- pentanone and cis/trans-(R,S)-2-acetamido-5-phenyl-4-penten-3-one - were synthesized and shown to have significant anticonvulsant activity in the MES test. C1 Dalhousie Univ, Dept Med Neurol, Halifax, NS B3H 4J3, Canada. Dalhousie Univ, Dept Chem, Halifax, NS B3H 4J3, Canada. Dalhousie Univ, Dept Biomed Engn, Halifax, NS B3H 4J3, Canada. Queens Univ, Dept Med Neurol, Kingston, ON K7L 3N6, Canada. Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Chapel Hill, NC 27599 USA. Midwestern Univ, Sch Pharm, Downers Grove, IL 60515 USA. NINDS, Epilepsy Branch, NIH, Rockville, MD 20852 USA. RP Weaver, DF (reprint author), Dalhousie Univ, Dept Med Neurol, Halifax, NS B3H 4J3, Canada. EM donald.weaver@dal.ca NR 47 TC 6 Z9 6 U1 0 U2 4 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA, ONTARIO K1A 0R6, CANADA SN 0008-4042 J9 CAN J CHEM JI Can. J. Chem.-Rev. Can. Chim. PD JAN PY 2005 VL 83 IS 1 BP 37 EP 45 DI 10.1139/V04-160 PG 9 WC Chemistry, Multidisciplinary SC Chemistry GA 898JL UT WOS:000227073000006 ER PT J AU Pinsky, PF Marcus, PM Kramer, BS Freedman, M Nath, H Kvale, P Reding, D AF Pinsky, PF Marcus, PM Kramer, BS Freedman, M Nath, H Kvale, P Reding, D TI Diagnostic procedures after a positive spiral computed tomography lung carcinoma screen SO CANCER LA English DT Article DE low-radiation dose spiral computed tomography (LDCT); screening; modality; lung carcinoma; lung screening study (LSS); diagnostic workup ID CANCER ACTION PROJECT; CT AB BACKGROUND. Low-radiation dose spiral computed tomography (LDCT) currently is being evaluated as a screening modality for lung carcinoma in a randomized trial. Although several diagnostic algorithms for the workup of positive LDCT screens have been proposed, to the authors' knowledge there i sno widely accepted standard to date and there are few nationwide data concerning how such diagnostic workups are actually being performed outside a research protocol setting. METHODS. The Lung Screening Study (LSS) was a multicenter feasibility trial that randomized 1660 subjects to undergo LDCT and an equivalent number to undergo chest X-ray. Subjects with positive screens were referred to their own health care providers for diagnostic follow-up LSS did not specify a diagnostic algorithm. LSS collected and abstracted medical records regarding procedures employed in the diagnostic workup of positive screens. RESULTS. Of the 522 subjects with a positive LDCT screen at baseline or at Year One, 12% underwent biopsy. Biopsy was less likely to be performed in subjects with 4-9-mm nodules (5%) than in subjects with nodules measuring 10+ mm (25%) or in subjects with no nodules but other suspicious findings (15%). Among 63% of the subjects who underwent chest CT on follow-up, the median time between screening and first follow-up chest CT was 82 days. Only a minority of subjects received diagnostic workups that were consistent with published algorithms. CONCLUSIONS. The data from the current study represent the experience of subjects followed by their health care providers in five different U.S. metropolitan areas and one rural area. As such, they provide some indication of practices in the U.S. with regard to the diagnostic workup of patients with positive spiral CT screens. Published 2004 by die American Cancer Society.*. C1 NCI, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. NIH, Off Dis Prevent, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA. Univ Alabama, Dept Radiol, Birmingham, AL USA. Henry Ford Hlth Syst, Detroit, MI USA. Marshfield Clin Res Fdn, Dept Hematol & Oncol, Marshfield, WI USA. RP Pinsky, PF (reprint author), NCI, Div Canc Prevent, NIH, 6130 Execut Blvd,EPN 3064, Bethesda, MD 20892 USA. EM pp4f@nih.gov NR 10 TC 12 Z9 12 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 2005 VL 103 IS 1 BP 157 EP 163 DI 10.1002/cncr.20746 PG 7 WC Oncology SC Oncology GA 886OA UT WOS:000226237000020 PM 15529306 ER PT J AU Roy-Burman, P Tindall, DJ Robins, DM Greenberg, NM Hendrix, MJC Mohla, S Getzenberg, RH Isaacs, JT Pienta, KJ AF Roy-Burman, P Tindall, DJ Robins, DM Greenberg, NM Hendrix, MJC Mohla, S Getzenberg, RH Isaacs, JT Pienta, KJ TI Androgens and prostate cancer: Are the descriptors valid? SO CANCER BIOLOGY & THERAPY LA English DT Editorial Material AB The term androgen-independent cancer has now become a misnomer. Given that the androgen receptor can be activated by even low androgen concentrations or via protein modifications or other protein-protein interactions, a growing prostate cancer has the chance of assuming an androgen depletion-independent state, without necessarily bypassing the androgen signaling processes. It is thus suggested that "androgen-independent (Al)" cancer should be more accurately termed "androgen depletion-independent (ADI)" cancer. C1 Univ So Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA. Mayo Clin & Mayo Fdn, Dept Biochem & Mol Biol, Rochester, MN 55905 USA. Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA. Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA. Northwestern Univ, Feinberg Sch Med, Childrens Mem Res Ctr, Chicago, IL 60611 USA. NCI, Div Canc Biol, Rockville, MD USA. Univ Pittsburgh, Inst Canc, Dept Urol, Pittsburgh, PA USA. Johns Hopkins Univ, Sidney Kimmel Canc Ctr, Div Expt Therapeut, Baltimore, MD USA. Univ Michigan, Ctr Canc, Dept Internal Med, Ann Arbor, MI 48109 USA. Univ Michigan, Ctr Canc, Dept Urol, Ann Arbor, MI 48109 USA. RP Roy-Burman, P (reprint author), Univ So Calif, Keck Sch Med, Dept Pathol, 2011 Zonal Ave, Los Angeles, CA 90033 USA. EM roayburma@usc.edu RI Pienta, Kenneth/E-7679-2015 OI Robins, Diane M./0000-0001-6727-6309; Pienta, Kenneth/0000-0002-4138-2186 NR 3 TC 36 Z9 39 U1 1 U2 1 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD JAN PY 2005 VL 4 IS 1 BP 4 EP 5 PG 2 WC Oncology SC Oncology GA 948RF UT WOS:000230732700002 PM 16052746 ER PT J AU Ling, BC Wu, JQ Miller, SJ Monk, KR Shamekh, R Rizvi, TA DeCourten-Myers, G Vogel, KS DeClue, JE Ratner, N AF Ling, BC Wu, JQ Miller, SJ Monk, KR Shamekh, R Rizvi, TA DeCourten-Myers, G Vogel, KS DeClue, JE Ratner, N TI Role for the epidermal growth factor receptor in neurofibromatosis-related peripheral nerve tumorigenesis SO CANCER CELL LA English DT Article ID SCHWANN-CELL PROLIFERATION; MOUSE-TUMOR MODEL; SHEATH TUMORS; TYPE-1 GENE; TRANSGENIC MICE; POINT MUTATION; NF1; ACTIVATION; EXPRESSION; PROTEIN AB Benign neurofibromas and malignant peripheral nerve sheath tumors are serious complications of neurofibromatosis type 1. The epidermal growth factor receptor is not expressed by normal Schwann cells, yet is overexpressed in subpopulations of Nf1 mutant Schwann cells. We evaluated the role of EGFR in Schwann cell tumorigenesis. Expression of EGFR in transgenic mouse Schwann cells elicited features of neurofibromas: Schwann cell hyperplasia, excess collagen, mast cell accumulation, and progressive dissociation of non-myelin-forming Schwann cells from axons. Mating EGFR transgenic mice to Nf1 hemizygotes did not enhance this phenotype. Genetic reduction of EGFR in Nf1(+/-);p53(+/-) mice that develop sarcomas significantly improved survival. Thus, gain- and loss-of-function experiments support the relevance of EGFR to peripheral nerve tumor formation. C1 Univ Cincinnati, Coll Med, Dept Cell Biol, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Neurobiol, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Anat, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Pathol, Cincinnati, OH 45267 USA. Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA. NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA. RP Ratner, N (reprint author), Univ Cincinnati, Coll Med, Dept Cell Biol, Cincinnati, OH 45267 USA. EM noncy.ratner@cchmc.org FU NCI NIH HHS [T32 CA059268]; NINDS NIH HHS [R01 NS028840-09, NS28840, R01 NS028840] NR 56 TC 75 Z9 77 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1535-6108 J9 CANCER CELL JI Cancer Cell PD JAN PY 2005 VL 7 IS 1 BP 65 EP 75 DI 10.1016/j.ccr.2004.10.016 PG 11 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 890TF UT WOS:000226533000008 PM 15652750 ER PT J AU Ifon, ET Pang, ALY Johnson, W Cashman, K Zimmerman, S Muralidhar, S Chan, WY Casey, J Rosenthal, LJ AF Ifon, Ekwere T. Pang, Alan L. Y. Johnson, Warren Cashman, Kathleen Zimmerman, Sharon Muralidhar, Sumitra Chan, Wai-Yee Casey, John Rosenthal, Leonard Jason TI U94 alters FN1 and ANGPTL4 gene expression and inhibits tumorigenesis of prostate cancer cell line PC3 SO CANCER CELL INTERNATIONAL LA English DT Article AB Background: Insensitivity of advanced-stage prostate cancer to androgen ablation therapy is a serious problem in clinical practice because it is associated with aggressive progression and poor prognosis. Targeted therapeutic drug discovery efforts are thwarted by lack of adequate knowledge of gene(s) associated with prostate tumorigenesis. Therefore there is the need for studies to provide leads to targeted intervention measures. Here we propose that stable expression of U94, a tumor suppressor gene encoded by human herpesvirus 6A (HHV-6A), could alter gene expression and thereby inhibit the tumorigenicity of PC3 cell line. Microarray gene expression profiling on U94 recombinant PC3 cell line could reveal genes that would elucidate prostate cancer biology, and hopefully identify potential therapeutic targets. Results: We have shown that stable expression of U94 gene in PC3 cell line inhibited its focus formation in culture, and tumorigenesis in nude mice. Moreover gene expression profiling revealed dramatic upregulation of FN 1 (fibronectin, 91 +/- 16-fold), and profound downregulation of ANGPTL 4 (angiopoietin-like-4, 20 +/- 4-fold) in U94 recombinant PC3 cell line. Quantitative real-time polymerase chain reaction (QRT-PCR) analysis showed that the pattern of expression of FN 1 and ANGPTL 4 mRNA were consistent with the microarray data. Based on previous reports, the findings in this study implicate upregulation of FN 1 and downregulation of ANGPTL 4 in the anti tumor activity of U94. Genes with cancer inhibitory activities that were also upregulated include SERPINE 2 (serine/cysteine protease inhibitor 2, 7 +/- 1-fold increase) and ADAMTS 1 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif, 7 +/- 2-fold increase). Additionally, SPUVE 23 (serine protease 23) that is protumorigenic was significantly downregulated (10 +/- 1-fold). Conclusion: The dramatic upregulation of FN 1 and downregulation of ANGPTL 4 genes in PC3 cell line stably expressing U94 implicate up-regulation of FN 1 and downregulation of ANGPTL 4 in anti tumor activity of U94. Further studies are necessary to determine functional roles of differentially expressed genes in U94 recombinant PC3 cell line, and hopefully provide leads to potential therapeutic targets in prostate cancer. C1 [Ifon, Ekwere T.; Cashman, Kathleen; Zimmerman, Sharon; Muralidhar, Sumitra; Casey, John; Rosenthal, Leonard Jason] Georgetown Univ, Med Ctr, Dept Microbiol & Immunol, Washington, DC 20057 USA. [Pang, Alan L. Y.; Johnson, Warren; Chan, Wai-Yee] NICHD, Lab Clin Genom, NIH, Bethesda, MD 20892 USA. [Chan, Wai-Yee] Georgetown Univ, Med Ctr, Dept Pediat, Washington, DC 20057 USA. [Chan, Wai-Yee] Georgetown Univ, Med Ctr, Dept Cell Biol, Washington, DC 20057 USA. [Chan, Wai-Yee] Georgetown Univ, Med Ctr, Dept Biochem & Mol Biol, Washington, DC 20057 USA. RP Rosenthal, LJ (reprint author), Georgetown Univ, Med Ctr, Dept Microbiol & Immunol, 3900 Reservoir Rd NW, Washington, DC 20057 USA. EM eti@georgetown.edu; panga@mail.nih.gov; johnsowa@mail.nih.gov; kac2@georgetown.edu; zimmersk@georgetown.edu; sumitra.muralidhar@hq.med.va.gov; chanwy@mail.nih.gov; caseyj@georgetown.edu; rosenthl@georgetown.edu FU National Institutes of Health (NIH; Bethesda, MD, USA) [CA 78120]; PHS/NIH [CA 78120]; National Foundation for Cancer Research (Bethesda, MD, USA) FX ETI was supported by a Minority Supplement (CMBB/NCI/NIH) to Public Health Service (PHS) grant CA 78120 from the National Institutes of Health (NIH; Bethesda, MD, USA). This work was supported in part by PHS/NIH grant CA 78120, and a Contract from the National Foundation for Cancer Research (Bethesda, MD, USA) awarded to LJR. Assistance with the tumorigenicity assays was provided by the Lombardi Cancer Research Center Animal Care Facility. Special thanks to: Dr. Yan A. Su, Department of Pathology, Loyola University Medical Center, Maywood, IL, USA for fabricating glass slide microarrays for NICHD/NIH; and Michael Sheridan, Sc. D., Consulting Epidemiologist, Inova Health System & Director, Epidemiology & Biostatistics, Department of Medicine, Inova Fairfax Hospital, VA, USA, for performing the ANOVA. NR 79 TC 29 Z9 32 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1475-2867 J9 CANCER CELL INT JI Cancer Cell Int. PY 2005 VL 5 AR 19 DI 10.1186/1475-2867-5-19 PG 13 WC Oncology SC Oncology GA V24IU UT WOS:000208404900019 PM 15972109 ER PT J AU Eiseman, JL Lan, J Lagattuta, TF Hamburger, DR Joseph, E Covey, JM Egorin, MJ AF Eiseman, JL Lan, J Lagattuta, TF Hamburger, DR Joseph, E Covey, JM Egorin, MJ TI Pharmacokinetics and pharmacodynamics of 17-demethoxy 17-[[(2-dimethylamino)ethyl]amino]geldanamycin (17DMAG, NSC 707545) in C.B-17 SCID mice bearing MDA-MB-231 human breast cancer xenografts SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE geldanamycin; heat shock proteins; pharmacokinetics; pharmacodynamics ID HEAT-SHOCK-PROTEIN; HSP90 MOLECULAR CHAPERONE; IN-VIVO; ANTIPROLIFERATIVE ACTIVITY; SIGNAL-TRANSDUCTION; TISSUE DISTRIBUTION; CRYSTAL-STRUCTURE; ANTITUMOR AGENT; GROWTH ARREST; DT-DIAPHORASE AB Purpose: 17-demethoxy 17-[[(2-dimethylamino) ethyl] amino] geldanamycin (17DMAG, NSC 707545) is a water-soluble analogue of 17-( allylamino)-17-demethoxygeldanamycin (17AAG), a compound currently in clinical trials. These preclinical studies: ( 1) characterized 17DMAG concentrations in plasma, normal tissues, and tumor after i.v. delivery to mice; and ( 2) correlated tumor and normal tissue 17DMAG concentrations with alterations in heat shock protein 90 (HSP90) and selected HSP90-chaperoned proteins. Methods: At specified times after i.v. administration of 75 mg/kg 17DMAG, SCID mice bearing s.c. MDA-MB-231 human breast xenografts were killed and plasma and tissues were retained. 17DMAG concentrations were determined by HPLC. Raf-1, heat shock protein 70 (HSP70), and HSP90 in tissues were determined by Western blotting. Results: Peak plasma 17DMAG concentration was 15.4 +/- 1.4 mug/ ml. The area under the plasma 17DMAG concentration versus time curve was 1072 mug/ml min, corresponding to a total body clearance of 70 ml/kg/min. Peak 17DMAG concentrations in liver (118.8 +/- 5.7 mug/g), kidney (122.9 +/- 10.6 mug/g), heart (81.3 +/- 8.1 mug/g), and lung (110.6 +/- 25.4 mug/g) occurred at 5 - 10 min, while peak concentrations in spleen (70.6 +/- 9.6 mug/g) and tumor (9.0 +/- 1.0 mug/g) occurred at 30 - 45 min. At 48 h, 17DMAG was detectable in tumor but not in any normal tissue. Raf-1 in tumors of 17DMAG-treated mice killed at 4, 7, 24 and 48 h was about 20% lower than in tumors from vehicle-treated mice. HSP90 and HSP70 in tumors of 17DMAG-treated animals were significantly lower than in tumors of control animals at 4, 7, and 24 h. Hepatic Raf-1 was decreased by more than 60% at all times after 17DMAG treatment; however, hepatic HSP90 was not affected. HSP70 was undetectable in livers of vehicle-treated mice or mice killed at 2 or 4 h after 17DMAG treatment, but was detected in livers at 7, 24 and 48 h. 17DMAG did not affect renal Raf-1. In contrast, renal HSP70 and HSP90 were decreased by more than 50% at 2 and 4 h after 17DMAG treatment. Renal HSP70 increased approximately twofold above that in kidneys from vehicle-treated control mice at 7 and 24 h, while HSP90 relative protein concentration was no different from that in controls. Conclusions: Plasma pharmacokinetics of 17DMAG in tumor-bearing mice were similar to those previously reported in nontumor-bearing mice. 17DMAG was distributed widely to tissues but was retained for longer in tumors than normal tissues. Raf-1, HSP90, and HSP70 were altered to different degrees in tumors, livers, and kidneys of 17DMAG-treated animals. These data illustrate the complex nature of the biological responses to 17DMAG. C1 Univ Pittsburgh, Inst Canc, Mol Therapeut Drug Discovery Program, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15213 USA. NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. Univ Pittsburgh, Sch Med, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15213 USA. RP Eiseman, JL (reprint author), Univ Pittsburgh, Inst Canc, Mol Therapeut Drug Discovery Program, G27B Hillman Res Pavil,5117 Ctr Ave, Pittsburgh, PA 15213 USA. EM eisemanj@msx.upmc.edu FU NCI NIH HHS [N01-CM07106, 2P30 CA47904] NR 71 TC 101 Z9 105 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD JAN PY 2005 VL 55 IS 1 BP 21 EP 32 DI 10.1007/s00280-004-0865-3 PG 12 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 873TO UT WOS:000225304200003 PM 15338192 ER PT J AU Orem, J Otieno, MW Banura, C Katongole-Mbidde, E Johnson, JL Ayers, L Ghannoum, M Fu, P Feigal, EG Black, J Whalen, C Lederman, M Remick, SC AF Orem, J Otieno, MW Banura, C Katongole-Mbidde, E Johnson, JL Ayers, L Ghannoum, M Fu, P Feigal, EG Black, J Whalen, C Lederman, M Remick, SC TI Capacity building for the clinical investigation of AIDS malignancy in East Africa SO CANCER DETECTION AND PREVENTION LA English DT Review DE AIDS malignancies; capacity building; East Africa (Uganda, Kenya); Fogarty training; clinical trials ID HUMAN-IMMUNODEFICIENCY-VIRUS; NON-HODGKINS-LYMPHOMA; ACTIVE ANTIRETROVIRAL THERAPY; ORAL COMBINATION CHEMOTHERAPY; EPSTEIN-BARR-VIRUS; SARCOMA-ASSOCIATED HERPESVIRUS; ENDEMIC KAPOSIS-SARCOMA; A-4 DISODIUM PHOSPHATE; LARGE-CELL LYMPHOMA; PHASE-I AB Purpose: To build capacity in the resource-poor setting to support the clinical investigation and treatment of AIDS-related malignancies in a region of the world hardest hit by the AIDS pandemic. Methods: An initial MEDLINE database search for international collaborative partnerships dedicated to AIDS malignancies in developing countries failed to identify any leads. This search prompted us to report progress on our collaboration in this aspect of the epidemic. Building on the formal Uganda-Case Western Reserve University (Case) Research Collaboration dating back to 1987, established NIH-supported centers of research excellence at Case, and expanding activities in Kenya, scientific and training initiatives, research capital amongst our institutions are emerging to sustain a international research enterprise focused on AIDS and other viral-related malignancies. Results: A platform of clinical research trials with pragmatic design has been developed to further enhance clinical care and sustain training initiatives with partners in East Africa and the United States. An oral chemotherapy feasibility trial in AIDS lymphoma is near completion; a second lymphoma trial of byrostatin and vincristine is anticipated and a feasibility trial of indinavir for endemic Kaposi's sarcoma is planned. Conclusions: In the absence of published reports of evolving international partnerships dedicated to AIDS malignancy in resource constrained settings, we feel it important for such progress on similar or related international collaborative pursuits to be published. The success of this effort is realized by the long-term international commitment of the collaborating investigators and institutions to sustain this effort in keeping with ethical and NIH standards for the conduct of research; the provision of formal training of investigators and research personnel on clinical problems our East African partners are faced with in practice and the development of pragmatic clinical trials and therapeutic intervention to facilitate technology transfer and enhance clinical practice. (c) 2004 Published by Elsevier Ltd on behalf of International Society for Preventive Oncology. C1 Case Western Reserve Univ, Case Sch Med, Fogarty AIDS Int Training & Res Program, Cleveland, OH 44106 USA. Case Western Reserve Univ, Case Sch Med, Dept Med, Div Hematol Oncol, Cleveland, OH 44106 USA. Case Western Reserve Univ, Case Sch Med, Ctr AIDS Res, Cleveland, OH 44106 USA. Mulago Hosp, Uganda Canc Inst, Kampala, Uganda. Makerere Univ, Sch Med, Kampala, Uganda. Univ Nairobi, Kenyatta Natl Hosp, Coll Hlth Sci, Dept Haematol & Blood Transfus, Nairobi, Kenya. Case Western Reserve Univ, Dept Med, Div Infect Dis, Cleveland, OH 44106 USA. Case Western Reserve Univ, Tuberculosis Res Unit, Cleveland, OH 44106 USA. Ohio State Univ, Dept Pathol AIDS & Canc Specimen Resource, Columbus, OH 43210 USA. Case Western Reserve Univ, Case Sch Med, Med Mycol Ctr, Skin Dis Res Ctr, Cleveland, OH 44106 USA. Case Western Reserve Univ, Case Sch Med, Dept Biostat & Epidemiol, Cleveland, OH 44106 USA. Univ Hosp Cleveland, CASE Comprehens Canc Ctr, Cleveland, OH 44106 USA. NCI, Fiv Canc Treatment & Diag, Bethesda, MD 20892 USA. RP Remick, SC (reprint author), Case Western Reserve Univ, Case Sch Med, Fogarty AIDS Int Training & Res Program, Cleveland, OH 44106 USA. EM scr@cwru.edu NR 115 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 2005 VL 29 IS 2 BP 133 EP 145 DI 10.1016/j.cdp.2004.10.001 PG 13 WC Oncology SC Oncology GA 921JJ UT WOS:000228760100004 PM 15829373 ER PT J AU Man, YG Shen, T Weisz, J Berg, PE Schwartz, AM Mulshine, JL Sang, QXA Nieburgs, HE AF Man, YG Shen, T Weisz, J Berg, PE Schwartz, AM Mulshine, JL Sang, QXA Nieburgs, HE TI A subset of in situ breast tumor cell clusters lacks expression of proliferation and progression related markers but shows signs of stromal and vascular invasion SO CANCER DETECTION AND PREVENTION LA English DT Article DE estrogen receptor; myoepithelial cells; anti-mitotic agents; stromal and vascular invasion; stem cells; breast tumor cells; ductal carcinoma in situ; morphologic features; progression-related markers; tumor invasion and metastasis; vascular invasion; immunostataining; matrix metalloproteinase-26; c-erb-B2 protein; cytokeratin; basement membrane disruption; genetic alterations ID MAMMARY EPITHELIAL-CELLS; STEM-CELLS; SUBMANDIBULAR GLANDS; LAYER DISRUPTIONS; CANCER INVASION; CARCINOMA; CD44; GENE; DIFFERENTIATION; LOCALIZATION AB Background: Our previous studies in pre-invasive mammary tumors revealed that estrogen receptor negative cell clusters (ER NCC) overlying focally disrupted myoepithelial (ME) cell layers showed a significantly higher rate of genetic abnormalities and cell proliferation than adjacent cells without ME cell layer disruptions. A subset of these ER NCC, however, completely lacked expression of Ki-67, a most commonly used marker for cell proliferation. The purpose of this study was to further elucidate the immunohistochemical and morphological profiles of these ER NCC. Methods: Fifteen cases with such ER NCC were selected from our previous studies and assessed with a panel of commonly used biomarkers for cell proliferation, tumor progression, and normal stem cells. Results: Immunohistochemically, in addition to Ki-67 and ER. these ER NCC completely lacked expression of all other proliferation and progression related markers that were distinctly expressed in adjacent cells within the same duct but overlying the non-disrupted ME cell layer. These ER NCC also lacked expression of all normal stem cell-related markers tested. These cell clusters, however, showed a higher and atypical expression of c-erb-B2, compared to their adjacent counterparts. Morphologically, these ER NCC were generally arranged as triangle shaped structures penetrating into the stroma, similar to micro-invasive lesions. About 15% of these ER NCC appeared to directly spread into blood vessel-like structures. These ER NCC and their possible derivatives within the stroma and blood vessels-like structures shared the same morphologic and immunohistochemical features. No comparable ER positive cell clusters were identified in any of the cases. Conclusions: These findings suggest that these ER NCC and their possible derivatives are likely regulated by yet to be defined molecules and mechanisms, and they are unlikely to respond to currently available anti-mitotic agents. (c) 2005 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved. C1 Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, Washington, DC 20306 USA. Amer Registry Pathol, Washington, DC 20306 USA. Temple Univ Hosp & Med Sch, Dept Pathol, Philadelphia, PA 19140 USA. Penn State Univ Med Scholl, Dept Obstet & Gynecol, Hershey, PA USA. George Washington Univ, Med Ctr, Dept Biochem & Mol Biol, Washington, DC 20037 USA. George Washington Univ, Med Ctr, Dept Pathol, Washington, DC 20037 USA. NCI, Intervent Sect, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. Florida State Univ, Dept Chem & Biochem, Tallahassee, FL 32306 USA. Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA. RP Man, YG (reprint author), Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, 6825 16th St,NW, Washington, DC 20306 USA. EM man@afip.osd.mil FU NCI NIH HHS [CA78646, CA91149, CA65532] NR 55 TC 14 Z9 15 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 2005 VL 29 IS 4 BP 323 EP 331 DI 10.1016/j.cdp.2005.06.010 PG 9 WC Oncology SC Oncology GA 972MV UT WOS:000232458800003 PM 16122886 ER PT J AU Rusiecki, JA Holford, TR Zahm, SH Zheng, T AF Rusiecki, JA Holford, TR Zahm, SH Zheng, T TI Breast cancer risk factors according to joint estrogen receptor and progesterone receptor status SO CANCER DETECTION AND PREVENTION LA English DT Article DE breast cancer; risk factor; estrogen receptor; progesterone receptor; hormone; age; menarche; lactation; menopausal status; BMI; alcohol intake; smoking; family history; race ID HORMONE-RECEPTOR; REPRODUCTIVE FACTORS; ALCOHOL-CONSUMPTION; AVOIDABLE CAUSES; ASSOCIATION; EPIDEMIOLOGY; DISEASE; AGE; CARCINOMA; WOMEN AB Background: We investigated risk factor patterns for Subtypes of breast cancer characterized by joint estrogen receptor (ER) and progesterone receptor (PR) status in a hospital-based case-control Study. Methods: ER and PR tumor status were determined immunohisotchemically. Risk factors of interest were entered into a multiple polychotomous logistic regression model simultaneously; odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Using this model, cases in the four tumor subtypes (ER+PR+, ER-PR-, ER+PR-, ER-PR+) were compared Simultaneously to controls. A Wald test for heterogeneity across the four subtypes was conducted, as well as a case-case comparison between the two most biologically disparate subtypes, ER+PR+ and ER-PR-. Results: The receptor status distribution was as follows: 33% ER+PR+, 34% ER-PR-. 20% ER+PR-, and 13% ER-PR. Among 317 cases and 401 control,,;, we found significant heterogeneity across the four tumor subtypes for older age at first full-term pregnancy (p = 0.04) and post-menopausal status (p = 0.04). For older age at first full-term pregnancy, an elevated risk was found for the ER+PR- subtype (OR = 2.5; 95% CI: 1.2-5. 1). For post-menopausal status, elevated risks were found for both the ER+PR+ (OR = 2.4; 95% CI: 1.1-4.9) and ER+PR- (OR = 7.2; 95% CI: 2.4-21.7) subtypes. From the case-case comparisons, we found that cases, who had consumed alcohol for more than 1 year were 3.4 times more likely to have ER+PR+ tumors than ER-PR- tumors (95% CI: 1.4-8.4). Conclusions: Certain breast cancer risk factors may vary by ER and PR status, and joint ER/PR status should be taken into account in future studies of risk factor estimates. (c) 2005 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved. C1 NCI, Occupat Epidemiol Branch, US Dept HHS, Div Canc Epidemiol & Genet,NIH, Bethesda, MD 20892 USA. Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA. RP Rusiecki, JA (reprint author), NCI, Occupat Epidemiol Branch, US Dept HHS, Div Canc Epidemiol & Genet,NIH, 6120 Execut Blvd,EPS 8111,MSC 7240, Bethesda, MD 20892 USA. EM rusieckj@mail.nih.gov RI Zahm, Shelia/B-5025-2015 NR 51 TC 30 Z9 31 U1 0 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 2005 VL 29 IS 5 BP 419 EP 426 DI 10.1016/j.cdp.2005.07.004 PG 8 WC Oncology SC Oncology GA 977RY UT WOS:000232822100004 PM 16185815 ER PT J AU Bonner, MR Han, DW Nie, L Rogerson, P Vena, JE Muti, P Trevisan, M Edge, SB Freudenheim, JL AF Bonner, MR Han, DW Nie, L Rogerson, P Vena, JE Muti, P Trevisan, M Edge, SB Freudenheim, JL TI Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID ATOMIC-BOMB SURVIVORS; AIR-POLLUTION; LUNG-CANCER; MOLECULAR EPIDEMIOLOGY; CARCINOGENESIS AB Polycyclic aromatic hydrocarbons (PAH) are ubiquitous in the environment. We hypothesized that early life exposure to PAHs may have particular importance in the etiology of breast cancer. We conducted a population-based, case-control study of ambient exposure to PAHs in early life in relation to the risk of breast cancer. Total suspended particulates (TSP), a measure of ambient air pollution, was used as a proxy for PAHs exposure. Cases (n = 1,166) were women with histologically confirmed, primary, incident breast cancer. Controls (it = 2,105) were frequency matched by age, race, and county of residence to cases. Annual average TSP concentrations (1959-1997) by location were obtained from the New York State Department of Environmental Conservation for Erie and Niagara Counties. Based on the monitor readings, prediction maps of TSP concentrations were generated with ArcGIS 8.0 (ESRI, Inc., Redlands, CA) usin- inverse distance squared weighted interpolation. Unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals. In postmenopausal women, exposure to high concentrations of TSP (>140 mug/m(3)) at birth was associated with an adjusted odds ratio of 2.42 (95% confidence interval, 0.97-6.09) compared with exposure to loiv concentrations (<84 mug/m(3)). However, in premenopausal women, where exposures were generally lower, the results were inconsistent with our hypothesis and in some instances were suggestive of a reduction in the risk of breast cancer. Our study suggests that exposure in early life to high levels of PAHs may increase the risk of postmenopausal breast cancer; however, other confounders related to geography cannot be ruled out. C1 SUNY Buffalo, Sch Publ Hlth & Hlth Profess, Dept Social & Prevent Med, Buffalo, NY USA. SUNY Buffalo, Dept Geog, Buffalo, NY USA. Roswell Pk Canc Inst, Dept Breast & Soft Tissue Surg, Buffalo, NY 14263 USA. Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA. RP Bonner, MR (reprint author), NCI, Occupat & Environm Epidemiol Branch, 6120 Execut Blvd,EPS 8121,MSC 7240, Bethesda, MD 20892 USA. EM bormerm@mail.nih.gov RI Han, Daikwon/D-2950-2016 OI Han, Daikwon/0000-0001-7509-015X FU NCI NIH HHS [5R21 CA8713802, CA09051]; NIEHS NIH HHS [ES 09816] NR 33 TC 81 Z9 88 U1 2 U2 9 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 EI 1538-7755 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 53 EP 60 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000007 PM 15668476 ER PT J AU Gram, IT Braaten, T Terry, PD Sasco, AJ Adami, HO Lund, E Weiderpass, E AF Gram, IT Braaten, T Terry, PD Sasco, AJ Adami, HO Lund, E Weiderpass, E TI Breast cancer risk among women who start smoking as teenagers SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID CIGARETTE-SMOKING; ALCOHOL-CONSUMPTION; PASSIVE SMOKING; EPIDEMIOLOGIC EVIDENCE; AROMATIC-HYDROCARBONS; CALIFORNIA TEACHERS; HEALTH COHORT; LIFE-STYLE; TOBACCO; CONTRACEPTIVES AB Objective: To examine the effect of smoking on breast cancer risk in a large population-based cohort of women, many of whom started smoking as teenagers. Methods: We followed 102,098 women, ages 30 to 50 years, completing a mailed questionnaire at recruitment to the Norwegian-Swedish Cohort Study in 1991/1992, through December 2000. We used Cox proportional hazard regression models to estimate relative risk (RR) of breast cancer associated with different measures of smoking initiation, duration, and intensity adjusting for confounding variables. We conducted analyses on the entire study population, among women who had smoked for at least 20 years, among nondrinkers, and separately for each country. Results: Altogether, 1,240 women were diagnosed with incident, invasive breast cancer. Compared with never smokers, women who smoked for at least 20 years and who smoked 10 cigarettes or more daily had a RR of 1.34 (95% CI, 1.06-1.70). Likewise, those who initiated smoking prior to their first birth (1.27, 1.00-1.62), before menarche (1.39, 1.03-1.87), or before age 15 (1.48, 1.03-2.13) had an increased risk. In contrast, women who had smoked for at least 20 years, but started after their first birth, did not experience an increased breast cancer risk. The increased RR associated with smoking was observed among nondrinkers of alcohol, women with and without a family history of breast cancer, premenopausal and postmenopausal women, and in both countries.. Conclusion: Our results support the notion that women who start smoking as teenagers and continue to smoke for at least 20 years may increase their breast cancer risk. C1 Univ Tromso, Inst Community Med, N-9037 Tromso, Norway. NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Int Agcy Res Canc, F-69372 Lyon, France. INSERM, F-69008 Lyon, France. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Finnish Canc Registry, FIN-00170 Helsinki, Finland. RP Gram, IT (reprint author), Univ Tromso, Inst Community Med, N-9037 Tromso, Norway. EM inger.gram@ism.uit.no RI Weiderpass, Elisabete/M-4029-2016 OI Weiderpass, Elisabete/0000-0003-2237-0128 FU NCI NIH HHS [CA 52449] NR 37 TC 81 Z9 81 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 61 EP 66 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000008 PM 15668477 ER PT J AU Flood, A Peters, U Chatterjee, N Lacey, JV Schairer, C Schatzkin, A AF Flood, A Peters, U Chatterjee, N Lacey, JV Schairer, C Schatzkin, A TI Calcium from diet and supplements is associated with reduced risk of colorectal cancer in a prospective cohort of women SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID EPITHELIAL-CELL PROLIFERATION; RECTAL MUCOSAL PROLIFERATION; RANDOMIZED CONTROLLED-TRIAL; CONTROLLED CLINICAL-TRIAL; VITAMIN-D; COLON-CANCER; UNITED-STATES; ADENOMA RECURRENCE; SPORADIC ADENOMA; DAIRY-PRODUCTS AB We investigated the association between calcium intake and colorectal cancer in a prospective cohort of 45,354 women without a history of colorectal cancer who successfully completed a 62-item National Cancer Institute/Block food-frequency questionnaire. Women were followed for an average of 8.5 years, during which time 482 subjects developed colorectal cancer. We used Cox proportional hazards models, with age as the underlying time metric, to estimate risk of colorectal cancer. Cut points between quintiles of energy-adjusted dietary calcium were 412, 529, 656, and 831 mg/day. We created categories for calcium from supplements as follows: 0 mg/day (n = 25,441), 0 to 400 mg/ day (n = 9,452), 401 to 800 mg/day (n = 4,176), and >800 mg/ day (n =6,285). Risk ratios and confidence intervals (95% CI) for increasing quintiles of dietary calcium relative to the lowest quintile were 0.79 (0.60-1.04), 0.77 (0.59-1.02), 0.78 (0.60-1.03), and 0.74 (0.56-0.98), P-trend = 0.05. For increasing categories of calcium from supplements, the risk ratios (and 95% CI) relative to no supplement use were 1.08 (0.87-1.34), 0.96 (0.70-1.32), and 0.76 (0.56-1.02), P-trend = 0.09. Simultaneously high consumption of calcium from diet and calcium from supplements resulted in even further risk reduction, RR = 0.54 (95% CI, 0.37-0.79) compared with low consumption of both sources of calcium. These data indicate that a difference of < 400 to > 800 mg of calcium per day was associated with an approximately 25% reduction in risk of colorectal cancer, and this reduction in risk occurred regardless of the source of the calcium (i.e., diet or supplements). C1 Univ Minnesota, Div Epidemiol, Minneapolis, MN 55454 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Flood, A (reprint author), Univ Minnesota, Div Epidemiol, 1300 S 2nd St,Suite 300, Minneapolis, MN 55454 USA. EM flood@epi.umn.edu NR 54 TC 53 Z9 56 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 126 EP 132 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000016 PM 15668485 ER PT J AU Huang, WY Chatterjee, N Chanock, S Dean, M Yeager, M Schoen, RE Hou, LF Berndt, SI Yadavalli, S Johnson, CC Hayes, RB AF Huang, WY Chatterjee, N Chanock, S Dean, M Yeager, M Schoen, RE Hou, LF Berndt, SI Yadavalli, S Johnson, CC Hayes, RB TI Microsomal epoxide hydrolase polymorphisms and risk for advanced colorectal adenoma SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID POLYCYCLIC AROMATIC-HYDROCARBONS; COLON-CANCER; LUNG-CANCER; SMOKING; SUSCEPTIBILITY; EXPRESSION; FREQUENCY; ENZYMES; METABOLITES; CARCINOGENS AB Cigarette smoking is a risk factor for colorectal adenoma, a precursor of colorectal cancer. Microsomal epoxide hydrolase (EPHX1) metabolizes polycyclic aromatic hydrocarbons, carcinogens found in cigarette smoke. Nonsynonymous variants of EPHX1 at Tyr(113)His (exon 3) and His(139)Arg (exon 4) are associated, respectively, with low ((113)His) and high ((139)Arg) predicted activity. Among participants randomized to the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we evaluated risks for advanced adenoma in relation to cigarette use and these two EPHX1 variants. We compared 772 cases with advanced adenoma (adenoma 2:1 cm or containing high-grade dysplasia or villous, including tubulovillous, elements) of the distal colon (left-sided, descending colon and sigmoid or rectum) to 777 gender- and age-matched controls who were screen-negative for left-sided adenoma. Compared to those with homozygous genotypes predicting low EPHX1 activity, advanced adenoma risks tended to be elevated for carriers of (113)TyrTyr [odds ratios (OR), 1.5; 95% confidence intervals (CI), 1.0-2.2] and (139)ArgArg (OR, 1.4; 95% CI, 0.8-2.5) and for subjects who carried a greater number of the alleles ((113)Tyr or (139)Arg) associated with high predicted enzymatic activity (P-trend = 0.03). The increased risk associated with the increasing number of putative high-activity alleles was most apparent among current and recent (quit <10 years) cigarette smokers (P-trend = 0.02). In conclusion, EPHX1 variants at codon 113 and 139 associated with high predicted enzymatic activity appear to increase risk for colorectal adenoma, particularly among recent and current smokers. C1 NCI, Div Canc Epidemiol & Genet, Ctr Canc Res, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NCI, Pediat Oncol Branch, Ctr Canc Res, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NCI, Lab Genom Divers, Frederick, MD 21701 USA. NCI, Core Genotyping Facil, Ctr Adv Technol, Gaithersburg, MD USA. Univ Pittsburgh, Div Gastroenterol, Pittsburgh, PA 15260 USA. Henry Ford Hlth Sci Ctr, Josephine Ford Canc Ctr, Detroit, MI USA. RP Huang, WY (reprint author), NCI, Div Canc Epidemiol & Genet, Ctr Canc Res, NIH,Dept Hlth & Human Serv, EPS 8113,MSC 7240, Bethesda, MD 20892 USA. EM huangw@mail.nih.gov OI Johnson, Christine Cole/0000-0002-6864-6604; Dean, Michael/0000-0003-2234-0631 NR 42 TC 40 Z9 44 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 152 EP 157 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000020 PM 15668489 ER PT J AU McGlynn, KA Sakoda, LC Hu, Y Schoen, RE Bresalier, RS Yeager, M Chanock, S Hayes, RB Buetow, KH AF McGlynn, KA Sakoda, LC Hu, Y Schoen, RE Bresalier, RS Yeager, M Chanock, S Hayes, RB Buetow, KH TI Hernochromatosis gene mutations and distal adenomatous colorectal polyps SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID BODY IRON STORES; HEMOCHROMATOSIS HFE GENE; HEREDITARY HEMOCHROMATOSIS; SERUM FERRITIN; COLON-CANCER; TRANSFERRIN SATURATION; INCREASED RISK; UNITED-STATES; FREE-RADICALS; DIETARY IRON AB Iron has been suggested to be a risk factor for colorectal neoplasia. Some individuals who are heterozygous for mutations in the hemochromatosis gene (HFE) have higher than average serologic measures of iron. We therefore investigated whether heterozygosity for HFE mutations was related to risk of advanced distal adenoma and whether the relationship was affected by dietary iron intake. In the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, 679 persons with advanced distal adenoma and 697 control persons were genotyped for the two major HFE mutations (C282Y and H63D), one HFE polymorphism (IVS2+4), and one polymorphism (G142S) in the transferrin receptor gene (TFRC). HFE haplotypes were also created to examine the effect of haplotype on risk. Food frequency questionnaire data were used to estimate daily iron intake. There was no relationship between any HFE genotype or haplotype and advanced adenoma. Stratification of HFE genotype by TFRC genotype did not change the results. In addition, there was no relationship between dietary iron intake and risk of adenoma or between HFE genotype and risk of adenoma, stratified by iron intake. These results do not support a relationship between HFE heterozygosity and risk of advanced distal adenoma. C1 NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA. NCI, Ctr Canc Res, NIH, US Dept HHS, Rockville, MD 20852 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. RP McGlynn, KA (reprint author), NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, EPS-7060,6120 Execut Blvd, Rockville, MD 20852 USA. EM mcglynnk@mail.nih.gov NR 57 TC 12 Z9 12 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 158 EP 163 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000021 PM 15668490 ER PT J AU Mahabir, S Leitzmann, MF Virtanen, MJ Virtamo, J Pietinen, P Albanes, D Taylor, PR AF Mahabir, S Leitzmann, MF Virtanen, MJ Virtamo, J Pietinen, P Albanes, D Taylor, PR TI Prospective study of alcohol drinking and renal cell cancer risk in a cohort of Finnish male smokers SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID HIGH-DENSITY-LIPOPROTEIN; POPULATION-BASED COHORT; DIABETES-MELLITUS; INSULIN-RESISTANCE; CIGARETTE-SMOKING; KIDNEY CANCER; CONSUMPTION; CARCINOMA; 8-HYDROXYDEOXYGUANOSINE; HYPERTENSION AB Of the few studies that have examined alcohol consumption in relation to risk of renal cell cancer (RCC), most are case-control studies. The extent to which alcohol affects RRC risk is unclear. We prospectively examined the association between total alcohol intake as well as specific types of alcoholic beverage and RCC in a large cohort of Finnish male smokers. Men from the Alpha-Tocopherol, BetaCarotene (ATBC) Cancer Prevention Study were followed for 12 years and RCC cases were identified. Alcohol consumption was assessed at baseline using a questionnaire previously shown to be both reproducible and valid. Cox proportional hazards modeling was used to adjust simultaneously for known or suspected risk factors for RCC. We ascertained 195 incident cases of RCC. In multivariate analysis, the relative risks and 95% confidence intervals (CI) of RCC according to increasing quartiles of total alcohol intake were 1.0, 0.91 (0.62-1.33), 0.94 (0.64-1.38), and 0.53 (0.34-0.83), respectively (P value for trend = 0.005); for spirit consumption, 1.0, 0.93 (0.63-1.39), 0.84 (0.58-1.20), and 0.55 (0.36-0.85) (P for trend = 0.02); and for beer intake, 1.0, 1.22 (0.85-1.76), 0.83 (0.57-1.22), and 0.55 (0.36-0.85) (P for trend = 0.003). Too few people in this cohort drank wine to assess its association with risk of RCC. These data suggest that alcohol consumption is associated with decreased risk of RCC in male smokers. Because most of the risk reductions were seen at the highest quartile of alcohol intake and alcohol is a risk factor for a number of cancers particularly among smokers, these data should be interpreted with caution. C1 NCI, Canc Prevent Studies Branch, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Nutrit Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. RP Mahabir, S (reprint author), NCI, Canc Prevent Studies Branch, Ctr Canc Res, 6116 Execut Blvd,Suite 705,MSC 8314, Bethesda, MD 20892 USA. EM mahabirs@mail.nih.gov RI Mahabir, Somdat/A-9788-2008; Albanes, Demetrius/B-9749-2015 FU NCI NIH HHS [N01 CN45165, N01 CN45035] NR 49 TC 32 Z9 32 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 170 EP 175 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000023 PM 15668492 ER PT J AU Falk, RT Fears, TR Xu, X Hoover, RN Pike, MC Wu, AH Nomura, AMY Kolonel, LN West, DW Sepkovic, DW Bradlow, HL Ziegler, RG AF Falk, RT Fears, TR Xu, X Hoover, RN Pike, MC Wu, AH Nomura, AMY Kolonel, LN West, DW Sepkovic, DW Bradlow, HL Ziegler, RG TI Urinary estrogen metabolites and their ratio among Asian American women SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID BREAST-CANCER RISK; POSTMENOPAUSAL WOMEN; ETHNIC-DIFFERENCES; HEALTHY WOMEN; PREMENOPAUSAL WOMEN; 2-HYDROXYESTRONE; 16-ALPHA-HYDROXYESTRONE; 2-ALPHA-HYDROXYLATION; CARCINOGENESIS; PREVENTION AB Controversy persists regarding the role of a low ratio of 2-hydroxyestone (2-OHE1)/16alpha-hydroxyestrone (16alpha-OHE1) as a potential estrogen metabolism marker of increased risk for breast cancer. Most of the evidence has been provided by case-control studies, where tumor effects on hormone metabolism are not known. Studies in populations at various risk of breast cancer are not consistent, with some suggesting that levels of the ratio may be altered by changes in diet and exercise. We studied Asian American women participating as controls in a case-control study of breast cancer in which migration history-a composite of the subject's place of birth, type of residence in Asia (urban or rural), length of time living in the West, and grandparents' place of birth-was associated with a 6-fold risk gradient that paralleled the historical differences in incidence rates between the United States and Asian countries. This population offered the possibility to address whether the ratio of 2-OHE1:16alpha-OHE1 differs according to recognized breast cancer risk factors, including migration history. Overnight 12-hour urines were obtained from 368 premenopausal and 143 naturally postmenopausal women of Chinese, Japanese, or Filipino descent who donated urines between 1985 and 1988. The estrogen metabolites 2-OH-E-1 and 16alpha-OHE1 were measured with an ELISA kit and adjusted for creatinine levels. In each ethnic group, the ratio of 2-OHE1:16alpha-OHE1 was consistently lower in women born in the West than in those who had migrated from Asia. For premenopausal women, the ratio declined 20% due to lower levels of 2-OHE1. Among postmenopausal women, the ratio was 23% lower in those born in the West, but no consistent patterns based on place of birth were observed for either 2-OHE1 or 16alpha-OHE1. The ratio did not vary with most recognized breast cancer risk factors, except for lower metabolite ratios in women with a younger age at first birth and more children, which runs contrary to the hypothesis, because both characteristics reduce breast cancer risk. Our study suggests that the ratio of 2-OHE1:16alpha-OHE1 may be a marker for lifestyle influences on estrogen metabolism associated with westernization. C1 NCI, Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA. Univ Hawaii, Etiol Program, Ctr Canc Res, Honolulu, HI USA. No Calif Canc Ctr, Union City, CA USA. Hackensack Univ Med Ctr, Alice & David Jurist Inst Res, Hackensack, NJ USA. RP Falk, RT (reprint author), NCI, Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC-7234,Suite 7070, Bethesda, MD 20892 USA. EM falkr@exchange.nih.gov OI Bradlow, H Leon/0000-0002-2397-3679 NR 39 TC 22 Z9 23 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 221 EP 226 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000030 PM 15668498 ER PT J AU Castle, PE Schiffman, M Herrero, R Hildesheim, A Rodriguez, AC Bratti, MC Wacholder, S Kendal, H Breheny, AM Prior, A Pfeiffer, R Burk, RD AF Castle, PE Schiffman, M Herrero, R Hildesheim, A Rodriguez, AC Bratti, MC Wacholder, S Kendal, H Breheny, AM Prior, A Pfeiffer, R Burk, RD TI PCR testing of pooled longitudinally collected cervical specimens of women to increase the efficiency of studying human papillomavirus infection SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID HIGH-RISK; CANCER; WORLDWIDE; ASSAY; HPV AB In large active cohort studies of women investigating human papillomavirus (HPV) and cervical neoplasia, many women will be HPV-negative at all time points and testing of all their cervical specimens is an inefficient use of laboratory resources. The aim of this pilot study was to evaluate whether pooling cervical specimens from the same woman might provide a useful pretest of specimens from women unlikely to have high-grade cervical neoplasia or significant HPV exposure. We selected women (n = 187) participating in the Guanacaste Project for whom we already had HPV testing data on all their specimens from multiple visits (median = 8 visits), who were HPV DNA-negative at enrollment and at their 5- to 7-year exit from the cohort, and had no evidence of high-grade cervical neoplasia. Equal aliquots of cervical specimens from these women were pooled to create a proportional pooled specimen. Aliquots of pooled specimens were tested in a masked fashion by MY09/11 L1 consensus primer PCR. Second aliquots of some pooled specimens (n = 83) were included to assess the reliability of pooled testing. Results were compared with the predicted (expected) results based on the obtained test results of the individual specimens collected at interim visits. There was good overall agreement between observed and expected HPV DNA positivity, with a kappa of 0.63 [95% confidence interval (95% CI), 0.51-0.75] and a percent agreement of 83.4% (95% Cl, 77.3-88.5%) although the HPV DNA positivity in the pooled specimen was less than expected (P = 0.001). The agreement between observed and expected HPV DNA positivity was related to the number of aliquots pooled, suggesting that positivity was related to viral genome concentrations. The K and percent agreement for intra-batch reliability of testing pooled specimens were 0.68 (95% Cl, 0.53-0.84) and 84.3% (95% CI, 74.7-91.4%), respectively. We conclude that pooling specimens and testing by PCR may be useful for discriminating HPV DNA-positive from completely negative specimen sets in women who are likely to have been HPV DNA-negative. C1 NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA. Proyecto Epidemiol Guanacaste, San Jose, Costa Rica. Albert Einstein Coll Med, Bronx, NY 10467 USA. RP Castle, PE (reprint author), NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Room 7074,6120 Execut Blvd,EPS MSC 7234, Bethesda, MD 20892 USA. EM castlep@mail.nih.gov RI Pfeiffer, Ruth /F-4748-2011 FU NCI NIH HHS [CA78527] NR 20 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2005 VL 14 IS 1 BP 256 EP 260 PG 5 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 890TP UT WOS:000226534000035 PM 15668503 ER PT J AU Espina, V Geho, D Mehta, AI Petricoin, EF Liotta, LA Rosenblatt, KP AF Espina, V Geho, D Mehta, AI Petricoin, EF Liotta, LA Rosenblatt, KP TI Pathology of the future: Molecular profiling for targeted therapy SO CANCER INVESTIGATION LA English DT Review DE laser capture microdissection; microarray; pathology; protein; proteomics; tissue; translational research ID GENE-EXPRESSION PROFILES; CATALYZED REPORTER DEPOSITION; B-CELL LYMPHOMA; LASER CAPTURE MICRODISSECTION; ACUTE LYMPHOBLASTIC-LEUKEMIA; HUMAN BREAST-CANCER; PROSTATE-CANCER; SIGNAL AMPLIFICATION; PROTEIN MICROARRAYS; OVARIAN-CANCER AB Recent evidence suggests that each patient's cancer has a unique subset of molecular pathogenetic derangements. These derangements may both genetic and proteomic alterations. Genomic and proteomic research tools enable genome-wide assessment of gene expression as well as kinase driven cell signaling events. These tools are illuminating the molecular derangements of individual tumors, even if these tumors have similar morphological characteristics. A combination of laser capture microdissection with multiplexed phosphoproteomic analysis using reverse phase protein microarray technology is being used to identify protein molecular signatures of individual tumors. The in vivo state of multiple kinase driven signal pathways may be evaluated by reverse phase protein microarray with a panel of specific antibodies developed based upon our knowledge of biological processes. Molecular profiling of individual patient's tumors is currently being evaluated in clinical trials at the National Institutes of Health, National Cancer Institute for monitoring Epidermal Growth Factor (EGF) cell signaling events for patients with breast and ovarian cancer. C1 NCI, Pathol Lab, Bethesda, MD 20892 USA. Howard Hughes Med Inst, NIH, Bethesda, MD 20817 USA. US FDA, Ctr Biol Evaluat & Res, Off Cellular & Gene Therapy, Bethesda, MD 20014 USA. SW Texas State Univ, Pathol Lab, Dallas, TX USA. RP Espina, V (reprint author), 9000 Rockville Pike,Bldg 10,Room BIB53, Bethesda, MD 20982 USA. OI Espina, Virginia/0000-0001-5080-5972 NR 81 TC 45 Z9 49 U1 1 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 1 BP 36 EP 46 DI 10.1081/CNV-200046434 PG 11 WC Oncology SC Oncology GA 906JE UT WOS:000227636200008 PM 15779867 ER PT J AU Linet, MS AF Linet, MS TI Etiology of childhood leukemia: Environment, genes, controversies, and conundrums SO CANCER INVESTIGATION LA English DT Editorial Material ID CANCER C1 NCI, Bethesda, MD 20892 USA. RP Linet, MS (reprint author), NCI, 6120 Execut Blvd,EPS Room 7048, Bethesda, MD 20892 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0735-7907 EI 1532-4192 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 1 BP 99 EP 99 DI 10.1081/CNV-200046392 PG 1 WC Oncology SC Oncology GA 906JE UT WOS:000227636200014 PM 15779873 ER PT J AU Moore, LE Wilson, RT Campleman, SL AF Moore, LE Wilson, RT Campleman, SL TI Lifestyle factors, exposures, genetic susceptibility, and renal cell cancer risk: A review SO CANCER INVESTIGATION LA English DT Review DE kidney cancer; exposures; genetic susceptibility; review ID TUMOR-SUPPRESSOR GENE; DRY-CLEANING WORKERS; LEAD SMELTER WORKERS; OIL REFINERY WORKERS; NEW-SOUTH-WALES; CHLORINATED ALIPHATIC-HYDROCARBONS; RETROSPECTIVE COHORT MORTALITY; CADMIUM PRODUCTION WORKERS; REDUCTION PLANT WORKERS; HIPPEL-LINDAU-DISEASE AB Malignant kidney tumors account for approximately 2% of all new primary cancer cases diagnosed in the United States, with an estimated 30,000 cases occurring annually. Although a variety of agents, chemical and biological, have been implicated as causal agents in the development of renal cell carcinoma (RCC), the etiology remains enigmatic. The strongest association has been developed between cigarette smoking and renal cancer however consistent, positive associations between RCC and obesity, diabetes, and hypertension have also been reported. In addition, more recent investigations of familial kidney cancer syndromes indicate that a strong genetic component contributes to RCC development. Several genes have been identified through investigation of familial kidney cancer syndromes. This review article describes recent trends in RCC incidence and the currently identifiable etiological causes that account for approximately half of the RCC cases diagnoses. The remainder of this review then focuses on additional risk factors that have thus far not been well examined but may be helpful in explaining the increasing incidence trends and the geographic or racial variation observed nationally and worldwide. C1 Natl Canc Inst, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. Inst Publ Hlth, Calif Canc Registry, Sacramento, CA USA. RP Moore, LE (reprint author), Natl Canc Inst, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. EM moorele@mail.nih.gov NR 230 TC 72 Z9 75 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 3 BP 240 EP 255 DI 10.1081/CNV-200055962 PG 16 WC Oncology SC Oncology GA 932IK UT WOS:000229547200007 PM 15945510 ER PT J AU Engels, EA AF Engels, EA TI Does simian virus 40 cause non-Hodgkin lymphoma? A review of the laboratory and epidemiological evidence SO CANCER INVESTIGATION LA English DT Article DE simian virus 40; non-Hodgkin lymphoma; poliovirus vaccines; SV40 antibody ID JC VIRUS; BK VIRUS; LYMPHOPROLIFERATIVE DISORDERS; PLEURAL MESOTHELIOMA; POLIOVIRUS VACCINES; VACUOLATING VIRUS; HUMAN CANCER; SV40; ASSOCIATION; INFECTION AB Recently, several studies have reported the detection of DNA from simian virus 40 (SV40), a macaque polyomavirus, in tumor tissues obtained from non-Hodgkin lymphoma (NHL) patients. SV40 accidentally contaminated poliovirus vaccines administered to millions of individuals in 1955-1962. A link between SV40 and NHL is biologically plausible because SV40 causes hematological malignancies in laboratory rodents. However, detection of SV40 DNA in human NHL tumors has not been confirmed by other laboratories. Casting doubt on an association between SV40 and NHL, follow-up studies of recipients of SV40-contaminated poliovirus vaccines have not revealed these individuals to be at increased risk of NHL. Furthermore, 2 recent case-control studies of NHL documented only infrequent SV40 antibody reactivity among NHL cases, and the prevalence of SV40 antibodies was similar in cases and controls. This review summarizes recent laboratory and epidemiological studies bearing on the question of whether SV40 is a cause of NHL in humans. The strengths and weaknesses of these data are discussed, and a framework for considering the collected evidence is presented. Many of the considerations raised in this review apply to the evaluation of data regarding other cancers, such as mesothelioma, brain tumors, and various sarcomas, for which an etiologic link with SV40 also has been proposed. C1 NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Engels, EA (reprint author), NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8010, Bethesda, MD 20892 USA. EM engelse@exchange.nih.gov NR 40 TC 6 Z9 8 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 6 BP 529 EP 536 DI 10.1080/07357900500202820 PG 8 WC Oncology SC Oncology GA 970WL UT WOS:000232343000007 PM 16203661 ER PT J AU Forman, MR Cantwell, MM Ronckers, C Zhang, YW AF Forman, MR Cantwell, MM Ronckers, C Zhang, YW TI Through the looking glass at early-life exposures and breast cancer risk SO CANCER INVESTIGATION LA English DT Review DE breast cancer risk; early-life exposures ID GROWTH-FACTOR-I; UMBILICAL-CORD SERUM; FACTOR-BINDING PROTEIN-1; INFANT BIRTH-WEIGHT; WORLD-WAR-II; FETAL-GROWTH; YOUNG-WOMEN; SUBSEQUENT RISK; UNITED-STATES; BODY-SIZE AB The global increase in the proportion of women diagnosed with breast cancer, inadequate access to screening and high cost of treatment for breast cancer argue strongly for a greater focus on preventive strategies. But at what age is it appropriate to begin targeting preventive approaches? The recognized role of perinatal nutrition in neurologic development and the relation of maternal nutritional status to birthweight and subsequent risk of hypertension, diabetes, and cardiovascular disease identify pregnancy and early childhood as potential phases for prevention. This review examines indicators of hormonal and nutritional exposures in early life and breast cancer risk through the lens of the life course paradigm integrated with maternal and child health research and methodology. Compared to women who were normal birthweight (2500-3999 g), women who weighed >= 4,000 g at birth have a 20 percent to 5-fold increased risk of premenopausal breast cancer. Women born preterm and likely to be small- or large-for-date also have an increased risk. Birth length is directly associated with risk and has a larger magnitude of effect than birthweight. Prior preeclamptics and their daughters have a lower risk of breast cancer than comparable normotensives. An association between infant feeding practices and breast cancer is unclear without improved exposure assessment and analysis. Rapid childhood and pubertal linear growth increases breast cancer risk, while greater body fat over the same periods reduces risk. Growth data thus far have not been calculated in Z-scores from reference growth curves for comparison across studies. Events and secular trends influencing birth cohorts may not be adequately addressed, thereby limiting C1 NCI, Ctr Canc Res, Lab Biosyst & Canc, Bethesda, MD 20892 USA. NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NCI, Hormone Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Forman, MR (reprint author), NCI, Ctr Canc Res, Lab Biosyst & Canc, 6116 Execut Blvd,Suite 702, Bethesda, MD 20892 USA. EM mf63p@nih.gov NR 139 TC 45 Z9 46 U1 0 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 7 BP 609 EP 624 DI 10.1080/07357900500283093 PG 16 WC Oncology SC Oncology GA 995AP UT WOS:000234072600008 PM 16305989 ER PT J AU Alavanja, MCR Bonner, MR AF Alavanja, MCR Bonner, MR TI Pesticides and human cancers SO CANCER INVESTIGATION LA English DT Review DE pesticides; cancer; multi-disciplinary studies; toxicology; molecular epidemiology ID NON-HODGKINS-LYMPHOMA; SHORT-TERM TESTS; SISTER-CHROMATID EXCHANGES; SALMONELLA-MICROSOME TEST; SOFT-TISSUE SARCOMA; NESTED CASE-CONTROL; BREAST-CANCER; PANCREATIC-CANCER; AGRICULTURAL HEALTH; GENETIC TOXICITY AB The potential for human carcinogenicity of almost all pesticides currently on the market has been poorly evaluated and is inadequately understood. Generating mechanistic data in both animal studies and epidemiology will play an increasingly important role in the future. Improved exposure assessment, in large prospective studies that generate reliable exposure-response data that focus on individual pesticide exposures are needed. One of the greatest opportunities to make more rapid progress will be to foster more multi-disciplinary collaborations between toxicologists and epidemiologists. Collaborations on molecular epidemiology investigations offers such opportunities to both toxicologists and epidemiologists that were not possible even a decade ago. C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Rockville, MD USA. RP Alavanja, MCR (reprint author), NCI, Occupat & Environm Epidemiol Branch, NIH, DHHS, 6120 Execut Blvd,EPS 8000,MSC 7240, Bethesda, MD 20892 USA. EM alavanjm@mail.nih.gov NR 140 TC 20 Z9 22 U1 1 U2 10 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 2005 VL 23 IS 8 BP 700 EP 711 DI 10.1080/07357900500360008 PG 12 WC Oncology SC Oncology GA 997MF UT WOS:000234248900008 PM 16377589 ER PT J AU Liu, XM Campbell, MR Pittman, GS Faulkner, EC Watson, MA Bell, DA AF Liu, XM Campbell, MR Pittman, GS Faulkner, EC Watson, MA Bell, DA TI Expression-based discovery of variation in the human glutathione S-transferase M3 promoter and functional analysis in a glioma cell line using allele-specific chromatin immunoprecipitation SO CANCER RESEARCH LA English DT Article ID SINGLE-NUCLEOTIDE POLYMORPHISMS; RISK-FACTORS; TISSUE DISTRIBUTION; GSTM3 LOCUS; IN-VIVO; CANCER; GENE; PHARMACOGENOMICS; IDENTIFICATION; DETOXICATION AB Discovery and functional evaluation of biologically significant regulatory single nucleotide polymorphisms (SNP) in carcinogen metabolism genes is a difficult challenge because the phenotypic consequences may be both transient and subtle. We have used a gene expression screening approach to identify a functional regulatory SNP in glutathione S-transferase M3 (GSTM3). Anttila et al. proposed that variation in GSTM3 expression was affected by exposure to cigarette smoke and inheritance of the GSTM1-null genotype. To investigate the mechanism of GSTM3 expression variation, we measured GSTM3 expression in lymphoblast cells from a human Centre d'Etude du Polymorphisme Humain family and observed a low expression phenotype. Promoter sequencing revealed two novel GSTM3 promoter SNPs: A/C and A/G SNPs, 63 and 783 bp upstream of the codon 1 start site, respectively. In this pedigree, the two children homozygous for the -63C/C genotype had 8-fold lower GSTM3 expression relative to the two children with the -63A/A genotype, with no association between A-783G SNP and GSTM3 expression. Further evaluation using genotyped glioma cell lines and with luciferase reporter constructs showed that the -63C allele was associated,with lower GSTM3 expression (P < 0.0001 and,P < 0.003). RNA pol II chromatin immunoprecipitation was combined with quantitative probed-based allelic discrimination genotyping to provide direct evidence of a 9-fold reduced RNA pol 11 binding capacity for the -63C allele. These results show that the GSTM3 -63C allele strongly affects gene expression in human cell lines and suggests that individuals who carry the low expression allele may be deficient in glutathione transferase catalyzed biological functions. C1 Natl Inst Environm Hlth Sci, Environm Genom Sect, NIH, Res Triangle Pk, NC 27709 USA. Natl Inst Environm Hlth Sci, Lab Computat Biol & Risk Anal, NIH, Res Triangle Pk, NC 27709 USA. RP Bell, DA (reprint author), Natl Inst Environm Hlth Sci, Environm Genom Sect, NIH, C3-03 POB 12233, Res Triangle Pk, NC 27709 USA. EM bell1@niehs.nih.gov NR 34 TC 21 Z9 26 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 2005 VL 65 IS 1 BP 99 EP 104 PG 6 WC Oncology SC Oncology GA 884JF UT WOS:000226080200014 PM 15665284 ER PT J AU Chen, YC Pohl, G Wang, TL Morin, PJ Risberg, B Kristensen, GB Yu, A Davidson, B Shih, IM AF Chen, YC Pohl, G Wang, TL Morin, PJ Risberg, B Kristensen, GB Yu, A Davidson, B Shih, IM TI Apolipoprotein E is required for cell proliferation and survival in ovarian cancer SO CANCER RESEARCH LA English DT Article ID BONE-MARROW-TRANSPLANTATION; E-DEFICIENT MICE; GENE-EXPRESSION; EFFUSION CYTOLOGY; TRANSPORT PROTEIN; SEROUS CARCINOMA; SERIAL ANALYSIS; NERVOUS-SYSTEM; RECEPTOR; ATHEROSCLEROSIS AB Apolipoprotein E (ApoE) has been recently identified as a potential tumor-associated marker in ovarian cancer by serial analysis of gene expression. ApoE has long been known to play a key role in lipid transport, and its specific isoforms may participate in atherosclerogenesis. However, its role in human cancer is not known. In this study, apoE expression was frequently detected in ovarian serous carcinomas, the most common and lethal type of ovarian cancer. It was not detected in serous borderline tumors and normal ovarian surface epithelium. Inhibition of apoE expression using art apoE-specific siRNA led to G(2) cell cycle arrest and apoptosis in an apoE-expressing ovarian cancer cell line, OVCAR3, buit not in apoE-negative cell lines. Furthermore, the phenotype of apoE siRNA-treated OVCAR3 cells was reversed by expressing engineered mutant apoE with introduced silent mutations in the siRNA target sequence. Expression of apoE in nuclei was significantly associated with a better survival in patients who presented peritoneal effusion at the time of diagnosis (5-year follow-up, P = 0.004). This study suggests a new role of apoE in cancer as apoE expression is important for the proliferation and survival in apoE-expressing ovarian cancer cells. C1 Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21231 USA. Johns Hopkins Med Inst, Dept Gynecol & Oncol, Baltimore, MD 21231 USA. NIA, Baltimore, MD 21224 USA. Univ Oslo, Norwegian Radium Hosp, Dept Pathol, Oslo, Norway. Univ Oslo, Norwegian Radium Hosp, Dept Gynecol Oncol, Oslo, Norway. RP Shih, IM (reprint author), Johns Hopkins Med Inst, Dept Pathol, 1503 E Jefferson St,Room B-315, Baltimore, MD 21231 USA. EM ishih@jhmi.edu RI Risberg, Bjorn/A-6447-2008 FU NCI NIH HHS [R01 CA103937, CA103937, R01 CA103937-03] NR 42 TC 67 Z9 72 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 2005 VL 65 IS 1 BP 331 EP 337 PG 7 WC Oncology SC Oncology GA 884JF UT WOS:000226080200041 PM 15665311 ER PT J AU Tian, E Qiang, YW Zhan, F Yaccoby, S Zangari, M Tricot, G Barlogie, B Rudikoff, S Shaughnessy, J AF Tian, E Qiang, YW Zhan, F Yaccoby, S Zangari, M Tricot, G Barlogie, B Rudikoff, S Shaughnessy, J TI Toward elucidation of the role of altered Wnt signaling in myeloma and myeloma bone disease and development of corresponding therapeutic interventions SO CANCER TREATMENT REVIEWS LA English DT Meeting Abstract CT 5th International Conference on Cancer Induced Bone Disease (CIBD) CY MAR 20-24, 2005 CL Davos, SWITZERLAND C1 Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA. NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND SN 0305-7372 J9 CANCER TREAT REV JI Cancer Treat. Rev. PY 2005 VL 31 SU 1 MA 05 BP S13 EP S13 PG 1 WC Oncology SC Oncology GA 921NJ UT WOS:000228771000006 ER PT J AU Hays, T Rusyn, I Burns, AM Kennett, MJ Ward, JM Gonzalez, FJ Peters, JM AF Hays, T Rusyn, I Burns, AM Kennett, MJ Ward, JM Gonzalez, FJ Peters, JM TI Role of peroxisome proliferator-activated receptor-alpha (PPAR alpha) in bezafibrate-induced hepatocarcinogenesis and cholestasis SO CARCINOGENESIS LA English DT Article ID TARGETED DISRUPTION; BILE-ACIDS; LIPID HOMEOSTASIS; DEFICIENT MICE; MOUSE-LIVER; EXPRESSION; GENES; GAMMA; RAT; INDUCTION AB Prolonged administration of peroxisome proliferators to rodents typically leads to hepatocarcinogenesis. Peroxisome proliferator-activated receptor-alpha (PPARalpha) is required to mediate alterations in PPARalpha target gene expression, repress apoptosis, enhance replicative DNA synthesis, oxidative stress to DNA and hepatocarcinogenesis induced by the relatively specific PPARalpha agonist, Wy-14,643. Interestingly, administration of the less specific PPARalpha agonist, bezafibrate, leads to a modest induction of PPARalpha target genes in the absence of PPARalpha expression. In these studies, the role of PPARalpha in modulating hepatocarcinogenesis induced by long-term feeding of 0.5% bezafibrate was examined in wild-type (+/+) and PPARalpha-null (-/-) mice. The average liver weight was significantly higher in (+/+) and (-/-) mice fed bezafibrate than controls, but this effect was considerably less in (-/-) mice as compared with similarly treated (+/+) mice. Increased levels of mRNA encoding cell cycle regulatory proteins and DNA repair enzymes were found in (+/+) mice fed bezafibrate, and this effect was not found in (-/-) mice. In mice fed bezafibrate for 1 year, preneoplastic foci, adenomas and a hepatocellular carcinoma were found in (+/+) mice, while only a single microscopic adenoma was found in one (-/-) mouse. This effect was observed in both Sv/129 and C57BL/6N strains of mice, although only preneoplastic foci were observed in the latter strain. Interestingly, hepatic cholestasis was observed in 100% of the bezafibrate-fed (-/-) mice, and this was accompanied by significantly elevated hepatic expression of mRNA encoding bile salt export pump and lower expression of mRNA encoding cytochrome P450 7A1, consistent with enhanced activation of the bile acid receptor, farnesoid X receptor. Results from these studies demonstrate that the PPARalpha is required to mediate hepatocarcinogenesis induced by bezafibrate, and that PPARalpha protects against potential cholestasis. C1 Penn State Univ, Dept Vet Sci, University Pk, PA 16802 USA. Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA. Univ N Carolina, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA. NIAID, Infect Dis Pathogenesis Sect, Comparat Med Branch, Bethesda, MD 20892 USA. NIAID, SoBran Inc, Bethesda, MD 20892 USA. NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA. RP Peters, JM (reprint author), Penn State Univ, Dept Vet Sci, University Pk, PA 16802 USA. EM jmp21@psu.edu RI Peters, Jeffrey/D-8847-2011; Rusyn, Ivan/S-2426-2016 FU NCI NIH HHS [CA89607, CA97999] NR 35 TC 79 Z9 82 U1 1 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 2005 VL 26 IS 1 BP 219 EP 227 DI 10.1093/carcin/bgh285 PG 9 WC Oncology SC Oncology GA 885WB UT WOS:000226186800026 PM 15447978 ER PT J AU Ponten, I Sayer, JM Jerina, DM AF Ponten, Ingrid Sayer, Jane M. Jerina, Donald M. BE Luch, A TI In Memoriam: Anthony Dipple (1940-1999) SO CARCINOGENIC EFFECTS OF POLYCYCLIC AROMATIC HYDROCARBONS LA English DT Biographical-Item; Book Chapter C1 [Ponten, Ingrid] AstraZeneca R&D Sodertalje, Safety Assessment, S-15185 Sodertalje, Sweden. [Sayer, Jane M.; Jerina, Donald M.] NIDDK, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA. RP Ponten, I (reprint author), AstraZeneca R&D Sodertalje, Safety Assessment, S-15185 Sodertalje, Sweden. EM ingrid.ponten@astrazeneca.com; jmsayer@helix.nih.gov; dmjerina@nih.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU IMPERIAL COLL PRESS PI COVENT GARDEN PA 57 SHELTON STREET, COVENT GARDEN WC2H 9HE, ENGLAND BN 978-1-86094-933-3 PY 2005 BP XI EP XIII D2 10.1142/9781860949333 PG 3 WC Biochemistry & Molecular Biology; Oncology; Toxicology SC Biochemistry & Molecular Biology; Oncology; Toxicology GA BYR28 UT WOS:000299841300002 ER PT J AU Shizukuda, Y Piekarz, RL Bates, SE Sachdev, V Finkel, T Rosing, DR AF Shizukuda, Y Piekarz, RL Bates, SE Sachdev, V Finkel, T Rosing, DR TI Effect of a histone deacetylase inhibitor on human cardiac mass SO CARDIOVASCULAR DRUGS AND THERAPY LA English DT Letter DE histone diacetylase inhibitor; chemotherapy; heart; cardiac mass ID DEPSIPEPTIDE FR901228; HYPERTROPHY C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Shizukuda, Y (reprint author), NHLBI, Cardiovasc Branch, NIH, 10 Ctr Dr,MSC-1454,Bldg 10-CRC,Rm 6-3142, Bethesda, MD 20892 USA. EM shizukuy@nhlbi.nih.gov FU Intramural NIH HHS NR 6 TC 4 Z9 4 U1 1 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-3206 J9 CARDIOVASC DRUG THER JI Cardiovasc. Drugs Ther. PD JAN PY 2005 VL 19 IS 1 BP 89 EP 90 DI 10.1007/s10557-005-6901-7 PG 2 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA 924SS UT WOS:000229001300012 PM 15883760 ER PT J AU Mastin, JP AF Mastin, JP TI Environmental cardiovascular disease SO CARDIOVASCULAR TOXICOLOGY LA English DT Article DE environmental; cardiovascular disease; air pollution; arsenic; dioxin ID EXHAUST PARTICLE CHEMICALS; PARTICULATE AIR-POLLUTION; OXIDATIVE STRESS; HEART-DISEASE; ASSOCIATION; MORTALITY; POPULATION; ZEBRAFISH; EXPOSURE; MARKERS AB The last decade has seen a remarkable growth in the evidence establishing exposure to environmental agents as a risk factor for cardiovascular disease (CVD). Most of this has come from research linking exposure to ambient particulate matter with CVD, although more recent evidence suggests that the ozone might also be contributing factor. Research on the cardiovascular toxicity of other pollutants, notably arsenic, has also grown during this period. In addition to their effects in adults, environmental agents, such as dioxin, have also been shown to adversely affect development of the heart in laboratory animals. Taken together, these results suggest that environmental exposure must be considered as an important risk factor for CVD and that further research to determine mechanisms of action and susceptible populations is needed. This research will require interdisciplinary approaches, and should yield data not only on the toxic effects of pollutants on the cardiovascular system, but on the basic pathophysiology of cardiovascular diseases as well. C1 Natl Inst Environm Hlth, Res Triangle Pk, NC 27709 USA. RP Mastin, JP (reprint author), Natl Inst Environm Hlth, 111 TW Alexander dr,EC-23, Res Triangle Pk, NC 27709 USA. EM mastin@niehs.nih.gov NR 23 TC 30 Z9 30 U1 2 U2 8 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1530-7905 J9 CARDIOVASC TOXICOL JI Cardiovasc. Toxicol. PY 2005 VL 5 IS 2 BP 91 EP 94 DI 10.1385/CT:5:2:091 PG 4 WC Cardiac & Cardiovascular Systems; Toxicology SC Cardiovascular System & Cardiology; Toxicology GA 036PC UT WOS:000237085900001 PM 16046786 ER PT J AU Jokinen, MP Lieuallen, WG Johnson, CL Dunnick, J Nyska, A AF Jokinen, MP Lieuallen, WG Johnson, CL Dunnick, J Nyska, A TI Characterization of spontaneous and chemically induced cardiac lesions in rodent model systems - The National Toxicology Program Experience SO CARDIOVASCULAR TOXICOLOGY LA English DT Article DE heart; cardiotoxicity; rat; mouse; pathology; mechanism ID ADVERSE CARDIOVASCULAR EVENTS; TOPICAL APPLICATION EXPOSURES; EARLY MYOCARDIAL-INFARCTION; MITOCHONDRIAL-FUNCTION; THIODIGLYCOLIC ACID; DRINKING-WATER; METHYL-BROMIDE; F344 RATS; TOXICITY; DIETHANOLAMINE AB Induction of heart disease can be related to exposure to a number of agents, including environmental chemicals. Studies with laboratory rodents are commonly used to identify cardiotoxic agents and to investigate mechanisms of toxicity. This study was conducted to characterize spontaneous and chemically-induced rodent heart lesions. A retrospective light-microscopic evaluation was performed on the hearts of F344 rats and B60F1 mice from National Toxicology Program studies of six chemicals in which chemically-induced myocardial toxicity was present: oxymetholone, monochloroacetic acid, 3,3'-4,4'-tetrachoroazoxybenzene, diethanolamine, urethane, and methyl bromide. Two myocardial lesions were observed: cardiomyopathy (multifocal myofiber degeneration that could occur spontaneously or as a treatment effect) and degeneration (diffuse myofiber degeneration that was clearly related to treatment). Oxymetholone produced cardiotoxicity that was apparent as an increase in the incidence and average severity of cardiomyopathy. The remaining five chemicals produced degeneration, which appeared morphologically similar with each of the chemicals. Based on available information concerning possible mechanisms by which each of these chemicals may induce cardiotoxicity, this evaluation indicated it may be possible to place the chemicals into two main categories: (1) those that primarily affected the coronary vasculature with secondary effects on the myocardium (oxymetholone), and (2) those that had a direct toxic effect on the myocardial cells (the remaining five chemicals). Beyond this, however, light-microscopic findings did not indicate any specific mechanisms. Additional morphologic evaluations, such as electron microscopy or special histochemical or immunostains, may help identify specific subcellular sites of toxic damage, which in turn can indicate appropriate types of molecular mechanistic studies. C1 NIEHS, Lab Expt Pathol, Res Triangle Pk, NC 27709 USA. NIEHS, Toxicol Operat Branch, Res Triangle Pk, NC 27709 USA. Chalk River Labs, Pathol Associates Div, Cary, NC 27513 USA. RP Nyska, A (reprint author), NIEHS, Lab Expt Pathol, MD B3-06,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. EM nyska@nichs.nih.gov NR 40 TC 14 Z9 14 U1 0 U2 3 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1530-7905 J9 CARDIOVASC TOXICOL JI Cardiovasc. Toxicol. PY 2005 VL 5 IS 2 BP 227 EP 244 DI 10.1385/CT:5:2:227 PG 18 WC Cardiac & Cardiovascular Systems; Toxicology SC Cardiovascular System & Cardiology; Toxicology GA 036PC UT WOS:000237085900011 PM 16046796 ER PT J AU Divi, RL Leonard, SL Kuo, MM Walker, BL Orozco, CC St Claire, MC Nagashima, K Harbaugh, SW Harbaugh, JW Thamire, C Sable, CA Poirier, MC AF Divi, RL Leonard, SL Kuo, MM Walker, BL Orozco, CC St Claire, MC Nagashima, K Harbaugh, SW Harbaugh, JW Thamire, C Sable, CA Poirier, MC TI Cardiac mitochondrial compromise in 1-yr-old Erythrocebus patas monkeys perinatally-exposed to nucleoside reverse transcriptase inhibitors SO CARDIOVASCULAR TOXICOLOGY LA English DT Article ID HIV-INFECTED WOMEN; IMMUNODEFICIENCY-VIRUS TYPE-1; MATERNAL-INFANT TRANSMISSION; IN-UTERO; CORD BLOOD; ZIDOVUDINE TREATMENT; UNINFECTED INFANTS; SKELETAL-MUSCLE; PREGNANT-WOMEN; UNITED-STATES AB Hearts from 1-yr-old Erythrocebus patas monkeys were examined after in utero and 6-wk-postbirth exposure to antiretroviral nucleoside reverse transcriptase inhibitors (NRTIs). Protocols were modeled on those given to human immunodeficiency virus (HIV)-1-infected pregnant women. NRTIs were administered daily to the dams for the last 20% or 50% of gestation, and to the infants for 6 wk after birth. Exposures included: no drug (n = 4); Zidovudine, 3'-azido-3'-deoxythymidine (AZT; n = 4); AZT/Lamivudine, (-)-beta-L-2', 3'-Dideoxy-3'-thiacytidine (Epivir, 3TC) (n = 4); AZT/Didanosine (Videx, ddl) (n = 4); and Stavudine (Zerit, d4T)/3TC (n = 4). Echocardiograms and clinical chemistry showed no drug-related changes, but the d4T/3TC-exposed fetuses at 6 and 12 mo had increased white cell counts (p < 0.05). At I yr of age, oxidative phosphorylation (OXPHOS) enzyme activities were similar in heart mitochondria from all groups. Mitochondrial pathology, that included clones of damaged mitochondria (p < 0.05), was found in hearts of all 1-yr drug-exposed infants. Levels of mtDNA were elevated (p < 0.05) in hearts of all NRTI-exposed monkeys in the following order: control < d4T/3TC < AZT < AZT/3TC < AZT/ddl. The clinical status of NRTI-exposed infants, as evidenced by behavior, clinical chemistry, OXPHOS activity and echocardiogram, was normal. However, extensive mitochondrial damage with clusters of similar-appearing damaged heart mitochondria observed by electron microscopy, and an increase in mtDNA quantity, that persisted at 1 yr of age, suggest the potential for cardiotoxicity later in life. C1 NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Bioqual Incorp, Rockville, MD 20850 USA. SAIC Frederick, Frederick Canc Res & Dev Ctr, Image Anal Lab, NCI, Ft Detrick, MD 21702 USA. Childrens Natl Med Ctr, Div Cardiol, Washington, DC 20010 USA. Univ Maryland, Dept Mech Engn, College Pk, MD 20742 USA. RP Poirier, MC (reprint author), NCI, Ctr Canc Res, NIH, Bldg 37,Rm 4032,37 Convent Dr, Bethesda, MD 20892 USA. EM poirierm@exchange.nih.gov NR 43 TC 32 Z9 33 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1530-7905 J9 CARDIOVASC TOXICOL JI Cardiovasc. Toxicol. PY 2005 VL 5 IS 3 BP 333 EP 346 DI 10.1385/CT:5:3:333 PG 14 WC Cardiac & Cardiovascular Systems; Toxicology SC Cardiovascular System & Cardiology; Toxicology GA 036PD UT WOS:000237086000009 PM 16244378 ER PT J AU Bretz, WA Corby, PMA Hart, TC Costa, S Coelho, MQ Weyant, RJ Robinson, M Schork, NJ AF Bretz, WA Corby, PMA Hart, TC Costa, S Coelho, MQ Weyant, RJ Robinson, M Schork, NJ TI Dental caries and microbial acid production in twins SO CARIES RESEARCH LA English DT Article DE dental caries; microbial acid production; twins ID SURFACES; CHILDREN; ENAMEL; MUTANS; ROOT; PH AB Objective: To determine the relative contribution of genetic and environmental stimuli on dental caries traits and microbial acid production in a twin model. Methods: Dental caries examinations and microbial acid production assays were performed on 388 pairs of twins 1.58 years old from the city of Montes Claros, Brazil. Genotyping 8 polymorphic DNA markers determined zygosity. Caries exams followed NIDCR criteria modified to distinguish white spot lesions from cavitated lesions. Surface-based caries prevalence rates (SBCPR) were computed and lesion severity was determined by a weighted index (LSI). Biofilm samples were collected from the tongue using a lactic acid indicator swab. Assay scores were categorized based on acid formation as 1 = low, 2 = medium, and 3 = high. Heritability analyses were performed using the SOLAR software package. Results: Heritability estimates for SBCPRs, LSI and for microbial acid production were H = 76.3 (p < 0.001), H = 70.6 (p < 0.001), H = 16.2 (p = 0.0078), respectively. Treating microbial acid production as a covariate in the SBCPR and LSI models did not significantly alter the heritability estimates, i.e. H = 76.5 (p < 0.001) and H = 70.8 (p < 0.001), respectively. Conclusions: These results suggest that variation in dental caries surface traits has a significant genetic contribution and that microbial acid production is modulated by the environment. Copyright (C) 2005 S. Karger AG, Basel. C1 Univ Pittsburgh, Sch Dent Med, Pittsburgh, PA 15261 USA. NIDCR, NIH, Bethesda, MD USA. Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. Univ Estadual Montes Claros UNIMONTES, Montes Claros, Brazil. RP Bretz, WA (reprint author), Univ Pittsburgh, Sch Dent Med, 380 Salk Hall,3501 Terrace St, Pittsburgh, PA 15261 USA. EM wab2@pitt.edu FU NIDCR NIH HHS [DE 014528, DE 15351] NR 15 TC 33 Z9 33 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6568 J9 CARIES RES JI Caries Res. PY 2005 VL 39 IS 3 BP 168 EP 172 DI 10.1159/000084793 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 927YG UT WOS:000229237700002 PM 15914976 ER PT S AU Van Uitert, R Bitter, I Butman, JA AF Van Uitert, R Bitter, I Butman, JA BE Lemke, HU Inamura, K Doi, K Vannier, MW Farman, AG TI Semi-automatic spinal cord segmentation and quantification SO CARS 2005: Computer Assisted Radiology and Surgery SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 19th International Congress and Exhibition on Computer Assisted Radiology and Surgery CY JUN 22-25, 2005 CL Berlin, GERMANY DE spinal cord; semi-automatic segmentation; level sets; quantification; length measurement; area measurement AB Delineation of objects within medical images is very hard to perform reproducibly, unless at least semi-automatic segmentation is available. This paper presents a semi-automatic process for determining the total length and area of the spinal cord, and the length and area of the spinal cord between adjacent pairs of intervertebral discs. We performed these measurements on 20 segments from C-1 to L-1 with three sets of user-selected landmarks. Our results show that the average spinal cord segment area was 852.3 mm(2) with a standard deviation of 0.7%, and the average spinal cord segment length was 57.4 mm with a standard deviation of 0.3%. Our method has been demonstrated to be potentially insensitive to intra- and inter-user variability. (c) 2005 CARS & Elsevier B.V. All rights reserved. C1 NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA. RP Van Uitert, R (reprint author), NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA. OI Butman, John/0000-0002-1547-9195 NR 4 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-51872-X J9 INT CONGR SER PY 2005 VL 1281 BP 224 EP 229 DI 10.1016/j.ics.2005.03.181 PG 6 WC Computer Science, Interdisciplinary Applications; Multidisciplinary Sciences; Radiology, Nuclear Medicine & Medical Imaging; Surgery SC Computer Science; Science & Technology - Other Topics; Radiology, Nuclear Medicine & Medical Imaging; Surgery GA BDG65 UT WOS:000233416000043 ER PT J AU Sinha, N Smith-Gill, SJ AF Sinha, N Smith-Gill, SJ TI Molecular dynamics simulation of a high-affinity antibody-protein complex - The binding site is a mosaic of locally flexible and preorganized rigid regions SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE protein-protein interactions; flexibility; binding affinity; structure-function relationship ID STRUCTURAL PLASTICITY; NONPOLAR CAVITY; LIGAND-BINDING; T4 LYSOZYME; ANTIGEN; FLEXIBILITY; SPECIFICITY; ENERGY; KINASE; DOMAIN AB One nanosecond molecular dynamic (MD) simulation of anti-hen egg white lysozyme (HEL) antibody HyHEL63 (HH63) complexed with HEL reveals rigid and flexible regions of the HH63 binding site. Fifty conformations, extracted from the MD trajectory at regular time intervals were superimposed on HH63-HEL X-ray crystal structure, and the root mean squared deviations (RMSDs) and deviations in C, atom positions between the X-ray structure and the MID conformer were measured. Residue positions showing the large deviations in both light chain and heavy chain of the antibody were same in all the MD conformers. The residue positions showing smallest deviations were same for all the conformers in the case of light chain, whereas relatively variable in the heavy chain. Positions of large and small deviations fell in the complementarity determining regions (CDRs), for both heavy and light chains. The larger deviations were in CDR-2 of light and CDR-1 of heavy chain. Smaller deviations were in CDR-3 of light and CDR-2 and CDR-3 of heavy chains. The large and small deviating regions highlight flexible and rigid regions of HH63 binding site and suggest a mosaic binding mechanism, including both "induced fit" and preconfigured "lock-and-key" type of binding. Combined "induced fit" and "lock-and-key" binding would be a better definition for the formation of large complexes, which bury larger surface area on binding, as in the case of antibody-HEL complex. We further show that flexible regions, comprising mostly charged and polar residues, form intermolecular interactions with HEL, whereas rigid regions do not. Electrostatic complementarity between HH63 and HEL also imply optimized binding affinity. Flexible and rigid regions of a high-affinity antibody are selected during the affinity maturation of the antibody and have specific functional significance. The functional importance of local inherently flexible regions is to establish intermolecular contacts or they play a key role in molecular recognition, whereas local rigid regions provide the structural framework. C1 Johns Hopkins Univ, Baltimore, MD 21218 USA. NCI, Struct Biophys Lab, Canc Res Ctr, NIH, Ft Detrick, MD 21702 USA. RP Sinha, N (reprint author), Johns Hopkins Univ, 106 Mudd Hall,3400 N Charles St, Baltimore, MD 21218 USA. EM nsinha1@jhu.edu NR 51 TC 21 Z9 22 U1 1 U2 8 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 2005 VL 43 IS 2 BP 253 EP 273 DI 10.1385/CBB:43:2:253 PG 21 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 958EG UT WOS:000231426900005 PM 16049350 ER PT J AU Zhan, M Miura, T Xu, XR Rao, MS AF Zhan, M Miura, T Xu, XR Rao, MS TI Conservation and variation of gene regulation in embryonic stem cells assessed by comparative genomics SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE embryonic stem cells; comparative genomics; regulatory pathway; transcriptional factors; reverse transcriptase-polymerase chain reaction (RT-PCR); LIF; Sox2 ID TRANSCRIPTION FACTOR; MOLECULAR SIGNATURE; HOMEOBOX GENES; MOUSE EMBRYOS; SELF-RENEWAL; ES CELLS; EXPRESSION; DIFFERENTIATION; PROMOTER; ENHANCER AB We have examined the gene structure and regulatory regions of octamer-binding transcription factor 3/4 (Oct 3/4), sex determining region Y box 2 (Sox2), signal transducer and activator of transcription 3 (Stat3), embryonal stem cell-specific gene 1 (ESG), Nanog homeobox (Nanog), and several other genes highly expressed in embryonic stem (ES) cells across different species. Our analysis showed that ES cell-expressed Ras (ERAS) was orthologous to a human pseudogene Harvey Ras (HRASP) and that the promoter and other regulatory sequences were highly divergent. No ortholog of (ES) cell-derived homeobox containing gene (Ehox) could be identified in human, and the closest paralogs PEPP gene subfamily 1 (PEPP1), PEPP2, and extraembryonic, spermatogenesis, homeobox 1 (Esx1) were not expressed by ES cells and shared little homology. The Sox2 promoter was the most conserved across species and the Oct3/4 promoter region showed significant homology particularly in the distal enhancer active in ES cells. Analysis suggested common and divergent pathways of regulation. Conserved Oct3/4 and Sox2 co-binding domains were identified in most ES expressed genes, highlighting the importance of this transcriptional pathway. Conserved fibroblast growth factor response element sites were identified in regulatory regions, suggesting a potential parallel pathway for regulation by FGFs. A central role of Stat3 activation in self-renewal and in a regulatory feedback loop was suggested by the identification of the conserved binding sites in most pathways. Although most pathways were evolutionarily conserved, promoters and genomic structure of the leukemia inhibitory factor (LIF) pathway components were divergent, likely explaining the differential requirement of LIF for human and rodent cells. Our analysis further suggested that the Nanog regulatory pathway was relatively independent of the LIF/Oct pathway and may interact with the Nodal/transforming growth factor-beta pathway. These results provide a framework for examining the current reported differences between rodent and human ES cells and define targets for future perturbation studies. C1 NIA, Bioinformat Unit, Branch Res Resources, NIH, Baltimore, MD 21224 USA. NIA, Stem Cell Sect, Neurosci Lab, NIH, Baltimore, MD 21224 USA. NIA, Cellular & Mol Neurosci Sect, Neurosci Lab, NIH, Baltimore, MD 21224 USA. RP Rao, MS (reprint author), NIA, Bioinformat Unit, Branch Res Resources, NIH, Baltimore, MD 21224 USA. EM zhanmi@grc.nia.nih.gov; raomah@grc.nia.nih.gov NR 77 TC 17 Z9 18 U1 1 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 EI 1559-0283 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 2005 VL 43 IS 3 BP 379 EP 405 DI 10.1385/CBB:43:3:379 PG 27 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 982QD UT WOS:000233175800004 PM 16244364 ER PT J AU Zhu, GZ Liu, Y Shaw, S AF Zhu, GZ Liu, Y Shaw, S TI Protein kinase specificity - A srategic collaboration between kinase peptide specificity and substrate recruitment SO CELL CYCLE LA English DT Article DE kinase; phosphorylation; substrate; recruitment; peptide specificity ID CONSENSUS SEQUENCES; PHOSPHORYLATION; PHOSPHATASES; DETERMINANTS; PREDICTION; ACTIVATION; RECEPTOR; GENOME AB Specificity of phosphorylation by protein kinases is essential to the integrity of biological signal transduction. Specificity is determined by two critical elements: ( 1) peptide specificity of the kinase, i.e., preferential phosphorylation of S/T/Y residues surrounded by particular patterns of amino acids; and ( 2) recruitment, i.e., increasing the frequency of encounter between kinase and substrate. Historically, the importance of peptide specificity was studied first, but it has been somewhat overshadowed by emerging emphasis on the importance of recruitment. Recent studies confirm and extend understanding of the relative contribution of these two elements. Peptide specificity always constrains the range of sites that can be phosphorylated by a kinase. Only when recruitment is very strong, as in the case with autophosphorylation, can markedly suboptimal substrates be phosphorylated. C1 NCI, Expt Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Shaw, S (reprint author), NCI, Expt Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM shaws@mail.nih.gov NR 20 TC 35 Z9 35 U1 0 U2 2 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2005 VL 4 IS 1 BP 52 EP 56 DI 10.4161/cc.4.1.1353 PG 5 WC Cell Biology SC Cell Biology GA 902SG UT WOS:000227376200016 PM 15655379 ER PT J AU DePamphilis, ML AF DePamphilis, ML TI Cell cycle dependent regulation of the origin recognition complex SO CELL CYCLE LA English DT Review DE ORC; Orc1; replication origins; cell division cycle; ubiquitination; Cdk; phosphorylation ID EUKARYOTIC DNA-REPLICATION; XENOPUS EGG EXTRACTS; MINICHROMOSOME MAINTENANCE PROTEINS; EPSTEIN-BARR-VIRUS; SCHIZOSACCHAROMYCES-POMBE; FISSION YEAST; SACCHAROMYCES-CEREVISIAE; METAZOAN CHROMOSOMES; MAMMALIAN-CELLS; ADENINE/THYMINE STRETCHES AB The eukaryotic origin recognition complex (ORC) not only selects the sites where prereplication complexes are assembled and DNA replication begins, it is the first in a series of multiple coherent pathways that determines when prereplication complexes are assembled. Data from yeast, frogs, flies and mammals present a compelling case that one or more of the six ORC subunits undergoes cell cycle dependent modifications involving phosphorylation and ubiquitination that repress ORC activity during S, G(2) and M-phases. ORC activity is not restored until mitosis is complete and a nuclear membrane is present. In yeast, frogs and mammals, the same cyclin-dependent protein kinase [Cdk1(Cdc2)] that initiates mitosis also inhibits assembly of functional ORC/chromatin sites. In yeast, ORC remains bound to chromatin throughout cell division, but in the metazoa either ORC or the Orc1 subunit appears to cycle on and off the chromatin. Thus, this "ORC cycle" is the premier step in preventing rereplication of DNA during a single cell division cycle. C1 NICHHD, NIH, Bethesda, MD 20892 USA. RP DePamphilis, ML (reprint author), NICHHD, NIH, Bldg 6,Room 3A-15,9000 Rockville Pike, Bethesda, MD 20892 USA. EM depamphm@mail.nih.gov NR 124 TC 82 Z9 84 U1 1 U2 3 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2005 VL 4 IS 1 BP 70 EP 79 DI 10.4161/cc.4.1.1333 PG 10 WC Cell Biology SC Cell Biology GA 902SG UT WOS:000227376200020 PM 15611627 ER PT J AU Fei, PW Yin, JH Wang, WD AF Fei, PW Yin, JH Wang, WD TI New advances in the DNA damage response network of Fanconi anemia and BRCA proteins - FAAP95 replaces BRCA2 as the true FANCB protein SO CELL CYCLE LA English DT Review DE Fanconi anemia; BRCA1; BRCA2; ubiquitin; FANCB; FANCD2 ID NUCLEAR-COMPLEX; HOMOLOGOUS RECOMBINATION; POSITIONAL CLONING; PANCREATIC-CANCER; UBIQUITIN LIGASE; GENE-PRODUCT; IN-VIVO; PATHWAY; CELLS; RAD51 AB Fanconi anemia ( FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2. In response to DNA damage or replication signals, a nuclear FA core complex of at least 6 FA proteins ( FANCA, FANCC, FANCE, FANCF, FANCG and FANCL) is activated and leads to monoubiquitination of the downstream FA protein, FANCD2. One puzzling question for this pathway is the role of BRCA2. A previous study has proposed that BRCA2 could be identical to two FA proteins: FANCD1, which functions either downstream or in a parallel pathway; and FANCB, which functions upstream of the FANCD2 monoubiquitination. Now, a new study shows that the real FANCB protein is not BRCA2, but a previously uncharacterized component of the FA core complex, FAAP95, suggesting that BRCA2 does not act upstream of the FA pathway. Interestingly, the newly discovered FANCB gene is X-linked and subject to X-inactivation. The presence of a single active copy of FANCB and its essentiality for a functional FA-BRCA pathway make it a potentially vulnerable component of the cellular machinery that maintains genomic integrity. C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. RP Wang, WD (reprint author), NIA, Genet Lab, NIH, 333 Cassell Dr,TRIAD Ctr Room 3000, Baltimore, MD 21224 USA. EM wangw@grc.nia.nih.gov NR 67 TC 31 Z9 33 U1 0 U2 3 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2005 VL 4 IS 1 BP 80 EP 86 DI 10.4161/cc.4.1.1358 PG 7 WC Cell Biology SC Cell Biology GA 902SG UT WOS:000227376200021 PM 15611632 ER PT J AU Strunnikov, AV AF Strunnikov, AV TI A case of selfish nucleolar segregation SO CELL CYCLE LA English DT Article DE nucleolus; condensin; FEAR; Cdc14; rDNA; chromosome segregation; mitosis ID RNA-POLYMERASE-I; YEAST SACCHAROMYCES-CEREVISIAE; FUNCTIONAL PROTEOMIC ANALYSIS; BUDDING YEAST; CHROMOSOME CONDENSATION; RIBOSOMAL DNA; FISSION YEAST; CDC14 PHOSPHATASE; CHROMATID SEGREGATION; MITOTIC EXIT AB Mitotic segregation of nucleolus in fission and budding yeast proceeds without disassembling its complex structure, creating challenging problems for transmission of nucleolus-organizing regions during nuclear division. The SMC complex called condensin, which plays a leading role in organizing mitotic structure of chromosomes in all eukaryotes, is essential for nucleolar segregation in budding yeast, where rDNA chromatin is the main target of mitotic condensin activity. Mitosis-specific condensin targeting to the nucleolus presents an attractive model to study mechanisms controlling condensin binding to specific chromatin domains. Recent reports suggest that the early-anaphase release of Cdc14 from the nucleolus ( FEAR pathway) controls the proficiency of nucleolar segregation by promoting the mitotic condensin function in rDNA. This finding uncovers an essential function for the FEAR pathway and postulates the unique nucleolar self-regulatory mechanism, which evolved to recruit two essential enzymatic activities, Cdc14 phosphatase and condensin ATP-dependent supercoiling, for the specific task of segregating nucleoli without their disassembly. C1 NICHD, NIH, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA. RP Strunnikov, AV (reprint author), NICHD, NIH, Lab Gene Regulat & Dev, 18T Lib Dr,Room 106, Bethesda, MD 20892 USA. EM strunnik@mail.nih.gov OI Strunnikov, Alexander/0000-0002-9058-2256 NR 92 TC 11 Z9 13 U1 0 U2 2 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2005 VL 4 IS 1 BP 113 EP 117 DI 10.4161/cc.4.1.1488 PG 5 WC Cell Biology SC Cell Biology GA 902SG UT WOS:000227376200027 PM 15655374 ER PT J AU Lee, AC Fernandez-Capetillo, O Pisupati, V Jackson, SP Nussenzweig, A AF Lee, AC Fernandez-Capetillo, O Pisupati, V Jackson, SP Nussenzweig, A TI Specific association of mouse MDC1/NFBD1 with NBS1 at sites of DNA-damage SO CELL CYCLE LA English DT Article DE DNA damage response; KIAA0170; NFBD1; MDC1; mediator of DNA damage checkpoint 1; MRN complex ID DOUBLE-STRAND BREAKS; DEPENDENT NUCLEAR-DYNAMICS; MRE11 COMPLEX; IONIZING-RADIATION; SIGNALING PATHWAYS; CHECKPOINT; PROTEIN; REPAIR; 53BP1; MDC1 AB Human MDC1/NFBD1 has been found to interact with key players of the DNA-damage response machinery. Here, we identify and describe a functional homologue of MDC1/ NFBD1 in Mus musculus. The mouse homologue, mMDC1, retains the key motifs identified in the human protein and in response to ionizing radiation forms foci that co-localize with the MRE11-RAD50-NBS1 (MRN) complex and factors such as gammaH2AX and 53BP1. In addition, mMDC1 is associated with DNA damage sites generated during meiotic recombination as well as the X and Y chromosomes during the late stages of meiotic prophase I. Finally, whereas MDC1 shows strong colocalization with the MRN complex in response to DNA damage it does not co-localize with the MRN complex on replicating chromatin. These data suggest that mMDC1 is a marker for both exogenously and endogenously generated DNA double-stranded breaks and that its interaction with the MRN complex is initiated exclusively by DNA damage. C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. Wellcome Trust & Canc Res UK Gurdon Inst, Cambridge, England. Univ Cambridge, Dept Zool, Cambridge, England. RP Nussenzweig, A (reprint author), NCI, Expt Immunol Branch, NIH, 10 Ctr Dr Room 4B4, Bethesda, MD 20892 USA. EM s.jack-son@gurdon.cam.ac.uk; andre_nussenzweig@nih.gov RI Dry, Kate/I-2328-2014; Fernandez-Capetillo, Oscar/H-3508-2015 OI Fernandez-Capetillo, Oscar/0000-0002-2690-6885 NR 35 TC 24 Z9 27 U1 0 U2 1 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2005 VL 4 IS 1 BP 177 EP 182 DI 10.4161/cc.4.1.1354 PG 6 WC Cell Biology SC Cell Biology GA 902SG UT WOS:000227376200037 PM 15611643 ER PT J AU Bugnard, E Zaal, KJM Ralston, E AF Bugnard, E Zaal, KJM Ralston, E TI Reorganization of microtubule nucleation during muscle differentiation SO CELL MOTILITY AND THE CYTOSKELETON LA English DT Article DE centrosome; gamma-tubulin; pericentrin; ninein; myogenesis ID GAMMA-TUBULIN COMPLEXES; GOLGI-COMPLEX; EPITHELIAL-CELLS; ENDOPLASMIC-RETICULUM; ORGANIZING CENTERS; MAMMALIAN-CELLS; IN-VITRO; CENTROSOME; PROTEIN; PERICENTRIN AB Skeletal muscle differentiation involves a complete reorganization of the microtubule network. Nearly 20 years ago, Tassin et al. [1985: J Cell Biol 100:35-46] suggested a mechanism for this reorganization by showing a redistribution of the microtubule organizing center from the centrosome to the nuclear membrane. Little progress has been made since. It is still not clear whether centrosomal proteins are redistributed together, whether microtubules are nucleated at the nuclear membrane or transported there post-nucleation, and whether gamma-tubulin (gammatub) remains necessary for nucleation in myotubes. To investigate these questions, we have examined the redistribution of the centrosomal proteins pericenttin (PC), gammatub, and ninein in the C2 muscle cell line. Immunofluorescence of differentiated myotubes shows PC along the nuclear membrane whereas gammatub is only detected there after pre-fixation detergent extraction. After expression of a GFP-tagged gammatub, we observe a weak fluorescence along the nuclear membrane, confirming the presence of gammatub at a low concentration relative to PC. Microinjection of anti-gammatub antibodies into myotubes blocks microtubule growth from both nuclear membranes and centrosomal sites. The centrosomal microtubule-anchoring protein, ninein, is found at the nuclear membrane as well and its distribution appears independent of microtubule integrity. We conclude that centrosomal proteins are redistributed independently during muscle differentiation, to sites that nucleate microtubules both along the nuclear membranes and through the cytoplasm. (dagger)Published 2004 Wiley-Liss, Inc. C1 NIAMSD, Light Imaging Sect, NIH, Bethesda, MD 20892 USA. RP Ralston, E (reprint author), NIAMSD, Light Imaging Sect, NIH, Bethesda, MD 20892 USA. EM ralstone@mail.nih.gov NR 52 TC 65 Z9 67 U1 1 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0886-1544 J9 CELL MOTIL CYTOSKEL JI Cell Motil. Cytoskeleton PD JAN PY 2005 VL 60 IS 1 BP 1 EP 13 DI 10.1002/cm.20042 PG 13 WC Cell Biology SC Cell Biology GA 885KS UT WOS:000226156100001 PM 15532031 ER PT J AU Singh, SR Chen, X Hou, SX AF Singh, SR Chen, X Hou, SX TI JAK/STAT signaling regulates tissue outgrowth and male germline stem cell fate in Drosophila SO CELL RESEARCH LA English DT Review DE cell signaling; JAK/STAT signal transduction pathway; cell regulation; Drosophila; stem cell fate; tissue outgrowth ID JAK-STAT PATHWAY; SELF-RENEWAL; TRANSDUCTION PATHWAY; MODEL ORGANISMS; ACTIVATION; CDK4; EYE; SPERMATOGENESIS; IDENTIFICATION; PROLIFERATION AB In multicellular organisms, biological activities are regulated by cell signaling. The various signal transduction pathways regulate cell fate, proliferation, migration, and polarity. Miscoordination of the communicative signals will lead to disasters like cancer and other fatal diseases. The JAK/STAT signal transduction pathway is one of the pathways, which was first identified in vertebrates and is highly conserved throughout evolution. Studying the JAK/STAT signal transduction pathway in Drosophila provides an excellent opportunity to understand the molecular mechanism of the cell regulation during development and tumor formation. In this review, we discuss the general overview of JAK/STAT signaling in Drosophila with respect to its functions in the eye development and stem cell fate determination. C1 NCI, Immunobiol Lab, NIH, Frederick, MD 21702 USA. RP Hou, SX (reprint author), NCI, Immunobiol Lab, NIH, Frederick, MD 21702 USA. EM shou@mail.ncifcrf.gov RI Singh, Shree Ram/B-7614-2008 OI Singh, Shree Ram/0000-0001-6545-583X FU Intramural NIH HHS [Z99 CA999999] NR 40 TC 22 Z9 24 U1 1 U2 10 PU SCIENCE CHINA PRESS PI BEIJING PA 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA SN 1001-0602 J9 CELL RES JI Cell Res. PD JAN PY 2005 VL 15 IS 1 BP 1 EP 5 DI 10.1038/sj.cr.7290255 PG 5 WC Cell Biology SC Cell Biology GA 896UY UT WOS:000226960600001 PM 15686618 ER PT J AU Liu, ZG AF Liu, ZG TI Molecular mechanism of TNF signaling and beyond SO CELL RESEARCH LA English DT Review DE TNF; ROS; necrosis; apoptosis; JNK ID NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; DOMAIN KINASE RIP; INDUCED CELL-DEATH; DNA-DAMAGE; OXIDATIVE STRESS; FREE-RADICALS; ACTIVATION; PROTEIN; APOPTOSIS AB Tumor necrosis factor (TNF) is a proinflammatory cytokine that plays a critical role in diverse cellular events, including cell proliferation, differentiation and apoptosis. TNF is also involved in many types of diseases. In recent years, the molecular mechanisms of TNF functions have been intensively investigated. Studies from many laboratories have demonstrated that the TNF-mediated diverse biological responses are achieved through activating multiple signaling pathways. Especially the activation of transcription factors NF-kappaB and AP-1 plays a critical role in mediating these cellular responses. Several proteins, including FADD, the death domain kinase RIP and the TNF receptor associated factor TRAF2 have been identified as the key effectors of TNF signaling. Recently, we found that the effector molecules of TNF signaling, such as RIP and TRAF2, are also involved in other cellular responses. These finding suggests that RIP and TRAF2 serve a broader role than as just an effector of TNF signaling. C1 NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Liu, ZG (reprint author), NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM zgliu@helix.nih.gov NR 38 TC 133 Z9 146 U1 0 U2 8 PU SCIENCE CHINA PRESS PI BEIJING PA 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA SN 1001-0602 J9 CELL RES JI Cell Res. PD JAN PY 2005 VL 15 IS 1 BP 24 EP 27 DI 10.1038/sj.cr.7290259 PG 4 WC Cell Biology SC Cell Biology GA 896UY UT WOS:000226960600005 PM 15686622 ER PT J AU Yin, JJ Pollock, CB Kelly, K AF Yin, JJ Pollock, CB Kelly, K TI Mechanisms of cancer metastasis to the bone SO CELL RESEARCH LA English DT Review DE cancer; bone metastases; osteolytic metastasis; osteoblastic metastasis ID HORMONE-RELATED PROTEIN; HUMAN PROSTATE-CANCER; BREAST-CANCER; CELL-LINES; IN-VIVO; TGF-BETA; ENDOTHELIN-1; INTERLEUKIN-6; GROWTH; ADENOCARCINOMA AB Some of the most common human cancers, including breast cancer, prostate cancer, and lung cancer, metastasize with avidity to bone. What is the basis for their preferential growth within the bone microenvironment? Bidirectional interactions between tumor cells and cells that make up bone result in a selective advantage for tumor growth and can lead to bone destruction or new bone matrix deposition. This review discusses our current understanding of the molecular components and mechanisms that are responsible for those interactions. C1 NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. RP Kelly, K (reprint author), NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. EM kkelly@helix.nih.gov NR 50 TC 101 Z9 111 U1 4 U2 15 PU SCIENCE CHINA PRESS PI BEIJING PA 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA SN 1001-0602 J9 CELL RES JI Cell Res. PD JAN PY 2005 VL 15 IS 1 BP 57 EP 62 DI 10.1038/sj.cr.7290266 PG 6 WC Cell Biology SC Cell Biology GA 896UY UT WOS:000226960600012 PM 15686629 ER EF