FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Thompson, B Jacob, RG Frederick, M Geller, NV Hunsberger, S AF Thompson, B Jacob, RG Frederick, M Geller, NV Hunsberger, S TI Innovative designs in behavioural trials SO STATISTICS IN MEDICINE LA English DT Article; Proceedings Paper CT 9th International Symposium on Long-Term Clinical Trials CY JUN 19-20, 2000 CL LONDON, ENGLAND DE clinical trial; missing data; non-specific effects; patient dropout; statistical design; behavioural treatments ID PSYCHOTHERAPY-RESEARCH; METHODOLOGICAL ISSUES; PLACEBO; PHARMACOTHERAPY AB Clinical trials that compare pharmacological and behavioural treatments require extra attention to design on the part of the investigators. Many of the standard control mechanisms for comparison of active drug to placebo and behavioural therapy to control therapy create problems when the two types of interventions are combined. The most important of these problems is the introduction of non-specific effects introduced by behavioural therapists and physicians that can bias the study. Solutions to these problems require procedures that are common to both types of studies and the introduction of more complex statistical designs to adequately control the proposed comparisons. It may also be necessary to have a robust statistical method to address informative censoring since patients assigned to behavioural therapy may drop out of the study for different reasons than patients who drop out of a pharmacological trial. In this paper we use the design of the Raynand's Treatment Study to demonstrate methods that can be used to control for non-specific effects and differential drop-out from the study. Copyright (C) 2002 John Wiley Sons, Ltd. C1 Clin Trials & Surveys Corp, Baltimore, MD 21210 USA. Univ Pittsburgh, Sch Med, Dept Psychiat & Otolaryngol, Pittsburgh, PA 15213 USA. NHLBI, Off Biostat Res, Rockledge Ctr 2, Bethesda, MD 20892 USA. NCI, Clin Trials Sect, Bethesda, MD 20892 USA. RP Thompson, B (reprint author), Clin Trials & Surveys Corp, Suite 350,Village Cross Keys, Baltimore, MD 21210 USA. FU NHLBI NIH HHS [HC-25127, HC-25119, HC-25120, HC-25121, HC-25122, HC-25123] NR 11 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0277-6715 J9 STAT MED JI Stat. Med. PD OCT 15 PY 2002 VL 21 IS 19 BP 2981 EP 2989 DI 10.1002/sim.1302 PG 9 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA 599WG UT WOS:000178357700023 PM 12325114 ER PT J AU Hoffmann, SC Kampen, RL Amur, S Sharaf, MA Kleiner, DE Hunter, K Swanson, SJ Hale, DA Mannon, RB Blair, PJ Kirk, AD AF Hoffmann, SC Kampen, RL Amur, S Sharaf, MA Kleiner, DE Hunter, K Swanson, SJ Hale, DA Mannon, RB Blair, PJ Kirk, AD TI Molecular and immunohistochemical characterization of the onset and resolution of human renal allograft ischemia-reperfusion injury SO TRANSPLANTATION LA English DT Article ID DELAYED GRAFT FUNCTION; QUANTITATIVE RT-PCR; ACUTE REJECTION; SUBCLINICAL REJECTION; TRANSPLANTED KIDNEYS; ADHESION MOLECULES; GENE-EXPRESSION; UP-REGULATION; BIOPSIES; HYPERTENSION AB Background. Following allotransplantation, renal ischemia-reperfusion (I/R) injury initiates a series of events that provokes counter-adaptive immunity. Though T cells clearly mediate allospecific immunity, the manner in which reperfusion events augment their activation has not been established. In addition, comprehensive analysis of I/R injury in humans has been limited. Methods. To evaluate the earliest events occurring following allograft reperfusion and gain insight into those factors linking reperfusion to alloimmunity, we examined human renal allografts 30 to 60 minutes postreperfusion (n=10) and compared them with allografts with normal function that had resolved their I/R injury insult (>1 month posttransplant, n=6) and to normal kidneys (living donor kidneys before procurement, n=8). Biopsies were processed both for immunohistochemical analysis as well as for transcript analysis by real-time quantitative polymerase chain reaction (RT-PCR). Results. Reperfusion injury was characterized by increased levels of gene transcripts known to be involved in cellular adhesion, chemotaxis, apoptosis, and monocyte recruitment and activation. T-cell-associated transcripts were generally absent. However, recovered allografts exhibited increased levels of T-cell and costimulation-related gene transcripts despite normal allograft function. Consistent with these findings, the immediate postreperfusion state was characterized histologically by tubular injury and monocyte infiltration, while the stable posttransplant state was notable for T-cell infiltration. Conclusions. These data suggest that monocytes and, transcripts related to their recruitment dominate the immediate postreperfusion state. This gives way to a T-cell dominant milieu even in grafts selected for their stable function and absence of rejection. These data have implications for understanding the fundamental link between I/R injury and alloimmunity. C1 NIDDKD, Bethesda, MD 20892 USA. USN, Transplantat & Autoimmun Branch, Bethesda, MD 20084 USA. Appl Biosyst Inc, Foster City, CA 94404 USA. NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. Walter Reed Army Med Ctr, Organ Transplant Serv, Washington, DC 20307 USA. RP Kirk, AD (reprint author), Room 11S-219,Bldg 10,Ctr Dr, Bethesda, MD 20892 USA. RI Kirk, Allan/B-6905-2012; OI Kleiner, David/0000-0003-3442-4453 NR 39 TC 73 Z9 79 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 15 PY 2002 VL 74 IS 7 BP 916 EP 923 DI 10.1097/01.TP.0000031932.83993.E9 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 604WX UT WOS:000178645000003 PM 12394831 ER PT J AU Xu, H Tadaki, DK Elister, EA Burkly, LC Berning, JD Cruzata, F Kampen, RL Montgomery, SP Patterson, NB Harlan, DM Kirk, AD AF Xu, H Tadaki, DK Elister, EA Burkly, LC Berning, JD Cruzata, F Kampen, RL Montgomery, SP Patterson, NB Harlan, DM Kirk, AD TI Humanized ANTI-CD154 antibody therapy for the treatment of allograft rejection in nonhuman primates SO TRANSPLANTATION LA English DT Article ID ENDOTHELIAL-CELLS; CD40 LIGAND; EXPRESSION AB The anti-CD154 antibody hu5C8 prevents acute allograft rejection and prolongs allograft survival after withdrawal of therapy in nonhuman primates. This study describes the use of hu5C8 as a rescue agent for rejection developing after the withdrawal of hu5C8. Twelve rhesus monkeys that had received renal allografts under hu5C8 induction and subsequently rejected were studied. Rescue with hu5C8 was analyzed based on the histological character of the rejection (acute versus chronic) and whether conventional therapy was received at the time of rescue or induction. The diagnosis of rejection and response to therapy was based on allograft function and histology. Four monkeys that had acute rejection associated with conventional immunosuppression and hu5C8 were not reversed by hu5C8 rescue. Four animals with isolated chronic rejection following prolonged rejection-free survival after the withdrawal of hu5C8 did not respond to hu5C8 rescue therapy. Hu5C8 rescue therapy effectively reversed acute rejection occurring in two monkeys after hu5C8 withdrawal. One of two animals with combined acute on chronic rejection responded to hu5C8 rescue therapy. Hu5C8 effectively reverses acute but not chronic allograft rejection and appears to have no synergistic effect with conventional rescue agents. C1 USN, NIDDK, Transplantat & Autoimmun Branch, Bethesda, MD USA. Biogen Inc, Cambridge, MA 02142 USA. RP Kirk, AD (reprint author), Room 11S-219,Bldg 10,Ctr Dr, Bethesda, MD 20892 USA. RI Kirk, Allan/B-6905-2012 FU NIAID NIH HHS [AI 43900] NR 10 TC 26 Z9 28 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 15 PY 2002 VL 74 IS 7 BP 940 EP 943 DI 10.1097/00007890-200210150-00007 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 604WX UT WOS:000178645000007 PM 12394834 ER PT J AU Karev, GP Wolf, YI Rzhetsky, AY Berezovskaya, FS Koonin, EV AF Karev, Georgy P. Wolf, Yuri I. Rzhetsky, Andrey Y. Berezovskaya, Faina S. Koonin, Eugene V. TI Birth and death of protein domains: A simple model of evolution explains power law behavior SO BMC EVOLUTIONARY BIOLOGY LA English DT Article AB Background: Power distributions appear in numerous biological, physical and other contexts, which appear to be fundamentally different. In biology, power laws have been claimed to describe the distributions of the connections of enzymes and metabolites in metabolic networks, the number of interactions partners of a given protein, the number of members in paralogous families, and other quantities. In network analysis, power laws imply evolution of the network with preferential attachment, i.e. a greater likelihood of nodes being added to pre-existing hubs. Exploration of different types of evolutionary models in an attempt to determine which of them lead to power law distributions has the potential of revealing non-trivial aspects of genome evolution. Results: A simple model of evolution of the domain composition of proteomes was developed, with the following elementary processes: i) domain birth (duplication with divergence), ii) death (inactivation and/or deletion), and iii) innovation (emergence from non-coding or non-globular sequences or acquisition via horizontal gene transfer). This formalism can be described as a birth, death and innovation model (BDIM). The formulas for equilibrium frequencies of domain families of different size and the total number of families at equilibrium are derived for a general BDIM. All asymptotics of equilibrium frequencies of domain families possible for the given type of models are found and their appearance depending on model parameters is investigated. It is proved that the power law asymptotics appears if, and only if, the model is balanced, i. e. domain duplication and deletion rates are asymptotically equal up to the second order. It is further proved that any power asymptotic with the degree not equal to -1 can appear only if the hypothesis of independence of the duplication/deletion rates on the size of a domain family is rejected. Specific cases of BDIMs, namely simple, linear, polynomial and rational models, are considered in details and the distributions of the equilibrium frequencies of domain families of different size are determined for each case. We apply the BDIM formalism to the analysis of the domain family size distributions in prokaryotic and eukaryotic proteomes and show an excellent fit between these empirical data and a particular form of the model, the second-order balanced linear BDIM. Calculation of the parameters of these models suggests surprisingly high innovation rates, comparable to the total domain birth (duplication) and elimination rates, particularly for prokaryotic genomes. Conclusions: We show that a straightforward model of genome evolution, which does not explicitly include selection, is sufficient to explain the observed distributions of domain family sizes, in which power laws appear as asymptotic. However, for the model to be compatible with the data, there has to be a precise balance between domain birth, death and innovation rates, and this is likely to be maintained by selection. The developed approach is oriented at a mathematical description of evolution of domain composition of proteomes, but a simple reformulation could be applied to models of other evolving networks with preferential attachment. C1 [Karev, Georgy P.; Wolf, Yuri I.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. [Rzhetsky, Andrey Y.] Columbia Univ, Columbia Genome Ctr, New York, NY 10032 USA. [Berezovskaya, Faina S.] Howard Univ, Dept Math, Washington, DC 20059 USA. RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. EM karev@ncbi.nlm.nih.gov; wolf@ncbi.nlm.nih.gov; ar345@columbia.edu; fberezovskaya@howard.edu; koonin@ncbi.nlm.nih.gov NR 43 TC 101 Z9 103 U1 0 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1471-2148 J9 BMC EVOL BIOL JI BMC Evol. Biol. PD OCT 14 PY 2002 VL 2 AR 18 DI 10.1186/1471-2148-2-18 PG 26 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA V13DF UT WOS:000207646800001 PM 12379152 ER PT J AU Yang, JS Lee, SY Gao, MG Bourgoin, S Randazzo, PA Premont, RT Hsu, VW AF Yang, JS Lee, SY Gao, MG Bourgoin, S Randazzo, PA Premont, RT Hsu, VW TI ARFGAP1 promotes the formation of COPI vesicles, suggesting function as a component of the coat SO JOURNAL OF CELL BIOLOGY LA English DT Article DE GAP; COPI; ARF1; vesicular transport; Golgi complex ID GTPASE-ACTIVATING PROTEIN; ADP-RIBOSYLATION FACTOR; ENDOPLASMIC-RETICULUM; NUCLEOTIDE-EXCHANGE; GUANINE-NUCLEOTIDE; BINDING PROTEIN; KDEL RECEPTOR; NONCATALYTIC DOMAIN; TRANSPORT VESICLES; RETROGRADE CARGO AB The role of GTPase-activating protein (GAP) that deactivates ADP-ribosylation factor 1 (ARF1) during the formation of coat protein I (COPI) vesicles has been unclear. GAP is originally thought to antagonize vesicle formation by triggering uncoating, but later studies suggest that GAP promotes cargo sorting, a process that occurs during vesicle formation. Recent models have attempted to reconcile these seemingly contradictory roles by suggesting that cargo proteins suppress GAP activity during vesicle formation, but whether GAP truly antagonizes coat recruitment in this process has not been assessed directly. We have reconstituted the formation of COPI vesicles by incubating Golgi membrane with purified soluble components, and find that ARFGAP1 in the presence of GTP promotes vesicle formation and cargo sorting. Moreover, the presence of GTPgammaS not only blocks vesicle uncoating but also vesicle formation by preventing the proper recruitment of GAP to nascent vesicles. Elucidating how GAP functions in vesicle formation, we find that the level of GAP on the reconstituted vesicles is at least as abundant as COPI and that GAP binds directly to the dilysine motif of cargo proteins. Collectively, these findings suggest that ARFGAP1 promotes vesicle formation by functioning as a component of the COPI coat. C1 Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Ctr Hosp Univ Quebec, Quebec City, PQ G1V 4G2, Canada. NCI, Cellular Oncol Lab, Div Basic Sci, Bethesda, MD 20892 USA. Duke Univ, Med Ctr, Dept Med, Div Gastroenterol, Durham, NC 27710 USA. RP Hsu, VW (reprint author), Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA. NR 49 TC 113 Z9 115 U1 1 U2 10 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT 14 PY 2002 VL 159 IS 1 BP 69 EP 78 DI 10.1083/jcb.200206015 PG 10 WC Cell Biology SC Cell Biology GA 605HJ UT WOS:000178671800007 PM 12379802 ER PT J AU Sansom, MSP Shrivastava, IH Bright, JN Tate, J Capener, CE Biggin, PC AF Sansom, MSP Shrivastava, IH Bright, JN Tate, J Capener, CE Biggin, PC TI Potassium channels: structures, models, simulations SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES LA English DT Review DE potassium channel; simulation; molecular structure ID MOLECULAR-DYNAMICS SIMULATIONS; SHAKER K+ CHANNEL; ION PERMEATION; STREPTOMYCES-LIVIDANS; BROWNIAN DYNAMICS; TETRAETHYLAMMONIUM ION; SELECTIVITY FILTER; BETA-SUBUNIT; TRANSMEMBRANE HELICES; CYTOPLASMIC DOMAINS AB Potassium channels have been studied intensively in terms of the relationship between molecular structure and physiological function. They provide an opportunity to integrate structural and computational studies in order to arrive at an atomic resolution description of mechanism. we review recent progress in K channel structural studies, focussing on the bacterial channel KcsA. Structural studies can be extended via use of computational (i.e. molecular simulation) approaches in order to provide a perspective on aspects of channel function such as permeation, selectivity, block and gating. Results from molecular dynamics simulations are shown to be in good agreement with recent structural studies of KcsA in terms of the interactions of K+ ions with binding sites within die selectivity filter of the channel, and in revealing the importance of filter flexibility in channel function. we discuss how the KcsA structure may be used as a template for developing structural models of other families of K channels. Progress in this area is explored via two examples: inward rectifier (Kir) and voltage-gated (Kv) potassium channels. A brief account of structural studies of ancillary domains and subunits of K channels is provided, (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Oxford, Dept Biochem, Lab Mol Biophys, Oxford OX1 3QU, England. NCI, LECB, Bethesda, MD 20892 USA. EMBL Outstn Hinxton, European Bioinformat Inst, Cambridge CB10 1SD, England. RP Sansom, MSP (reprint author), Univ Oxford, Dept Biochem, Lab Mol Biophys, Rex Richards Bldg,S Parks Rd, Oxford OX1 3QU, England. OI Sansom, Mark/0000-0001-6360-7959 NR 110 TC 89 Z9 94 U1 1 U2 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0005-2736 J9 BBA-BIOMEMBRANES JI Biochim. Biophys. Acta-Biomembr. PD OCT 11 PY 2002 VL 1565 IS 2 BP 294 EP 307 AR PII S0005-2736(02)00576-X DI 10.1016/S0005-2736(02)00576-X PG 14 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 612PP UT WOS:000179084900012 PM 12409202 ER PT J AU Louet, JF Hayhurst, G Gonzalez, FJ Girard, J Decaux, JF AF Louet, JF Hayhurst, G Gonzalez, FJ Girard, J Decaux, JF TI The coactivator PGC-1 is involved in the regulation of the liver carnitine palmitoyltransferase I gene expression by cAMP in combination with HNF4 alpha and cAMP-response element-binding protein (CREB) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACTIVATED RECEPTOR-ALPHA; BROWN ADIPOSE-TISSUE; CYCLIC-AMP; CPT-I; TRANSCRIPTIONAL REGULATION; FATTY-ACIDS; KINASE-A; RAT HEPATOCYTES; C-FOS; PROMOTER AB Liver carnitine palmitoyltransferase I catalyzes the transfer of long-chain fatty acids into mitochondria. L-CPT I is considered the rate-controlling enzyme in fatty acid oxidation. Expression of the L-CPT I gene is induced by starvation in response to glucagon secretion from the pancreas, an effect mediated by cAMP. Here, the molecular mechanisms underlying the induction of L-CPT I gene expression by cAMP were characterized. We demonstrate that the cAMP response unit of the L-CPT I gene is composed of a cAMP-response element motif and a DR1 sequence located 3 kb upstream of the transcription start site. Our data strongly suggest that the coactivator PGC-1 is involved in the regulation of this gene expression by cAMP in combination with HNF4alpha and cAMP-response element-binding protein (CREB). Indeed, (i) cotransfection of CREB or HNF4alpha dominant negative mutants completely abolishes the effect of cAMP on the L-CPT I promoter, and (ii) the cAMP-responsive unit binds HNF4alpha and CREB through the DR1 and the cAMP-response element sequences, respectively. Moreover, cotransfection of PGC-1 strongly activates the L-CPT I promoter through HNF4alpha bound at the DR1 element. Finally, we show that the transcriptional induction of the PGC-1 gene by glucagon through cAMP in hepatocytes precedes that of L-CPT-1. In addition to the key role that PGC-1 plays in glucose homeostasis, it may also be critical for lipid homeostasis. Taken together these observations suggest that PGC-1 acts to coordinate the process of metabolic adaptation in the liver. C1 Inst Cochin, Dept Endocrinol, F-75014 Paris, France. Inst Pasteur, Dept Dev Biol, Unite Genet Differenciat, F-75015 Paris, France. NCI, Lab Metab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Decaux, JF (reprint author), Inst Cochin, Dept Endocrinol, 24 Rue Faubourg St Jacques, F-75014 Paris, France. OI Louet, Jean-Francois/0000-0002-1626-7098 NR 50 TC 93 Z9 104 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 11 PY 2002 VL 277 IS 41 BP 37991 EP 38000 DI 10.1074/jbc.M205087200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600005 PM 12107181 ER PT J AU Yang, KS Kang, SW Woo, HA Hwang, SC Chae, HZ Kim, K Rhee, SG AF Yang, KS Kang, SW Woo, HA Hwang, SC Chae, HZ Kim, K Rhee, SG TI Inactivation of human peroxiredoxin I during catalysis as the result of the oxidation of the catalytic site cysteine to cysteine-sulfinic acid SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALKYL HYDROPEROXIDE REDUCTASE; THIOL-SPECIFIC ANTIOXIDANT; MAMMALIAN PEROXIREDOXIN; SALMONELLA-TYPHIMURIUM; CRYSTAL-STRUCTURE; ANGSTROM RESOLUTION; NADH PEROXIDASE; SULFENIC ACIDS; SACCHAROMYCES-CEREVISIAE; TRYPAREDOXIN PEROXIDASE AB By following peroxiredoxin I (Prx I)-dependent NADPH oxidation spectrophotometrically, we observed that Prx I activity decreased gradually with time. The decay in activity was coincident with the conversion of Prx I to a more acidic species as assessed by two-dimensional gel electrophoresis. Mass spectral analysis and studies with Cys mutants determined that this shift in pI was due to selective oxidation of the catalytic site Cys(51)-SH to Cys(51)-SO2H. Thus, Cys(51)-SOH generated as an intermediate during catalysis appeared to undergo occasional further oxidation to Cys(51)-SO2H, which cannot be reversed by thioredoxin. The presence of H2O2 alone was not sufficient to cause oxidation of Cys(51) to Cys(51)-SO2H. Rather, the presence of complete catalytic components (H2O2, thioredoxin, thioredoxin reductase, and NADPH) was necessary, indicating that such hyperoxidation occurs only when Prx I is engaged in the catalytic cycle. Likewise, hyperoxidation of Cys(172)/Ser(172) mutant Prx I required not only H2O2, but also a catalysis-supporting thiol (dithiothreitol). Kinetic analysis of Prx I inactivation in the presence of a low steady-state level (< 1 μM) of H2O2 indicated that Prx I was hyperoxidized at a rate of 0.072% per turnover at 30 &DEG;C. Hyperoxidation of Prx I was also detected in HeLa cells treated with H2O2. C1 NHLBI, Lab Cell Signaling, NIH, Bethesda, MD 20892 USA. RP Rhee, SG (reprint author), NHLBI, Lab Cell Signaling, NIH, Bldg 50,Rm 3523,South Dr,MSC 8015, Bethesda, MD 20892 USA. OI Hwang, Sung Chul/0000-0003-2401-619X NR 43 TC 276 Z9 287 U1 0 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 11 PY 2002 VL 277 IS 41 BP 38029 EP 38036 DI 10.1074/jbc.M206626200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600009 PM 12161445 ER PT J AU Kim, J Cantwell, CA Johnson, PF Pfarr, CM Williams, SC AF Kim, J Cantwell, CA Johnson, PF Pfarr, CM Williams, SC TI Transcriptional activity of CCAAT/enhancer-binding proteins is controlled by a conserved inhibitory domain that is a target for sumoylation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LONG-TERM FACILITATION; DNA-BINDING; C/EBP-BETA; COVALENT MODIFICATION; SUMO-1 MODIFICATION; ACTIVATION DOMAINS; NUCLEAR-BODIES; C-MYB; CCAAT; UBIQUITIN AB CCAAT/enhancer-binding proteins (C/EBPs) are basic region/leucine zipper transcription factors that function as regulators of cell growth and differentiation in numerous cell types. We previously localized transcriptional activation and inhibitory regions in one family member, C/EBPepsilon. Here we describe the further characterization of a C/EBPepsilon inhibitory domain termed regulatory domain 1. We show that functionally related domains are present in C/EBPalpha, C/EBPbeta, and C/EBPdelta. These domains contain an evolutionarily conserved five-amino acid motif (the regulatory domain motif (RDM)) that conforms to the consensus sequence (I/V/ L)KXEP. Mutagenesis studies revealed that the residues at positions 1, 2, and 4 of the RDM are critical for inhibitory domain function. Data base searches identified RDM-like sequences in a number of nuclear proteins. We found that small regions from c-Jun, JunB, and JunD containing this sequence also function as transcriptional inhibitory domains. Importantly, the RDM is similar to the recognition sequence for attachment of the ubiquitin-like protein, small ubiquitin-like modifier-1 (SUMO-1), and the conserved lysine residue of each C/EBP RDM served as an attachment site for SUMO-1. SUMO-1 attachment decreased the inhibitory effect of the C/EBPepsilon regulatory domain, suggesting that sumoylation may play an important role in modulating C/EBPepsilon activity as well as that of the other C/EBP family members. C1 Texas Tech Univ, Hlth Sci Ctr, Dept Biochem & Cell Biol, Lubbock, TX 79430 USA. UMC Lubbock, SW Canc Ctr, Lubbock, TX 79430 USA. NCI Frederick, Regulat Cell Growth Lab, Frederick, MD 21702 USA. RP Williams, SC (reprint author), Texas Tech Univ, Hlth Sci Ctr, Dept Biochem & Cell Biol, Lubbock, TX 79430 USA. RI Johnson, Peter/A-1940-2012 OI Johnson, Peter/0000-0002-4145-4725 NR 50 TC 114 Z9 118 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 OCT 11 PY 2002 VL 277 IS 41 BP 38037 EP 38044 DI 10.1074/jbc.M207235200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600010 PM 12161447 ER PT J AU Wechsler, J Choi, YH Krall, J Ahmad, F Manganiello, VC Movsesian, MA AF Wechsler, J Choi, YH Krall, J Ahmad, F Manganiello, VC Movsesian, MA TI Isoforms of cyclic nucleotide phosphodiesterase PDE3A in cardiac myocytes SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INHIBITED CAMP-PHOSPHODIESTERASE; DEPENDENT PROTEIN-KINASE; CARDIOMYOCYTES IN-VITRO; SARCOPLASMIC-RETICULUM; DILATED CARDIOMYOPATHY; ROLIPRAM INHIBITION; PHOSPHORYLATION; ACTIVATION; INSULIN; IDENTIFICATION AB PDE3A cyclic nucleotide phosphodiesterases regulate cAMP- and cGMP-mediated intracellular signaling in cardiac myocytes. We used antibodies to different regions of PDE3A to demonstrate the presence of three PDE3A isoforms in these cells. These isoforms, whose apparent molecular weights are 136,000, 118,000, and 94,000 ("PDE3A-136,"PDE3A-118," and "PDE3A-94"), are identical save for the deletion of different lengths of N-terminal sequence containing two membrane-association domains and sites for phosphorylation/activation by protein kinase B ("PK-B") and protein kinase A ("PK-A"). PDE3A-136 contains both membrane-association domains and the PK-B and PK-A sites. PDE3-118 contains only the downstream membrane-association domain and the PK-A sites. PDE3A-94 lacks both membrane localization domains and the PK-B and PK-A sites. The three isoforms are translated from two mRNAs derived from the PDE3A1 gene: PDE3A-136 is translated from PDE3A1 mRNA, whereas PDE3A-118 and PDE3A-94 are translated from PDE3A2 mRNA. Experiments involving in vitro transcription/translation indicate that PDE3A-118 and PDE3A-94 may be translated from different AUGs in PDE3A2 mRNA. These findings suggest that alternative transcriptional and post-transcriptional processing of the PDE3A gene results in the generation of two mRNAs and three protein isoforms in cardiac myocytes that differ with respect to intracellular localization and may be regulated through different signaling pathways. C1 Vet Affairs Salt Lake City Hlth Care Syst, Cardiol Sect, Salt Lake City, UT 84148 USA. Univ Utah, Sch Med, Dept Internal Med Cardiol, Salt Lake City, UT 84132 USA. Univ Utah, Sch Med, Dept Pharmacol, Salt Lake City, UT 84132 USA. NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. RP Movsesian, MA (reprint author), Vet Affairs Salt Lake City Hlth Care Syst, Cardiol Sect 111C, 500 Foothill Blvd, Salt Lake City, UT 84148 USA. NR 40 TC 66 Z9 69 U1 1 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 OCT 11 PY 2002 VL 277 IS 41 BP 38072 EP 38078 DI 10.1074/jbc.M203647200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600014 PM 12154085 ER PT J AU Huang, XL Pawliczak, R Cowan, MJ Gladwin, MT Madara, P Logun, C Shelhamer, JH AF Huang, XL Pawliczak, R Cowan, MJ Gladwin, MT Madara, P Logun, C Shelhamer, JH TI Epidermal growth factor induces p11 gene and protein expression and down-regulates calcium ionophore-induced arachidonic acid release in human epithelial cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYTOSOLIC PHOSPHOLIPASE A(2); ANNEXIN-II TETRAMER; GLOMERULAR MESANGIAL CELLS; PROSTAGLANDIN GENERATION; PLASMINOGEN ACTIVATION; BINDING PROTEINS; KINASE; PHOSPHORYLATION; INHIBITION; PLATELETS AB p11, a member of the S-100 family of proteins, is the cellular ligand of annexin II and also interacts with the C-terminal region of cytosolic phospholipase A(2) (cPLA(2)), inhibiting cPLA(2) activity and arachidonic acid (AA) release. It has been reported that epidermal growth factor (EGF) induces cPLA(2), activation or cPLA(2) expression and subsequent AA release. It was of interest to study the effect of EGF on p11 production and on AA release in human epithelial cells (HeLa). EGF (20 ng/ml) treatment of HeLa cells increased the cellular p11. protein and the steady-state levels of p11 mRNA in a time- and dose-dependent manner but did not affect cPLA(2) protein expression over a 4-48-h incubation time. Transient transfection experiments of a reporter gene construct containing 1498 bp of the 5'-flanking region of p11 promoter demonstrated that EGF induced p11. gene expression at the transcriptional level. EGF caused a rapid phosphorylation of p44/42 and p38 kinases with a maximum level at 10 min. AG 1478 (EGF receptor tyrosine kinase inhibitor), PD 98059 (ERK1/2 inhibitor), and SB 203580 (p38 inhibitor) significantly inhibited EGF-induced p11. expression. EGF-induced AA release was significantly suppressed by AG 1478, PD 98059, SB 203580, and methyl arachidonyl fluorophosphate (a specific cPLA2 inhibitor). Methyl arachidonyl fluorophosphate (50 pm) also significantly inhibited EGF-induced p11 expression, demonstrating that the activation of cPLA(2) may have a role in the EGF-induced p11. expression. Immunoprecipitation experiments showed that EGF induced increased p11 binding to cPLA(2) in a time- and dose-dependent manner. EGF treatment for 30 min increased A23187-induced AA release, whereas EGF treatment for 24 h inhibited A23187-induced AA release. These results suggest that EGF treatment increased p11. bound to cPLA(2), may lead to the late suppression of AA release induced by EGF. C1 NIH, Dept Crit Care Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. Med Univ Lodz, Dept Allergy & Clin Immunol, PL-92213 Lodz, Poland. RP Shelhamer, JH (reprint author), NIH, Dept Crit Care Med, Warren G Magnuson Clin Ctr, Bldg 10,Rm 7D43,10 Ctr Dr,MSC1662, Bethesda, MD 20892 USA. RI Pawliczak, Rafal/S-9649-2016; OI Pawliczak, Rafal/0000-0001-6784-453X NR 34 TC 13 Z9 14 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 OCT 11 PY 2002 VL 277 IS 41 BP 38431 EP 38440 DI 10.1074/jbc.M207406200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600057 PM 12163506 ER PT J AU Lee, DK Kim, BC Kim, IY Cho, EA Satterwhite, DJ Kim, SJ AF Lee, DK Kim, BC Kim, IY Cho, EA Satterwhite, DJ Kim, SJ TI The human papilloma virus E7 oncoprotein inhibits transforming growth factor-beta signaling by blocking binding or the Smad complex to its target sequence SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-CYCLE ARREST; TGF-BETA; TRANSCRIPTIONAL ACTIVATION; TUMOR-SUPPRESSOR; PROTEINS; TGF-BETA-1; EXPRESSION; GENE; PHOSPHORYLATION; INACTIVATION AB The human papillomavirus (HPV) oncoprotein E7 is implicated in the etiology of cervical cancer associated with infection by HPV. HPV-positive cells develop resistance to TGF-beta growth inhibitory activity through the inhibition of hypophosphorylation of pRb by papillomavirus type 16 E7 oncoprotein. In this study, we examined whether E7, in addition to its well known effects on pRb, might directly target the Smad proteins that mediate TGF-beta signaling. Here, we show that E7 significantly blocks both Smad transcriptional activity and the ability of TGF-beta to inhibit DNA synthesis. We found that E7 interacts constitutively with Smad2, Smad3, and Smad4. Confocal microscopic studies confirm that E7 and Smads co-localize in vivo. Using a canonical Smad DNA binding sequence, we found that E7 blocks Smad3 binding to its target sequence on DNA. These results suggest that suppression of Smad-mediated signaling by E7 may contribute to HPV-associated carcinogenesis. C1 NIH, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. Univ Utah, Div Neonatol, Salt Lake City, UT 84132 USA. RP Kim, SJ (reprint author), NIH, Lab Cell Regulat & Carcinogenesis, Bldg 10, Bethesda, MD 20892 USA. NR 36 TC 47 Z9 61 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 11 PY 2002 VL 277 IS 41 BP 38557 EP 38564 DI 10.1074/jbc.M206786200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600072 PM 12145312 ER PT J AU Bannach, FG Gutierrez, A Fowler, BJ Bugge, TH Degen, JL Parmer, RJ Miles, LA AF Bannach, FG Gutierrez, A Fowler, BJ Bugge, TH Degen, JL Parmer, RJ Miles, LA TI Localization of regulatory elements mediating constitutive and cytokine-stimulated plasminogen gene expression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article; Proceedings Paper CT 2nd Annual Conference on Arteriosclerosis, Thrombosis and Vascular Biology CY MAY 11-13, 2001 CL ARLINGTON, VIRGINIA ID ACUTE-PHASE RESPONSE; FIBRINOLYTIC SYSTEM; MICE; DEFICIENCY; PROMOTER; ACTIVATION; FAMILY; LIVER; ATHEROSCLEROSIS; HEPATOCYTES AB The activity of plasmin, the major enzyme responsible for dissolving fibrin clots, is regulated by plasminogen activators, plasminogen activator inhibitors, alpha(2)-antiplasmin, and inflammatory mediators. Recent studies suggest that plasmin activity can be regulated also at the level of plasminogen gene expression. In this study, we characterized the murine plasminogen promoter and 5'-flanking region. The major transcription start site was identified at -83 bp relative to the ATG translational initiation codon. A series of 5'-flanking sequences up to 2400 bp upstream of the transcription initiation site were fused to the luciferase reporter gene and transfected into hepatocytic cells. A 106-bp 5'-flanking region of the murine plasminogen gene demonstrated sufficient functional promoter activity in plasminogen-expressing cells. IL-6 treatment stimulated luciferase activity driven by the 5'-flanking region, and an intact consensus IL-6-responsive element at -791, was required for maximal stimulation by this cytokine. These results indicate the presence of regulatory elements in the 5'-flanking region of the murine plasminogen promoter that may regulate murine plasminogen gene expression and, hence, plasmin activity. C1 Scripps Res Inst, Dept Cell Biol, Div Vasc Biol CVN26, La Jolla, CA 92037 USA. NIDCR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. Childrens Hosp Res Fdn, Cincinnati, OH 45229 USA. Univ Calif San Diego, Dept Med, San Diego, CA 92161 USA. Vet Adm Med Ctr, San Diego, CA 92161 USA. RP Bannach, FG (reprint author), Scripps Res Inst, Dept Cell Biol, Div Vasc Biol CVN26, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA. EM fbannach@ucsd.edu OI Gutierrez-Fernandez, Ana/0000-0002-9287-8843 FU NHLBI NIH HHS [HL-45934, HL-38272, HL-47826, HL-50398, HL-63194] NR 50 TC 11 Z9 12 U1 1 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 OCT 11 PY 2002 VL 277 IS 41 BP 38579 EP 38588 DI 10.1074/jbc.M202509200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600075 PM 12149246 ER PT J AU Qian, SB Ott, DE Schubert, U Bennink, JR Yewdell, JW AF Qian, SB Ott, DE Schubert, U Bennink, JR Yewdell, JW TI Fusion proteins with COOH-terminal ubiquitin are stable and maintain dual functionality in vivo SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SHORT-LIVED PROTEIN; A-FACTOR RECEPTOR; DEGRADATION SIGNAL; TAGGED UBIQUITIN; ANTIGEN; RECOGNITION; SUBUNIT; HIV-1; INTERNALIZATION; LOCALIZATION AB The ubiquitin (Ub) fusion degradation pathway functions to degrade fusion proteins containing a nonremovable Ub moiety at their NH2 terminus (Johnson, E. S., Ma, P. C., Ota, I. M., and Varshavsky, A. (1995) J. Biol. Chem. 270, 17442-17456). Here we show that ubiquitin fusion degradation also targets proteins for proteasomal degradation when Ub is present in the middle of fusion proteins (X-Ub-Y), in a process that entails polyubiquitylation of Ub Lys(48). By contrast, fusion proteins bearing COOH-terminal Ub (X-Ub) are metabolically stable. Such fusion proteins, either newly biosynthesized or generated by Ub hydrolases, are reversibly conjugated to heterogeneous target proteins in a manner similar to wild-type Ub. Most importantly, the NH2-terminal fusion partner (X) can maintain its structure and function in the formed X-Ub conjugates as inferred from the fluorescence of green fluorescent protein-Ub conjugates and the incorporation of human immunodeficiency virus type 1 Gag-Ub into viral particles. These findings strongly suggest that 26S proteasomes exhibit spatial discrimination of Ub-conjugated proteins, sparing domains extended from the NH2 terminus of Ub from unfolding and degradation. The multifunctionality of X-Ub fusion proteins opens the possibility for a number of novel practical applications, including the imaging of Ub conjugate formation in living cells. C1 NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. NCI, AIDS Vaccine Program, NIH, Frederick, MD 21702 USA. RP Yewdell, JW (reprint author), NIAID, Viral Dis Lab, NIH, Rm 205,Bldg 4,4 Ctr Dr, Bethesda, MD 20892 USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 FU NCI NIH HHS [N01-CO-12400] NR 42 TC 37 Z9 37 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 OCT 11 PY 2002 VL 277 IS 41 BP 38818 EP 38826 DI 10.1074/jbc.M205547200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600103 PM 12163494 ER PT J AU Gao, HW Parkin, S Johnson, PF Schwartz, RC AF Gao, HW Parkin, S Johnson, PF Schwartz, RC TI C/EBP gamma has a stimulatory role on the IL-6 and IL-8 promoters SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NF-KAPPA-B; MONOCYTE CHEMOATTRACTANT PROTEIN-1; MACROPHAGE INFLAMMATORY PROTEIN-2; LYMPHOBLASTIC CELL-LINE; BINDING-PROTEIN; GENE-EXPRESSION; LEUCINE-ZIPPER; TRANSCRIPTIONAL ACTIVATORS; INTERLEUKIN-8 PRODUCTION; MESSENGER-RNA AB CCAAT/enhancer-binding protein gamma (C/EBPgamma) is an ubiquitously expressed member of the C/EBP family of transcription factors that has been shown to be an inhibitor of C/EBP transcriptional activators and has been proposed to act as a buffer against C/EBP-mediated activation. We have now unexpectedly found that C/EBPgamma dramatically augments the activity of C/EBPbeta in lipopolysaccharide induction of the interleukin-6 and interleukin-8 promoters in a B lymphoblast cell line. This activating role for C/EBPgamma is promoter-specific, neither being observed in the regulation of a simple C/EBP-dependent promoter nor the TNFalpha promoter. C/EBPgamma activity also shows cell-type specificity with no activity observed in a macrophage cell line. Studies with chimeric C/EBP proteins implicate the formation of a heterodimeric leucine zipper between C/EBPbeta and C/EBPgamma as the critical structural feature required for C/EBPgamma stimulatory activity. These findings suggest a unique role for C/EBPgamma in B cell gene regulation and, along with our previous observation of the ability of C/EBP basic region-leucine zipper domains to confer lipopolysaccharide inducibility of interleukin-6, suggest that the C/EBP leucine zipper domain has a role in C/EBP function beyond allowing dimerization between C/EBP family members. C1 Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA. NCI, Eukaryot Transcript Regulat Sect, Regulat Cell Growth Lab, Frederick, MD 21702 USA. RP Schwartz, RC (reprint author), Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA. RI Johnson, Peter/A-1940-2012 OI Johnson, Peter/0000-0002-4145-4725 NR 44 TC 34 Z9 34 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 11 PY 2002 VL 277 IS 41 BP 38827 EP 38837 DI 10.1074/jbc.M206224200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 602XK UT WOS:000178529600104 PM 12177065 ER PT J AU Du, QZ Cai, WJ Xia, M Ito, YC AF Du, QZ Cai, WJ Xia, M Ito, YC TI Purification of (+)-dihydromyricetin from leaves extract of Ampelopsis grossedentata using high-speed countercurrent chromatograph with scale-up triple columns SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article DE countercurrent chromatography; Ampelopsis grossedentata; preparative chromatography; dihydromyricetin AB Purification of (+)-dihydromyricetin from an extract (16 g) of leaves of Ampelopsis grossedentata was performed using a, preparative triple-column countercurrent chromatograph. With a solvent system composed of n-hexane-ethyl acetate-methanol-water (1:3:2:4, v/v) 11.3 g of (+)-dihydromyricetin was obtained at a high purity of over 99% by HPLC at 254 nm in 9 h. (C) 2002 Elsevier Science B.V. All rights reserved. C1 NHLBI, Biophys Chem Lab, NIH, Bethesda, MD 20892 USA. Hangzhou Univ Commerce, Inst Food & Biol Engn, Hangzhou 310035, Peoples R China. RP Ito, YC (reprint author), NHLBI, Biophys Chem Lab, NIH, Bldg 50,Rm 3334,50 South Dr, Bethesda, MD 20892 USA. NR 8 TC 29 Z9 35 U1 2 U2 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD OCT 11 PY 2002 VL 973 IS 1-2 BP 217 EP 220 AR PII S0021-9673(02)01092-0 DI 10.1016/S0021-9673(02)01092-0 PG 4 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 604UH UT WOS:000178639100023 PM 12437181 ER PT J AU Brank, AS Eritja, R Garcia, RG Marquez, VE Christman, JK AF Brank, AS Eritja, R Garcia, RG Marquez, VE Christman, JK TI Inhibition of HhaI DNA (cytosine-C5) methyltransferase by oligodeoxyribonucleotides containing 5-aza-2 '-deoxycytidine: Examination of the intertwined roles of co-factor, target, transition state structure and enzyme conformation SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE DNA methyltransferase; methylation inhibitor; 5-azacytidine; gene activation; epigenetics ID AZACYTOSINE-CONTAINING DNA; PHASE-II; HYPOMETHYLATING AGENT; CELL-CYCLE; METHYLATION; 5-AZACYTIDINE; DECITABINE; LEUKEMIA; CANCER; EXPRESSION AB The presence of 5-azacytosine (ZCyt) residues in DNA leads to potent inhibition of DNA (cytosine-C5) methyltranferases (C5-MTases) in vivo and in vitro.. Enzymatic methylation of cytosine in mammalian DNA is an epigenetic modification that can alter gene activity and chromosomal stability, influencing both differentiation and tumorigenesis. Thus, it is important to understand the critical mechanistic determinants of ZCyt's inhibitory action. Although several DNA C5-MTases have been reported to undergo essentially irreversible binding to ZCyt in DNA, there is little agreement as to the role of AdoMet and/or methyl transfer in stabilizing enzyme interactions with ZCyt. Our results demonstrate that formation of stable complexes between Hha I methyltransferase (M.Hha I) and oligo-deoxyribonucleotides containing ZCyt at the target position for methylation (ZCyt-ODNs) occurs in both the absence and presence of co-factors, AdoMet and AdoHcy. Both binary and ternary complexes survive SDS-PAGE under reducing conditions and take on a compact conformation that increases their electrophoretic mobility in comparison to free M.Hha I. Since methyl transfer can occur only in the presence of AdoMet these results suggest (1) that the inhibitory capacity of ZCyt in DNA is based on its ability to induce a stable, tightly closed conformation of M.Hha I that prevents DNA and co-factor release and (2) that methylation of ZCyt in DNA is not required for inhibition of M.Hha L (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Nebraska, Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA. CSIC, Ctr Invest & Desarrollo, E-08034 Barcelona, Spain. NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA. Univ Nebraska, Med Ctr, Eppley Canc Ctr, Omaha, NE 68198 USA. RP Christman, JK (reprint author), Univ Nebraska, Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA. RI eritja, ramon/B-5613-2008 OI eritja, ramon/0000-0001-5383-9334 NR 53 TC 14 Z9 14 U1 0 U2 3 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 11 PY 2002 VL 323 IS 1 BP 53 EP 67 DI 10.1016/S0022-2836(02)00918-X PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 606MF UT WOS:000178737200006 PM 12368098 ER PT J AU Steingart, RA Heldenberg, E Pinhasov, A Brenneman, DE Fridkin, M Gozes, I AF Steingart, RA Heldenberg, E Pinhasov, A Brenneman, DE Fridkin, M Gozes, I TI A vasoactive intestinal peptide receptor analog alters the expression of homeobox genes SO LIFE SCIENCES LA English DT Article DE HT 29 cell line; vasoactive intestinal peptide (VIP); stearyl-Nle(17)-neurotensin(6-11)VIP(7-28) (SNH); homeobox genes ID BREAST-CANCER CELLS; RETINOIC ACID; LUNG-CANCER; NEUROBLASTOMA-CELLS; BINDING-SITE; HUMAN TUMORS; LINE HT-29; VIP HYBRID; GROWTH; ANTAGONIST AB A lipophilic analog of vasoactive intestinal peptide (VIP), stearyl-Nle(17)-neurotensin(6-11)VIP(7-28) (SNE), that inhibited lung cancer growth, has been previously described. The mechanism of SNH inhibition of cancer growth is still being elucidated. The present study examined the effects of SNH on homeobox genes in the colon cancer cell line HT 29 that expresses VIP receptors. Homeobox genes contain a characteristic DNA sequence, coding for a stretch of 61 amino acid homeodomain that binds specific DNA motifs. While the HOX gene family contains a single homeodomain, the POU gene family contains an additional DNA binding homeodomain. HT 29 cells were incubated with SNH; RNA was extracted and subjected to reverse-transcription-polymerase chain reaction (RTPCR) with primers that matched the conserved area of the various HOX or POU genes. The PCR products that were altered by SNE treatment were sequenced. Three candidate SNH-responsive genes, the HOX A4, the HOX 135 and the PUO V transcription factor I (Oct-3) were identified. Semi-quantitative RT-PCR with specific primers confirmed the increase in HOX A4 and the decrease in Oct-3 expression levels following SNH treatment. Thus, the HOX A4 and the Oct-3 homeobox genes may partially mediate SNH activity on cancer cells. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NICHHD, Lab Dev Neurobiol, Sect Dev & Mol Pharmacol, Bethesda, MD 20892 USA. Weizmann Inst Sci, Dept Organ Chem, IL-76100 Rehovot, Israel. RP Gozes, I (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NR 43 TC 10 Z9 11 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0024-3205 J9 LIFE SCI JI Life Sci. PD OCT 11 PY 2002 VL 71 IS 21 BP 2543 EP 2552 AR PII S0024-3205(02)02082-9 DI 10.1016/S0024-3205(02)02082-9 PG 10 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 599ZH UT WOS:000178365100009 PM 12270759 ER PT J AU Li, XW DePetrillo, PB AF Li, XW DePetrillo, PB TI Corticosterone increases serotonin type-3 receptor mRNA in rat pheochromocytoma-12 cells SO NEUROSCIENCE LETTERS LA English DT Article DE receptors; serotonin; corticosterone; gene expression; pheochromocytoma-12 cells; ethanol ID PITUITARY-ADRENAL AXIS; PC12 CELLS; ETHANOL; ALCOHOL; EXPRESSION; CHANNEL; TOLERANCE; GENOTYPE; PROTEIN AB Serotonin type-3 (5-HT3) receptors are cation permeable membrane receptors which are involved in modulation of calcium entry in neuronal cells. Along with other ion-channels such as the N-methyl-D-aspartate receptor, it appears to be a target for the actions of ethanol and has been the focus of considerable work in this regard. Since in animals, ethanol exposure results in elevations of corticosteroids in both acute and chronic conditions, we studied the effects of both ethanol and corticosteroid exposure on 5-HT3 gene expression in an in situ pheochromocytoma-12 (PC12) cell model. We found that ethanol exposure alone (80 mM x 4 days) did not significantly alter target gene expression. Corticosterone (CORT) (50, 150, and 300 ng/ml) resulted in significant increases in 5-HT3 expression which were attenuated by mife-prestone (50 ng/ml). Ethanol in combination with CORT did not significantly alter the increase in 5-HT3 mRNA seen with CORT alone. We conclude that in PC12 cells, exposure to CORT at physiologically relevant concentrations increases 5-HT3 gene expression. (C) 2002 Published by Elsevier Science Ireland Ltd. C1 NIAAA, Clin Studies Lab, Unit Clin & Biochem Pharmacol, Div Intramural Clin & Biochem Res,NIH, Bethesda, MD 20892 USA. RP DePetrillo, PB (reprint author), NIAAA, Clin Studies Lab, Unit Clin & Biochem Pharmacol, Div Intramural Clin & Biochem Res,NIH, 10-3C103,10 Ctr Dr,MSC 1256, Bethesda, MD 20892 USA. NR 19 TC 3 Z9 3 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD OCT 11 PY 2002 VL 331 IS 2 BP 143 EP 145 AR PII S0304-3940(02)00870-4 DI 10.1016/S0304-3940(02)00870-4 PG 3 WC Neurosciences SC Neurosciences & Neurology GA 605UW UT WOS:000178696300018 PM 12361860 ER PT J AU Towner, RA Mason, RP Reinke, LA AF Towner, RA Mason, RP Reinke, LA TI In vivo detection of aflatoxin-induced lipid free radicals in rat bile SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS LA English DT Article DE aflatoxin B1; spin trapping; lipid radical; desferoxamine mesylate; SKF 525A ID MURINE PERITONEAL-MACROPHAGES; IN-VIVO; SPIN TRAPS; B-1; METABOLISM; SUPPRESSION; INHIBITION; METHYL; PHOTOLYSIS; OXIDATION AB Aflatoxin B1 (AFB1), a potent hepatotoxin and hepatocarcinogen, is metabolized in the liver via cytochrome P-450 to an AFB1-8,9-epoxide intermediate. The formation of the A-FB1-8,9-epoxide correlates with the pathological changes observed in numerous mammalian species. Oxidative damage has been postulated to play a major role in the mechanisms associated with AFB1-induced cytotoxicity and carcinogenecity in mammalian species. The aim of this study was to detect and identify free radical intermediates from the hepatic metabolism of AFB1 in vivo. Rat bile ducts were cannulated and rats were treated simultaneously with AFB1 (3 mg/kg i.p.) and the spin trapping agent 4-POBN (alpha-(4-pyridyl-1-oxide)-N-tert-butyl nitrone) (1 g/kg i.p.), and bile was collected over a period of 2 h at 20-min intervals. ESR spectroscopy was used to detect a carbon-centered radical adduct of 4-POBN in rat bile. The effect of metabolic inhibitors, such as deferoxamine mesylate (DFO), an iron chelator, and SKF 525A, a cytochrome P-450 inhibitor, on in vivo aflatoxin-induced free radical formation were also studied. It was found that there was a significant decrease in free radical formation by pre-treatment with both DFO and SKF 525A. This indicates that oxidation of AFB1 generates free radical species via CYP metabolism and an iron-mediated redox mechanism. (C) 2002 Elsevier Science B.V. All rights reserved. C1 James Cook Univ N Queensland, Sch Biomed Sci, N Queensland Magnet Resonance Ctr, Townsville, Qld 4811, Australia. James Cook Univ N Queensland, Sch Biomed Sci, Dept Physiol & Pharmacol, Townsville, Qld 4811, Australia. NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Dept Pharmaceut Sci, Oklahoma City, OK 73190 USA. RP Towner, RA (reprint author), James Cook Univ N Queensland, Sch Biomed Sci, N Queensland Magnet Resonance Ctr, Mol Sci Bldg, Townsville, Qld 4811, Australia. NR 33 TC 19 Z9 20 U1 3 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-4165 J9 BBA-GEN SUBJECTS JI Biochim. Biophys. Acta-Gen. Subj. PD OCT 10 PY 2002 VL 1573 IS 1 BP 55 EP 62 AR PII S0304-4165(02)00326-4 DI 10.1016/S0304-4165(02)00326-4 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 604FY UT WOS:000178607300009 PM 12383942 ER PT J AU Kovalchuk, AL Janz, S AF Kovalchuk, AL Janz, S TI Isotype switch-mediated C-H deletions are a recurrent feature of MYC/C-H translocations in peritoneal plasmacytomas in mice SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID IMMUNOGLOBULIN HEAVY-CHAIN; SITU HYBRIDIZATION ANALYSIS; CHROMOSOMAL TRANSLOCATIONS; BALB/C PLASMACYTOMA; CELL; LYMPHOMA; REARRANGEMENTS; RECOMBINATION; T(12-15); MYELOMA AB Oncogene activating chromosomal translocations that interrupt IGH switch (S) regions at 14q32 are thought to be caused by misguided IGH isotype switching in postgerminal center B-cell lymphomas and plasma cell myelomas in humans. Aberrant switching also seems to be involved in altering the fine structure of the translocation in some of these tumors, but the significance of these changes is not known. Here we report on 3 cases of IL-6 transgenic mouse plasmacytomas (PCT) that harbor T(12;15) translocations that had been modified by frustrated switch attempts that result in C. deletions. When considered together with 6 similar cases of PCT described previously, our observations suggest that secondary deletions in C-H are a regular feature in the molecular evolution of T(12;15) translocations and, thereby, in the progression of PCT. We propose that the T(12;15)(+) mouse PCT offers a uniquely valuable model system for elucidating the dual role of abnormal isotype switching in causation and,'remodeling' of chromosomal translocations. (C) 2002 Wiley-Liss, Inc. C1 NCI, Genet Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Janz, S (reprint author), NCI, Genet Lab, Ctr Canc Res, NIH, Bldg 37,Room 2B10, Bethesda, MD 20892 USA. NR 25 TC 5 Z9 5 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 10 PY 2002 VL 101 IS 5 BP 423 EP 426 DI 10.1002/ijc.10638 PG 4 WC Oncology SC Oncology GA 593LH UT WOS:000177992400004 PM 12216069 ER PT J AU Cushman, M Mohanakrishnan, AK Hollingshead, M Hamel, E AF Cushman, M Mohanakrishnan, AK Hollingshead, M Hamel, E TI The effect of exchanging various substituents at the 2-position of 2-methoxyestradiol on cytotoxicity in human cancer cell cultures and inhibition of tubulin polymerization SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ENDOGENOUS ESTROGEN METABOLITE; MAMMALIAN METABOLITE; 17-BETA-ESTRADIOL METABOLITES; ENDOTHELIAL-CELLS; TERMINAL ALKYNES; APOPTOSIS; ANGIOGENESIS; INDUCTION; ANALOGS; GROWTH AB A new set of estradiol derivatives bearing various substituents at the 2-position were synthesized in order to further elucidate the structural parameters associated with the antitubulin activity and cytotoxicity of 2-substituted estradiols. The potencies of the new compounds as inhibitors of tubulin polymerization were determined, and the cytotoxicities of the analogues in human cancer cell cultures were investigated. The substituents introduced into the 2-position of estradiol included E-3'-hydroxy-1'-propenyl, 2'-hydroxyethoxy, 3-N,N-dimethylaminoethylideneamino, 2'-hydroxyethylineneamino, (beta-3,4,5-trimethoxyphenyl)ethenyl, phenylethynyl, ethynly, 1'-propynyl, and cyano. The substituents conferring the ability to inhibit tubulin polymerization included E-3'-hydroxy-1'-propenyl, 2'-hydroxyethoxy, ethynyl, and 1'-propynyl. The remaining compounds were all inactive as inhibitors of tubulin polymerization when tested at concentrations of up to 40 muM. All of the compounds were cytotoxic in a panel of 55 human cancer cell cultures, and in general, the most cytotoxic compounds were also the most potent as inhibitors of tubulin polymerization. 2-(1'-Propynyl)estradiol displayed significant anticancer activity in the in vivo hollow fiber animal model. C1 Purdue Univ, Sch Pharm & Pharmacal Sci, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47907 USA. NCI, Div Canc Treatment & Diagnosis, Dev Therapeut Program, Biol Testing Branch,Fairview Ctr,NIH, Frederick, MD 21701 USA. NCI, Div Canc Treatment & Diagnosis, Div Canc, Dev Therapeut Program,Screening Technol Branch,NI, Ft Detrick, MD 21702 USA. RP Cushman, M (reprint author), Purdue Univ, Sch Pharm & Pharmacal Sci, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47907 USA. FU NCI NIH HHS [N01-CM-12400, N01-CM-67260] NR 46 TC 39 Z9 39 U1 1 U2 4 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 OCT 10 PY 2002 VL 45 IS 21 BP 4748 EP 4754 DI 10.1021/jm020218r PG 7 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 601UL UT WOS:000178466600018 PM 12361402 ER PT J AU LeTiran, A Stables, JP Kohn, H AF LeTiran, A Stables, JP Kohn, H TI Design and evaluation of affinity labels of functionalized amino acid anticonvulsants SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ANTIEPILEPTIC DRUG DEVELOPMENT; N-BENZYLACETAMIDE DERIVATIVES; OPIOID RECEPTORS; ALPHA; AGENTS; ISOTHIOCYANATES; HETEROGENEITY; LYSINES; LIGANDS; SERINE AB Studies have shown that functionalized amino acids (FAA) exhibit outstanding activity in the maximal electroshock-induced seizure (MES) test in rodents. Affinity labels patterned in part after the potent antiepileptic (R)-N-benzyl-2-acetamido-3-methoxypropionamide ((R)-2) have been prepared as mechanistic probes to learn the pharmacological basis for FAA function. The chemical reactivity of the affinity labels with nucleophiles was assessed, and the labels were evaluated in in vitro radioligand assays and in the MES tests in rodents. The affinity labels did not bind to receptors known to effect seizure spread. Three affinity labels, (R,S)-N-benzyl-2-acetamido-6-isothiocyanatohexanamide ((R,S)-5), (R)-N-(4-isothiocyanatobenzyl)-2-acetamido-3-methoxy-propionamide ((R)-6), and (R)-N-(3-isothiocyanatobenzyl)-2-acetamido-3-methoxy-propionamide ((R)-7), possessed excellent in vivo anticonvulsant activity and exhibited maximal activity at later time periods than typically observed for FAA. The anticonvulsant activity of 6 and 7 resided primarily in the (R)-enantiomer and the activity of (R)-6 and (R)-7 in rats (po) exceeded that of phenytoin. The chemical properties, pharmacological profile, and marked stereospecificity associated with 6 and 7 anticonvulsant activity make these compounds useful pharmacological tools for the study of the mode of action of FAA. C1 Univ Houston, Dept Chem, Houston, TX 77204 USA. NINDS, Epilepsy Branch, NIH, Bethesda, MD 20892 USA. Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Chapel Hill, NC 27599 USA. RP Kohn, H (reprint author), Univ Houston, Dept Chem, Univ Pk, Houston, TX 77204 USA. EM harold_kohn@unc.edu FU NIMH NIH HHS [K02MH01366] NR 54 TC 24 Z9 25 U1 0 U2 3 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 OCT 10 PY 2002 VL 45 IS 21 BP 4762 EP 4773 DI 10.1021/jm020225f PG 12 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 601UL UT WOS:000178466600020 PM 12361404 ER PT J AU Mu, FR Lee, DJ Pryor, DE Hamel, E Cushman, M AF Mu, FR Lee, DJ Pryor, DE Hamel, E Cushman, M TI Synthesis and investigation of conformationally restricted analogues of lavendustin A as cytotoxic inhibitors of tubulin polymerization SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID PROTEIN-TYROSINE KINASE; SOLID-PHASE SYNTHESIS; IN-VITRO; ACETYLENES; SERIES; CELLS; HYDROSTANNATION; CATALYST; AGENTS; DESIGN AB A series of conformationally restricted analogues were synthesized in order to elucidate the possible effects of different amide conformations of lavendustin A derivatives on cytotoxicity in cancer cell cultures and on inhibition of tubulin polymerization. The conformationally restricted analogues were based on the oxazinedione and isoindolone ring systems. In addition, the amide bond was replaced by both cis and trans alkene moieties. Surprisingly, the results indicated very little effect of conformational. restriction on biological activity. Because all of the compounds synthesized had similar cytotoxicities and potencies as tubulin polymerization inhibitors, the side chain present on the aniline ring system does not appear to be important in the biological effects of the lavendustins. The hydroquinone ring of lavendustin A may be a more important determinant of the biological activity than the structure surrounding the aniline ring. C1 Natl Canc Inst, Div Canc Treatment & Diagnosis, Dev Therapeut Program, Screening Technol Branch, Ft Detrick, MD 21702 USA. RP Cushman, M (reprint author), Purdue Univ, Sch Pharm & Pharmacal Sci, W Lafayette, IN 47907 USA. NR 41 TC 11 Z9 12 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 10 PY 2002 VL 45 IS 21 BP 4774 EP 4785 DI 10.1021/jm0202270 PG 12 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 601UL UT WOS:000178466600021 PM 12361405 ER PT J AU Wise, RA AF Wise, RA TI Brain reward circuitry: Insights from unsensed incentives SO NEURON LA English DT Review ID VENTRAL TEGMENTAL AREA; MEDIAL FOREBRAIN-BUNDLE; NUCLEUS-ACCUMBENS DOPAMINE; INDUCED BEHAVIORAL SENSITIZATION; IN-VIVO MICRODIALYSIS; SELF-STIMULATION; DRUG-ADDICTION; D-AMPHETAMINE; MOLECULAR MECHANISMS; INTRAVENOUS COCAINE AB The natural incentives that shape behavior reach the central circuitry of motivation trans-synaptically, via the five senses, whereas the laboratory rewards of intracranial stimulation or drug injections activate reward circuitry directly, bypassing peripheral sensory pathways. The unsensed incentives of brain stimulation and intracranial drug injections thus give us tools to identify reward circuit elements within the associational portions of the CNS. Such studies have implicated the mesolimbic dopamine system and several of its afferents and efferents in motivational function. Comparisons of natural and laboratory incentives suggest hypotheses as to why some habits become compulsive and give insights into the roles of reinforcement and of prediction of reinforcement in habit formation. C1 NIDA, Behav Neurosci Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA. RP Wise, RA (reprint author), NIDA, Behav Neurosci Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA. EM rwise@intra.nida.nih.gov RI Wise, Roy/A-6465-2012 NR 188 TC 498 Z9 513 U1 6 U2 50 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0896-6273 J9 NEURON JI Neuron PD OCT 10 PY 2002 VL 36 IS 2 BP 229 EP 240 DI 10.1016/S0896-6273(02)00965-0 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 603JA UT WOS:000178554700005 PM 12383779 ER PT J AU Watts, DH AF Watts, DH TI Human immunodeficiency virus in pregnancy - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. RP Watts, DH (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 10 PY 2002 VL 347 IS 15 BP 1209 EP 1209 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 601TW UT WOS:000178465100026 ER PT J AU Furuta, S Miura, K Copeland, T Shang, WH Oshima, A Kamata, T AF Furuta, S Miura, K Copeland, T Shang, WH Oshima, A Kamata, T TI Light Chain 3 associates with a Sos1 guanine nucleotide exchange factor: its significance in the Sos1-mediated Rac1 signaling leading to membrane ruffling SO ONCOGENE LA English DT Article DE Sos1; Rac1; light chain 3 ID PROTEIN; BINDING; RAS; AUTOPHAGOSOME; ACTIVATION; DOMAIN; YEAST; MSOS1 AB A 19 kDa protein was identified to associate with the Dbl oncogene homology domain of Sos1 (Sos-DH) and was purified from rat brains by GST-Sos-DH affinity chromatography. Peptide sequencing revealed that the protein is identical to light chain 3 (LC3), a microtubule-associated protein. LC3 coimmunoprecipitated with Sos1, and GST-LC3 was capable of forming complexes with Sos1 in in vitro GST-pull down assay. Furthermore, LC3 was colocalized with Sos1 in cells, as determined by immunohistochemistry. While Sos1 stimulated the guanine nucleotide exchange reaction on Rac1, LC3 suppressed the ability of Sos1 to activate Rac1 in in vitro experiments using COS cell lysates. Consistent with this, overexpression of LC3 decreased the level of active GTP-bound Rac1 in COS cells. Sos1 expression induced membrane ruffling, a downstream target for Rac1, but LC3 expression inhibited this biological effect of Sos1. These findings suggest that LC3 interacts with Sos1 and thereby negatively regulates the Sos1-dependent Rac1 activation leading to membrane ruffling. C1 Shinshu Univ, Sch Med, Dept Biochem & Mol Biol, Matsumoto, Nagano 3908621, Japan. NCI, Frederick Canc Res & Dev Ctr, IRSP, SAIC Frederick, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Wlodawers Program Struct Biol, Frederick, MD 21702 USA. RP Kamata, T (reprint author), Shinshu Univ, Sch Med, Dept Biochem & Mol Biol, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan. NR 15 TC 10 Z9 12 U1 2 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 OCT 10 PY 2002 VL 21 IS 46 BP 7060 EP 7066 DI 10.1038/sj.onc.1205790 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 601AX UT WOS:000178424900009 PM 12370828 ER PT J AU Sherman, MP Schubert, U Williams, SA de Noronha, CMC Kreisberg, JF Henklein, P Greene, WC AF Sherman, MP Schubert, U Williams, SA de Noronha, CMC Kreisberg, JF Henklein, P Greene, WC TI HIV-1 Vpr displays natural protein-transducing properties: Implications for viral pathogenesis SO VIROLOGY LA English DT Article DE protein transduction; HIV; Vpr; cell cycle ID HUMAN-IMMUNODEFICIENCY-VIRUS; CELL-CYCLE ARREST; TYPE-1 PREINTEGRATION COMPLEXES; NUCLEAR-LOCALIZATION SIGNAL; N-TERMINAL DOMAIN; T-CELLS; TAT PROTEIN; INFECTED-CELLS; IN-VIVO; REGULATORY PROTEIN AB The 14-kDa Vpr protein of human immunodeficiency virus type 1 (HIV-1) serves multiple functions in the retroviral life cycle, including the enhancement of viral replication in nondividing macrophages, the induction of G2 cell-cycle arrest in proliferating T lymphocytes, and the modulation of HIV-1-induced apoptosis. Extracellular Vpr has been detected in the sera and cerebral spinal fluid of HIV-infected patients. However, it is not known whether such forms of Vpr are biologically active. Vpr contains a carboxy-terminal basic amino acid rich segment stretch that is homologous to domains that mediate the energy- and receptor-independent cellular uptake of polypeptides by a process termed protein transduction. Similar functional protein-transducing domains are present in HIV-1 Tat, herpes simplex virus-1 DNA-binding protein VP22, and the Drosophila antennapedia homeotic transcription factor. We now demonstrate effective transduction of biologically active, synthetic Vpr (sVpr) as well as the Vpr-beta-galactosidase fusion protein. However, in contrast to other transducing proteins, Vpr transduction is not enhanced by protein denaturation, and Vpr's carboxy-terminal basic domain alone is not sufficient for its transduction across biological membranes. In contrast, the full-length Vpr protein effectively transduces a broad array of cells, leading to dose-dependent G2 cell-cycle arrest and apoptosis. Addition of Vpr into the extracellular medium also rescues the replication of Vpr-deficient strains of HIV-1 in human macrophage cultures. Native Vpr may thus be optimized for protein transduction, a feature that might enhance and extend the pathological effects of HIV infection. (C) 2002 Elsevier Science (USA). C1 Gladstone Inst Virol & Immunol, San Francisco, CA 94141 USA. NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. Univ Hamburg, Heinrich Pette Inst Expt Virol & Immunol, D-2000 Hamburg, Germany. Humboldt Univ, Inst Biochem, D-10115 Berlin, Germany. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA. RP Greene, WC (reprint author), Gladstone Inst Virol & Immunol, POB 419100, San Francisco, CA 94141 USA. FU NIAID NIH HHS [R01 AI45234-01A2]; NIDDK NIH HHS [R01 DK59537-01]; NIMH NIH HHS [P30 MH59037] NR 93 TC 68 Z9 70 U1 1 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD OCT 10 PY 2002 VL 302 IS 1 BP 95 EP 105 DI 10.1006/viro.2002.1576 PG 11 WC Virology SC Virology GA 605NE UT WOS:000178683300009 PM 12429519 ER PT J AU Gourdier, I Del Rio, M Crabbe, L Candeil, L Copois, V Ychou, M Auffray, C Martineau, P Mechti, N Pommier, Y Pau, B AF Gourdier, I Del Rio, M Crabbe, L Candeil, L Copois, V Ychou, M Auffray, C Martineau, P Mechti, N Pommier, Y Pau, B TI Drug specific resistance to oxaliplatin is associated with apoptosis defect in a cellular model of colon carcinoma SO FEBS LETTERS LA English DT Article DE oxaliplatin; drug resistance; apoptosis; Bax; colorectal cancer ID PERMEABILITY TRANSITION PORE; COLORECTAL-CANCER; CISPLATIN; AGENTS; CELLS; DNA; REPAIR; BAX AB To investigate acquired resistance to oxaliplatin, we selected two resistant clones from the HCT116 cell line. We found that the resistant phenotype was associated with resistance to oxaliplatin-induced apoptosis as demonstrated by FACS analysis and by Western blotting of caspase 3 activation. In addition, the resistant phenotype showed a concomitant resistance to lonidamine and arsenic trioxide which are inducers of mitochondrial apoptosis. Furthermore, a complete loss of Bax expression due to a frameshift mutation was observed in the most resistant clone. Taken together, these findings suggest that altered mitochondrial-mediated apoptosis could play a role in oxaliplatin resistance. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved. C1 Fac Pharm Montpellier, CNRS, UMR 5094, F-34093 Montpellier, France. Ctr Reg Lutte Contre Canc Val Aurelle, Serv Oncol Digest, F-34298 Montpellier, France. CNRS FRE 2376, F-94801 Villejuif, France. Natl Canc Inst, Mol Pharmacol Lab, Bethesda, MD 20890 USA. RP Pau, B (reprint author), Fac Pharm Montpellier, CNRS, UMR 5094, 15 Ave Charles Flahaut,POB 14491, F-34093 Montpellier, France. NR 24 TC 42 Z9 42 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD OCT 9 PY 2002 VL 529 IS 2-3 BP 232 EP 236 AR PII S0014-5793(02)03347-1 DI 10.1016/S0014-5793(02)03347-1 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 604GE UT WOS:000178608000016 PM 12372606 ER PT J AU Castellanos, FX Lee, PP Sharp, W Jeffries, NO Greenstein, DK Clasen, LS Blumenthal, JD James, RS Ebens, CL Walter, JM Zijdenbos, A Evans, AC Giedd, JN Rapoport, JL AF Castellanos, FX Lee, PP Sharp, W Jeffries, NO Greenstein, DK Clasen, LS Blumenthal, JD James, RS Ebens, CL Walter, JM Zijdenbos, A Evans, AC Giedd, JN Rapoport, JL TI Developmental trajectories of brain volume abnormalities in children and adolescents with attention-deficit/hyperactivity disorder SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; CHILDHOOD-ONSET SCHIZOPHRENIA; CORPUS-CALLOSUM MORPHOLOGY; MORPHOMETRIC ANALYSIS; QUANTITATIVE MORPHOLOGY; CAUDATE-NUCLEUS; BASAL GANGLIA; MRI; ASYMMETRY; VOXEL AB Context Various anatomic brain abnormalities have been reported for attention-deficit/hyperactivity disorder (ADHD), with varying methods, small samples, cross-sectional designs, and without accounting for stimulant drug exposure. Objective To compare regional brain volumes at initial scan and their change over time in medicated and previously unmedicated male and female patients with ADHD and healthy controls. Design, Setting, and Participants Case-control study conducted from 19912001 at the National Institute of Mental Health, Bethesda, Md, of 152 children and adolescents with ADHD (age range, 5-18 years) and 139 age- and sex-matched controls (age range, 4.5-19 years) recruited from the local community, who contributed 544 anatomic magnetic resonance images. Main Outcome Measures Using completely automated methods, initial volumes and prospective age-related changes of total cerebrum, cerebellum, gray and white matter for the 4 major lobes, and caudate nucleus of the brain were compared in patients and controls. Results On initial scan, patients with ADHD had significantly smaller brain volumes in all regions, even after adjustment for significant covariates. This global difference was reflected in smaller total cerebral volumes (-3.2%, adjusted F-1,F-280=8.30, P=.004) and in significantly smaller cerebellar volumes (-3.5%, adjusted F-1,F-280=12.29, P=.001). Compared with controls, previously unmedicated children with ADHD demonstrated significantly smaller total cerebral volumes (overall F-2,F-288=6.65; all pairwise comparisons Bonferroni corrected, -5.8%; P=.002) and cerebellar volumes (-6.2%, F-2,F-288=8.97, P<.001). Unmedicated children with ADHD also exhibited strikingly smaller total white matter volumes (F-2,F-288= 11.65) compared with controls (-10.7%, P<.001) and with medicated children with ADHD (-8.9%, P<.001). Volumetric abnormalities persisted with age in total and regional cerebral measures (P=.002) and in the cerebellum (P=.003). Caudate nucleus volumes were initially abnormal for patients with ADHD (P=.05), but diagnostic differences disappeared as caudate volumes decreased for patients and controls during adolescence. Results were comparable for male and female patients on all measures. Frontal and temporal gray matter, caudate, and cerebellar volumes correlated significantly with parent- and clinician-rated severity measures within the ADHD sample (Pearson coefficients between -0.16 and -0.26; all P values were <.05). Conclusions Developmental trajectories for all structures, except caudate, remain roughly parallel for patients and controls during childhood and adolescence, suggesting that genetic and/or early environmental influences on brain development in ADHD are fixed, nonprogressive, and unrelated to stimulant treatment. C1 NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. NINDS, Biostat Branch, NIH, Bethesda, MD 20892 USA. McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada. RP Castellanos, FX (reprint author), NYU, Ctr Child Study, 577 1st Ave, New York, NY 10016 USA. RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015 OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978 NR 53 TC 795 Z9 812 U1 23 U2 106 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 9 PY 2002 VL 288 IS 14 BP 1740 EP 1748 DI 10.1001/jama.288.14.1740 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 602BJ UT WOS:000178484700027 PM 12365958 ER PT J AU Gollust, SE Hull, SC Wilfond, BS AF Gollust, SE Hull, SC Wilfond, BS TI Limitations of direct-to-consumer advertising for clinical genetic testing SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PRESCRIPTION DRUGS; ALZHEIMER-DISEASE; OVARIAN-CANCER; BREAST-CANCER; RISK; PHYSICIANS; PRACTITIONERS; INFORMATION; KNOWLEDGE; MEDICINE AB Although direct-to-consumer (DTC) advertisements for pharmaceuticals have been appearing in the mass media for 20 years, DTC advertisements for genetic testing have only recently appeared. Advertisements for genetic testing can provide both consumers and physicians with information about test availability in an expanding market. However, 3 factors limit the value and appropriateness of advertisements: complex information, a complicated social context surrounding genetics, and a lack of consensus about the clinical utility of some tests. Consideration of several advertisements suggests that they overstate the value of genetic testing for consumers' clinical care. Furthermore, advertisements may provide misinformation about genetics, exaggerate consumers' risks, endorse a deterministic relationship between genes and disease, and reinforce associations between diseases and ethnic groups. Advertising motivated by factors other than evidence of the clinical value of genetic tests can manipulate consumers' behavior by exploiting their fears and worries. At this time, DTC advertisements are inappropriate, given the public's limited sophistication regarding genetics and the lack of comprehensive premarket review of tests or oversight of advertisement content. Existing Federal Trade Commission and Food and Drug Administration regulations for other types of health-related advertising should be applied to advertisements for genetic tests. C1 NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA. NIH, Warren G Magnuson Clin Ctr, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Hull, SC (reprint author), NHGRI, Med Genet Branch, NIH, Bldg 10,Room 1C118,9000 Rockville Pike,MSC 1156, Bethesda, MD 20892 USA. NR 66 TC 114 Z9 115 U1 1 U2 12 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 9 PY 2002 VL 288 IS 14 BP 1762 EP 1767 DI 10.1001/jama.288.14.1762 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 602BJ UT WOS:000178484700030 PM 12365961 ER PT J AU Segurado, R Detera-Wadleigh, SD Gill, M Levinson, DF Lewis, CL AF Segurado, R Detera-Wadleigh, SD Gill, M Levinson, DF Lewis, CL TI Meta-analysis of genome scans for bipolar affective disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Dublin Trinity Coll, Dept Genet, Dublin 2, Ireland. NIMH, NIH, Bethesda, MD 20892 USA. St James Hosp, Dept Psychiat, Trinity Ctr Hlth Sci, Dublin 8, Ireland. Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA. Guys Kings & St Thomas Sch Med, Div Med & Mol Genet, London, England. RI Segurado, Ricardo/K-6116-2014 OI Segurado, Ricardo/0000-0002-3547-6733 NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA SL3 BP 701 EP 701 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400011 ER PT J AU Parsian, A Cloninger, CR Sinha, R Zhang, ZH AF Parsian, A Cloninger, CR Sinha, R Zhang, ZH TI Functional variation in promoter region of MAO-A gene and subtypes of alcoholism: Haplotype analysis SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Louisville, Dept Mol & Cellular Biol, Louisville, KY 40292 USA. Washington Univ, Dept Psychiat, St Louis, MO USA. NIH, Bethesda, MD 20892 USA. RI Cloninger, Claude/F-5357-2012 OI Cloninger, Claude/0000-0003-3096-4807 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O17 BP 718 EP 718 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400060 ER PT J AU Schulze, TG Chen, YS Akula, N Hennessy Badner, JA McInnis, MG DePaulo, JR Schumacher, J Cichon, S Propping, P Maier, W Rietschel, M Nothen, MM McMahon, FJ AF Schulze, TG Chen, YS Akula, N Hennessy Badner, JA McInnis, MG DePaulo, JR Schumacher, J Cichon, S Propping, P Maier, W Rietschel, M Nothen, MM McMahon, FJ TI Can long-range microsatellite data be used to predict short-range linkage disequilibrium? SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 NIMH, Bethesda, MD 20892 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Bonn, Dept Psychiat, D-5300 Bonn, Germany. Johns Hopkins Univ, Dept Psychiat, Baltimore, MD USA. Univ Bonn, Inst Human Genet, D-5300 Bonn, Germany. Univ Antwerp, Dept Med Genet, B-2020 Antwerp, Belgium. Cent Inst Mental Hlth, D-6800 Mannheim, Germany. RI McMahon, Francis/A-7290-2009; McInnis, Melvin/F-6963-2012; Schulze, Thomas/H-2157-2013; Cichon, Sven/H-8803-2013; Cichon, Sven/B-9618-2014 OI McInnis, Melvin/0000-0002-0375-6247; Cichon, Sven/0000-0002-9475-086X; Cichon, Sven/0000-0002-9475-086X NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O30 BP 723 EP 723 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400073 ER PT J AU Schalling, M Johansson, C Willeit, M Smedh, C Ekholm, J Paunio, T Lichtermann, D Praschak-Rieder, N Neumeister, A Nilsson, LG Kasper, S Peltonen, L Levitan, R Del Favero, J Masellis, M Basile, V Zill, P Bondy, B Van Broeckhoven, C Lam, R Adolfsson, R Partonen, T AF Schalling, M Johansson, C Willeit, M Smedh, C Ekholm, J Paunio, T Lichtermann, D Praschak-Rieder, N Neumeister, A Nilsson, LG Kasper, S Peltonen, L Levitan, R Del Favero, J Masellis, M Basile, V Zill, P Bondy, B Van Broeckhoven, C Lam, R Adolfsson, R Partonen, T TI Circadian clock related polymorphisms and the serotonin transporter promoter in seasonal affective disorder and seasonality SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Karolinska Hosp & Inst, Dept Mol Med, Neurogenet Unit, Stockholm, Sweden. Univ Vienna, Dept Gen Psychiat, A-1010 Vienna, Austria. Umea Univ, Dept Clin Sci, Div Psychiat, S-90187 Umea, Sweden. Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Bonn, Dept Psychiat, D-5300 Bonn, Germany. NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA. Univ Stockholm, Dept Psychol, S-10691 Stockholm, Sweden. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA USA. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. Univ Antwerp, Dept Biochem, B-2020 Antwerp, Belgium. Univ Munich, Dept Neurochem, Munich, Germany. Univ British Columbia, Dept Psychiat, Vancouver, BC, Canada. Natl Publ Hlth Inst, Dept Mental Hlth & Alcohol Res, Helsinki, Finland. RI Partonen, Timo/G-1105-2012; Schalling, Martin/F-1518-2015 OI Partonen, Timo/0000-0003-1951-2455; Schalling, Martin/0000-0001-5011-2922 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O41 BP 727 EP 728 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400084 ER PT J AU Hashimoto, R Matsumoto, M Shannon-Weickert, C Hyde, TM Kleinman, JE Weinberger, DR Straub, RE AF Hashimoto, R Matsumoto, M Shannon-Weickert, C Hyde, TM Kleinman, JE Weinberger, DR Straub, RE TI Expression analysis of the 6p22.3 gene dysbindin (DTNBP1), a positional candidate susceptibility gene for schizophrenia. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA. RI Matsumoto, Mitsuyuki/G-3207-2012; Hashimoto, Ryota/P-8572-2014 OI Matsumoto, Mitsuyuki/0000-0002-1172-2354; Hashimoto, Ryota/0000-0002-5941-4238 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O77 BP 741 EP 741 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400120 ER PT J AU Rotondo, A Rucci, P Gonnelli, C Bouanani, S Pardini, L Carlini, M Mazzanti, C Goldman, D Cassano, GB Dell'Osso, L AF Rotondo, A Rucci, P Gonnelli, C Bouanani, S Pardini, L Carlini, M Mazzanti, C Goldman, D Cassano, GB Dell'Osso, L TI Association of serotonin transporter and tryptophan hydroxylase genes with personality traits in self-harm behaviors SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Pisa, Dept Psychiat, I-56100 Pisa, Italy. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA O106 BP 752 EP 752 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400149 ER PT J AU Roca, CA Harlow, BL Davis, C Schmidt, PJ Goldman, D Rubinow, DR AF Roca, CA Harlow, BL Davis, C Schmidt, PJ Goldman, D Rubinow, DR TI Role of polymorphisms in the estrogen receptor alpha gene in premenstrual dysphoric disorder (PMDD) SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 NIMH, Behav Endocrinol Branch, Bethesda, MD 20892 USA. Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA. NIAAA, Neurogenet Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P46 BP 770 EP 770 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400197 ER PT J AU Toyota, T Yamada, K Yoshikawa, T Detera-Wadleigh, SD AF Toyota, T Yamada, K Yoshikawa, T Detera-Wadleigh, SD TI Family-based association analysis of AKT1 gene, a candidate gene of mood disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 RIKEN, Brain Sci Inst, Lab Mol Psychiat, Wako, Saitama 35101, Japan. Tokyo Med & Dent Univ, Dept Neuropsychiat, Tokyo, Japan. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P59 BP 775 EP 775 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400210 ER PT J AU Sommer, SS Feng, J Chen, J Yan, J Craddock, N Jones, I Cook, E Goldman, D Heston, LL AF Sommer, SS Feng, J Chen, J Yan, J Craddock, N Jones, I Cook, E Goldman, D Heston, LL TI Comprehensive mutation scanning of RAR/RXR and vitamin D receptor genes in patients with schizophrenia and other psychiatric diseases SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Univ Birmingham, Queen Elizabeth Psychiat Hosp, Div Neurosci, Birmingham, W Midlands, England. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. NIAAA, Dept Psychiat, NIH, Bethesda, MD 20892 USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RI Jones, Ian/B-4925-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P146 BP 807 EP 807 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400297 ER PT J AU Webb, BT Straub, RE Wormley, B York, TP Kendler, KS Riley, BP Neale, MC AF Webb, BT Straub, RE Wormley, B York, TP Kendler, KS Riley, BP Neale, MC TI No association between schizophrenia and a novel trinucleotide repeat polymorphism in ATP6B2 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Virginia Commonwealth Univ, Dept Human Genet, Richmond, VA USA. Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA. Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA. NIMH, Clin Brain Disorders Branch, IRP, NIH, Bethesda, MD 20892 USA. RI Neale, Michael/B-1418-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P150 BP 808 EP 809 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400301 ER PT J AU Hamshere, ML Hollingworth, P Holmans, P Wavrant-De Vrieze, F Myers, A Marshall, H Rice, F Jones, L O'Donovan, M Lovestone, S Goate, A Hardy, J Owen, MJ Williams, J AF Hamshere, ML Hollingworth, P Holmans, P Wavrant-De Vrieze, F Myers, A Marshall, H Rice, F Jones, L O'Donovan, M Lovestone, S Goate, A Hardy, J Owen, MJ Williams, J TI A genome screen to identify loci that modify the age-of-onset of Alzheimer's disease SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Univ Wales Coll Cardiff, Dept Psychol Med, Cardiff CF4 4XN, S Glam, Wales. MRC, Biostat Unit, Cambridge CB2 2BW, England. NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. Washington Univ, Dept Psychiat, St Louis, MO USA. Inst Psychiat, London, England. RI Lovestone, Simon/E-8725-2010; Myers, Amanda/B-1796-2010; Holmans, Peter/F-4518-2015 OI Myers, Amanda/0000-0002-3100-9396; Holmans, Peter/0000-0003-0870-9412 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P211 BP 831 EP 831 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400362 ER PT J AU Fanous, AH Straub, RE Neale, MC Webb, BT Walsh, D O'Neill, AF Kendler, KS AF Fanous, AH Straub, RE Neale, MC Webb, BT Walsh, D O'Neill, AF Kendler, KS TI A family-based association study of several candidate genes and clinical features of schizophrenia SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA. Virginia Commonwealth Univ, Dept Human Genet, Richmond, VA USA. Virginia Inst Psychiat & Behav Genet, Richmond, VA USA. NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA. Mater Hosp, Belfast, Antrim, North Ireland. St Lomans Hosp, Dublin, Ireland. RI Neale, Michael/B-1418-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P261 BP 848 EP 848 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400412 ER PT J AU Matsumoto, M Weinberger, DR Straub, RE AF Matsumoto, M Weinberger, DR Straub, RE TI Molecular cloning, sequencing, and characterization of a novel 500 kilobase gene (MRDS1) from 6p24, a schizophrenia candidate region SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA. RI Matsumoto, Mitsuyuki/G-3207-2012 OI Matsumoto, Mitsuyuki/0000-0002-1172-2354 NR 0 TC 2 Z9 2 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P288 BP 857 EP 858 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400439 ER PT J AU York, TP Sullivan, P Webb, BT Kendler, KS Riley, B Straub, RE Eaves, LJ AF York, TP Sullivan, P Webb, BT Kendler, KS Riley, B Straub, RE Eaves, LJ TI Multivariate adaptive regression spline (MARS) analysis of schizophrenia genotypes SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 Virginia Commonwealth Univ, Dept Human Genet, Richmond, VA USA. Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA. Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA. NIMH, Clin Brain Disorders Branch, IRP, NIH, Bethesda, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P347 BP 879 EP 879 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400498 ER PT J AU Bocklandt, S Hamer, DH AF Bocklandt, S Hamer, DH TI Genomic imprinting, X-inactivation and male sexual orientation SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract CT 10th World Congress of Psychiatric Genetics CY OCT 09-13, 2002 CL BRUSSELS, BELGIUM C1 NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 8 PY 2002 VL 114 IS 7 MA P363 BP 885 EP 886 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 600WH UT WOS:000178414400514 ER PT J AU Brosh, RM Driscoll, HC Dianov, GL Sommers, JA AF Brosh, RM Driscoll, HC Dianov, GL Sommers, JA TI Biochemical characterization of the WRN-FEN-1 functional interaction SO BIOCHEMISTRY LA English DT Article ID WERNER-SYNDROME PROTEIN; CELL NUCLEAR ANTIGEN; EUKARYOTIC DNA-REPLICATION; SINGLE-STRANDED-DNA; FLAP ENDONUCLEASE-1; SACCHAROMYCES-CEREVISIAE; SYNDROME GENE; HELICASE ACTIVITY; POLYMERASE-DELTA; EXCISION-REPAIR AB Werner Syndrome is a premature aging disorder characterized by chromosomal instability. Recently we reported a novel interaction of the WRN gene product with human 5' flap endonuclease/5'-3' exonuclease (FEN-1), a DNA structure-specific nuclease implicated in pathways of DNA metabolism that are important for genomic stability. To characterize the mechanism for WRN stimulation of FEN-1 cleavage, we have determined the effect of WRN on the kinetic parameters of the FEN-1 cleavage reaction. WRN enhanced the efficiency of FEN-1 cleavage rather than DNA substrate binding. WRN effectively stimulated FEN-1 cleavage on a flap DNA substrate with streptavidin bound to the terminal 3' nucleotide at the end of the upstream duplex, indicating that WRN does not require a free upstream end to stimulate FEN-1 cleavage of the 5' flap substrate. These results indicate that the mechanism whereby WRN stimulates FEN-1 cleavage is distinct from that proposed for the functional interaction between proliferating cell nuclear antigen and FEN-1. To understand the potential importance of the WRN-FEN-1(1) interaction in DNA replication, we have tested the effect of WRN on FEN-1 cleavage of several DNA substrate intermediates that may arise during Okazaki fragment processing. WRN stimulated FEN-1 cleavage of flap substrates with a terminal monoribonucleotide, a long 5' ssDNA tract, and a pseudo-Y structure. The ability of WRN to facilitate FEN-1 cleavage of DNA replication/repair intermediates may be important for the role of WRN in the maintenance of genomic stability. C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. MRC, Radiat & Genome Stabil Unit, Harwell OX11 0RD, Oxon, England. RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 74 TC 53 Z9 53 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 8 PY 2002 VL 41 IS 40 BP 12204 EP 12216 DI 10.1021/bi026031j PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601XF UT WOS:000178473600031 PM 12356323 ER PT J AU Mi, QW Cui, BL Silva, GL Lantvit, D Lim, E Chai, HY Hollingshead, MG Mayo, JG Kinghorn, AD Pezzuto, JM AF Mi, QW Cui, BL Silva, GL Lantvit, D Lim, E Chai, HY Hollingshead, MG Mayo, JG Kinghorn, AD Pezzuto, JM TI Pervilleines B and C, new tropane alkaloid aromatic esters that reverse the multidrug-resistance in the hollow fiber assay SO CANCER LETTERS LA English DT Article DE pervilleines B and C; multidrug-resistance; hollow fiber test; cancer chemotherapy; MDR1 gene; verapamil ID IN-VIVO REVERSAL; P-GLYCOPROTEIN; CYCLOSPORINE-A; P388 LEUKEMIA; TUMOR-MODEL; CELLS; TRANSPORTER; VINCRISTINE; VERAPAMIL; AGENTS AB P-Glycoprotein (Pgp)-mediated drug efflux can yield a multidrug-resistance phenotype that is associated with poor response to cancer chemotherapy. Pervilleines B and C (PB and PC), two new tropane alkaloid aromatic esters obtained from a chloroform extract of the roots of Erythroxylum pervillei as the result of bioactivity-guided fractionation, were found to restore the vinblastine (VLB) sensitivity of cultured multidrug-resistant KB-V1 cells, with 50% inhibitory concentration values of 0.17 muM in each case. To explore the potential relevance of this response, KB-V1 cells were placed in hollow fibers and implanted into NCr nu/nu mice. Cell growth was not significantly inhibited when VLB or PB or PC were administered as single agents, but when used in combination with vinblastine inhibition of up to 77.7% was observed. Equimolar doses of verapamil were less effective. These data suggest that PB and PC are effective inhibitors of Pgp and should be further evaluated for clinical utility. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Univ Illinois, Coll Pharm MC 877, Program Collaborat Res Pharmaceut Sci, Chicago, IL 60612 USA. Univ Illinois, Coll Pharm MC 781, Dept Med Chem & Pharmacognosy, Chicago, IL 60612 USA. NCI, Frederick Canc Res & Dev Ctr, Biol Testing Branch, Dev Therapeut Program,Div Canc Treatment & Diag, Frederick, MD 21701 USA. RP Pezzuto, JM (reprint author), Univ Illinois, Coll Pharm MC 877, Program Collaborat Res Pharmaceut Sci, 833 S Wood St, Chicago, IL 60612 USA. OI Silva, Gloria/0000-0002-0763-8096; Kinghorn, A. Douglas/0000-0002-6647-8707 NR 32 TC 23 Z9 24 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD OCT 8 PY 2002 VL 184 IS 1 BP 13 EP 20 AR PII S0304-3835(02)00202-1 DI 10.1016/S0304-3835(02)00202-1 PG 8 WC Oncology SC Oncology GA 595WB UT WOS:000178130600003 PM 12104043 ER PT J AU Doerge, DR Twaddle, NC Banks, EP Jefferson, WN Newbold, RR AF Doerge, DR Twaddle, NC Banks, EP Jefferson, WN Newbold, RR TI Pharmacokinetic analysis in serum of genistein administered subcutaneously to neonatal mice SO CANCER LETTERS LA English DT Article DE genistein; soy; pharmacokinetics; mass spectrometry; phytoestrogen; uterine cancer ID SPRAGUE-DAWLEY RATS; UDP-GLUCURONOSYLTRANSFERASE; UTERINE ADENOCARCINOMA; ISOFLAVONE GENISTEIN; HUMAN-LIVER; SOY; GLUCURONIDATION; ESTROGENS; DIETARY; MODEL AB Genistein, the principal soy isoflavone, was Previously shown to induce uterine adenocarcinomas by 18 months of age in female CD-1 mice following administration by subcutaneous injections on postnatal days 1-5. A serum pharmacokinetic analysis of genistein in male and female mice treated identically showed that: maximal concentrations of total (conjugated + aglycone) genistein in females (6.8 +/- 1.4 muM) and males (3.8 +/- 1.1 muM, mean +/- SD) were comparable to those previously reported from dietary exposures in adult rats or in human infants consuming soy formulas; the average fraction present as active aglycone (31%) was similar to those in fetal and neonatal rats from placental and lactational exposures; and elimination half-times were longer than those in rats (three- to seven-fold) and adult humans (two- to three-fold). These results are consistent with a diminished capacity for enzymatic conjugation of genistein, based on the ontogeny, as an important determinant of estrogenicity in neonatal mice. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA. NIEHS, Dev Endocrinol Sect, Mol Toxicol Lab, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA. RP Doerge, DR (reprint author), Natl Ctr Toxicol Res, Div Biochem Toxicol, 3900 NCTR Rd, Jefferson, AR 72079 USA. NR 23 TC 46 Z9 46 U1 0 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD OCT 8 PY 2002 VL 184 IS 1 BP 21 EP 27 AR PII S0304-3835(02)00200-8 DI 10.1016/S0304-3835(02)00200-8 PG 7 WC Oncology SC Oncology GA 595WB UT WOS:000178130600004 PM 12104044 ER PT J AU Akiyama, Y Maruyama, K Nara, N Hojo, T Cheng, JY Mori, T Wiltrout, RH Yamaguchi, K AF Akiyama, Y Maruyama, K Nara, N Hojo, T Cheng, JY Mori, T Wiltrout, RH Yamaguchi, K TI Antitumor effects induced by dendritic cell-based immunotherapy against established pancreatic cancer in hamsters SO CANCER LETTERS LA English DT Article DE hamster dendritic cell; DEC205; DC SIGN; hamster pancreatic cancer; cytotoxic T lymphocyte ID SURGICAL-TREATMENT; IMMUNE-RESPONSES; ANTIGEN-UPTAKE; VACCINATION; PEPTIDES; ADENOCARCINOMA; IDENTIFICATION; EXPERIENCE; MUTATIONS; CARCINOMA AB Because the prognosis of patients with pancreatic cancer is very poor, development of a novel approach for treatment of this disease is vital. In the present study, we investigated the effect of dendritic cell (DC)-based immunotherapy against established syngeneic hamster pancreatic cancer named HPD1NR. Hamster enriched DCs were prepared from bone marrow (BM) by a culture for 7 days in the presence of mouse GM-CSF and mouse IL-4, and characterized by the expression of specific DC markers (DEC205, DC-SIGN) mRNA using in situ hybridization (ISH). DCs pulsed with tumor lysate and N-[1-(2,3-dioleoyloxy)propyl]-N,N,N-trimethylammonium methylsulfate (DOTAP) or DCs alone were injected s.c. weekly into HPDINR-bearing hamsters three times. Tumor growth was significantly inhibited by 82% in hamsters treated with tumor lysate and DOTAP-pulsed DCs when compared with the PBS vehicle-treated group. These findings suggest that DC-based immunotherapy may be a useful approach for the treatment of pancreatic cancers. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Natl Canc Ctr, Res Inst, Div Growth Factor, Chuo Ku, Tokyo 1040045, Japan. Nara Med Univ, RI Ctr, Kashihara, Nara 6348521, Japan. NCI, Frederick Canc Res & Dev Ctr, Expt Therapeut Sect, Expt Immunol Lab, Frederick, MD 21702 USA. RP Akiyama, Y (reprint author), Natl Canc Ctr, Res Inst, Div Growth Factor, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan. NR 19 TC 11 Z9 13 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD OCT 8 PY 2002 VL 184 IS 1 BP 37 EP 47 AR PII S0304-3835(02)00189-1 DI 10.1016/S0304-3835(02)00189-1 PG 11 WC Oncology SC Oncology GA 595WB UT WOS:000178130600006 PM 12104046 ER PT J AU Raja, SN Haythornthwaite, JA Pappagallo, M Clark, MR Travison, TG Sabeen, S Royall, RM Max, MB AF Raja, SN Haythornthwaite, JA Pappagallo, M Clark, MR Travison, TG Sabeen, S Royall, RM Max, MB TI Opioids versus antidepressants in postherpetic neuralgia - A randomized, placebo-controlled trial SO NEUROLOGY LA English DT Article ID NEUROPATHIC PAIN; LIDOCAINE PATCH; HIP FRACTURE; DRUG-USE; AMITRIPTYLINE; MORPHINE; RESPONSIVENESS; NORTRIPTYLINE; CONSEQUENCES; GABAPENTIN AB Background: Tricyclic antidepressants (TCA) provide less than satisfactory pain relief for postherpetic neuralgia (PHN), and the role of opioids is controversial. Objective: To compare the analgesic and cognitive effects of opioids with those of TCA and placebo in the treatment of PHN. Methods: Seventy-six patients with PHN were randomized in a double-blind, placebo-controlled, crossover trial. Each subject was scheduled to undergo three treatment periods (opioid, TCA, and placebo), approximately 8 weeks' duration each. Doses were titrated to maximal relief or intolerable side effects. The primary outcome measures were pain intensity (0 to 10 scale), pain relief (0 to 100%), and cognitive function. Analyses included patients who provided any pain ratings after having received at least a single dose of a study medication. Results: Fifty patients completed two periods, and 44 patients completed all three. Mean daily maintenance doses were morphine 91 mg or methadone 15 mg and nortriptyline 89 mg or desipramine 63 mg. Opioids and TCA reduced pain (1.9 and 1.4) more than placebo (0.2; p < 0.001), with no appreciable effect on any cognitive measure. The trend favoring opioids over TCA fell short of significance (p = 0.06), and reduction in pain with opioids did not correlate with that following TCA. Treatment with opioids and TCA resulted in greater pain relief (38 and 32%) compared with placebo (11%; p < 0.001). More patients completing all three treatments preferred opioids (54%) than TCA (30%; p = 0.02). Conclusions: Opioids effectively treat PHN without impairing cognition. Opioids and TCA act via independent mechanisms and with varied individual effect. C1 Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA. NIDCD, Pain & Neurosensory Mechanisms Branch, NIH, Bethesda, MD USA. RP Raja, SN (reprint author), Johns Hopkins Univ Hosp, Osler 292,600 N Wolfe St, Baltimore, MD 21287 USA. OI Yang, Shuman/0000-0002-9638-0890 FU NCRR NIH HHS [RR0052]; NINDS NIH HHS [NS 32386] NR 40 TC 305 Z9 318 U1 3 U2 14 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD OCT 8 PY 2002 VL 59 IS 7 BP 1015 EP 1021 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 601HP UT WOS:000178440600010 PM 12370455 ER PT J AU Leon-Sarmiento, FE Prada, LJ Torres-Hillera, M AF Leon-Sarmiento, FE Prada, LJ Torres-Hillera, M TI The first sign of Babinski SO NEUROLOGY LA English DT Editorial Material C1 NINDS, Brain Stimulat Unit, NIH, Bethesda, MD 20892 USA. RP Leon-Sarmiento, FE (reprint author), NINDS, Brain Stimulat Unit, NIH, 10 Ctr Dr,Bldg 10-5N234, Bethesda, MD 20892 USA. NR 1 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD OCT 8 PY 2002 VL 59 IS 7 BP 1067 EP 1067 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 601HP UT WOS:000178440600018 PM 12370463 ER PT J AU Wei, CQ Li, BH Guo, RB Yang, DJ Burke, TR AF Wei, CQ Li, BH Guo, RB Yang, DJ Burke, TR TI Development of a phosphatase-stable phosphotyrosyl mimetic suitably protected for the synthesis of high-affinity Grb2 SH2 domain-binding ligands SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID INHIBITORS; DESIGN AB Synthesis of (2R)-2-carboxymethyl-3-(4-(phosphonomethyl)phenyl) proprionic acid (5) in tert-butyl-protected form (6) and its use for the preparation of a Grb2 SH2 domain-directed tripeptide (8a) is reported. In extracellular ELISA-based assays, 8a exhibits potent Grb2 SH2 domain binding affinity (IC50=8 nM). Against cultures of MDA-MB-453 breast cancer cells, which overexpress erbB-2 tyrosine kinase, 8a is also antimitogenic at concentrations equivalent to those required to inhibit intracellular association of Grb2 protein with phosphorylated p185(erbB-2) protein (IC50=8 muM). Analogue 6 may be useful for the preparation of a variety of phosphatase-stable SH2 domain-directed ligands. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 NCI Frederick, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA. Georgetown Univ, Med Ctr, Lombardi Canc Ctr, Washington, DC 20007 USA. RP Burke, TR (reprint author), NCI Frederick, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA. RI Burke, Terrence/N-2601-2014 NR 16 TC 27 Z9 27 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD OCT 7 PY 2002 VL 12 IS 19 BP 2781 EP 2784 AR PII S0960-894X(02)00527-9 DI 10.1016/S0960-894X(02)00527-9 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA 595NM UT WOS:000178115700026 PM 12217375 ER PT J AU Robles, AI Linke, SP Harris, CC AF Robles, AI Linke, SP Harris, CC TI The p53 network in lung carcinogenesis SO ONCOGENE LA English DT Review DE p73; p14(ARF); mutational spectrum; mutational hotspots; tobacco smoke ID INTRACHROMOSOMAL HOMOLOGOUS RECOMBINATION; POLYCYCLIC AROMATIC-HYDROCARBONS; CANCER MUTATIONAL HOTSPOTS; TUMOR-SUPPRESSOR P53; KINASE C-ABL; DNA-DAMAGE; P53-MEDIATED APOPTOSIS; MAMMALIAN-CELLS; TRANSCRIPTIONAL TARGET; FUNCTIONAL INTERACTION AB The p53 tumor suppressor gene lies at the crossroads of multiple cellular response pathways that control a cell's fate in response to endogenous or exogenous stresses. Positive and negative regulatory loops both upstream and downstream of p53 cooperate to finely tune its functions as a transcription factor, a DNA damage sensor, and possibly, a protein-assembly scaffold. Through this plethora of activities, p53 is a major determinant of cell survival and a safeguard against genetic instability. Functional inactivation of p53 pathways through genetic and epigenetic events affecting the p53 gene itself and/or its interacting partners occur with a high frequency in lung cancer. The p53 mutational spectrum provides molecular evidence of the etiology of lung cancer and supports abundant epidemiological data indicating the role of tobacco smoke in the causation of this disease. C1 NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. RP Harris, CC (reprint author), 37 Convent Dr,Bldg 37,Room 2C05, Bethesda, MD 20892 USA. NR 119 TC 96 Z9 98 U1 0 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 7 PY 2002 VL 21 IS 45 BP 6898 EP 6907 DI 10.1038/sj.onc.1205563 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 604UV UT WOS:000178640200005 PM 12362272 ER PT J AU Kaye, FJ AF Kaye, FJ TI RB and cyclin dependent kinase pathways: defining a distinction between RB and p16 loss in lung cancer SO ONCOGENE LA English DT Article DE retinoblastoma; cyclin dependent kinase; pl6INK4; p27Kipl; lung cancer; neuroendocrine ID RETINOBLASTOMA SUSCEPTIBILITY GENE; SMALL-CELL CARCINOMA; LARGE T-ANTIGEN; TUMOR-SUPPRESSOR PROTEIN; RAS ONCOGENE MUTATIONS; N-MYC GENE; P16(INK4) PROTEIN; IN-VIVO; EXPRESSION; LINES AB The genetic components of the RB:CDK:cyclin:p16 tumor suppressor pathway undergo mutational and epigenetic alterations in a wide range of human cancers and serve as critical targets for inactivation by the transforming oncoproteins of several DNA tumor viruses. Lung cancer has been a useful model system for these studies as it was the first tumor to demonstrate an important role for RB in the genesis of a common adult malignancy and was also the first human cancer to demonstrate genetic evidence for a multi-component RB:p16 tumor suppressor pathway. Lung tumorigenesis, however, is a complex disease process that requires longstanding carcinogen exposure in order to acquire somatic alterations at many distinct genetic loci. Understanding the multifunctional properties of RB to regulate cell proliferation, differentiation, and apoptosis and how they relate to the sequential accumulation of other clonal gene defects will be essential in order to understand the specific patterns of gene inactivation observed in different subtypes of lung cancer and to fulfill the promise of 'molecular target' therapeutics. C1 Natl Naval Med Res Inst, NCI Navy Oncol, Bethesda, MD 20889 USA. NCI, Genet Branch, Canc Res Ctr, NIH, Bethesda, MD 20889 USA. RP Kaye, FJ (reprint author), Natl Naval Med Res Inst, NCI Navy Oncol, Bldg 8,Room 5101, Bethesda, MD 20889 USA. EM fkaye@helix.nih.gov RI kaye, frederic/E-2437-2011 NR 90 TC 84 Z9 89 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 OCT 7 PY 2002 VL 21 IS 45 BP 6908 EP 6914 DI 10.1038/sj.onc.1205834 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 604UV UT WOS:000178640200006 PM 12362273 ER PT J AU Zabarovsky, ER Lerman, MI Minna, JD AF Zabarovsky, ER Lerman, MI Minna, JD TI Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers SO ONCOGENE LA English DT Review DE lung cancer; tumor supressor gene; human chromosome 3; deletion mapping; preneoplasia; gene therapy ID RENAL-CELL CARCINOMA; JAAGSIEKTE SHEEP RETROVIRUS; 3P21.3 HOMOZYGOUS DELETION; ARGININE-RICH PROTEIN; FHIT-DEFICIENT MICE; ABERRANT PROMOTER METHYLATION; EPITHELIAL OVARIAN-TUMORS; ACID RECEPTOR BETA-2; SHORT ARM; BREAST-CANCER AB Loss of heterozygosity (LOH) involving several chromosome 3p regions accompanied by chromosome 3p deletions are detected in almost 100% of small (SCLCs) and more than 90% of non-small (NSCLCs) cell lung cancers. In addition, these changes appear early in the pathogenesis of lung cancer and are found as clonal lesions in the smoking damaged respiratory epithelium including histologically normal epithelium as well as in epithelium showing histologic changes of preneoplasia. These 3p genetic alterations lead to the conclusion that the short arm of human chromosome 3 contains several tumor suppressor gene(s) (TSG(s)). Although the first data suggesting that 3p alterations were involved in lung carcinogenesis were published more than 10 years ago, only recently has significant progress been achieved in identifying the candidate TSGs and beginning to demonstrate their functional role in tumor pathogenesis. Some of the striking results of these findings has been the discovery of multiple 3p TSGs and the importance of tumor acquired promoter DNA methylation as an epigenetic mechanism for inactivating the expression of these genes in lung cancer. This progress, combined with the well known role of smoking as an environmental causative risk factor in lung cancer pathogenesis, is leading to the development of new diagnostic and therapeutic strategies which can be translated into the clinic to combat and prevent the lung cancer epidemic. It is clear now that genetic and epigenetic abnormalities of several genes residing in chromosome region 3p are important for the development of lung cancers but it is still obscure how many of them exist and which of the numerous candidate TSGs are the key players in lung cancer pathogenesis. We review herein our current knowledge and describe the most credible candidate genes. C1 Karolinska Inst, Ctr Microbiol & Tumor Biol, S-17177 Stockholm, Sweden. Karolinska Inst, Ctr Genomics & Bioinformat, S-17177 Stockholm, Sweden. NCI, Immunobiol Lab, Ctr Canc Res, Frederick, MD 21702 USA. Univ Texas, SW Med Ctr, Hamon Ctr Therapeut Oncol Res, Dallas, TX 75390 USA. RP Zabarovsky, ER (reprint author), Karolinska Inst, MTC, Box 280, S-17177 Stockholm, Sweden. RI Zabarovsky, Eugene/A-6645-2010 FU NCI NIH HHS [CA71618, P50 CA70907] NR 198 TC 244 Z9 272 U1 2 U2 14 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 7 PY 2002 VL 21 IS 45 BP 6915 EP 6935 DI 10.1038/sj.onc.1205835 PG 21 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 604UV UT WOS:000178640200007 PM 12362274 ER PT J AU Rappaport, SM Yeowell-O'Connell, K Smith, MT Dosemeci, M Hayes, RB Zhang, LP Li, GL Yin, SN Rothman, N AF Rappaport, SM Yeowell-O'Connell, K Smith, MT Dosemeci, M Hayes, RB Zhang, LP Li, GL Yin, SN Rothman, N TI Non-linear production of benzene oxide-albumin adducts with human exposure to benzene SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES LA English DT Article DE benzene oxide; albumin; benzene ID HUMAN LIVER-MICROSOMES; BIOLOGICAL MARKERS; HEMOGLOBIN; METABOLISM; 1,4-BENZOQUINONE; TOXICOKINETICS; IDENTIFICATION; PHENOL; BLOOD; MOUSE AB Benzene is initially metabolized to benzene oxide, which either undergoes further metabolism or reacts with macromolecules including proteins. Previously reported levels of benzene oxide-albumin adducts (BO-Alb) are analyzed from 30 workers exposed to 0.2-302 ppm benzene and 43 controls from Shanghai, China. Although both exposed workers and controls had significant levels of BO-Alb in their blood, exposed subjects' adduct levels (GM=378 pmol/g protein) were much greater than those of controls (GM=115 pmol/g protein). When the natural logarithm of the BO-Alb level was regressed upon the natural logarithm of exposure among the 30 exposed subjects, a strong effect of benzene exposure was observed (R-2=0.612; p<0.0001). Because the slope of the relationship between BO-Alb and benzene exposure was significantly less than one in log-space, we infer that production of benzene oxide was less than proportional to benzene exposure. Since benzene is a substrate for CYP2E1, these results are consistent with saturation of CYP450 metabolism. They indicate that deviations from linear metabolism began at or below benzene exposures of 10 ppm and that pronounced saturation was apparent at 40-50 ppm. To our knowledge, this is the first study to investigate the linearity of human metabolism of a carcinogen based upon protein adducts. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ N Carolina, Sch Publ Hlth, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. Chinese Acad Prevent Med, Inst Occupat Med, Beijing 100050, Peoples R China. RP Rappaport, SM (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Environm Sci & Engn, CB 7400, Chapel Hill, NC 27599 USA. FU NIEHS NIH HHS [P42ES05948, P42ES04705] NR 26 TC 23 Z9 24 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1570-0232 J9 J CHROMATOGR B JI J. Chromatogr. B PD OCT 5 PY 2002 VL 778 IS 1-2 BP 367 EP 374 AR PII S0378-4347(01)00457-1 DI 10.1016/S0378-4347(01)00457-1 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 609ZP UT WOS:000178936500029 PM 12376141 ER PT J AU Bar-Noy, S Moskovitz, J AF Bar-Noy, S Moskovitz, J TI Mouse methionine sulfoxide reductase B: effect of selenocysteine incorporation on its activity and expression of the seleno-containing enzyme in bacterial and mammalian cells SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE methionine sulfoxide reductase; selenoproteins; methionine oxidation; methionine sulfoxide; selenocysteine ID ESCHERICHIA-COLI; THIOREDOXIN REDUCTASE; CATALYTIC ACTIVITY; OXIDATIVE DAMAGE; GENE; OVEREXPRESSION; IDENTIFICATION; PROTEIN; CLONING; SECIS AB The mammalian methionine sulfoxide reductase B (MsrB) has been found to be a selenoprotein which can reduce R form of both free and protein-incorporated methionine sulfoxide to methionine. Together with MsrA, which reduces specifically the S form of methionine sulfoxide, the living cell can repair methionine-dam aged proteins and salvage free methionine under oxidative stress conditions. Here, we report about the pivotal role of the selenocysteine residue in the protein putative active site by site-directed mutagenesis directed to the selenocysteine codon. Using the Escherichia coli SECIS (selenocysteine insertion sequence) element, needed for the recognition of the UGA codon as a selenocysteine codon in E. coli, we expressed the seleno-MsrB as a recombinant selenoprotein in E. coli. The recombinant seleno-MsrB has been shown to be much more active than the cysteine mutant, whereas the mutations to alanine and serine rendered the protein inactive. Although the yields of expression of the full-length N-terminus and C-terminus His-tagged seleno-MsrB were only 3% (of the total MsrB expressed), the C-terminus His-tagged protein enabled us to get a pure preparation of the seleno-MsrB. Using both recombinant selenoproteins, the N-terminus His-tagged and the C-terminus His-tagged proteins, we were able to determine the specific activities of the recombinant seleno-MsrB, which were found to be much higher than the cysteine mutant homologue. This finding confirmed our suggestion that the selenocysteine is essential for maintaining high reducing activity of MsrB. In addition, using radioactive selenium we were able to determine the in vivo presence of MsrB as a selenoprotein in mammalian cell cultures. (C) 2002 Elsevier Science (USA). All rights reserved. C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Moskovitz, J (reprint author), NHLBI, Biochem Lab, NIH, Bldg 3, Bethesda, MD 20892 USA. NR 24 TC 39 Z9 42 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 4 PY 2002 VL 297 IS 4 BP 956 EP 961 AR PII S0006-291X(02)02314-8 DI 10.1016/S0006-291X(02)02314-8 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 603PY UT WOS:000178569700039 PM 12359247 ER PT J AU Neufeld, EB Demosky, SJ Stonik, JA Combs, C Remaley, AT Duverger, N Santamarina-Fojo, S Brewer, HB AF Neufeld, EB Demosky, SJ Stonik, JA Combs, C Remaley, AT Duverger, N Santamarina-Fojo, S Brewer, HB TI The ABCA1 transporter functions on the basolateral surface of hepatocytes SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE ABCA1; ABC transporters; GFP; apoA-1 ID BINDING CASSETTE TRANSPORTER-1; TANGIER-DISEASE; TRANSGENIC MICE; CHOLESTEROL; GENE; MUTATIONS; TRAFFICKING AB ABCA1 on the cell surface and in endosomes plays an essential role in the cell-mediated lipidation of apoA-1 to form nascent HDL. Our previous studies of transgenic mice overexpressing ABCA1 suggested that ABCA1 in the liver plays a major role in regulating plasma HDL levels. The site of function of ABCA1 in the polarized hepatocyte was currently assessed by expression of an adenoviral construct encoding a human ABCA1-GFP fusion protein in the polarized hepatocyte-like WIF-B cell line. Consistent with localization of ABCA1 at the basolateral (vascular) cell surface, expression of ABCA1-GFP stimulated apoA-1 mediated efflux of WIF-B cell cholesterol into the culture medium. Confocal fluorescence microscopy revealed that ABCA1-GFP was expressed solely on the basolateral surface and associated endocytic vesicles. These findings suggest an important role for hepatocyte basolateral membrane ABCA1 in the regulation of the levels of intracellular hepatic cholesterol, as well as plasma HDL. (C) 2002 Elsevier Science (USA). All rights reserved. C1 NHLBI, Mol Dis Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA. Aventis Pharma, F-94403 Vitry Sur Seine, France. RP Neufeld, EB (reprint author), NHLBI, Mol Dis Branch, NIH, 10-7N115,10 Ctr Dr, Bethesda, MD 20892 USA. NR 24 TC 52 Z9 53 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 4 PY 2002 VL 297 IS 4 BP 974 EP 979 AR PII S0006-291X(02)02274-X DI 10.1016/S0006-291X(02)02274-X PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 603PY UT WOS:000178569700042 PM 12359250 ER PT J AU Trievel, RC Beach, BM Dirk, LMA Houtz, RL Hurley, JH AF Trievel, RC Beach, BM Dirk, LMA Houtz, RL Hurley, JH TI Structure and catalytic mechanism of a SET domain protein methyltransferase SO CELL LA English DT Article ID RIBULOSE-1,5-BISPHOSPHATE CARBOXYLASE OXYGENASE; MULTIPLE ISOMORPHOUS REPLACEMENT; N-EPSILON-METHYLTRANSFERASE; HISTONE H3 METHYLATION; ARGININE METHYLTRANSFERASE; PARTIAL-PURIFICATION; NEUROSPORA-CRASSA; CRYSTAL-STRUCTURE; LYSINE 9; EXPRESSION AB Protein lysine methylation by SET domain enzymes regulates chromatin structure, gene silencing, transcriptional activation, plant metabolism, and other processes. The 2.6 Angstrom resolution structure of Rubisco large subunit methyltransferase in a pseudo-bisubstrate complex with S-adenosylhomocysteine and a HEPES ion reveals an all-beta architecture for the SET domain embedded within a larger alpha-helical enzyme fold. Conserved regions of the SET domain bind S-adenosylmethionine and substrate lysine at two sites connected by a pore. We propose that methyl transfer is catalyzed by a conserved Tyr at a narrow pore connecting the sites. The cofactor enters by a "back door" on the opposite side of the enzyme from substrate, promoting highly specific protein recognition and allowing addition of multiple methyl groups. C1 NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Kentucky, Dept Hort, Plant Physiol Biochem Mol Biol Program, Lexington, KY 40546 USA. RP Hurley, JH (reprint author), NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NR 60 TC 152 Z9 159 U1 1 U2 15 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0092-8674 J9 CELL JI Cell PD OCT 4 PY 2002 VL 111 IS 1 BP 91 EP 103 DI 10.1016/S0092-8674(02)01000-0 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 601RQ UT WOS:000178461900011 PM 12372303 ER PT J AU Berkin, A Coxon, B Pozsgay, V AF Berkin, A Coxon, B Pozsgay, V TI Towards a synthetic glycoconjugate vaccine against Neisseria meningitidis A SO CHEMISTRY-A EUROPEAN JOURNAL LA English DT Article DE Diels-Alder reaction; glycoconjugates; immunology; Neisseria meningitidis; vaccines ID GROUP-A; POLYSACCHARIDE; CONJUGATE; CHILDREN; FRAGMENT; UNITS; MICE AB Albumin conjugates of synthetic fragments of the capsular polysaccharide of the Gram-negative bacterium Neisseria meningitidis serogroup A were prepared. The fragments include monosaccharides 1 [alpha-D-ManpNAc(1--> 0)-(CH2)(2)NH2] and 2 [6-O-P(O)-(O-)(2)-alpha-D-ManpNAc-(1 --> O)-(CH2)(2)NH2] ,disaccharide 3 [alpha-D-ManpNAc[1-->O-P(O)(O-) --> 6]-alpha-D-ManpNAc(1 --> O)-(CH2)(2)NH2], and trisaccharide 4 [alpha-D-ManpNAc-[1 -->O-P(O)(O-)--> 6]-alpha-D-ManpNAc-[1 -->O-P(O)(O-)--> 6]-alpha-D-ManpNAc-(1 --> O)-(CH2)(2)NH2]. Two monosaccharide blocks were employed as key intermediates. The reduc-ing-end mannose unit featured the NHAc group at C-2, and contained the aminoethyl spacer as the aglycon for the final bioconjugation. The interresidual phosphodiester linkages were fashioned from an anomerically positioned H-phosphonate group in a 2-azido-man-nose building block. The spacer-linked saccharides 1-4 were N-acylated with hepta-4,6-dienoic acid and the resulting conjugated diene-equipped saccharides were subjected to Diels-Alder-type addition with maleimidobutyryl-group functionalized human serum albumin to form covalent conjugates containing up to 26 saccharide haptens per albumin molecule. Complete H-1, C-13, and P-31 NMR assignments for 1-4 are given. Antigenicity of the neoglycoconjugates containing 1-4 was demonstrated by a double immunodiffusion assay which indicated that a fragment as small as a monosaccharide is recognized by a polyclonal meningococcus group A antiserum and that the O-acetyl group(s) present in the natural capsular material is not essential for antigenicity. C1 NICHHD, Dev & Mol Immun Lab, NIH, Bethesda, MD 20892 USA. RP Pozsgay, V (reprint author), NICHHD, Dev & Mol Immun Lab, NIH, 6 Ctr Dr,MSC 2720, Bethesda, MD 20892 USA. NR 25 TC 27 Z9 27 U1 0 U2 11 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0947-6539 J9 CHEM-EUR J JI Chem.-Eur. J. PD OCT 4 PY 2002 VL 8 IS 19 BP 4424 EP 4433 DI 10.1002/1521-3765(20021004)8:19<4424::AID-CHEM4424>3.0.CO;2-1 PG 10 WC Chemistry, Multidisciplinary SC Chemistry GA 603CV UT WOS:000178542000009 PM 12355530 ER PT J AU Patino, WD Mian, OY Hwang, PM AF Patino, WD Mian, OY Hwang, PM TI Serial analysis of gene expression - Technical considerations and applications to cardiovascular biology SO CIRCULATION RESEARCH LA English DT Review DE expression; gene; cardiovascular ID SAGE; IDENTIFICATION; CANCER; APOPTOSIS; GENOME; CELLS; TRANSCRIPTOMES; PROFILES; CDNAS AB It has been 7 years since serial analysis of gene expression (SAGE) and microarray hybridization techniques were simultaneously introduced to allow the screening of thousands of expressed genes. Both techniques have stood up to the test of time as evidenced by their widespread use, and both have been used for studying cardiovascular diseases. SAGE has been used more extensively to study cancer cells, but it has also been used to examine gene expression in systems as divergent as rice seedlings, yeast, and Caenorhabditis elegans. In this review, a summary of the advances in SAGE technology and its unique attributes and potential applications to the cardiovascular system will be presented. C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. RP Hwang, PM (reprint author), NHLBI, Cardiovasc Branch, NIH, Bldg 10,Rm 7B15,10 Ctr Dr, Bethesda, MD 20892 USA. EM hwangp@nhlbi.nih.gov OI Mian, Omar/0000-0002-8133-8120 NR 42 TC 35 Z9 38 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7330 J9 CIRC RES JI Circ.Res. PD OCT 4 PY 2002 VL 91 IS 7 BP 565 EP 569 DI 10.1161/01.RES.0000036018.76903.18 PG 5 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA 604HF UT WOS:000178610800004 PM 12364383 ER PT J AU Deem, S Kim, JU Manjula, BN Acharya, AS Kerr, ME Patel, RP Gladwin, MT Swenson, ER AF Deem, S Kim, JU Manjula, BN Acharya, AS Kerr, ME Patel, RP Gladwin, MT Swenson, ER TI Effects of S-nitrosation and cross-linking of hemoglobin on hypoxic pulmonary vasoconstriction in isolated rat lungs SO CIRCULATION RESEARCH LA English DT Article DE hemoglobin; nitric oxide; hypoxic pulmonary vasoconstriction; S-nitrosohemoglobin ID EXHALED NITRIC-OXIDE; PERFUSED RABBIT LUNGS; OXYGEN-BINDING; BIOCHEMICAL-CHARACTERIZATION; VASCULAR REACTIVITY; BIOLOGICAL-ACTIVITY; NITROSOHEMOGLOBIN; NO; INHIBITION; RELEASE AB Free hemoglobin (Hb) and red blood cells augment hypoxic pulmonary vasoconstriction (HPV) by scavenging nitric oxide (NO). S-nitrosation of Hb (SNO-Hb) may confer vasodilatory properties by allowing release of NO during deoxygenation and/or by interaction with small-molecular weight thiols. Likewise, cross-linking of free Hb may limit its vasoconstrictive effect by preventing abluminal movement of the molecule. We compared the effects of free SNO-Hb and Hb intramolecularly cross-linked at the beta-cysteine 93 residue [Bis(maleidophenyl)-polyethylene glycol2000HbA (Bis-Mal-PEGHb)] to those of free oxyHb on pulmonary artery pressure (PAP), HPV, and exhaled NO (eNO) in isolated, perfused rat lungs. Ventilation of lungs with anoxic gas for 5 minutes reduced perfusate Po-2 to 11 +/- 1.0 Torr. Addition of SNO-Hb or Bis-Mal-PEPHb (100 mumol/L) to buffer perfusate increased normoxic PAP and augmented HPV in similar magnitude as free oxyHb, but had no effect on eNO. Addition of the allosteric modulator inositol hexaphosphate to increase Hb P50 and the thiol glutathione (GSH) to allow removal of NO from Hb via transnitrosation to the perfusate did not reduce augmentation of HPV by SNO-Hb or increase eNO. GSH resulted in an approximate to50% reduction in perfusate [S-nitrosothiol], in association with an increase in perfusate [metHb]. Free SNO-Hb is a net NO scavenger and pulmonary vasoconstrictor in this model, although thiol-mediated release of NO from SNO-Hb does occur. However, release of NO from SNO-Hb was not influenced by deoxygenation-mediated allosteric changes in Hb across a broad range of oxyHb saturation. Cross-linking of Hb does not limit its pulmonary vasoconstrictor effects. C1 Univ Washington, Harborview Med Ctr, Dept Anesthesiol, Seattle, WA 98104 USA. Univ Washington, Dept Med Pulm & Crit Care, Seattle, WA 98104 USA. Vet Affairs Puget Sound Hlth Care Ctr, Seattle, WA USA. Univ Ulsan, Dept Anesthesiol, Coll Med, Asan Med Ctr, Seoul, South Korea. Albert Einstein Coll Med, Dept Physiol & Biophys, Bronx, NY 10467 USA. Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA. NIH, Warren G Magnuson Clin Ctr, Dept Crit Care Med, Bethesda, MD 20892 USA. RP Deem, S (reprint author), Univ Washington, Harborview Med Ctr, Dept Anesthesiol, Box 359724, Seattle, WA 98104 USA. OI Patel, Rakesh/0000-0002-1526-4303 FU NHLBI NIH HHS [HL03796-01, HL45571] NR 44 TC 30 Z9 31 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7330 J9 CIRC RES JI Circ.Res. PD OCT 4 PY 2002 VL 91 IS 7 BP 626 EP 632 DI 10.1161/01.RES.0000036268.47509.02 PG 7 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA 604HF UT WOS:000178610800012 PM 12364391 ER PT J AU Paolini, R Molfetta, R Beitz, LO Zhang, J Scharenberg, AM Piccoli, M Frati, L Siraganian, R Santoni, A AF Paolini, R Molfetta, R Beitz, LO Zhang, J Scharenberg, AM Piccoli, M Frati, L Siraganian, R Santoni, A TI Activation of Syk tyrosine kinase is required for c-Cbl-mediated ubiquitination of Fc epsilon RI and Syk in RBL cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR SIGNAL-TRANSDUCTION; NATURAL-KILLER-CELLS; HUMAN NK CELLS; ANTIGEN RECEPTOR; HIGH-AFFINITY; NEGATIVE REGULATOR; IMMUNOGLOBULIN-E; BETA-SUBUNIT; ZETA-CHAIN; LIGASE ACTIVITY AB Engagement of the high affinity receptor for IgE (FcepsilonRI) on mast cells and basophils results in FcepsilonRI beta and gamma subunits ubiquitination by an as yet undefined mechanism. Here we show that, upon FcepsilonRI engagement on RBL-2H3 cells Syk undergoes ubiquitination and Syk kinase activity is required for its own ubiquitination and that of FcepsilonRI beta and gamma chains. This requirement was demonstrated by overexpression of Syk wild-type or its kinase-dead mutant in RBL cells or using an Syk-deficient RBL-derived cell line transfected with wild-type or a kinase inactive form of Syk. We also identify c-Cbl as the E3 ligase responsible for both Syk and receptor ubiquitination. Furthermore, we demonstrate that Syk controls tyrosine phosphorylation of Syk-associated Cbl induced after receptor engagement. These data suggest a mutual regulation between Syk and Cbl activities. Finally, we show that a selective inhibitor of proteasome degradation induces persistence of tyrosine-phosphorylated receptor complexes, of activated Syk, and of FcepsilonRI-triggered degranulation. Our results provide a molecular mechanism for down-regulation of engaged receptor complexes by targeting ubiquitinated FcepsilonRI and activated Syk to the proteasome for degradation. C1 Univ Roma La Sapienza, Dept Expt Med & Pathol, Inst Pasteur, Fdn Cenci Bolognetti, I-00161 Rome, Italy. Univ Washington, Dept Pediat Rheumatol, Seattle, WA 98195 USA. Univ Washington, Dept Immunol, Seattle, WA 98195 USA. NIDCR, Receptors & Signal Transduct Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. Mediterranean Inst Neurosci Neuromed, I-86077 Pozzilli, IS, Italy. RP Paolini, R (reprint author), Univ Roma La Sapienza, Dept Expt Med & Pathol, Inst Pasteur, Fdn Cenci Bolognetti, Viale Regina Elena 324, I-00161 Rome, Italy. RI Molfetta, Rosa/N-4529-2015; santoni, angela/K-8997-2016 OI Molfetta, Rosa/0000-0003-2904-6371; santoni, angela/0000-0003-1206-7731 NR 54 TC 63 Z9 64 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 4 PY 2002 VL 277 IS 40 BP 36940 EP 36947 DI 10.1074/jbc.M204948200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100006 PM 12145291 ER PT J AU Chariot, A Leonardi, A Muller, J Bonif, M Brown, K Siebenlist, U AF Chariot, A Leonardi, A Muller, J Bonif, M Brown, K Siebenlist, U TI Association of the adaptor TANK with the I kappa B kinase (IKK) regulator NEMO connects IKK complexes with IKK epsilon and TBK1 kinases SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR-ASSOCIATED FACTOR-2; SEVERE LIVER DEGENERATION; EMBRYONIC LETHALITY; DEFICIENT MICE; TAX PROTEIN; T-CELLS; ACTIVATION; ALPHA; PHOSPHORYLATION; SUBUNIT AB Canonical activation of NF-kappaB is mediated via phosphorylation of the inhibitory IkappaB proteins by the IkappaB kinase complex (IKK). IKK is composed of a heterodimer of the catalytic IKKalpha and IKKbeta subunits and a presumed regulatory protein termed NEMO (NF-kappaB essential modulator) or IKKgamma. NEMO/IKKgamma is indispensable for activation of the IKKs in response to many signals, but its mechanism of action remains unclear. Here we identify TANK (TRAF family member-associated NF-kappaB activator) as a NEMO/IKKgamma-interacting protein via yeast two-hybrid analyses. This interaction is confirmed in mammalian cells, and the domains required are mapped. TANK was previously shown to assist NF-kappaB activation in a complex with TANK-binding kinase 1 (TBK1) or IKKepsilon, two kinases distantly related to IKKalpha/beta, but the underlying mechanisms remained unknown. Here we show that TBK1 and IKKepsilon synergize with TANK to promote interaction with the IKKs. The TANK binding domain within NEMO/IKKgamma is required for proper functioning of this IKK subunit. These results indicate that TANK can synergize with IKKepsilon or TBK1 to link them to IKK complexes, where the two kinases may modulate aspects of NF-kappaB activation. C1 NIAID, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA. CHU Sart Tilman, Med Chem Lab, Ctr Cellular & Mol Therapy Pathol, B-4000 Liege, Belgium. RP Siebenlist, U (reprint author), NIAID, Lab Immunoregulat, NIH, Bldg 10,Rm 11B16, Bethesda, MD 20892 USA. NR 41 TC 111 Z9 126 U1 0 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 4 PY 2002 VL 277 IS 40 BP 37029 EP 37036 DI 10.1074/jbc.M205069200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100018 PM 12133833 ER PT J AU Shimizu, K Hashimoto, K Kirchner, JM Nakai, W Nishikawa, H Resnick, MA Sugino, A AF Shimizu, K Hashimoto, K Kirchner, JM Nakai, W Nishikawa, H Resnick, MA Sugino, A TI Fidelity of DNA polymerase epsilon holoenzyme from budding yeast Saccharomyces cerevisiae SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL NUCLEAR ANTIGEN; 5' EXONUCLEASE ACTIVITY; SCHIZOSACCHAROMYCES-POMBE; CATALYTIC DOMAINS; REPLICATION FORK; CHROMOSOMAL DNA; S-PHASE; DELTA; SUBUNIT; GENE AB DNA polymerases delta and epsilon (pol delta and epsilon) are the major replicative polymerases and possess 3'-5' proofreading exonuclease activities that correct errors arising during DNA replication in the yeast Saccharomyces cerevisiae. This study measures the fidelity of the holoenzyme of wild-type pol epsilon, the 3'-5' exonuclease-deficient pol2-4, a +1 frameshift mutator for homonucleotide runs, pol2C1089Y, and pol2C1089Y pol2-4 enzymes using a synthetic 30-mer primer/100-mer template. The nucleotide substitution rate for wild-type pol epsilon was 0.47 x 10(-5) for G:G mismatches, 0.15 x 10(-5) for T:G mismatches, and less than 0.01 x 10(-5) for A:G mismatches. The accuracy for A opposite G was not altered in the exonuclease-deficient pol2-4 pol epsilon; however, G:G and T:G misincorporation rates increased 40- and 73-fold, respectively. The pol2C1089Y pol c mutant also exhibited increased G:G and T:G misincorporation rates, 22- and 10-fold, respectively, whereas A:G misincorporation did not differ from that of wild type. Since the fidelity of the double mutant pol2-4 pol2C1089Y was not greatly decreased, these results suggest that the proofreading 3'-5' exonuclease activity of pol2C1089Y pol epsilon is impaired even though it retains nuclease activity and the mutation is not in the known exonuclease domain. C1 Osaka Univ, Dept Biochem & Mol Biol, Microbial Dis Res Inst, Osaka 5650871, Japan. NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Sugino, A (reprint author), Osaka Univ, Labs Biomol Networks, Grad Sch Frontier Biosci, 3-1 Yamada Oka, Osaka 5650871, Japan. NR 40 TC 28 Z9 32 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 OCT 4 PY 2002 VL 277 IS 40 BP 37422 EP 37429 DI 10.1074/jbc.M204476200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100066 PM 12124389 ER PT J AU Harndahl, L Jing, XJ Ivarsson, R Degerman, E Ahren, B Manganiello, VC Renstrom, E Holst, LS AF Harndahl, L Jing, XJ Ivarsson, R Degerman, E Ahren, B Manganiello, VC Renstrom, E Holst, LS TI Important role of phosphodiesterase 3B for the stimulatory action of cAMP on pancreatic beta-cell exocytosis and release of insulin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE; PROTEIN-KINASE-A; ISLET HORMONE-SECRETION; GLUCAGON-LIKE PEPTIDE-1; ADENYLATE-CYCLASE; IN-VITRO; RAT; AMP; EXPRESSION; ACTIVATION AB Cyclic AMP potentiates glucose-stimulated insulin release and mediates the stimulatory effects of hormones such as glucagon-like peptide 1 (GLP-1) on pancreatic beta-cells. By inhibition of cAMP-degrading phosphodiesterase (PDE) and, in particular, selective inhibition of PDE3 activity, stimulatory effects on insulin secretion have been observed. Molecular and functional information on beta-cell PDE3 is, however, scarce. To provide such information, we have studied the specific effects of the PDE3B isoform by adenovirus-mediated overexpression. In rat islets and rat insulinoma cells, approximate 10-fold overexpression of PDE3B was accompanied by a 6-8-fold increase in membrane-associated PDE3B activity. The cAMP concentration was significantly lowered in transduced cells (INS-1(832/13)), and insulin secretion in response to stimulation with high glucose (11.1 mM) was reduced by 40% (islets) and 50% (INS-1). Further, the ability of GLP-1 (100 nM) to augment glucose-stimulated insulin secretion was inhibited by similar to30% (islets) and 70% (INS-1). Accordingly, when stimulating with cAMP, a substantial decrease (65%) in exocytotic capacity was demonstrated in patch-clamped single beta-cells. In untransduced insulinoma cells, application of the PDE3-selective inhibitor OPC3911 (10 muM) was shown to increase glucose-stimulated insulin release as well as cAMP-enhanced exocytosis. The findings suggest a significant role of PDE3B as an important regulator of insulin secretory processes. C1 Lund Univ, Dept Cell & Mol Biol, Ctr Biomed, SE-22184 Lund, Sweden. NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. Lund Univ, Dept Med, Biomed Ctr, SE-22184 Lund, Sweden. Lund Univ, Dept Physiol Sci, Biomed Ctr, SE-22184 Lund, Sweden. RP Harndahl, L (reprint author), Lund Univ, Dept Cell & Mol Biol, Ctr Biomed, C11, SE-22184 Lund, Sweden. NR 49 TC 56 Z9 57 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 OCT 4 PY 2002 VL 277 IS 40 BP 37446 EP 37455 DI 10.1074/jbc.M205401200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100069 PM 12169692 ER PT J AU Hoover, DM Boulegue, C Yang, D Oppenheim, JJ Tucker, K Lu, WY Lubkowski, J AF Hoover, DM Boulegue, C Yang, D Oppenheim, JJ Tucker, K Lu, WY Lubkowski, J TI The structure of human macrophage inflammatory protein-3 alpha/CCL20 - Linking antimicrobial and CC chemokine receptor-6-binding activities with human beta-defensins SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MONOCYTE CHEMOTACTIC PROTEIN-1; CRYSTAL-STRUCTURE; RECEPTOR-BINDING; DENDRITIC CELLS; 3-DIMENSIONAL STRUCTURE; SELECTIVE RECRUITMENT; HUMAN BETA-DEFENSIN-2; T-CELLS; IDENTIFICATION; MIP-3-ALPHA AB Human macrophage inflammatory protein-3alpha (MIP-3alpha; CCL20) is a CC-type chemokine that binds to and activates CC chemokine receptor-6 (CCR6). Although MIP-3a does not share the binding site of CCR6 with any other chemokine, human beta-defensin-1 and -2, small cationic antimicrobial peptides, have also been found to bind to and activate CCR6. Conversely, we have found that MIP-3a possesses antibacterial activity of greater potency than human beta-defensin-1 and -2 against Escherichia coli ATCC 25922 and Staphylococcus aureus ATCC 29213, while having no activity against the fungus Candida albicans. There is no clear sequence similarity between,beta-defensins and the chemokine MIP-3alpha, beyond an abundance of cationic residues and the presence of disulfide bonds. Nonetheless, there are structural similarities between these three proteins that allow their overlap of chemotactic and antimicrobial activities. In this report, we describe the x-ray crystal structure of human MIP-3a refined to a resolution of 1.7 Angstrom and compare it with the crystal structures of human beta-defensin-1 and -2. Molecules of MIP-3alpha and the beta-defensins seem to share few structural motifs that are likely associated with their common biological activities. C1 NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA. NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. NCI, Opportunist Infect Lab, Div Canc Treatment, Centers & Diag Dev Therapeut Program, Frederick, MD 21702 USA. Univ Maryland, Inst Human Virol, Inst Biotechnol, Baltimore, MD 21201 USA. RP Lubkowski, J (reprint author), NCI, Macromol Crystallog Lab, POB B,Ft Detrick, Frederick, MD 21702 USA. RI Boulegue, Cyril/A-4092-2009; Lu, Wuyuan/B-2268-2010 FU NCI NIH HHS [N01-CO-1240] NR 74 TC 152 Z9 160 U1 1 U2 7 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 4 PY 2002 VL 277 IS 40 BP 37647 EP 37654 DI 10.1074/jbc.M203907200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100095 PM 12149255 ER PT J AU Lu, M Wang, T Yan, QS Yang, XB Dong, K Knepper, MA Wang, WH Giebisch, G Shull, GE Hebert, SC AF Lu, M Wang, T Yan, QS Yang, XB Dong, K Knepper, MA Wang, WH Giebisch, G Shull, GE Hebert, SC TI Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in ROMK (Bartter's) knockout mice SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-TYROSINE-PHOSPHATASE; POTASSIUM CHANNEL; RAT-KIDNEY; GENETIC-HETEROGENEITY; NACL TRANSPORT; MOUSE KIDNEY; HENLES-LOOP; MUTATIONS; SECRETION; TUBULE AB The ROMK (Kir1.1; Kcnj1) gene is believed to encode the apical small conductance K+ channels (SK) of the thick ascending limb (TAL) and cortical collecting duct (CCD). Loss-of-function mutations in the human ROMK gene cause Bartter's syndrome with renal Na+ wasting, consistent with the role of this channel in apical K+ recycling in the TAL that is crucial for NaCl reabsorption. However, the mechanism of renal K+ wasting and hypokalemia that develop in individuals with ROMK Bartter's syndrome is not apparent given the proposed loss of the collecting duct SK channel. Thus, we generated a colony of ROMK null mice with similar to25% survival to adulthood that provides a good model for ROMK Bartter's syndrome. The remaining 75% of null mice die in less than 14 days after birth. The surviving ROMK null mice have normal gross renal morphology with no evidence of significant hydronephrosis, whereas non-surviving null mice exhibit marked hydronephrosis. ROMK protein expression was absent in TAL and CCD from null mice but exhibited normal abundance and localization in wild-type littermates. ROMK null mice were polyuric and natriuretic with an elevated hematocrit consistent with mild extracellular volume depletion. SK channel activity in TAL and CCD was assessed by patch clamp analysis in ROMK wild-type ROMK(+/+), heterozygous ROMK(+/-), and null ROMK(-/-) mice. In 313 patches with successful seals from the three ROMK genotypes, SK channel activity in ROMK (+/+ and +/-) exhibited normal single channel kinetics. The expression frequencies are as follows: 67 (TAL) and 58% (CCD) in ROMK(+/+); about half that of the wild-type in ROMK(+/-), being 38 (TAL) and 25% (CCD); absent in both TAL or CCD in ROMK(-/-) between 2 and 5 weeks in 15 mice (61 and 66 patches, respectively). The absence of SK channel activity in ROMK null mice demonstrates that ROMK is essential for functional expression of SK channels in both TAL and CCD. Despite loss of ROMK expression, the normokalemic null mice exhibited significantly increased kaliuresis, indicating alternative mechanisms for K+ absorption/secretion in the nephron. C1 Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06520 USA. Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA. NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA. RP Hebert, SC (reprint author), Yale Univ, Sch Med, Dept Cellular & Mol Physiol, 333 Cedar St, New Haven, CT 06520 USA. FU Intramural NIH HHS [Z99 HL999999, Z01 HL001285-21]; NIDDK NIH HHS [R01 DK054999, R37 DK050594, R01 DK054983, R01 DK050594, DK54999, R01 DK054998, DK50594, DK54983, DK54998] NR 68 TC 117 Z9 118 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 OCT 4 PY 2002 VL 277 IS 40 BP 37881 EP 37887 DI 10.1074/jbc.M206644200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 601LH UT WOS:000178447100124 PM 12130653 ER PT J AU Ramelot, TA Cort, JR Yee, AA Liu, FR Goshe, MB Edwards, AM Smith, RD Arrowsmith, CH Dever, TE Kennedy, MA AF Ramelot, TA Cort, JR Yee, AA Liu, FR Goshe, MB Edwards, AM Smith, RD Arrowsmith, CH Dever, TE Kennedy, MA TI Myxoma virus immunomodulatory protein M156R is a structural mimic of eukaryotic translation initiation factor eIF2 alpha SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE eIF2 alpha; K3L; myxoma virus M156R; nuclear magnetic resonance; PKR ID SIDE-CHAIN RESONANCES; KINASE PKR; ALPHA-SUBUNIT; GENE-PRODUCT; RIBOSOMAL PROTEIN-S1; BACKBONE AMIDE; DNA-SEQUENCE; K3L PROTEIN; FACTOR-II; RNA AB Phosphorylation of the translation initiation factor eIF2 on Ser51 of its alpha subunit is a key event for regulation of protein synthesis in all eukaryotes. M156R, the product of the myxoma virus M156R open reading frame, has sequence similarity to eIF2alpha as well as to a family of viral proteins that bind to the interferon-induced protein kinase PKR and inhibit phosphorylation of eIF2alpha. In this study, we demonstrate that, like eIF2alpha. M156R is an efficient substrate for phosphorylation by PKR and can compete with eIF2alpha. To gain insights into the substrate specificity of the eIF2alpha kinases, we have determined the nuclear magnetic resonance (NMR) structure of M156R, the first structure of a myxoma virus protein. The fold consists of a five-stranded antiparallel beta-barrel with two of the strands connected by a loop and an a-helix. The similarity between M156R and the beta-barrel structure in the N terminus of eIF2alpha suggests that the viral homologs mimic eIF2alpha structure in order to compete for binding to PKR. A homology-modeled structure of the well-studied vaccinia virus K3L was generated on the basis of alignment with M156R. Comparison of the structures of the K3L model, M156R, and human eIF2a indicated that residues important for binding to PKR are located at conserved positions on the surface of the beta-barrel and in the mobile loop, identifying the putative PKR recognition motif. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Pacific NW Natl Lab, Environm Mol Sci Lab, Richland, WA 99352 USA. Ontario Canc Inst, Div Mol & Struct Biol, Toronto, ON M4X 1K9, Canada. Univ Toronto, Dept Med Biophys, Toronto, ON M5G 1L7, Canada. NIH, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA. RP Kennedy, MA (reprint author), Pacific NW Natl Lab, Environm Mol Sci Lab, K8-98, Richland, WA 99352 USA. RI Smith, Richard/J-3664-2012; OI Smith, Richard/0000-0002-2381-2349; Dever, Thomas/0000-0001-7120-9678 FU NIGMS NIH HHS [P50-GM62413] NR 60 TC 26 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 4 PY 2002 VL 322 IS 5 BP 943 EP 954 DI 10.1016/S0022-2836(02)00858-6 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 605EQ UT WOS:000178664400004 PM 12367520 ER PT J AU Compton, D DeVrieze, FW Petersen, RC Tangalos, E Li, L Hardy, J AF Compton, D DeVrieze, FW Petersen, RC Tangalos, E Li, L Hardy, J TI Possible association between genetic variability at the apolipoprotein(a) locus and Alzheimer's disease in apolipoprotein E2 carriers SO NEUROSCIENCE LETTERS LA English DT Article DE apolipoprotein(a) locus; Alzheimer's disease; lipoprotein(a); cholesterol; polymorphisms; apolipoprotein(a); lipoprotein(a) ID E POLYMORPHISM; PLASMA-LEVELS; LIPOPROTEIN(A); CHOLESTEROL; RISK AB Apolipoprotein(a) (Apo(a)) is a glycoprotein that is linked by a disulfide bond to apolipoprotein B on low density lipoprotein particles to form lipoprotein(a) (Lp(a)). High plasma levels of Lp(a) are thought to contribute directly to the development of atherosclerosis. We tested a variant (T3888P) located in the Kringle-IV region of Apo(a) in a case-control series. Overall, there were no differences between case and controls. However, in the apoE2 positive subgroup, we noticed that the mutant allele is over-represented in the cases (P = 0.005). We suggest that this polymorphism and others at the Apo(a) locus be further studied in relation to Alzheimer's disease. (C) 2002 Published by Elsevier Science Ireland Ltd. C1 Mayo Clin, Dept Neurosci, Jacksonville, FL 32224 USA. NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. Mayo Clin, Dept Community Med, Rochester, MN 55055 USA. Mayo Clin, Dept Neurol, Rochester, MN 55055 USA. Univ Alabama, Dept Med, Arteriosclerosis Res Unit, Med Ctr, Birmingham, AL 35294 USA. UCL, Reta Lila Weston Inst Neurol Studies, London WC2, England. RP Hardy, J (reprint author), Mayo Clin, Dept Neurosci, Jacksonville, FL 32224 USA. RI Hardy, John/C-2451-2009 NR 17 TC 10 Z9 10 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 OCT 4 PY 2002 VL 331 IS 1 BP 60 EP 62 AR PII S0304-3940(02)00703-6 DI 10.1016/S0304-3940(02)00703-6 PG 3 WC Neurosciences SC Neurosciences & Neurology GA 604XN UT WOS:000178646500015 PM 12359323 ER PT J AU Aultman, KS Gottlieb, M Giovanni, MY Fauci, AS AF Aultman, KS Gottlieb, M Giovanni, MY Fauci, AS TI Anopheles gambiae genome: Completing the malaria triad SO SCIENCE LA English DT Editorial Material C1 NIAID, Parasitol & Int Programs Branch, NIH, Bethesda, MD 20892 USA. RP Aultman, KS (reprint author), NIAID, Parasitol & Int Programs Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 0 TC 11 Z9 13 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 13 EP 13 DI 10.1126/science.298.5591.13 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500003 PM 12364752 ER PT J AU Hamer, D AF Hamer, D TI Rethinking behavior genetics SO SCIENCE LA English DT Editorial Material ID MONOAMINE-OXIDASE; POLYMORPHISM; RISK C1 NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Hamer, D (reprint author), NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NR 12 TC 94 Z9 101 U1 2 U2 12 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 71 EP 72 DI 10.1126/science.1077582 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500028 PM 12364769 ER PT J AU Alphey, L Beard, CB Billingsley, P Coetzee, M Crisanti, A Curtis, C Eggleston, P Godfray, C Hemingway, J Jacobs-Lorena, M James, AA Kafatos, FC Mukwaya, LG Paton, M Powell, JR Schneider, W Scott, TW Sina, B Sinden, R Sinkins, S Spielman, A Toure, Y Collins, FH AF Alphey, L Beard, CB Billingsley, P Coetzee, M Crisanti, A Curtis, C Eggleston, P Godfray, C Hemingway, J Jacobs-Lorena, M James, AA Kafatos, FC Mukwaya, LG Paton, M Powell, JR Schneider, W Scott, TW Sina, B Sinden, R Sinkins, S Spielman, A Toure, Y Collins, FH TI Malaria control with genetically manipulated insect vectors SO SCIENCE LA English DT Editorial Material ID ANOPHELES-GAMBIAE; AEDES-AEGYPTI; TRANSFORMATION C1 Univ Oxford, Oxford OX1 2JD, England. Ctr Dis Control & Prevent, Natl Ctr Infect Dis, Atlanta, GA USA. Univ Aberdeen, Aberdeen AB9 1FX, Scotland. S African Inst Med Res, ZA-2000 Johannesburg, South Africa. Univ London Imperial Coll Sci Technol & Med, London, England. Univ London London Sch Hyg & Trop Med, London WC1E 7HT, England. Case Western Reserve Univ, Cleveland, OH 44106 USA. Univ Calif Irvine, Irvine, CA 92717 USA. European Mol Biol Lab, Heidelberg, Germany. Uganda Virus Res Inst, Entebbe, Uganda. Hlth & Safety Execut, HSC, Sheffield S3 7HQ, S Yorkshire, England. Yale Univ, New Haven, CT 06520 USA. US EPA, Washington, DC 20460 USA. Univ Calif Davis, Davis, CA 95616 USA. NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA. Harvard Univ, Sch Publ Hlth, Cambridge, MA 02138 USA. WHO, Special Programme Res & Training Trop Dis, Geneva, Switzerland. Univ Notre Dame, Notre Dame, IN 46556 USA. RP Alphey, L (reprint author), Univ Oxford, Oxford OX1 2JD, England. NR 15 TC 161 Z9 166 U1 4 U2 38 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 119 EP 121 DI 10.1126/science.1078278 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500043 PM 12364786 ER PT J AU Miller, LH Greenwood, B AF Miller, LH Greenwood, B TI Malaria - a shadow over Africa SO SCIENCE LA English DT Editorial Material ID RESISTANCE C1 NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1B 3DP, England. RP Miller, LH (reprint author), NIAID, Lab Malaria & Vector Res, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 14 TC 20 Z9 20 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 121 EP 122 DI 10.1126/science.1078048 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500044 PM 12364787 ER PT J AU Wellems, TE AF Wellems, TE TI Plasmodium chloroquine resistance and the search for a replacement antimalarial drug SO SCIENCE LA English DT Editorial Material ID HEMATIN POLYMERIZATION; FALCIPARUM; MALARIA; INHIBITION; MUTATIONS; BINDING C1 NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. RP Wellems, TE (reprint author), NIAID, Lab Malaria & Vector Res, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 23 TC 75 Z9 82 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 124 EP 126 DI 10.1126/science.1078167 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500046 PM 12364789 ER PT J AU Holt, RA Subramanian, GM Halpern, A Sutton, GG Charlab, R Nusskern, DR Wincker, P Clark, AG Ribeiro, JMC Wides, R Salzberg, SL Loftus, B Yandell, M Majoros, WH Rusch, DB Lai, ZW Kraft, CL Abril, JF Anthouard, V Arensburger, P Atkinson, PW Baden, H de Berardinis, V Baldwin, D Benes, V Biedler, J Blass, C Bolanos, R Boscus, D Barnstead, M Cai, S Center, A Chatuverdi, K Christophides, GK Chrystal, MA Clamp, M Cravchik, A Curwen, V Dana, A Delcher, A Dew, I Evans, CA Flanigan, M Grundschober-Freimoser, A Friedli, L Gu, ZP Guan, P Guigo, R Hillenmeyer, ME Hladun, SL Hogan, JR Hong, YS Hoover, J Jaillon, O Ke, ZX Kodira, C Kokoza, E Koutsos, A Letunic, I Levitsky, A Liang, Y Lin, JJ Lobo, NF Lopez, JR Malek, JA McIntosh, TC Meister, S Miller, J Mobarry, C Mongin, E Murphy, SD O'Brochta, DA Pfannkoch, C Qi, R Regier, MA Remington, K Shao, HG Sharakhova, MV Sitter, CD Shetty, J Smith, TJ Strong, R Sun, JT Thomasova, D Ton, LQ Topalis, P Tu, ZJ Unger, MF Walenz, B Wang, AH Wang, J Wang, M Wang, XL Woodford, KJ Wortman, JR Wu, M Yao, A Zdobnov, EM Zhang, HY Zhao, Q Zhao, SY Zhu, SPC Zhimulev, I Coluzzi, M della Torre, A Roth, CW Louis, C Kalush, F Mural, RJ Myers, EW Adams, MD Smith, HO Broder, S Gardner, MJ Fraser, CM Birney, E Bork, P Brey, PT Venter, JC Weissenbach, J Kafatos, FC Collins, FH Hoffman, SL AF Holt, RA Subramanian, GM Halpern, A Sutton, GG Charlab, R Nusskern, DR Wincker, P Clark, AG Ribeiro, JMC Wides, R Salzberg, SL Loftus, B Yandell, M Majoros, WH Rusch, DB Lai, ZW Kraft, CL Abril, JF Anthouard, V Arensburger, P Atkinson, PW Baden, H de Berardinis, V Baldwin, D Benes, V Biedler, J Blass, C Bolanos, R Boscus, D Barnstead, M Cai, S Center, A Chatuverdi, K Christophides, GK Chrystal, MA Clamp, M Cravchik, A Curwen, V Dana, A Delcher, A Dew, I Evans, CA Flanigan, M Grundschober-Freimoser, A Friedli, L Gu, ZP Guan, P Guigo, R Hillenmeyer, ME Hladun, SL Hogan, JR Hong, YS Hoover, J Jaillon, O Ke, ZX Kodira, C Kokoza, E Koutsos, A Letunic, I Levitsky, A Liang, Y Lin, JJ Lobo, NF Lopez, JR Malek, JA McIntosh, TC Meister, S Miller, J Mobarry, C Mongin, E Murphy, SD O'Brochta, DA Pfannkoch, C Qi, R Regier, MA Remington, K Shao, HG Sharakhova, MV Sitter, CD Shetty, J Smith, TJ Strong, R Sun, JT Thomasova, D Ton, LQ Topalis, P Tu, ZJ Unger, MF Walenz, B Wang, AH Wang, J Wang, M Wang, XL Woodford, KJ Wortman, JR Wu, M Yao, A Zdobnov, EM Zhang, HY Zhao, Q Zhao, SY Zhu, SPC Zhimulev, I Coluzzi, M della Torre, A Roth, CW Louis, C Kalush, F Mural, RJ Myers, EW Adams, MD Smith, HO Broder, S Gardner, MJ Fraser, CM Birney, E Bork, P Brey, PT Venter, JC Weissenbach, J Kafatos, FC Collins, FH Hoffman, SL TI The genome sequence of the malaria mosquito Anopheles gambiae SO SCIENCE LA English DT Article ID DROSOPHILA-MELANOGASTER; TRANSPOSABLE ELEMENTS; INCIPIENT SPECIATION; RESISTANCE; FAMILIES; LOCI; DIFFERENTIATION; REFRACTORINESS; IDENTIFICATION; EVOLUTION AB Anopheles gambiae is the principal vector of malaria, a disease that afflicts more than 500 million people and causes more than 1 million deaths each year. Tenfold shotgun sequence coverage was obtained from the PEST strain of A. gambiae and assembled into scaffolds that span 278 million base pairs. A total of 91% of the genome was organized in 303 scaffolds; the largest scaffold was 23.1 million base pairs. There was substantial genetic variation within this strain, and the apparent existence of two haplotypes of approximately equal frequency ("dual haplotypes") in a substantial fraction of the genome likely reflects the outbred nature of the PEST strain. The sequence produced a conservative inference of more than 400,000 single-nucleotide polymorphisms that showed a markedly bimodal density distribution. Analysis of the genome sequence revealed strong evidence for about 14,000 protein-encoding transcripts. Prominent expansions in specific families of proteins likely involved in cell adhesion and immunity were noted. An expressed sequence tag analysis of genes regulated by blood feeding provided insights into the physiological adaptations of a hematophagous insect. C1 Celera Genom, Rockville, MD 20850 USA. Genoscope Ctr Natl Sequencage, F-91057 Evry 06, France. CNRS, UMR 8030, F-91057 Evry 06, France. Cornell Univ, Ithaca, NY 14853 USA. NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. Bar Ilan Univ, Fac Life Sci, Ramat Gan, Israel. Inst Genom Res TIGR, Rockville, MD 20850 USA. CRG, UPF, IMIM, Grp Recerca Informat Biomed, Barcelona, Catalonia, Spain. Univ Calif Riverside, Dept Entomol, Riverside, CA 92521 USA. European Mol Biol Lab, D-69117 Heidelberg, Germany. Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA. Univ Notre Dame, Ctr Trop Dis Res & Training, Notre Dame, IN 46556 USA. Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England. Univ Maryland, Inst Biotechnol, Agr Biotechnol Ctr, College Pk, MD 20742 USA. Russian Acad Sci, Inst Cytol & Genet, Novosibirsk 630090, Russia. Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, GR-71110 Iraklion, Crete, Greece. Univ Crete, Dept Biol, GR-71110 Iraklion, Crete, Greece. European Bioinformat Inst, Cambridge CB10 1SD, England. Univ Roma La Sapienza, Dipartimento Sci Sanita Pubbl, Sez Parassitol, I-00185 Rome, Italy. Inst Pasteur, Unite Biochim & Biol Mol Insectes, F-75724 Paris 15, France. RP British Columbia Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Room 3427,600 W 10th Ave, Vancouver, BC V5Z 4E6, Canada. EM rholt@bcgsc.ca; frank.h.collins.75@nd.edu RI Letunic, Ivica/A-6032-2009; Louis, Christos/F-2527-2012; Holt, Robert/C-3303-2009; Zdobnov, Evgeny/K-1133-2012; Bork, Peer/F-1813-2013; Abril Ferrando, Josep/B-3877-2014; Tang, Macy/B-9798-2014; Meister, Stephan/M-6608-2014; Guigo, Roderic/D-1303-2010; Zhimulev, Igor/N-7978-2015; Kokoza, E l e n a /N-8507-2015; Salzberg, Steven/F-6162-2011; Gasull, Martina/A-6630-2013 OI Fraser, Claire/0000-0003-1462-2428; Ribeiro, Jose/0000-0002-9107-0818; Bork, Peer/0000-0002-2627-833X; Abril Ferrando, Josep/0000-0001-7793-589X; Meister, Stephan/0000-0003-2436-7037; Guigo, Roderic/0000-0002-5738-4477; Salzberg, Steven/0000-0002-8859-7432; FU NIAID NIH HHS [R01AI44273, U01AI48846, U01AI50687] NR 52 TC 1320 Z9 1638 U1 15 U2 159 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 129 EP + DI 10.1126/science.1076181 PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500048 PM 12364791 ER PT J AU Zdobnov, EM von Mering, C Letunic, I Torrents, D Suyama, M Copley, RR Christophides, GK Thomasova, D Holt, RA Subramanian, GM Mueller, HM Dimopoulos, G Law, JH Wells, MA Birney, E Charlab, R Halpern, AL Kokoza, E Kraft, CL Lai, ZW Lewis, S Louis, C Barillas-Mury, C Nusskern, D Rubin, GM Salzberg, SL Sutton, GG Topalis, P Wides, R Wincker, P Yandell, M Collins, FH Ribeiro, J Gelbart, WM Kafatos, FC Bork, P AF Zdobnov, EM von Mering, C Letunic, I Torrents, D Suyama, M Copley, RR Christophides, GK Thomasova, D Holt, RA Subramanian, GM Mueller, HM Dimopoulos, G Law, JH Wells, MA Birney, E Charlab, R Halpern, AL Kokoza, E Kraft, CL Lai, ZW Lewis, S Louis, C Barillas-Mury, C Nusskern, D Rubin, GM Salzberg, SL Sutton, GG Topalis, P Wides, R Wincker, P Yandell, M Collins, FH Ribeiro, J Gelbart, WM Kafatos, FC Bork, P TI Comparative genome and proteome analysis of anopheles gambiae and Drosophila melanogaster SO SCIENCE LA English DT Article ID DOSAGE-COMPENSATION; INNATE IMMUNITY; REGULATORY ELEMENTS; MALARIA MOSQUITO; GENE FAMILIES; FUGU-RUBRIPES; EVOLUTION; SEQUENCE; INSECTS; IDENTIFICATION AB Comparison of the genomes and proteomes of the two diptera Anopheles gambiae and Drosophila melanogaster, which diverged about 250 million years ago, reveals considerable similarities. However, numerous differences are also observed; some of these must reflect the selection and subsequent adaptation associated with different ecologies and life strategies. Almost half of the genes in both genomes are interpreted as orthologs and show an average sequence identity of about 56%, which is slightly lower than that observed between the orthologs of the pufferfish and human (diverged about 450 million years ago). This indicates that these two insects diverged considerably faster than vertebrates. Aligned sequences reveal that orthologous genes have retained only half of their intron/exon structure, indicating that intron gains or losses have occurred at a rate of about one per gene per 125 million years. Chromosomal arms exhibit significant remnants of homology between the two species, although only 34% of the genes colocalize in small "microsyntenic" clusters, and major interarm transfers as well as intra-arm shuffling of gene order are detected. C1 European Mol Biol Lab, D-69117 Heidelberg, Germany. Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Celera Genom, Rockville, MD 20850 USA. Univ London Imperial Coll Sci Technol & Med, Ctr Mol Microbiol & Infect, Dept Biol Sci, London SW7 2AZ, England. Univ Arizona, Tucson, AZ 85721 USA. European Bioinformat Inst, Cambridge CB10 1SD, England. Univ Calif Berkeley, Berkeley, CA 94720 USA. Russian Acad Sci, Inst Cytol & Genet, Sibirian Div, Novosibirsk 630090, Russia. Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, GR-71110 Iraklion, Crete, Greece. Univ Crete, GR-71110 Iraklion, Crete, Greece. Colorado State Univ, Ft Collins, CO 80523 USA. Inst Genome Res, Rockville, MD 20850 USA. Bar Ilan Univ, Fac Life Sci, Ramat Gan, Israel. Genoscope Ctr Natl Sequencage, F-91057 Evry 06, France. CNRS, UMR 8030, F-91057 Evry 06, France. Univ Notre Dame, Ctr Trop Dis Res & Training, Notre Dame, IN 46556 USA. NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. Harvard Univ, Cambridge, MA 02138 USA. RP Zdobnov, EM (reprint author), European Mol Biol Lab, Meyerhofstr 1, D-69117 Heidelberg, Germany. RI von Mering, Christian/B-3300-2008; Letunic, Ivica/A-6032-2009; Louis, Christos/F-2527-2012; Holt, Robert/C-3303-2009; Zdobnov, Evgeny/K-1133-2012; Bork, Peer/F-1813-2013; Tang, Macy/B-9798-2014; Kokoza, E l e n a /N-8507-2015; Salzberg, Steven/F-6162-2011; Torrents, David/G-5785-2015; OI Rubin, Gerald/0000-0001-8762-8703; Ribeiro, Jose/0000-0002-9107-0818; von Mering, Christian/0000-0001-7734-9102; Bork, Peer/0000-0002-2627-833X; Salzberg, Steven/0000-0002-8859-7432; Torrents, David/0000-0002-6086-9037; Dimopoulos, George/0000-0001-6755-8111; Lewis, Suzanna/0000-0002-8343-612X NR 66 TC 360 Z9 388 U1 2 U2 35 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD OCT 4 PY 2002 VL 298 IS 5591 BP 149 EP 159 DI 10.1126/science.1077061 PG 12 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 600BJ UT WOS:000178370500049 PM 12364792 ER PT J AU Hoshino, Y Jones, RW Chanock, RM Kapikian, AZ AF Hoshino, Y Jones, RW Chanock, RM Kapikian, AZ TI Generation and characterization of six single VP4 gene substitution reassortant rotavirus vaccine candidates: each bears a single human rotavirus VP4 gene encoding P serotype 1A[8] or 1B[4] and the remaining 10 genes of rhesus monkey rotavirus MMU18006 or bovine rotavirus UK SO VACCINE LA English DT Article DE single VP4 gene substitution rotavirus reassortants; rotavirus vaccine; rotavirus VP4 and VP7 ID MONOCLONAL-ANTIBODIES; HOSPITALIZED CHILDREN; BRAZILIAN CHILDREN; PRIMARY INFECTION; INDUCED DIARRHEA; IMMUNE-RESPONSE; CAPSID PROTEIN; YOUNG-CHILDREN; STRAINS; NEUTRALIZATION AB The global disease burden of rotavirus diarrhea in infants and young children has stimulated interest in the biological and clinical characteristics of these agents, leading to intensive efforts to develop a vaccine. A rhesus rotavirus (RRV)-based quadrivalent vaccine ("RotaShield") was licensed and administered to about 1 million infants and found to be highly effective. However, it was withdrawn because of a link with intussusception. This vaccine was developed according to a modified "Jennerian" approach in which one of the two major outer capsid proteins (VP7) shares neutralization specificity with one of the four epidemiologically important human rotavirus serotypes. The other outer capsid protein (VP4) is derived solely from RRV and is distinct from the VP4 of the four human rotavirus serotypes of epidemiologic importance. In an effort to further increase the immunogenicity of the existing VP7-based RRV quadrivalent vaccine, we generated three single VP4 gene substitution reassortant rotavirus candidate vaccines, each of which bears a single human rotavirus VP4 gene encoding P serotype I A[8] or I B [4] specificity while the remaining 10 genes are derived from the rhesus rotavirus. By incorporating one or two of these strains into the quadrivalent vaccine, a pentavalent or hexavalent RRV-based vaccine could be formulated thus providing antigenic coverage not only for VP7 serotype 1, 2, 3 and 4 but also for VP4 serotype 1A[8] or 1B[4], thus possibly augmenting its immunogenicity. Similarly, three single VP4 gene (P1A[8] or P1B[4]) substitution reassortants have also been generated in a background of 10 bovine (UK) rotavirus genes for addition to a second generation UK-based quadrivalent vaccine. Published by Elsevier Science Ltd. C1 NIAID, Epidemiol Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA. RP Hoshino, Y (reprint author), NIAID, Epidemiol Sect, Infect Dis Lab, NIH, Bldg 50,Room 6308,50 S Dr MSC 8026, Bethesda, MD 20892 USA. NR 79 TC 14 Z9 14 U1 0 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0264-410X J9 VACCINE JI Vaccine PD OCT 4 PY 2002 VL 20 IS 29-30 BP 3576 EP 3584 AR PII S0264-410X(02)00313-4 DI 10.1016/S0264-410X(02)00313-4 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 610AT UT WOS:000178939100019 PM 12297404 ER PT J AU Ulrich, CM Wallen, G Grady, C AF Ulrich, CM Wallen, G Grady, C TI The nursing shortage and the quality of care SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. RP Ulrich, CM (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 2 TC 6 Z9 6 U1 0 U2 1 PU MASSACHUSETTS MEDICAL SOC/NEJM PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 3 PY 2002 VL 347 IS 14 BP 1118 EP 1118 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 599KD UT WOS:000178332900027 PM 12362020 ER PT J AU Mamane, Y Grandvaux, N Hernandez, E Sharma, S Innocente, SA Lee, JM Azimi, N Lin, R Hiscott, J AF Mamane, Y Grandvaux, N Hernandez, E Sharma, S Innocente, SA Lee, JM Azimi, N Lin, R Hiscott, J TI Repression of IRF-4 target genes in human T cell leukemia virus-1 infection SO ONCOGENE LA English DT Review DE human T cell leukemia virus; interferon regulatory factors; cyclin B1; transcription ID INTERFERON REGULATORY FACTOR-4; NF-KAPPA-B; HUMAN-IMMUNODEFICIENCY-VIRUS; REPLICATION PROTEIN-A; TYPE-1 TAX PROTEIN; I HTLV-I; CYCLIN B1; TRANSCRIPTION FACTOR; KINASE IKK; MOLECULAR MECHANISM AB The human T cell leukemia/lymphotropic virus-1 (HTLV-I) is the etiologic agent of adult T cell leukemia (ATL), an aggressive and fatal leukemia of CD4+ T lymphocytes. Interferon regulatory factor-4 (IRF-4) was shown previously to be constitutively expressed in T cells infected with HTLV-1. In this study, we investigated the role of IRF-4 gene regulation in the context of HTLV-1 infection using gene array technology and IRF-4 expressing T cells. Many potential IRF-4 regulated genes were identified, the vast majority of which were repressed by IRF-4 expression. Cyclin B1, a G2-M checkpoint protein identified as an IRF-4 repressed gene in the array, was further characterized in the context of HTLV-1 infection. All HTLV-1 infected cell lines and ATL patient lymphocytes demonstrated a dramatic decrease in cyclin B1 levels; subsequent analysis of the cyclin B1 promoter identified two sites important in IRF-4 binding and repression of cyclin B1 expression. Furthermore, IRF-4-mediated repression of cyclin B1 led to a significant decrease in CDC2 kinase activity in HTLV-1 infected T cells. IRF-4 expression in HTLV-1 infected T cells also downregulated other genes implicated in the mitotic checkpoint as well as genes involved in actin cytoskeletal rearrangement, DNA repair, apoptosis, metastasis and immune recognition. Several of the identified genes are dysregulated in ATL and may provide important mechanistic information concerning pathways critical to the emergence of ATL. C1 McGill Univ, Lady Davis Inst Med Res, Terry Fox Mol Oncol Grp, Montreal, PQ H3T 1E2, Canada. McGill Univ, Dept Microbiol & Immunol, Montreal, PQ H3T 1E2, Canada. Hamilton Reg Canc Ctr, Hamilton, ON L8V 1C3, Canada. NCI, NIH, Bethesda, MD 20892 USA. RP Hiscott, J (reprint author), McGill Univ, Lady Davis Inst Med Res, Terry Fox Mol Oncol Grp, 3755 Cote Ste Catherine, Montreal, PQ H3T 1E2, Canada. RI Lin, Rongtuan/A-1442-2008 OI Lin, Rongtuan/0000-0002-2238-3503 NR 108 TC 17 Z9 17 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 3 PY 2002 VL 21 IS 44 BP 6751 EP 6765 DI 10.1038/sj.onc.1205843 PG 15 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 599CD UT WOS:000178315800005 PM 12360402 ER PT J AU Kopantzev, Y Heller, M Swaminathan, N Rudikoff, S AF Kopantzev, Y Heller, M Swaminathan, N Rudikoff, S TI IL-6 mediated activation of STAT3 bypasses Janus kinases in terminally differentiated B lineage cells SO ONCOGENE LA English DT Article DE IL-6; STAT3; MEK kinase; phosphorylation ID SIGNAL TRANSDUCER GP130; JAK-TYK KINASES; TYROSINE KINASE; SERINE PHOSPHORYLATION; CYTOKINE RECEPTORS; INTERLEUKIN-6 FAMILY; PROTEIN-KINASES; IN-VIVO; INHIBITOR; ASSOCIATION AB Cytokine signaling generally occurs through receptors lacking tyrosine kinase activity. Aggregation of receptors leads to activation of receptor associated Janus kinases (Jaks) which in turn phosphorylate members of a family of transcription factors (STATs) that translocate to the nucleus and regulate gene expression. In the case of Interleukin-6 (IL-6), the consensus for signaling in B lineage cells has been that Jak1, Jak2 and Tyk2 are all phosphorylated upon ligand binding and participate in activation of downstream elements, in particular STAT3. In other cell types, Jak1 has been demonstrated to be absolutely required for IL-6 mediated activation of STAT3. In the present studies, we have identified a series of end stage B cell (plasma cell) lines that fail to express Jak1, but phosphorylate STAT3 in response to IL-6. No evidence was found for a requirement of other Jak family members in the activation of STAT3. STAT3 tyrosine phosphorylation was inhibited in a dose dependent manner by the MEK inhibitor U0126, but not by inhibitors of PI-3K or Src kinases. Moreover, STAT3 phosphorylation was similarly inhibited in lines expressing Jak1 wherein Jak1 was phosphorylated upon IL-6 stimulation and Jakl phosphorylation was not inhibited by U0126. These results indicate that the MAPK pathway plays a critical role in IL-6 mediated tyrosine phosphorylation of STAT3 and suggests that Jak kinases may not be required in this cascade. Thus, it may be important to re-evaluate the role of Jak kinases in other cytokine signaling pathways as well. C1 NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Rudikoff, S (reprint author), NCI, Cellular & Mol Biol Lab, NIH, Bldg 37,Room 1D-18, Bethesda, MD 20892 USA. NR 38 TC 15 Z9 15 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 3 PY 2002 VL 21 IS 44 BP 6791 EP 6800 DI 10.1038/sj.onc.1205815 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 599CD UT WOS:000178315800009 PM 12360405 ER PT J AU Halcox, JPJ Nour, KRA Zalos, G Mincemoyer, R Waclawiw, MA Rivera, CE Willie, G Ellahham, S Quyyumi, AA AF Halcox, JPJ Nour, KRA Zalos, G Mincemoyer, R Waclawiw, MA Rivera, CE Willie, G Ellahham, S Quyyumi, AA TI The effect of sildenafil on human vascular function, platelet activation, and myocardial ischemia SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; COLD PRESSOR TEST; NITRIC-OXIDE; IN-VITRO; PHOSPHODIESTERASE-5 INHIBITOR; ENDOTHELIAL DYSFUNCTION; RELAXING FACTOR; P-SELECTIN; VASODILATION; ATHEROSCLEROSIS AB OBJECTIVES We studied the effects of sildenafil, a phosphodiesterase 5 inhibitor, on coronary and peripheral vascular function, platelet activation, and myocardial ischemia. BACKGROUND Nitric oxide vasodilates and inhibits platelet activation by generating cyclic guanosine 5'-monophosphate, which is metabolized by phosphodiesterase type 5. METHODS The effect of oral sildenafil on resting coronary vascular tone, endothelium-dependent and -independent function and platelet activation was measured in 24 patients. An additional 24 patients with coronary artery disease (CAD) and ischemia during exercise, and 12 control subjects received either 100 mg of sildenafil, 10 mg of isosorbide dinitrate (ISDN) or placebo during exercise on three separate days in a randomized, double-blind manner. Flow-mediated dilation of the brachial artery was measured, and CAD patients underwent treadmill exercise testing. RESULTS Sildenafil (100 mg) vasodilated epicardial coronary arteries (+6.9 +/- 1.3%, p < 0.0001). Coronary epicardial and microvascular responses with acetylcholine and cold-pressor testing improved, with a greater enhancement in patients with CAD and endothelial dysfunction. Verapamil responses were unchanged. Both resting and adenosine diphosphate-stimulated platelet IIb/IIIa receptor activation was inhibited by sildenafil (p < 0.05). Brachial arteries dilated in response to sildenafil in controls. Peak flow-mediated dilation was similar, but the duration of hyperemia was prolonged after sildenafil administration (p < 0.001). Compared with placebo, ISDN improved myocardial ischemia during exercise (p < 0.05), whereas the effect of sildenafil was intermediate between the two. CONCLUSIONS Sildenafil dilates epicardial coronary arteries, improves endothelial dysfunction and inhibits platelet activation in patients with CAD. It has an intermediate effect on myocardial ischemia compared with ISDN and placebo. (C) 2002 by the American College of Cardiology Foundation. C1 Washington Hosp Ctr, Dept Cardiol, Washington, DC 20010 USA. NIH, Dept Hematol, Bethesda, MD 20892 USA. NHLBI, Bethesda, MD 20892 USA. RP Quyyumi, AA (reprint author), Emory Univ Hosp, 1364 Clifton Rd NE,Suite F606, Atlanta, GA 30322 USA. OI Halcox, Julian/0000-0001-6926-2947 NR 33 TC 170 Z9 180 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT 2 PY 2002 VL 40 IS 7 BP 1232 EP 1240 AR PII S0735-1097(02)02139-3 DI 10.1016/S0735-1097(02)02139-3 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 599FX UT WOS:000178324400006 PM 12383570 ER PT J AU Correia, LCL Lakatta, EG O'Connor, FC Becker, LC Clulow, J Townsend, S Gerstenblith, G Fleg, JL AF Correia, LCL Lakatta, EG O'Connor, FC Becker, LC Clulow, J Townsend, S Gerstenblith, G Fleg, JL TI Attenuated cardiovascular reserve during prolonged submaximal cycle exercise in healthy older subjects SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID LEFT-VENTRICULAR FUNCTION; PLASMA-CATECHOLAMINES; EJECTION FRACTION; UPRIGHT EXERCISE; DYNAMIC EXERCISE; AGE; ADJUSTMENTS; RESPONSES; HUMANS; VOLUME AB OBJECTIVES The goal of this study was to determine the effect of age on the hemodynamic response to prolonged submaximal aerobic exercise in healthy volunteers. BACKGROUND Reductions in peak work rate, heart rate (HR), and left ventricular (LV) emptying but higher blood pressure (BP) and systemic vascular resistance occur in healthy older versus younger humans during short bursts of graded maximal aerobic exercise. However, the effect of aging on the cardiovascular response to prolonged exercise at submaximal work rates typical of daily aerobic activities remains unknown. METHODS We evaluated cardiovascular performance throughout prolonged submaximal upright cycle ergometry in 40 carefully screened healthy untrained volunteers, 8 men and 12 women <50 years old, mean = 37 +/- 8 years (younger), and 10 men and 10 women greater than or equal to50 years old, mean = 66 +/- 9 years (older), during upright cycle exercise at 70% of peak cycle oxygen consumption (VO2) to exhaustion or a maximum of 120 min. Cardiac volumes were acquired by gated blood pool scans with Tc-99m at rest and every 10 min throughout exercise. RESULTS Duration of exercise was similar in younger ([81 +/- 28 min] versus older [71 +/- 29 min] subjects, p = NS). At 10 min of exercise in the steady state, older subjects demonstrated lower VO2 (1.1 +/- 0.2 l/min vs. 1.3 +/- 0.3 l/min) and lower HR (118 +/- 17 vs. 135 +/- 11 beats/min, p < 0.001) but larger end-diastolic (80 +/- 11 ml/m(2) vs. 73 +/- 8 ml/m(2), p = 0.03) and end-systolic volume index (ESVI) 20 +/- 6 ml/m(2) Vs. 17 +/- 4 ml/m(2), p < 0.05) than younger ones. Between 10 min and exercise termination, with VO2 held constant in both groups, increases in HR (14.0 +/- 12.4 beats/min vs. 5.9 +/- 11.5 beats/min, p = 0.04), cardiac index (1.6 +/- 1.0 l/min/m(2) vs. 0.8 +/- 1.1 l/min/m(2), p = 0.03), and LV ejection fraction (7.1 +/- 4.0% vs. 2.9 +/- 4.4%, p = 0.003) were greater in younger than older subjects, respectively, as was the reduction in ESVI (-5.1 +/- 3.0 ml/m(2) vs. -1.8 +/- 3.3 ml/m(2), p = 0.002), despite similar declines in systolic BP (-12.3 +/- 6.3 mm Hg vs. -12.1 +/- 15.0 mm Hg, p = NS). CONCLUSIONS Thus, age-associated deficits in chronotropic and LV systolic reserve performance occur during prolonged submaximal upright cycle ergometry, analogous to those observed during graded maximal exercise. (C) 2002 by the American College of Cardiology Foundation. C1 Johns Hopkins Univ Hosp, Div Cardiol, Baltimore, MD 21287 USA. NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. RP Fleg, JL (reprint author), NHLBI, DECA, Rockledge 2,Room 8112,6701 Rockledge Dr,MSC 7936, Bethesda, MD 20892 USA. FU NIA NIH HHS [N01AG82109] NR 20 TC 16 Z9 16 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT 2 PY 2002 VL 40 IS 7 BP 1290 EP 1297 AR PII S0735-1097(02)02132-0 DI 10.1016/S0735-1097(02)02132-0 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 599FX UT WOS:000178324400013 PM 12383577 ER PT J AU Freed, LA Benjamin, EJ Levy, D Larson, MG Evans, JC Fuller, DL Lehman, B Levine, RA AF Freed, LA Benjamin, EJ Levy, D Larson, MG Evans, JC Fuller, DL Lehman, B Levine, RA TI Mitral valve prolapse in the general population - The benign nature of echocardiographic features in the Framingham Heart Study SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID PAPILLARY-MUSCLE TRACTION; TERM FOLLOW-UP; HYPERTROPHIC CARDIOMYOPATHY; DIMENSIONAL ECHOCARDIOGRAPHY; CLINICAL-FEATURES; REQUIRING SURGERY; YOUNG-WOMEN; REGURGITATION; PREVALENCE; MOTION AB OBJECTIVES The aim of this study was to examine the echocardiographic features and associations of mitral valve prolapse (MVP) diagnosed by current two-dimensional echocardiographic criteria in an unselected outpatient sample. BACKGROUND Previous studies of patients with MVP have emphasized the frequent occurrence of echocardiographic abnormalities such as significant mitral regurgitation (MR) and left atrial (LA) enlargement that are associated with clinical complications. These studies, however, have been limited by the use of hospital-based or referral series. METHODS We quantitatively studied all 150 subjects with possible MVP by echocardiography and 150 age- and gender-matched subjects without MVP from the 3,491 subjects in the Framingham Heart Study. Based on leaflet morphology, subjects were classified as having classic (n = 46), nonclassic (n = 37), or no MVP: RESULTS Leaflet length, MR degree, and LA and left ventricular size were significantly but mildly increased in MVP (p < 0.0001 to 0.004), with mean values typically within normal range. Average MR jet area was 15.1 +/- 1.4% (mild) in classic MVP and 8.9 +/- 1.5% (trace) in nonclassic MVP; MR was severe In only 3 of 46 (6.5%) subjects with classic MVP, and LA volume was increased in only 8.7% of those with classic MVP and 2.7% of those with nonclassic MVP. CONCLUSIONS Although the echocardiographic characteristics of subjects with MVP in the Framingham Heart Study differ from those without MVP, they display a far more benign profile of associated valvular, atrial, and ventricular abnormalities than previously reported in hospital-or referral-based series. Therefore, these findings may influence the perception of and approach to the outpatient with MVP. (C) 2002 by the American College of Cardiology Foundation. C1 Beth Israel Deaconess Med Ctr, Div Cardiol, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Div Clin Epidemiol, Boston, MA 02215 USA. NHLBI, Bethesda, MD 20892 USA. Boston Univ, Sch Med, Div Epidemiol & Prevent Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Div Cardiol, Boston, MA 02118 USA. Harvard Univ, Sch Med, Boston, MA USA. Massachusetts Gen Hosp, Cardiac Ultrasound Lab, Dept Med, Cardiac Unit, Boston, MA 02114 USA. NHLBI, Framingham Heart Study, Framingham, MA USA. RP Levine, RA (reprint author), Massachusetts Gen Hosp, Cardiac Ultrasound Lab, Dept Med, Cardiac Unit, 55 Fruit St,VBK 508, Boston, MA 02114 USA. OI Benjamin, Emelia/0000-0003-4076-2336 FU NHLBI NIH HHS [N01-HC-38038, HL38176, HL53702, K24 HL67434]; NINDS NIH HHS [5-R01-NS-17950-16] NR 74 TC 85 Z9 98 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT 2 PY 2002 VL 40 IS 7 BP 1298 EP 1304 AR PII S0735-1097(02)02161-7 DI 10.1016/S0735-1097(02)02161-7 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 599FX UT WOS:000178324400014 PM 12383578 ER PT J AU Bauer, F Jones, M Shiota, T Firstenberg, MS Qin, JX Tsujino, H Kim, YJ Sitges, M Cardon, LA Zetts, AD Thomas, JD AF Bauer, F Jones, M Shiota, T Firstenberg, MS Qin, JX Tsujino, H Kim, YJ Sitges, M Cardon, LA Zetts, AD Thomas, JD TI Left ventricular outflow tract mean systolic acceleration as a surrogate for the slope of the left ventricular end-systolic pressure-volume relationship SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID AORTIC BLOOD VELOCITY; SINGLE-BEAT ESTIMATION; CARDIAC-OUTPUT; HEART-RATE; CONTRACTILITY; PERFORMANCE; FAILURE; FLOW AB OBJECTIVES The goal of this study was to analyze left ventricular outflow tract systolic acceleration (LVOTAcc) during alterations in left ventricular (LV) contractility and LV filling. BACKGROUND Most indexes described to quantify LV systolic function, such as LV ejection fraction and cardiac output, are dependent on loading conditions. METHODS In 18 sheep (4 normal, 6 with aortic regurgitation, and 8 with old myocardial infarction), blood flow velocities through the LVOT were recorded using conventional pulsed Doppler. The LVOTAcc was calculated as the aortic peak velocity divided by the time to peak flow; LVOTAcc was compared with LV maximal elastance (E-m) acquired by conductance catheter under different loading conditions, including volume and pressure overload during an acute coronary occlusion (n = 10). In addition, a clinically validated lumped-parameter numerical model of the cardiovascular system was used to support our findings. RESULTS Left ventricular E-m and LVOTAcc decreased during ischemia (1.67 +/- 0.67 mm Hg(.)ml(-1) before vs. 0.93 +/- 0.41 min Hg(.)ml(-1) during acute coronary occlusion [p < 0.05] and 7.9 +/- 3.1 m(.)s(-2) before vs. 4.4 +/- 1.0 m(.)s(-2) during coronary occlusion [p < 0.05], respectively). Left ventricular outflow tract systolic acceleration showed a strong linear correlation with LV E-m (y = 3.84x + 1.87, r = 0.85, p < 0.001). Similar findings were obtained with the numerical modeling, which demonstrated a strong correlation between predicted and actual LV E-m (predicted = 0.98 [actual] -0.01, r = 0.86). By analysis of variance, there was no statistically significant difference in LVOTAcc under different loading conditions. CONCLUSIONS For a variety of hemodynamic conditions, LVOTAcc was linearly related to the LV contractility index LV E-m and was independent of loading conditions. These findings were consistent with numerical modeling. Thus, this Doppler index may serve as a good noninvasive index of LV contractility. (C) 2002 by the American College of Cardiology Foundation. C1 Cleveland Clin Fdn, Dept Cardiol, Cleveland, OH 44195 USA. NHLBI, Bethesda, MD 20892 USA. RP Shiota, T (reprint author), Cleveland Clin Fdn, Dept Cardiol, Desk F15,9500 Euclid Ave, Cleveland, OH 44195 USA. NR 23 TC 29 Z9 32 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT 2 PY 2002 VL 40 IS 7 BP 1320 EP 1327 AR PII S0735-1097(02)02138-1 DI 10.1016/S0735-1097(02)02138-1 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 599FX UT WOS:000178324400017 PM 12383581 ER PT J AU Hofmann, A Hess, S Noegel, AA Schleicher, M Wlodawer, A AF Hofmann, A Hess, S Noegel, AA Schleicher, M Wlodawer, A TI Crystallization of cyclase-associated protein from Dictyostelium discoideum SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY LA English DT Article ID YEAST ADENYLYL-CYCLASE; PROLINE-RICH REGION; SACCHAROMYCES-CEREVISIAE; RAS PROTEINS; MOLECULAR REPLACEMENT; CAP; IDENTIFICATION; HOMOLOG; ACTIN; GENE AB Cyclase-associated protein (CAP) is a conserved two-domain protein that helps to activate the catalytic activity of adenylyl cyclase in the cyclase-bound state through interaction with Ras, which binds to the cyclase in a different region. With its other domain, CAP can bind monomeric actin and therefore also carries a cytoskeletal function. The protein is thus involved in Ras/cAMP-dependent signal transduction and most likely serves as an adapter protein translocating the adenylyl cyclase complex to the actin cytoskeleton. Crystals belonging to the orthorhombic space group C222, with unit-cell parameters a = 71.2, b = 75.1, c = 162.9 Angstrom, have been obtained from Dictyostelium discoideum CAP carrying a C-terminal His tag. A complete native data set extending to 2.2 Angstrom resolution was collected from a single crystal using an in-house X-ray system. The asymmetric unit contains one molecule of CAP. C1 NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. NIDDK, Struct Mass Spectrometry Facil, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. Univ Cologne, Fak Med, Inst Biochem 1, D-5000 Cologne 41, Germany. Univ Munich, Adolf Butenandt Inst, D-80336 Munich, Germany. RP Hofmann, A (reprint author), NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA. RI Hofmann, Andreas/B-9515-2008 OI Hofmann, Andreas/0000-0003-4408-5467 NR 39 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0907-4449 J9 ACTA CRYSTALLOGR D JI Acta Crystallogr. Sect. D-Biol. Crystallogr. PD OCT PY 2002 VL 58 SI 2 BP 1858 EP 1861 DI 10.1107/S0907444902013306 PN 10 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics; Crystallography SC Biochemistry & Molecular Biology; Biophysics; Crystallography GA 597YJ UT WOS:000178248100020 PM 12351838 ER PT J AU Ehringer, MA Thompson, J Conroy, O Goldman, D Smith, TL Schuckit, MA Sikela, JM AF Ehringer, MA Thompson, J Conroy, O Goldman, D Smith, TL Schuckit, MA Sikela, JM TI Human alcoholism studies of genes identified through mouse quantitative trait locus analysis SO ADDICTION BIOLOGY LA English DT Article ID CROSS-FOSTERING ANALYSIS; ETHANOL SENSITIVITY; USE DISORDERS; DEPENDENCE; RISK; MEN; GENETICS; LEVEL; TWIN; SONS AB Coding region DNA sequence variants have been recently identified in several QTL candidate genes in a mouse model of differential sensitivity to alcohol [inbred long-sleep (ILS) and inbred short-sleep (ISS)]. This work has been extended into a human population characterized for their initial level of response to alcohol (LR). The coding region of one of the most promising of these candidate genes, zinc finger 133 (Znf133), has been sequenced completely in 50 individuals who participated in alcohol challenges at approximately age 20 and have been followed subsequently for the last 15 years. PCR products were obtained for the protein coding region of ZNF133 using human genomic DNA and directly sequenced using automated sequencers. Novel single nucleotide polymorphisms (SNPs) were detected by analyzing the sequence data using a suite of bioinformatics programs including Consed, Phred, Phrap and Polyphred. Five human SNPs were detected, two that correspond to amino acid changes in the protein, two that are silent DNA changes and one located in an intron. In this small sample, no significant association between any of the SNPs and alcohol diagnosis was detected. A follow-up of these SNPs in a larger sample should allow a more definitive conclusion to be reached. Significantly, the data presented here demonstrate the feasibility of directly testing genes in human alcoholic populations that had been identified first by comparative DNA sequencing of candidate genes located within mouse alcohol-related QTLs, even without detailed knowledge of the gene's function. C1 Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Human Med Genet Program, Denver, CO 80262 USA. Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. Vet Affairs Med Ctr, Alcohol Res Ctr, San Diego, CA 92161 USA. NIAAA, NIH, Rockville, MD 20852 USA. RP Sikela, JM (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, 4200 E 9th Ave C236, Denver, CO 80262 USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 FU NIAAA NIH HHS [2 AA 05526, AA 03527, AA 11853] NR 23 TC 3 Z9 4 U1 2 U2 3 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 1355-6215 J9 ADDICT BIOL JI Addict. Biol. PD OCT PY 2002 VL 7 IS 4 BP 365 EP 371 DI 10.1080/1355621021000005496 PG 7 WC Biochemistry & Molecular Biology; Substance Abuse SC Biochemistry & Molecular Biology; Substance Abuse GA 601UW UT WOS:000178467600002 PM 14578011 ER PT J AU Gibney, RTN Kimmel, PL Lazarus, M AF Gibney, RTN Kimmel, PL Lazarus, M TI The Acute Dialysis Quality Initiative - Part I: Definitions and reporting of CRRT techniques SO ADVANCES IN RENAL REPLACEMENT THERAPY LA English DT Article DE continuous hemofiltration; acute kidney failure; intensive care critical illness; sepsis ID RENAL REPLACEMENT THERAPIES; HIGH-VOLUME HEMOFILTRATION; ARTERIOVENOUS HEMOFILTRATION; SEPTIC SHOCK; HEMODIAFILTRATION; KINETICS; FAILURE AB Standard terminology has been developed for continuous renal replacement therapies (CRRTs). However, the field has continued to evolve. An international panel of experts reviewed the existing nomenclature for these therapies and proposed definitions for new modalities of CRRT. A set of minimal criteria for reporting CRRT techniques was also developed and will be critical in evaluating studies using CRRT and comparisons between continuous and intermittent renal replacement therapies. (C) 2002 by the National Kidney Foundation, Inc. C1 Univ Alberta, Div Crit Care Med, Edmonton, AB T6G 2B7, Canada. NIDDKD, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA. Fresenius Med Care N Amer, Lexington, MA USA. RP Gibney, RTN (reprint author), Univ Alberta, Div Crit Care Med, 3C1-16 WMC, Edmonton, AB T6G 2B7, Canada. OI GIBNEY, NOEL/0000-0003-3376-0535 NR 18 TC 2 Z9 2 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 1073-4449 J9 ADV RENAL REPLACE TH JI Adv. Renal Replace. Ther. PD OCT PY 2002 VL 9 IS 4 BP 252 EP 254 DI 10.1053/jarr.2002.35571 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA 672HV UT WOS:000182515900005 PM 12382226 ER PT J AU Bellomo, R Angus, D Star, RA AF Bellomo, R Angus, D Star, RA TI The Acute Dialysis Quality Initiative - Part II: Patient selection for CRRT SO ADVANCES IN RENAL REPLACEMENT THERAPY LA English DT Article DE hemofiltration; hemodialysis; continuous renal replacement therapy; critical illness; survival; mortality; uremia; intensive care unit; acute renal failure ID ACUTE-RENAL-FAILURE; CONTINUOUS ARTERIOVENOUS HEMOFILTRATION; CRITICALLY ILL PATIENTS; INTERMITTENT HEMODIALYSIS; REPLACEMENT THERAPY; INTRACRANIAL-PRESSURE; MULTIPLE ORGAN; HEART-FAILURE; MULTICENTER; HEMODIAFILTRATION AB The delivery of optimal acute dialytic support requires that the correct patients be selected for such treatment in a timely fashion and that such treatment be delivered at the appropriate dose, for an appropriate length of time, and for the appropriate indications. The Acute Dialysis Quality Initiative sought to address these issues through an expert-enhanced review of the literature. This article represents a condensation of its findings with regard to patients selection for CRRT, indications for initiation of treatment, transition to other treaatments, cessation of treatment, and availability of continuous therapy. The article offers recommendations for clinical practice based on the findings of the expert group. It also offers suggestions and sets priorities for future research in this important area of critical care nephrology. (C) 2002 by the National Kidney Foundation, Inc. C1 Austin & Repatriat Hosp, Dept Intens Care, Melbourne, Vic, Australia. Univ Pittsburgh, Sch Med, Div Crit Care Med, Pittsburgh, PA USA. NIDDK, NIH, Bethesda, MD 20892 USA. RP Bellomo, R (reprint author), Austin & Repatriat Hosp, Dept Intens Care, Melbourne, Vic, Australia. RI Angus, Derek/E-9671-2012 NR 33 TC 8 Z9 11 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 1073-4449 J9 ADV RENAL REPLACE TH JI Adv. Renal Replace. Ther. PD OCT PY 2002 VL 9 IS 4 BP 255 EP 259 DI 10.1053/jarr.2002.35570 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA 672HV UT WOS:000182515900006 PM 12382227 ER PT J AU Walsh, CR Cupples, LA Levy, D Kiel, DP Hannan, M Wilson, PWF O'Donnell, CJ AF Walsh, CR Cupples, LA Levy, D Kiel, DP Hannan, M Wilson, PWF O'Donnell, CJ TI Abdominal aortic calcific deposits are associated with increased risk for congestive, heart failure: The Framingham Heart Study SO AMERICAN HEART JOURNAL LA English DT Article ID LEFT-VENTRICULAR DYSFUNCTION; CORONARY-ARTERY DISEASE; CONVERTING-ENZYME INHIBITOR; MYOCARDIAL-INFARCTION; ATHEROSCLEROSIS; POPULATION; PROGRESSION; MORTALITY; PRESSURE; ULTRASOUND AB Objectives We sought to determine the association of aortic atherosclerosis, detected by calcific deposits in the abdominal aorta seen on lateral lumbar radiographs, with risk for congestive heart failure (CHF). Background Although the association between atherosclerotic coronary heart disease (CHID) and CHIF has been extensively studied, there are limited prospective data regarding the association of extracoronary atherosclerosis with CHF. Methods Lateral lumbar radiographs were obtained in 2467 Framingham Heart Study participants (1030 males and 1437 females) free of CHF in 1968. An abdominal aortic calcium (AAC) score was calculated for each subject based on the extent of calcium in the abdominal aorta. Proportional hazards models were used to test for associations between AAC score and CHF risk. Results There were 141 cases of CHF in men and 169 cases in women. In men, the multivariable-adjusted risk for CHF was increased for the second (hazards ratio [HR] 1.5, 95% CI 0.9-2.5) and third (HR 2.2, 95% CI 1.3-3.7) tertiles compared with the lowest tertile. Similarly, in women, the multivariable-adjusted risk for CHF was increased for the second (HR 1.8, 95% CI 1.1-2.9) and third (HR 3.2, 95% CI 2.0-5.1) tertiles compared with the lowest tertile. After further adjustment for CHID occurring prior to the onset of CHF, risk remained significantly increased for both men and women. Conclusions Atherosclerosis of the abdominal aorta is an important risk factor for CHF, independent of CHD and other risk factors. Noninvasive detection and quantification of atherosclerosis may be useful in identifying high-risk individuals likely to benefit from strategies aimed at preventing CHF. The possibility of a link between AAC and vascular compliance deserves further study. C1 Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA. Boston Univ, Dept Epidemiol & Biostat, Sch Publ Hlth, Boston, MA 02215 USA. Harvard Univ, Sch Med, Div Cardiol, Massachusetts Gen Hosp, Boston, MA 02115 USA. Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med, Boston, MA 02215 USA. Harvard Univ, Hebrew Rehabil Ctr Aged, Sch Med, Res & Training Inst,Div Aging, Boston, MA 02215 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RP O'Donnell, CJ (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA. OI Hannan, Marian/0000-0002-9586-6928; Kiel, Douglas/0000-0001-8474-0310 FU NHLBI NIH HHS [N01-HC-38038] NR 44 TC 66 Z9 68 U1 1 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 OCT PY 2002 VL 144 IS 4 BP 733 EP 739 DI 10.1067/mhj.2002.124404 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 600GU UT WOS:000178382900025 PM 12360172 ER PT J AU Heron, DE Karimpour, S Grigsby, PW AF Heron, DE Karimpour, S Grigsby, PW TI Anaplastic thyroid carcinoma - Comparison of conventional radiotherapy and hyperfractionation chemoradiotherapy in two groups SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE anaplastic thyroid carcinoma; surgery; radiation therapy; chemotherapy ID DOXORUBICIN; SURVIVAL; THERAPY; SURGERY; CANCER; GLAND AB Anaplastic thyroid carcinoma (ATC) is a highly aggressive neoplasm with a poor prognosis. Curative management of these tumors has been difficult secondary to delayed diagnosis and advanced disease at presentation. Treatment modalities including surgery and fractionated radiotherapy have had limited success in controlling these tumors. Median survival time is often measured in months. A review of all patients treated between 1952 and 1999 identified 32 patients with anaplastic or poorly differentiated thyroid carcinoma. Patients were divided into two groups: those treated between 1952 to 1980 (9 patients, group 1) and those treated between 1981 and 1999 (23 patients, group 2). Most group 1 patients received once-daily radiotherapy and most group 2 patients received twice-daily radiotherapy with concurrent chemotherapy. A variety of radiotherapy techniques were used. Chemotherapy consisted of doxorubicin, paclitaxel, vincristine, or cisplatin. Eleven patients presented with lymph node metastasis and two patients had distant metastases at diagnosis. The most common clinical presentation was a neck mass in 17 patients. In group 1, one patient was treated with surgery only, four with surgery and radiotherapy and four with radiotherapy alone. In group 2, 1 patient was treated with surgery only; 3 with surgery and radiotherapy; 10 with radiotherapy and chemotherapy; 5 with surgery, radiotherapy, and chemotherapy; and 5 with radiotherapy alone. Overall 2-year survival rates were 44% for group 1 and 52% for group 2. Two-year progression-free survival (PFS) was 53% for group 1 and 38% for group 2. Five (16%) patients died within 60 days of diagnosis. Severe side effects included skin sequelae (one patient) and osteoradionecrosis of the mandible (one patient). There were 10 (52%) long-term survivors (>2 years). Clinicopathologic features associated with extended survival were limited extent of disease and inclusion in group 2. Among patients with ATC surgery, hyperfractionated radiotherapy in conjunction with chemotherapy is associated with better survival but not PFS compared to conventional radiotherapy. C1 Univ Pittsburgh, Sch Med, Dept Radiat Oncol, Pittsburgh, PA USA. NIH, Dept Radiat Oncol, Bethesda, MD 20892 USA. Washington Univ, Mallinckrodt Inst Radiol, Dept Radiat Oncol, St Louis, MO USA. RP Heron, DE (reprint author), Univ Pittsburgh, Inst Canc, Shadyside Hosp, Dept Radiat Oncol, 5230 Ctr Ave, Pittsburgh, PA 15232 USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 21 TC 31 Z9 33 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0277-3732 J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD OCT PY 2002 VL 25 IS 5 BP 442 EP 446 DI 10.1097/01.COC.0000023060.34146.B3 PG 5 WC Oncology SC Oncology GA 603EY UT WOS:000178546900003 PM 12393980 ER PT J AU Barry, TS Jaffe, ES Kingma, DW Martin, AW Sorbara, L Raffeld, M Pittaluga, S AF Barry, TS Jaffe, ES Kingma, DW Martin, AW Sorbara, L Raffeld, M Pittaluga, S TI CD5+ follicular lymphoma - A clinicopathologic study of three cases SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE follicular lymphoma; CD5; t(14;18); bcl-2; IgH gene rearrangement; immunohistochemistry; flow cytometry ID B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMAS; MONOCLONAL-ANTIBODIES; PARAFFIN SECTIONS; T-CELL; LYMPHOPROLIFERATIVE DISORDERS; DIAGNOSTIC USEFULNESS; MALIGNANT-LYMPHOMAS; FLOW-CYTOMETRY; BONE-MARROW AB Follicular lymphoma (FL) is a low-grade lymphoma that typically lacks CD5 antigen expression. We report 3 cases of FL with unusual expression of CD5. All cases showed histologic features of FL, including effaced nodal architecture, follicular growth pattern, and a spectrum of grades from 1 to 3 using World Health Organization criteria. Inflow cytometric studies, all 3 cases showed a light chain-restricted, CD19+, CD20+ B-cell population coexpressing CD10 and low-level CD5. Immunohistochemical studies demonstrated an identical B-cell immunophenotype with weak expression of CD5 and coexpression of bcl-2 protein and the germinal center-associated markers, CD10 and bcl-6 protein. None of the cases showed expression of CD43, cyclin D1, or IgD. By molecular analysis, immunoglobulin heavy chain gene rearrangements were demonstrated in all 3 cases, and 2 of 3 cases had a t(14; 18). These cases highlight the difficulty classifying these lymphomas by flow cytometric studies alone and emphasize the importance of recognizing FL in the differential diagnosis of CD5+ B-cell lymphomas. C1 NCI, Hematopathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA. Univ Louisville, Sch Med, Louisville, KY 40292 USA. RP Pittaluga, S (reprint author), NCI, Hematopathol Sect, Pathol Lab, NIH, NIH Bldg 10,Room 2N202,10 Ctr Dr, Bethesda, MD 20892 USA. NR 46 TC 30 Z9 30 U1 0 U2 2 PU AMER SOC CLINICAL PATHOLOGY PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 2002 VL 118 IS 4 BP 589 EP 598 PG 10 WC Pathology SC Pathology GA 598XT UT WOS:000178302500015 PM 12375647 ER PT J AU Muenke, M Slavotinek, A Odent, S David, V Brown, S AF Muenke, M Slavotinek, A Odent, S David, V Brown, S CA Carter Centers for Holoprosencene TI Holoproesencephaly due to ZIC2 mutations: Clinical, neuroradiological, and molecular studies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. Univ Rennes, Rennes, France. Columbia Univ, New York, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 26 BP 169 EP 169 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800027 ER PT J AU Biesecker, BB McInerney-Leo, AM AF Biesecker, BB McInerney-Leo, AM TI Turner syndrome: Adaptation across the lifespan. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Med Genet Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 33 BP 170 EP 170 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800035 ER PT J AU Gollust, SE Hull, SC Wilfond, BS AF Gollust, SE Hull, SC Wilfond, BS TI "Bringing you the world of genetics": Direct-to-consumer genetic services on the Internet. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bioeth Res Sect, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 40 BP 171 EP 171 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800039 ER PT J AU Thomas, S Wideroff, L Breen, N Croyle, R Freedman, A AF Thomas, S Wideroff, L Breen, N Croyle, R Freedman, A TI Awareness of genetic testing for increased cancer risk in the year 2000 National Health Interview Survey. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. NCI, Canc Prevent Fellowship Program, Bethesda, MD 20892 USA. RI Hernandez, Jessica/G-6527-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 37 BP 171 EP 171 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800040 ER PT J AU Huizing, M Hermos, CR Vasconselos, OM Orvisky, E Krasnewich, D Dalakas, MC Gahl, WA AF Huizing, M Hermos, CR Vasconselos, OM Orvisky, E Krasnewich, D Dalakas, MC Gahl, WA TI Hereditary inclusion body myopathy due to mutations in the gene for UDP-Glc-NAc 2-epimerase/ManNAc kinase. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Bethesda, MD USA. NINDS, Bethesda, MD 20892 USA. NIMH, Bethesda, MD 20892 USA. NHGRI, Bethesda, MD 20892 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 47 BP 173 EP 173 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800050 ER PT J AU Porter, FD Wassif, CA Cozma, D Kratz, L Tsokos, M Hunter, AGW Kelley, RI Krakowiak, PA AF Porter, FD Wassif, CA Cozma, D Kratz, L Tsokos, M Hunter, AGW Kelley, RI Krakowiak, PA TI Lathosterol 5-desaturase deficiency: An inborn error of human and murine cholesterol biosynthesis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, HDB, NIH, Bethesda, MD USA. Kennedy Krieger Inst, Baltimore, MD USA. NCI, NIH, Bethesda, MD 20892 USA. Childrens Hosp Eastern Ontario, Ottawa, ON K1H 8L1, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 76 BP 179 EP 179 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800077 ER PT J AU Harris, EL Mellen, BG Adams, PC Acton, R Barton, JC McLaren, GD Dawkins, F Eckfeldt, JH Gordeuk, VR Lovato, L McLaren, CE Press, N Sholinsky, P Speechley, M Thomson, E AF Harris, EL Mellen, BG Adams, PC Acton, R Barton, JC McLaren, GD Dawkins, F Eckfeldt, JH Gordeuk, VR Lovato, L McLaren, CE Press, N Sholinsky, P Speechley, M Thomson, E TI Hemochromatosis and iron overload screening (HEIRS) study. Prevalence of elevated iron test levels by HFE genotype. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Kaiser Permanente Ctr Hlth Res, Portland, OR USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Univ Alabama, Birmingham, AL USA. Univ Calif Irvine, Irvine, CA USA. Howard Univ, Washington, DC 20059 USA. Univ Minnesota, Minneapolis, MN USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. NHLBI, Bethesda, MD 20892 USA. NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 83 BP 180 EP 180 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800085 ER PT J AU Huusko, P Wolf, M Ruiz, J Allinen, M Hautaniemi, S Chen, Y Mousses, S Kallioniemi, O AF Huusko, P Wolf, M Ruiz, J Allinen, M Hautaniemi, S Chen, Y Mousses, S Kallioniemi, O TI Genome-wide microarray screening for genes harboring truncating mutations based on non-sense-mediated RNA decay and comparative genomic hybridization (NMD-CGH). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD USA. Tampere Univ Technol, Inst Signal Proc, FIN-33101 Tampere, Finland. RI Kallioniemi, Olli/H-4738-2012; Kallioniemi, Olli/H-5111-2011 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 86 BP 181 EP 181 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800087 ER PT J AU Matyakhina, LD Lenherr, S Sandrini, F Kurschner, LS Dutra, A Pak, E Stratakis, CA AF Matyakhina, LD Lenherr, S Sandrini, F Kurschner, LS Dutra, A Pak, E Stratakis, CA TI Protein kinase A may be involved in chromosomal stability: Induction of cytogenetic abnormalities in mouse embryonic fibroblasts by PRKAR1A down- regulation. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Dept DEB, Bethesda, MD USA. NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 99 BP 183 EP 183 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800101 ER PT J AU Rosenberg, MJ Agarwala, R Bouffard, G Davis, J Fiermonte, G Hilliard, MS Koch, T Kalikin, LM Makalowska, I Morton, DH Petty, EM Weber, JL Palmieri, F Kelley, RI Schaffer, AA Biesecker, LG AF Rosenberg, MJ Agarwala, R Bouffard, G Davis, J Fiermonte, G Hilliard, MS Koch, T Kalikin, LM Makalowska, I Morton, DH Petty, EM Weber, JL Palmieri, F Kelley, RI Schaffer, AA Biesecker, LG TI Amish microcephaly is caused by mutation in the deoxynucleotide carrier DNC. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIH, Bethesda, MD 20892 USA. Univ Bari, Dept Pharmacobiol, Biochem & Mol Biol Lab, Bari, Italy. Logicon ROW Sci Corp, Rockville, MD USA. Konrad Zuse Zentrum Informat Tech, Berlin, Germany. Univ Michigan, Med Ctr, Dept Internal Med, Ann Arbor, MI 48109 USA. Clin Special Children, Strasburg, PA USA. Marshfield Med Res Fdn, Marshfield, WI 54449 USA. Johns Hopkins Univ, Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Dept Pediat, Baltimore, MD 21218 USA. RI Schaffer, Alejandro/F-2902-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 124 BP 188 EP 188 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800124 ER PT J AU Wang, T Zhang, L Obie, C Mousses, S Trent, J Valle, D AF Wang, T Zhang, L Obie, C Mousses, S Trent, J Valle, D TI Identification of genes responsible for X linked mental retardation (XLMR) using a human X chromosome specific cDNA microarray. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Johns Hopkins Univ, Inst Med Genet, Baltimore, MD USA. Johns Hopkins Univ, Dept Pediat, Baltimore, MD 21218 USA. Howard Hughes Med Inst, Bethesda, MD 20817 USA. NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 125 BP 188 EP 188 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800126 ER PT J AU Bourdeau, I Lacroix, A Kirschner, LS Costouros, NG Lorang, D Stratakis, CA AF Bourdeau, I Lacroix, A Kirschner, LS Costouros, NG Lorang, D Stratakis, CA TI Differential gene expression in sporadic macronodular adrenal hyperplasia compared to normal adrenals by microarrays : Dissecting the genetics of adrenocortical tumorigenesis SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, UGEN, DEB, NIH, Bethesda, MD USA. CHUM, Hotel Dieu, Montreal, PQ, Canada. NCI, Surg Br, Bethesda, MD 20892 USA. RI Levesque, Isabelle/A-1899-2012 NR 0 TC 1 Z9 1 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 127 BP 189 EP 189 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800130 ER PT J AU Chen, G Zhou, J Doumatey, A Amoah, A Acheampong, J Agyenim-Boateng, K Eghan, B Oli, J Okafor, G Ofoegbu, E Osotimehin, B Abbiyesuku, F Johnson, T Fasimade, O Chen, Y Daniel, H Furbert-Harris, P Dunston, G Collins, F Rotimi, C AF Chen, G Zhou, J Doumatey, A Amoah, A Acheampong, J Agyenim-Boateng, K Eghan, B Oli, J Okafor, G Ofoegbu, E Osotimehin, B Abbiyesuku, F Johnson, T Fasimade, O Chen, Y Daniel, H Furbert-Harris, P Dunston, G Collins, F Rotimi, C CA AADM Study TI Scanning the genome for obesity susceptibility genes in type 2 diabetes patients from West Africa. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Howard Univ, Natl Human Genome Ctr, Washington, DC 20059 USA. Univ Ghana, Accra, Ghana. Univ Nigeria, Enugu, Nigeria. UCH, Ibadan, Nigeria. Univ Lagos, Lagos, Nigeria. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 131 BP 189 EP 189 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800132 ER PT J AU Crabtree, JS Libutti, SK Lorang, D Ward, JM Garrett-Beal, L Scacheri, PC Hanahan, D Edlund, H Magnuson, MA Chandrasekharappa, SC Marx, SJ Spiegel, AM Collins, FS AF Crabtree, JS Libutti, SK Lorang, D Ward, JM Garrett-Beal, L Scacheri, PC Hanahan, D Edlund, H Magnuson, MA Chandrasekharappa, SC Marx, SJ Spiegel, AM Collins, FS TI A conditional mouse knockout model of Multiple Endocrine Neoplasia, type 1. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Umea Univ, Umea, Sweden. Vanderbilt Univ, Nashville, TN USA. NIDDK, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 128 BP 189 EP 189 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800128 ER PT J AU Scacheri, PC Caplen, N Shanmugarajah, D Crabtree, JS Chandrasekharappa, S Marx, S Spiegel, A Collins, FS AF Scacheri, PC Caplen, N Shanmugarajah, D Crabtree, JS Chandrasekharappa, S Marx, S Spiegel, A Collins, FS TI Using RNAi and microarrays to investigate the function of menin. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NIDDK, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 129 BP 189 EP 189 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800131 ER PT J AU Hattori, E Liu, C Badner, JA Christian, SL Maheshwari, M Detera-Wadleigh, SD Bonner, TI Gibbs, RA Gershon, ES AF Hattori, E Liu, C Badner, JA Christian, SL Maheshwari, M Detera-Wadleigh, SD Bonner, TI Gibbs, RA Gershon, ES TI Polymorphisms of LG72 (on 13q33) associated with Bipolar disorder by TDT and partition of linkage evidence. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA. NIMH, Bethesda, MD 20892 USA. RI Liu, Chunyu/G-7561-2012 OI Liu, Chunyu/0000-0002-5986-4415 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 153 BP 194 EP 194 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800155 ER PT J AU Edgemon, K Haluzik, M Cutler, DA Zamowski, MJ Gavrilova, O Londos, C Reitman, ML AF Edgemon, K Haluzik, M Cutler, DA Zamowski, MJ Gavrilova, O Londos, C Reitman, ML TI Transgenic mice with partial lipodystrophy due to expression of lamin A or C cDNA containing a Dunnigan-specific mutation. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDDK, NIH, Bethesda, MD USA. George Washington Univ, Genet Program, Washington, DC USA. NCI, NIH, Frederick, MD 21701 USA. Merck Res Labs, Rahway, NJ USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 157 BP 195 EP 195 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800160 ER PT J AU Eriksson, M Singer, J Scott, L Dutra, A Boehnke, M Collins, FS AF Eriksson, M Singer, J Scott, L Dutra, A Boehnke, M Collins, FS TI Uniparental isodisomy of chromosome 1q in a patient with Hutchinson-Gilford Progeria syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 176 BP 199 EP 199 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800177 ER PT J AU Bussey, K Chin, K Reinhold, WC Lababidi, S Gwadry, F Scherf, U Ajay Tonon, G Roschke, A Stover, K Kirsch, I Scudiero, DA Gray, JW Weinstein, JN AF Bussey, K Chin, K Reinhold, WC Lababidi, S Gwadry, F Scherf, U Ajay Tonon, G Roschke, A Stover, K Kirsch, I Scudiero, DA Gray, JW Weinstein, JN TI Correlating array CGH with gene expression and sensitivity to drugs in a panel of 60 human cancer cell lines. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Mol Pharmacol Lab, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. GeneLogic, Gaithersburg, MD USA. Celera Genom, Rockville, MD USA. NCI, Genet Lab, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 185 BP 200 EP 200 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800186 ER PT J AU Cabral, W Marini, JC AF Cabral, W Marini, JC TI Two mosaics for COL1A1 mutations causing type III and IV osteogenesis imperfecta have a high percent of mutant bone cells: Implications for cell/gene therapy. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, SCTD, HDB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 189 BP 201 EP 201 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800191 ER PT J AU Phomphutkul, C Introne, W Perry, M Bernardini, L Anderson, P Fitzpatrick, D D'Souza, M Huizing, M Anikster, Y Gerber, L Gahl, W AF Phomphutkul, C Introne, W Perry, M Bernardini, L Anderson, P Fitzpatrick, D D'Souza, M Huizing, M Anikster, Y Gerber, L Gahl, W TI Clinical, biochemical, molecular and therapeutic findings in alkaptonuria (AKU). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, HDB, NIH, Bethesda, MD USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 190 BP 201 EP 201 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800189 ER PT J AU Margulies, EH AF Margulies, EH TI Computational approaches for performing multi-species comparative sequence analysis: A platform for targeted studies of genome architecture, function, and evolution. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NISC, Comparat Sequencing Program, Bethesda, MD USA. NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 198 BP 203 EP 203 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800198 ER PT J AU Mohlke, KL Wiles, KR Wilkowski, J Jackson, AU Silander, K Erdos, MR Bennett-Baker, PE Scott, LJ Fingerlin, TE Wasson, J Permutt, MA Burke, DT Boehnke, M Collins, FS AF Mohlke, KL Wiles, KR Wilkowski, J Jackson, AU Silander, K Erdos, MR Bennett-Baker, PE Scott, LJ Fingerlin, TE Wasson, J Permutt, MA Burke, DT Boehnke, M Collins, FS TI High-throughput screening of allele frequency differences between DNA pools of cases and controls using four primer extension genotyping technologies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Washington Univ, Sch Med, St Louis, MO USA. Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 201 BP 203 EP 203 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800202 ER PT J AU Mykytyn, K Nishimura, DY Searby, C Yen, H Cornier, AS Cox, GF Carmi, R Chandrasekharappa, SC Collins, FS Stone, EM Sheffield, VC AF Mykytyn, K Nishimura, DY Searby, C Yen, H Cornier, AS Cox, GF Carmi, R Chandrasekharappa, SC Collins, FS Stone, EM Sheffield, VC TI Identification of the gene most commonly involved in Bardet-Biedl syndome (BBS1) and evaluation of triallelic inheritance involving the BBS1 gene. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Iowa, Dept Ophthalmol, Iowa City, IA 52242 USA. NHGRI, NIH, Bethesda, MD 20892 USA. Soroka Med Ctr, Genet Inst, IL-84101 Beer Sheva, Israel. Childrens Hosp, Boston, MA 02115 USA. Ponce Sch Med, Dept Biochem, Ponce, PR USA. Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 229 BP 209 EP 209 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800231 ER PT J AU McBride, KL Lewin, MB Pignatelli, R Fernbach, SD Combes, A Lam, W Bezold, L Ho, T Craigen, W Kaplan, N Towbin, JA Belmont, JW AF McBride, KL Lewin, MB Pignatelli, R Fernbach, SD Combes, A Lam, W Bezold, L Ho, T Craigen, W Kaplan, N Towbin, JA Belmont, JW TI Echocardiographic evaluation of parental and sibling risk associated with pediatric left ventricular outflow tract lesions. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Natl Inst Environm Sci, NIH, Bethesda, MD USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. Baylor Coll Med, Div Pediat Cardiol, Houston, TX 77030 USA. Univ Washington, Div Pediat Cardiol, Seattle, WA 98195 USA. Baylor Coll Med, Dept Human Mol Genet, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 238 BP 211 EP 211 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800238 ER PT J AU Hol, NC Brant, LJ Park, SS North, M Guarnieri, MJ Francomano, CA Carson, BS AF Hol, NC Brant, LJ Park, SS North, M Guarnieri, MJ Francomano, CA Carson, BS TI Living with achondroplasia: quality of life evaluation following cervico-medullary decompression. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Stat Methods & Expt Designs Sect, RRB, NIH, Baltimore, MD 21224 USA. NIA, Sect Human Genet & Integrat Med, LG, NIH, Baltimore, MD 21224 USA. Johns Hopkins Med Inst, Dept Pediat, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 245 BP 212 EP 212 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800246 ER PT J AU Toro, JR Nickerson, ML Warren, MB Glenn, G Turner, ML Duray, P Merino, M Choyke, P Walther, M Linehan, MW Zbar, B Schmidt, LS AF Toro, JR Nickerson, ML Warren, MB Glenn, G Turner, ML Duray, P Merino, M Choyke, P Walther, M Linehan, MW Zbar, B Schmidt, LS TI Mutations in fumarate hydratase cause uterine fibroids, cutaneous leiomyomas and aggressive renal neoplasia. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 SAIC Frederick, Intramural Res Support Program, Frederick, MD USA. Ctr Canc Res, Urol Oncol Branch, Bethesda, MD USA. Ctr Canc Res, Pathol Lab, Bethesda, MD USA. Ctr Canc Res, Dermatol Branch, Bethesda, MD USA. NCI, Immunol Lab, Frederick, MD 21701 USA. NCI, Genet Epidemiol Branch, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 248 BP 213 EP 213 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800248 ER PT J AU Lin, JP Cupples, LA Wilson, PWF Jaquish, CE O'Donnell, CJ AF Lin, JP Cupples, LA Wilson, PWF Jaquish, CE O'Donnell, CJ TI Evidence for a gene influencing serum bilirubin on chromosome 2q telomere: A genome-wide scan in the Framingham Offspring Study. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHLBI, Framingham Heart Study, Framingham, MA USA. Boston Univ, Sch Med, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Boston, MA USA. NHLBI, DECA, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 257 BP 215 EP 215 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800260 ER PT J AU Papanicolaou, GJ Platte, P Johnston, J Doheny, K Pugh, EW Roy-Gagnon, MH Stunkard, AJ Francomano, C Wilson, AF AF Papanicolaou, GJ Platte, P Johnston, J Doheny, K Pugh, EW Roy-Gagnon, MH Stunkard, AJ Francomano, C Wilson, AF TI Linkage and association of BMI to markers on 7q in the Old-Order Amish. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, NIH, Baltimore, MD 21224 USA. Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA. JHSPH, Dept Epidemiol, Baltimore, MD USA. JHU, SOM, CIDR, Baltimore, MD USA. NHGRI, NIH, Bethesda, MD 20892 USA. Univ Wurzburg, Wurzburg, Germany. NHGRI, Genometr Sect, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 258 BP 215 EP 215 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800258 ER PT J AU Zhang, J Rowe, W Buetow, K AF Zhang, J Rowe, W Buetow, K TI HapScope: a software system for automated and visual analysis of functional haplotypes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Populat Genet, Gaithersburg, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 282 BP 220 EP 220 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800283 ER PT J AU Barker, PE Pinsky, P Wang, W Srivastava, S Hocker, D Wu, X Spitz, MR AF Barker, PE Pinsky, P Wang, W Srivastava, S Hocker, D Wu, X Spitz, MR TI Estimates of consensus in cell selection and scoring of FISH data. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX USA. NCI, Canc Biomarkers Grp, Div Canc Prevent, Bethesda, MD 20892 USA. NIST, Div Biotechnol, DNA Technol Grp, Gaithersburg, MD 20899 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 294 BP 222 EP 222 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800294 ER PT J AU Sarraf, SA Tejada, R Dennis, T Oberst, M Simon, KC Blancato, JK AF Sarraf, SA Tejada, R Dennis, T Oberst, M Simon, KC Blancato, JK TI PA-1, a human ovarian teratocarcinoma cell line, deomonstrates a single chromosome abnormality, t(15;20)(p11.2;11.2): analysis with FISH, SKY and BAC microarray analysis SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Georgetown Univ, Washington, DC USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 310 BP 225 EP 225 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800311 ER PT J AU Wang, Z Lo, S Yang, H Gere, S Hu, Y Buetow, K Lee, M AF Wang, Z Lo, S Yang, H Gere, S Hu, Y Buetow, K Lee, M TI Computational screening and experimental validation of tumor related alternative splicing in human genome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Populat Genet, Gaithersburg, MD 20877 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 334 BP 229 EP 229 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800333 ER PT J AU Atha, DH Miller, K Sanow, AD Xu, J Hess, JL Wu, OC Wang, W Srivastava, S Highsmith, WE AF Atha, DH Miller, K Sanow, AD Xu, J Hess, JL Wu, OC Wang, W Srivastava, S Highsmith, WE TI High-throughput TRAP/PCR analysis of telomerase using capillary electrophoresis SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIST, Div Biotechnol, Gaithersburg, MD 20899 USA. Univ Maryland, Dept Pathol, Sch Med, Baltimore, MD 21201 USA. NCI, Div Canc Prevent, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 341 BP 230 EP 230 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800342 ER PT J AU Hadley, D Jenkins, J DeCarvalho, M Dimond, E Kirsch, I Palmer, CGS AF Hadley, D Jenkins, J DeCarvalho, M Dimond, E Kirsch, I Palmer, CGS TI Cancer screening practices following genetic counseling/testing in families with HNPCC. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NCI, CCR, NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 369 BP 235 EP 235 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800371 ER PT J AU Kilpivaara, O Vahteristo, P Syrjakoski, K Eerola, H Bartkova, J Aittomaki, K Heikkila, P Bartek, J Holli, K Blomqvist, C Kallioniemi, OP Nevanlinna, H AF Kilpivaara, O Vahteristo, P Syrjakoski, K Eerola, H Bartkova, J Aittomaki, K Heikkila, P Bartek, J Holli, K Blomqvist, C Kallioniemi, OP Nevanlinna, H TI A CHEK2 variant with increased breast cancer risk. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, Helsinki, Finland. Tampere Univ, Lab Canc Genet, Inst Med Technol, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Dept Oncol, Tampere, Finland. HUCH, Dept Oncol, Helsinki, Finland. Danish Canc Soc, Inst Canc Biol, Copenhagen, Denmark. HUCH, Dept Clin Genet, Helsinki, Finland. HUCH, Dept Pathol, Helsinki, Finland. Natl Human Genome Res Inst, Canc Genet Branch, Bethesda, MD USA. Univ Uppsala Hosp, Uppsala, Sweden. RI Kallioniemi, Olli/H-4738-2012; Kallioniemi, Olli/H-5111-2011; Bartek, Jiri/G-5870-2014 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332; NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 372 BP 236 EP 236 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800373 ER PT J AU McInerney-Leo, AM Biesecker, BB Hadley, D Kase, RG Giambarresi, TR Johnson, E Lerman, C Struewing, JP AF McInerney-Leo, AM Biesecker, BB Hadley, D Kase, RG Giambarresi, TR Johnson, E Lerman, C Struewing, JP TI How BRCA1/2 test results affect risk perception and beliefs among members of Hereditary Breast and Ovarian Cancer (HBOC) Families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. Westat Res, Rockville, MD USA. Johns Hopkins Biostats Ctr, Baltimore, MD USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 376 BP 236 EP 236 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800375 ER PT J AU McMaster, ML Griffith, GM Choyke, PL Glenn, GM Linehan, WM AF McMaster, ML Griffith, GM Choyke, PL Glenn, GM Linehan, WM TI Minimal expression of von Hippel-Lindau disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Genet Epidemiol Branch, DCEG, NIH, Bethesda, MD 20892 USA. NCI, Urol Oncol Branch, CCR, NIH, Bethesda, MD USA. NIH, Dept Diagnost Radiol, Warren Grant Magnuson Clin Ctr, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 398 BP 240 EP 240 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800398 ER PT J AU Ravnik-Glavac, M Potocnik, U Glavac, D AF Ravnik-Glavac, M Potocnik, U Glavac, D TI Identification of novel genes with somatic frameshift mutations within coding,mononucleotide repeats In colorectal tumors with high microsatellite instability. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Fac Med, Inst Pathol, Dept Mol Genet, Ljubljana, Slovenia. NCI, FCRDC, Lab Genom Divers, Frederick, MD USA. Fac Med, Inst Biochem, Ljubljana, Slovenia. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 404 BP 241 EP 241 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800404 ER PT J AU Yeager, M Packer, B Miller, E Welch, R Kiley, M Burke, M Strausberg, R Rothman, N Chanock, S AF Yeager, M Packer, B Miller, E Welch, R Kiley, M Burke, M Strausberg, R Rothman, N Chanock, S TI SNP500Cancer database and candidate SNP approach to genetic association studies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Pediat Oncol Branch, Sect Genom Variat, Bethesda, MD USA. NCI, FCRDC, Frederick, MD USA. SAIC, Intramural Res Support Program, Frederick, MD USA. NCI, Off Canc Genom, Bethesda, MD USA. NCI, DCEG, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 410 BP 242 EP 242 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800410 ER PT J AU Beck, JC Hopper, JL John, EM Knight, JA Neuhausen, SL Senie, RT Andrulis, IL Anton-Culver, H Buys, S West, D Whittemore, A Daly, MB Seminara, D AF Beck, JC Hopper, JL John, EM Knight, JA Neuhausen, SL Senie, RT Andrulis, IL Anton-Culver, H Buys, S West, D Whittemore, A Daly, MB Seminara, D TI The Breast Cancer Family Registry: 1997-2002. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Corielil Inst Med Res, Camden, NJ USA. Univ Melbourne, Melbourne, Vic, Australia. No Calif Canc Ctr, Union, CA USA. Canc Care, Toronto, ON, Canada. Univ Utah, Salt Lake City, UT USA. Columbia Univ, New York, NY USA. NCI, DCCPS, EGRP, NIH, Bethesda, MD USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 438 BP 247 EP 247 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800439 ER PT J AU Matrosova, V Nickerson, M Warren, M Sharma, N Schmidt, L Zbar, B AF Matrosova, V Nickerson, M Warren, M Sharma, N Schmidt, L Zbar, B TI Establishment of the physical map in the 17p11.2 critical region for BHD gene discovery. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Immunobiol Lab, NIH, Frederick, MD USA. SAIC Frederick Inc, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 440 BP 247 EP 247 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800440 ER PT J AU Hostetter, GH Kakareka, J Salem, G Hubbell, J Kononen, J Wagner, U Comelison, R Pohida, T Kallioniemi, OP AF Hostetter, GH Kakareka, J Salem, G Hubbell, J Kononen, J Wagner, U Comelison, R Pohida, T Kallioniemi, OP TI Automated construction of tissue miciroarrays from morphologically selected sites: a powerful method for studies of genetic heterogenel of cancer. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, Canc Genet Branch, NIH, Bethesda, MD USA. Ctr Informat Technol, NIH, Bethesda, MD USA. RI Kallioniemi, Olli/H-4738-2012; Kallioniemi, Olli/H-5111-2011 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 452 BP 249 EP 249 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800452 ER PT J AU Ghiorzo, P Gramigi, C Mantelli, M Pastorino, L Gargiulo, S Banelli, B Romani, M Villaggio, B Garre, C Bianchi-Scarra, G AF Ghiorzo, P Gramigi, C Mantelli, M Pastorino, L Gargiulo, S Banelli, B Romani, M Villaggio, B Garre, C Bianchi-Scarra, G TI Correlation between NF-kB/GM-CSF expression and functional status of the p16 melanoma susceptibility gene. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Genoa, Dept Oncol Biol, Genoa, Italy. Natl Canc Inst, Genoa, Italy. Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy. RI Bianchi Scarra, Giovanna/G-8933-2014 OI Bianchi Scarra, Giovanna/0000-0002-6127-1192 NR 0 TC 0 Z9 0 U1 1 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 460 BP 250 EP 250 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800459 ER PT J AU Potocnik, U Martin, MP Gold, B Gao, X Dean, M Carrington, M AF Potocnik, U Martin, MP Gold, B Gao, X Dean, M Carrington, M TI Genetic risk factors for progression to lymphoma in AIDS patients. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Lab Genom Divers, NCI Frederick, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 458 BP 250 EP 250 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800458 ER PT J AU Tilli, MT Frech, MS Hudgins, SL Renou, JP Heletz, I Hruska, KS Hennighausen, L Flaws, JA Furth, PA AF Tilli, MT Frech, MS Hudgins, SL Renou, JP Heletz, I Hruska, KS Hennighausen, L Flaws, JA Furth, PA TI The E2F binding partner DP-1 and its role in cancer progression and differentiation. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Maryland, Grad Program Human Genet, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA. NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD USA. Georgetown Univ, Dept Oncol, Lombardi Canc Ctr, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 466 BP 251 EP 251 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800465 ER PT J AU Griffin, KJ Bei, T Meck, J Wong, LJ Bondy, C Stratakis, CA AF Griffin, KJ Bei, T Meck, J Wong, LJ Bondy, C Stratakis, CA TI Gender ambiguity and fragile X: a new syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, UGEN, DEB, NIH, Bethesda, MD USA. Georgetown Univ, Inst Mol & Human Genet, Washington, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 573 BP 270 EP 270 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800576 ER PT J AU Solomon, BI McCullagh, L Krasnewich, D Smith, ACM AF Solomon, BI McCullagh, L Krasnewich, D Smith, ACM CA SMS Research Unit TI Oral motor, speech and voice functions in Smith Magenis Syndrome children: A research update. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIH, Dept Rehabil Med, WG Magnuson Clin Ctr, Bethesda, MD 20892 USA. NHGRI, Med Genet Branch, NIH, Bethesda, MD USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 583 BP 271 EP 271 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800584 ER PT J AU Ng, D Johnston, JJ Turner, JT Biesecker, LG AF Ng, D Johnston, JJ Turner, JT Biesecker, LG TI Gonadal mosaicism in Pallister-Hall syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 611 BP 276 EP 276 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800613 ER PT J AU Lacbawan, FL Davis, RL Collins, GH Kent, P Holohan, PD Shrimpton, AE Muenke, M Krasnewic, D AF Lacbawan, FL Davis, RL Collins, GH Kent, P Holohan, PD Shrimpton, AE Muenke, M Krasnewic, D TI Genotype governs the clinical spectrum of neuroserpinopathy SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 GWU, Childrens Natl Med Ctr, Med Genet, Washington, DC USA. NHGRI, Med Genet Br, NIH, Bethesda, MD 20892 USA. SUNY Upstate Med Univ, Syracuse, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 653 BP 283 EP 283 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800655 ER PT J AU Slavotinek, AM AF Slavotinek, AM TI Phenotypic diversity in human malformation syndromes are modifier genes important? SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 656 BP 284 EP 284 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800657 ER PT J AU Cozma, D Correa-Cerro, LS Krakowiak, PA Porter, FD AF Cozma, D Correa-Cerro, LS Krakowiak, PA Porter, FD TI Mutation analysis and phenotypic description of three severely affected Smith-Lemli-Opitz syndrome patients SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIH, Heritable Disorder Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 667 BP 285 EP 285 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800668 ER PT J AU Wright, BS Nwokoro, NA Waye, JS Wassif, CW Nowaczyk, MJ Porter, FD AF Wright, BS Nwokoro, NA Waye, JS Wassif, CW Nowaczyk, MJ Porter, FD TI Carrier frequency of the Smith-Lemli-Opitz IVS8-1GC mutation of the DHCR7 gene in African Americans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Heritable disorders Branch, NIH, Bethesda, MD USA. McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON L8S 4L8, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 669 BP 286 EP 286 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800672 ER PT J AU Kozma, C Slavotinek, A Meck, J AF Kozma, C Slavotinek, A Meck, J TI Segregation of a t(1;3) translocation in multiple affected family members with both types of adjacent-1 segregants. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Georgetown Univ, Dept Pediat, Dept Obstet & Gynecol, Washington, DC 20057 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 719 BP 295 EP 295 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800722 ER PT J AU Meck, JM Wray, A Ghidini, A Gorman, B Vallejo, P Dennis, T Haddad, B AF Meck, JM Wray, A Ghidini, A Gorman, B Vallejo, P Dennis, T Haddad, B TI True fetal mosaicism for a supernumerary de novo ring chromosome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Georgetown Univ Hosp, Dept Obstet Gynecol, Washington, DC 20007 USA. NHGRI, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20057 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 786 BP 306 EP 306 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800786 ER PT J AU Donarum, EA Hautaniemi, S Graff, J Cheng, Y Mousses, S Kallioniemi, O Natale, J Stephan, DA AF Donarum, EA Hautaniemi, S Graff, J Cheng, Y Mousses, S Kallioniemi, O Natale, J Stephan, DA TI Novel developmentally regulated gene circuits in murine brain regions: A template for understanding dysfunction and tumorigenesis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Childrens Res Inst, Med Genet Res Ctr, Washington, DC USA. NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA. RI Kallioniemi, Olli/H-4738-2012; Kallioniemi, Olli/H-5111-2011 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 818 BP 312 EP 312 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800821 ER PT J AU Karkera, JD Roessler, E Ouspenskaia, MV Dela Cruz, J Goldmuntz, E Bowers, P Towbin, J Belmont, J Shen, MM Muenke, M AF Karkera, JD Roessler, E Ouspenskaia, MV Dela Cruz, J Goldmuntz, E Bowers, P Towbin, J Belmont, J Shen, MM Muenke, M TI Mutations in the EGF-CFC genes, CFC1 and TDGF1, cause congenital cardiovascular malformations in humans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, Med Genet Br, NIH, Bethesda, MD 20892 USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. Yale Univ, Coll Med, New Haven, CT 06520 USA. Baylor Coll Med, Houston, TX 77030 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, CABM, Piscataway, NJ 08854 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 821 BP 313 EP 313 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800823 ER PT J AU Ouspenskaia, MV Karkera, JD Roessler, E Shen, MM Goldmunts, E Bowers, P Towbin, J Belmont, J Muenke, M AF Ouspenskaia, MV Karkera, JD Roessler, E Shen, MM Goldmunts, E Bowers, P Towbin, J Belmont, J Muenke, M TI Role of FAST1 gene in the development of holoprosencephaly (HPE) and congenital cardiac malformations in humans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, MGB, NIH, Bethesda, MD 20892 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, CABM, Piscataway, NJ 08854 USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. Yale Univ, Sch Med, New Haven, CT 06520 USA. Baylor Coll Med, Houston, TX 77030 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 822 BP 313 EP 313 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800826 ER PT J AU Cui, CY Durmowicz, M Tanaka, TS Hartung, AJ Tezuka, T Hashimoto, K Ko, MSH Srivastava, AK Schlessinger, D AF Cui, CY Durmowicz, M Tanaka, TS Hartung, AJ Tezuka, T Hashimoto, K Ko, MSH Srivastava, AK Schlessinger, D TI EDA targets revealed by skin gene expression profiles of wild-type, Tabby, and Tabby EDA-Al transgenic mice. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. Greenwood Genet Ctr, JC Self res Inst Human Genet, Greenwood, SC 29646 USA. Kinki Univ, Sch Med, Dept Dermatol, Osaka 589, Japan. Wayne State Univ, Sch Med, Dept Dermatol, Detroit, MI 48201 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 UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 829 BP 314 EP 314 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800830 ER PT J AU Wang, KS Grimes, P Dutra, A Favor, J Stambolian, D AF Wang, KS Grimes, P Dutra, A Favor, J Stambolian, D TI Localization of the mouse Tcm gene to a 1 Mb region on chromosome 4 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Penn, Dept Genet, Philadelphia, PA 19104 USA. Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA. NHGRI, NIH, Bethesda, MD 20892 USA. GSF, Inst Mammalian Genet, Natl Res Ctr Environm & Hlth, Neuherberg, Germany. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 836 BP 315 EP 315 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800839 ER PT J AU Mez, JB Karkera, JD Roessler, E Goldmuntz, E Bowers, P Towbin, JA Belmont, J Ekker, SC Muenke, M AF Mez, JB Karkera, JD Roessler, E Goldmuntz, E Bowers, P Towbin, JA Belmont, J Ekker, SC Muenke, M TI Mutations in GDF1 are associated with congenital cardiovascular malformations in humans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA. Childrens Hosp Philadelphia, Div Cardiol, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA. Univ Minnesota, Dept Genet Cell Biol & Dev, Inst Human Genet, Arnold & Mabel Beckman Ctr Transposon Res, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 853 BP 318 EP 318 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800854 ER PT J AU Yang, T Carmi, R Bayazit, Y Ramesh, A Kurima, K Cable, B Elbedour, K Srisailapathy, CRS Griffith, AJ Sheffield, VC Smith, RJH AF Yang, T Carmi, R Bayazit, Y Ramesh, A Kurima, K Cable, B Elbedour, K Srisailapathy, CRS Griffith, AJ Sheffield, VC Smith, RJH TI Mutation screening of TMC1 in DFNB7/11 families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Iowa, Genet Program, Iowa City, IA USA. Ben Gurion Univ Negev, Soroka Med Ctr, Genet Inst, Negev, Israel. Gaziantep Univ, Dept Otolaryngol Head & Neck Surg, Kolejtepe, Gaziantep, Turkey. Univ Madras, Dept Genet, Madras, Tamil Nadu, India. Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD USA. Univ Iowa, Howard Hughes Med Inst, Iowa City, IA 52242 USA. Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA. NR 0 TC 3 Z9 3 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 858 BP 319 EP 319 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800861 ER PT J AU Liu, PC Kaler, SG AF Liu, PC Kaler, SG TI Genomic organization and characterization of the human ATX1 homologue involved-in copper homeostasis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Unit Pediat Genet, Lab Clin Genom, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 884 BP 323 EP 323 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800886 ER PT J AU Annilo, T Chen, ZQ Shulenin, S Dean, M AF Annilo, T Chen, ZQ Shulenin, S Dean, M TI Evolutionary analysis of a cluster of ATP-binding cassette (ABC) genes reveals multiple gene duplication, gene deletion and gene conversion events. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA. SAIC, Intramural Res & Support Program, Frederick, MD 21702 USA. RI Annilo, Tarmo/J-2900-2013 OI Annilo, Tarmo/0000-0002-9588-3058 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 889 BP 324 EP 324 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800889 ER PT J AU Crisponi, L Uda, M Chiappe, F Delana, M Usala, GL Maronqiu, M Amati, P Bonneau, D Faravelli, F Tolmie, J Bisceglia, L Piemontese, MR Zelante, L Gasparini, P Crisponi, G Boccone, L Iolascon, A Percesepe, A Forabosco, A Pilia, G AF Crisponi, L Uda, M Chiappe, F Delana, M Usala, GL Maronqiu, M Amati, P Bonneau, D Faravelli, F Tolmie, J Bisceglia, L Piemontese, MR Zelante, L Gasparini, P Crisponi, G Boccone, L Iolascon, A Percesepe, A Forabosco, A Pilia, G CA FOXL2 Study Group TI Genetic basis for non-syndromic and syndromic, blepharophimosis/ptosis and epicantus inversus syndrome (BPES)-associated premature ovarian failure (POF). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 CNR, Inst Ric Talass Anemie Medit, Cagliari, Italy. Serv Genet Med, Poitiers, France. Univ Cagliari, Cagliari, Italy. Osped Galliera, Genoa, Italy. Duncan Guthrie Inst Med Genet, Glasgow G3 8SJ, Lanark, Scotland. IRCCS, San Giovanni Rotondo, Italy. Univ Bari, I-70121 Bari, Italy. Univ Modena, I-41100 Modena, Italy. NIA, NIH, Bethesda, MD 20892 USA. RI Iolascon, Achille/A-4461-2014; Bonneau, Dominique/K-6110-2015; Bisceglia, Luigi/B-8720-2017 OI Bisceglia, Luigi/0000-0001-5367-8518 NR 0 TC 2 Z9 2 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 885 BP 324 EP 324 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800887 ER PT J AU Erichsen, HC Eck, P Taylor, JG Yeager, M Hughes, A Levine, MA Chanock, SJ AF Erichsen, HC Eck, P Taylor, JG Yeager, M Hughes, A Levine, MA Chanock, SJ TI Genetic analysis of two sodium dependent vitamin C transporters, SLC 23A1 and SLC23A2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Ctr Adv Technol, Gaithersburg, MD USA. NIDDK, NIH, Bethesda, MD 20892 USA. Univ S Carolina, Dept Biol Sci, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 910 BP 328 EP 328 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800914 ER PT J AU Chae, JJ Chen, J Komarow, H Wood, G Raben, N Liu, PP Kastner, DL AF Chae, JJ Chen, J Komarow, H Wood, G Raben, N Liu, PP Kastner, DL TI Mice deficient in pyrin, the FMF protein, show increased sensitivity to endotoxin through a new pathway regulating IL-1 activation and apoptosis SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAMS, Genet & Genom Branch, NIH, Bethesda, MD USA. NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. NIAMS, Arthrit & Rheumatism Branch, NIH, Bethesda, MD USA. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 933 BP 332 EP 332 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800935 ER PT J AU Rogan, PK Svojanovsky, SR Hurwitz, I Schneider, TD Leeder, JS AF Rogan, PK Svojanovsky, SR Hurwitz, I Schneider, TD Leeder, JS TI Modeling splice site and transcription factor binding site variation by information theory. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Childrens Mercy Hosp, Kansas City, MO 64108 USA. NCI, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 942 BP 333 EP 333 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800945 ER PT J AU Crawford, GE Holt, I Robbins, CM Moses, T Wolfsberg, TG Collins, FS AF Crawford, GE Holt, I Robbins, CM Moses, T Wolfsberg, TG Collins, FS TI Generation of a genome-wide library of regulatory sequences through the use of a novel DNAse hypersensitive site cloning procedure. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 949 BP 334 EP 334 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800949 ER PT J AU Durmowicz, MC Cui, CY Schlessinger, D AF Durmowicz, MC Cui, CY Schlessinger, D TI Characterization of regulatory networks controlling ectodysplasin-A expression: Progress toward identification of enhancer-binding proteins. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 948 BP 334 EP 334 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800951 ER PT J AU Shulenin, S Annilo, T Dean, M AF Shulenin, S Annilo, T Dean, M TI Study of ABCG5 and ABCG8 genes regulation SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Frederick, MD USA. RI Annilo, Tarmo/J-2900-2013 OI Annilo, Tarmo/0000-0002-9588-3058 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 957 BP 336 EP 336 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801624 ER PT J AU Lipsky, RH Lu, FL Card, AS Marko, AJ AF Lipsky, RH Lu, FL Card, AS Marko, AJ TI Generation of reporter constructs for high throughput functional analysis of gene variants. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAAA, Dept Neurogenet, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 964 BP 337 EP 337 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025800962 ER PT J AU Chen, Q Reis, SE Kammerer, C Luedecking-Zimmer, E McNamara, DM Pauly, DF Sharai, B Holubkov, R Merz, NB Sopko, G Kamboh, MI AF Chen, Q Reis, SE Kammerer, C Luedecking-Zimmer, E McNamara, DM Pauly, DF Sharai, B Holubkov, R Merz, NB Sopko, G Kamboh, MI CA WISE Study TI Genetic variation in the oxidized LDL-receptor-1 (OLR1)gene and the risk of coronary artery disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Pittsburgh, Pittsburgh, PA 15260 USA. Univ Florida, Gainesville, FL 32611 USA. Brown Univ, Providence, RI 02912 USA. Univ Utah, Salt Lake City, UT 84112 USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RI Reis, Steven/J-3957-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1031 BP 348 EP 348 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801027 ER PT J AU Marroni, F Aretini, P Bailey-Wilson, JE Parmigiani, G Bevilacqua, G Presciuttini, S AF Marroni, F Aretini, P Bailey-Wilson, JE Parmigiani, G Bevilacqua, G Presciuttini, S CA Italian Consortium Hereditary Brea TI Performance of different models predicting BFICA-mutation carrier status in 570 Italian families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Pisa, Dept Biomed, I-56100 Pisa, Italy. Univ Pisa, Dept Oncol, I-56100 Pisa, Italy. NHGRI, NIH, Baltimore, MD USA. JHU, Dept Biostat, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1029 BP 348 EP 348 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801026 ER PT J AU Berthier-Schaad, Y Liu, Y Fink, N Klag, MJ Coresh, J Smith, MW AF Berthier-Schaad, Y Liu, Y Fink, N Klag, MJ Coresh, J Smith, MW TI Haplotype frequencies in the beta fibrinogen gene SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Genom Divers, Frederick, MD 21701 USA. Johns Hopkins Med Inst, Baltimore, MD 21205 USA. NCI, Basic Res Program, Frederick, MD 21701 USA. RI Smith, Michael/B-5341-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1080 BP 357 EP 357 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801076 ER PT J AU Modi, WS Jamba, M Roemer-Binns, B Winkler, C O'Brien, S AF Modi, WS Jamba, M Roemer-Binns, B Winkler, C O'Brien, S TI Haplotype map of the chromosome 17 CC chemokine gene cluster. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD 21701 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Genom Divers, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1090 BP 358 EP 358 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801084 ER PT J AU Liu, Y Berthier-Schaad, Y Fink, N Tracy, RP Klag, MJ Smith, MW Coresh, J AF Liu, Y Berthier-Schaad, Y Fink, N Tracy, RP Klag, MJ Smith, MW Coresh, J CA CHOICE Study TI Genetic variation in beta fibrinogen (FGB)and plasma fibrinogen levels in dialysis patients: The CHOICE study. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA. NCI, Lab Genom Divers, Frederick, MD 21701 USA. Univ Vermont, Burlington, VT USA. NCI, SAIC, Basic Res Program, Frederick, MD 21701 USA. RI Smith, Michael/B-5341-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1094 BP 359 EP 359 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801089 ER PT J AU Martin, MP Nelson, G Lee, JH Pellett, F Gao, X Wade, J Wilson, M Trowsdale, J Carrington, M AF Martin, MP Nelson, G Lee, JH Pellett, F Gao, X Wade, J Wilson, M Trowsdale, J Carrington, M TI Susceptibility to psoriatic arthritis: influence of activating killer immunoglobulin-like receptor genes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, SAIC, Frederick, MD 21701 USA. NCI, LGD, Frederick, MD 21701 USA. Toronto Western Res Inst, Toronto, ON, Canada. Toronto Western Hosp, Ctr Prognosis Studies Rheumat Dis, Toronto, ON M5T 2S8, Canada. Univ Toronto, Hlth Network, Reg HLA Lab, Toronto, ON, Canada. GlaxoSmithKline, Stevenage, Herts, England. Univ Cambridge, Cambridge, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1095 BP 359 EP 359 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801092 ER PT J AU Malik, S Abel, L Tooker, H Poon, A Simkin, L Girard, M Adams, G Starke, JR Connely-Smith, K Graviss, EA Musser, JM Schurr, E AF Malik, S Abel, L Tooker, H Poon, A Simkin, L Girard, M Adams, G Starke, JR Connely-Smith, K Graviss, EA Musser, JM Schurr, E TI Genetic risk factors for pediatric tuberculosis disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 McGill Ctr Study Host Resistance, Montreal, PQ, Canada. McGill Univ, Dept Med, Montreal, PQ, Canada. Hop Necker Enfants Malad, INSERM U550, Paris, France. Baylor Coll Med, Houston, TX 77030 USA. NIH, Lab Human Bacterial Pathogenesis, Hamilton, MT USA. McGill Univ, Dept Human Genet, Montreal, PQ H3A 2T5, Canada. NR 0 TC 0 Z9 0 U1 0 U2 3 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1100 BP 360 EP 360 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801095 ER PT J AU Lautenberger, JA Chretien, JP Coresh, J O'Brien, SJ Smith, MW AF Lautenberger, JA Chretien, JP Coresh, J O'Brien, SJ Smith, MW TI An SNP map for admixture linkage disequilibrium studies in African Americans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Genom Divers, Frederick, MD 21701 USA. Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA. NCI, SAIC Frederick, Basic Res Program, Frederick, MD 21701 USA. RI Smith, Michael/B-5341-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1106 BP 361 EP 361 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801101 ER PT J AU Mathias, RA Beaty, TH Bailey-Wilson, J Wilson, A Barnes, KC AF Mathias, RA Beaty, TH Bailey-Wilson, J Wilson, A Barnes, KC TI Segregation analysis of total serum IgE in a completely ascertained isolated island population. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Johns Hopkins Univ, Baltimore, MD USA. NHGRI, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1105 BP 361 EP 361 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801103 ER PT J AU Oleksyk, TK Sivtseva, T Danilova, AP Osakovskiy, VL O'Brien, SJ Goldfarb, LG Smith, MW AF Oleksyk, TK Sivtseva, T Danilova, AP Osakovskiy, VL O'Brien, SJ Goldfarb, LG Smith, MW TI Association between Viliuisk Encephalomyelitis syndrome in Sakha People of Siberia and the inflammation gene polymorphisms. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Genom Divers, NIH, Frederick, MD 21701 USA. Inst Hlth, Sakha Republ, Russia. NINDS, Clin Neurogenet Unit, NIH, Bethesda, MD 20892 USA. NCI, Basic Res Program, SAIC Frederick, NIH, Frederick, MD 21701 USA. RI Smith, Michael/B-5341-2012; Taras, Oleksyk/J-8805-2013 OI Taras, Oleksyk/0000-0002-8148-3918 NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1107 BP 361 EP 361 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801104 ER PT J AU Kovac, IP Wilson, AF Kinder, J Coe, BJ Coe, FL Asplin, JR AF Kovac, IP Wilson, AF Kinder, J Coe, BJ Coe, FL Asplin, JR TI Heritabilities of biochemical urine components in families with nephrolithiasis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, Baltimore, MD USA. Litholink Corp, Chicago, IL USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1123 BP 364 EP 364 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801121 ER PT J AU An, P Vlahov, D Maroglick, JB Phair, J OBrien, TR Lautenberger, J OBrien, SJ Winkler, CA AF An, P Vlahov, D Maroglick, JB Phair, J OBrien, TR Lautenberger, J OBrien, SJ Winkler, CA TI A TNF-alpha inducible promoter variant of interferon-gamma accelerates AIDS progression. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, SAIC, IRSP, Frederick, MD 21701 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Northwestern Univ, Sch Med, Comprehens AIDS Ctr, Chicago, IL 60611 USA. NCI, Viral Epidemiol Branch, DCEG, Bethesda, MD 20892 USA. NCI, Lab Genom Divers, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1136 BP 366 EP 366 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801131 ER PT J AU Bernig, T Foster, C Yeager, M Taylor, JG Chanock, S AF Bernig, T Foster, C Yeager, M Taylor, JG Chanock, S TI Characterization of genetic variants within the 10 kb mannose binding lectin (MBL2) locus. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, ATC, Pediat Oncol Branch, Gaithersburg, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1143 BP 367 EP 367 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801140 ER PT J AU Dogulu, CF Kansu, T Baxendale, V Wu, SM Ozguc, M Chan, WY Rennert, OM AF Dogulu, CF Kansu, T Baxendale, V Wu, SM Ozguc, M Chan, WY Rennert, OM TI Evidence for genetic susceptibility for Pseudotumor cerebri in Turkish population SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Lab Clin Genom, NIH, Bethesda, MD USA. Hacettepe Univ, Ankara, Turkey. RI Kansu, Tulay/B-6280-2012 OI Kansu, Tulay/0000-0002-1986-4680 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1152 BP 369 EP 369 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801148 ER PT J AU Klein, AP O'Neill, JA Bailey-Wilson, JE Klein, R Lee, KE Klein, BEK AF Klein, AP O'Neill, JA Bailey-Wilson, JE Klein, R Lee, KE Klein, BEK TI Genetic predisposition to nuclear cataract. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 IDRB, NH GRI, Stat Genet Sect, NIH, Baltimore, MD USA. Univ Wisconsin, Sch Med, Dept Ophthalmol & Visual Sci, Madison, WI 53706 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1181 BP 373 EP 373 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801177 ER PT J AU Grouse, LH AF Grouse, LH CA MGC Project Team TI Analysis of the human and mouse full-length cDNA clone sets generated by the NIH Mammalian Gene Collection. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1283 BP 390 EP 390 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801278 ER PT J AU Baptista, MJ O'Farrell, C Ahmad, R Cookson, MR AF Baptista, MJ O'Farrell, C Ahmad, R Cookson, MR TI Microarray analysis of a cell culture model of early onset dystonia linked to torsin A mutations. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MD SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Mayo Clin, Jacksonville, FL 32224 USA. Mayo Clin, Jacksonville, FL 32224 USA. NIH, NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 EI 1537-6605 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1289 BP 391 EP 391 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801284 ER PT J AU Chen, D Orthner, HF Sell, SM AF Chen, D Orthner, HF Sell, SM TI Software agent to automatically update genomic information. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Alabama, Genet Core Facil, NIDDK,Sch Hlth Related Profess, Clin Nutr Res Ctr,Dept Nutr Sci, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1287 BP 391 EP 391 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801283 ER PT J AU Francomano, CA Ho, NC Park, S Dudekula, D AF Francomano, CA Ho, NC Park, S Dudekula, D TI The skeletal gene database: A comprehensive resource for skeletal gene information. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1284 BP 391 EP 391 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801279 ER PT J AU Jia, L AF Jia, L CA CGAP Project Team TI Comprehensive resource: The Cancer Genome Anatomy Project. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Off Canc Genomics, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1292 BP 392 EP 392 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801286 ER PT J AU Liu, CY Bonner, TI Liu, YW Christian, SL Lyons, JL Gershon, ES AF Liu, CY Bonner, TI Liu, YW Christian, SL Lyons, JL Gershon, ES TI DNannotator: a web-based sequence annotation tool kit and its application on analyses of 13q32-33 sequence. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Cent S Univ, Natl Lab Med Genet China, Changsha, Peoples R China. NIMH, Genet Lab, Bethesda, MD 20892 USA. Univ Chicago, Dept Psychiat, Knapp Res Ctr, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1291 BP 392 EP 392 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801288 ER PT J AU Karaman, MW Chemnick, LG Houck, ML Sudano, D Chawannakul, D Nagpal, S Ryder, OA Hacia, JG AF Karaman, MW Chemnick, LG Houck, ML Sudano, D Chawannakul, D Nagpal, S Ryder, OA Hacia, JG TI Comparative analysis of gene expression patterns in human and African great ape cell lines. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. CRES, San Diego, CA USA. USC, IGM, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1317 BP 396 EP 396 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801313 ER PT J AU Liu, G Green, ED Eichler, EE AF Liu, G Green, ED Eichler, EE CA NISC TI Nature and pattern of primate genomic variation. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Case Western Reserve Univ, Dept Genet, Ctr Human Genet, Sch Med, Cleveland, OH 44106 USA. Case Western Reserve Univ, Ctr Computat Genom, Sch Med, Cleveland, OH 44106 USA. Univ Hosp Cleveland, Cleveland, OH 44106 USA. NIH, Intramural Sequencing Ctr, Gaithersburg, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1320 BP 397 EP 397 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801315 ER PT J AU Zhu, G Lipsky, RH Xu, K Ali, S Hyde, T Kleinman, J Akhtar, LA Mash, DC Goldman, D AF Zhu, G Lipsky, RH Xu, K Ali, S Hyde, T Kleinman, J Akhtar, LA Mash, DC Goldman, D TI RT-coupled 5' nuclease assay - A general and high throughput method for detection,of gene differential allele expression using transcribed SNPs as endogenous reporters SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAAA, NIH, Rockville, MD 20852 USA. NIMH, NIH, Bethesda, MD 20892 USA. Univ Miami, Dept Neurol, Miami, FL 33152 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1348 BP 401 EP 401 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801341 ER PT J AU Waeltz, P Brathwaite, M Schroeder, M Schlessinger, D Nagaraja, R AF Waeltz, P Brathwaite, M Schroeder, M Schlessinger, D Nagaraja, R TI Physical map and sequence analysis in the mouse t-complex inversion 2 region and comparison to the human syntenic region. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1369 BP 405 EP 405 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801366 ER PT J AU Fitzpatrick, DL Kleta, R Martin, RA Aughton, DJ Rivkin, MJ Orvisky, E Huizing, M Krasnewich, D Gahl, WA AF Fitzpatrick, DL Kleta, R Martin, RA Aughton, DJ Rivkin, MJ Orvisky, E Huizing, M Krasnewich, D Gahl, WA TI Molecular and biochemical diagnosis of lysosomal free sialic acid storage disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Sect Human Biochem Genet, HDB, NIH, Bethesda, MD USA. Washington Univ, Childrens Hosp, St Louis, MO 63130 USA. William Beaumont Hosp, Royal Oak, MI 48072 USA. Harvard Univ, Sch Med, Childrens Hosp, Boston, MA USA. NIMH, NSB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1414 BP 412 EP 412 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801407 ER PT J AU Orvisky, E Walker, JM Sidransky, E Martin, BM AF Orvisky, E Walker, JM Sidransky, E Martin, BM TI The identification of different tissue isoforms of glucocerebrosidase in patients with Gaucher disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIMH, Sect Mol Neurogenet, NIH, Bethesda, MD USA. NIMH, Lab Neurotoxicol, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1415 BP 412 EP 412 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801410 ER PT J AU Skovby, F Kleta, R Anikster, Y Christensen, R Gahl, WA AF Skovby, F Kleta, R Anikster, Y Christensen, R Gahl, WA TI Cystinosis in Denmark: Mutation analysis and treatment with cystamine, the disulfide of cysteamine. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Rigshosp, Dept Clin Genet, DK-2100 Copenhagen, Denmark. NICHD, Sect Human Biochem Genet, HDB, NIH, Bethesda, MD USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1420 BP 413 EP 413 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801413 ER PT J AU Bernardini, I Hermos, CR Blair, S Kaiser-Kupfer, M Kleta, R Gahl, WA AF Bernardini, I Hermos, CR Blair, S Kaiser-Kupfer, M Kleta, R Gahl, WA TI Keratopathy of multiple myeloma masquerading as the corneal crystals of ocular cystinosis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Sect Human Biochem Gened, HDB, NIH, Bethesda, MD USA. Riverside Methodist Hosp, Columbus, OH 43214 USA. NEI, Ophthalm Genet Branch, NIH, Bethesda, MD 20205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1427 BP 414 EP 414 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801422 ER PT J AU Hyman, T Huizing, M Anikster, Y Falic-Zaccai, TC Gahl, W AF Hyman, T Huizing, M Anikster, Y Falic-Zaccai, TC Gahl, W TI Use of cDNA microarrays to evaluate molecular mechanisms involved in gray platelet syndrome (GPS). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, LCCTP, Bethesda, MD 20892 USA. NICHD, Sect Human Biochem Genet, NIH, Bethesda, MD USA. Hosp Western Galillee Naharia, Rappaport Fac Med, Div Med Genet, Haifa, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1423 BP 414 EP 414 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801420 ER PT J AU Altarescu, G Moore, D Schiffmann, R AF Altarescu, G Moore, D Schiffmann, R TI Natural history of cardiac involvement in hemizygotes Fabry patients. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Shaare Zedek Med Ctr, Jerusalem, Israel. NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1428 BP 415 EP 415 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801423 ER PT J AU Krasnewich, D Orvisky, E LaMarca, M Andrews, D Tayebi, N Goker-Alpan, O Sidransky, E AF Krasnewich, D Orvisky, E LaMarca, M Andrews, D Tayebi, N Goker-Alpan, O Sidransky, E TI GenotypePhenotype analysis of American patients with congenital disorders of glycosylation-IA (CDG-1A). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA. NIMH, Sect Mol Neurogenet, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1433 BP 415 EP 415 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801428 ER PT J AU Walker, JM Tayebi, N Hanson, M Stubblefield, BK Sidransky, E AF Walker, JM Tayebi, N Hanson, M Stubblefield, BK Sidransky, E TI The association of Gaucher disease and Parkinsonism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIMH, Sect Mol Neurogenet, Bethesda, MD 20892 USA. NIA, Neurogenet Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1441 BP 417 EP 417 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801438 ER PT J AU Raben, N Jatkar, T Lee, A Plotz, P AF Raben, N Jatkar, T Lee, A Plotz, P TI Lessons learned from an attempt to rescue the phenotype in acid alpha-glucosiclase knockout mice. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAMS, ARB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1446 BP 418 EP 418 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801441 ER PT J AU Anikster, Y Huizing, M Kleta, R Anderson, PD Gahl, WA AF Anikster, Y Huizing, M Kleta, R Anderson, PD Gahl, WA TI A new approach for positional cloning using cDNA clones: The discovery of HPS3 and OPA3. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Chaim Sheba Med Ctr, Metab Dis Unit, IL-52621 Tel Hashomer, Israel. NICHD, NIH, Sect Human Biochem Genet, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1457 BP 419 EP 419 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801452 ER PT J AU LaMarca, ME Tayebi, N Sidransky, E AF LaMarca, ME Tayebi, N Sidransky, E TI A point mutation in metaxin 1 is associated with the N370S mutation in Gaucher disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIMH, NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1453 BP 419 EP 419 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801450 ER PT J AU Goker-Alpan, O Tayebi, N Kishani, PS Rosenbaum, H Rubinger, D Sidransky, E AF Goker-Alpan, O Tayebi, N Kishani, PS Rosenbaum, H Rubinger, D Sidransky, E TI Renal involvement in Gaucher disease: Pathogenesis and natural history. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIMH, NIH, Bethesda, MD 20892 USA. Duke Univ, Durham, NC USA. Rambam Med Ctr, Haifa, Israel. Hadassah Univ, Jerusalem, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1461 BP 420 EP 420 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801457 ER PT J AU Jeong, A Lalor, M Anderson, PD Kleta, R Skovby, F Huizing, M Gahl, W Anikster, Y AF Jeong, A Lalor, M Anderson, PD Kleta, R Skovby, F Huizing, M Gahl, W Anikster, Y TI 3-methylglutaconic aciduria type III in a non Iraqi-Jewish patient. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Sect Human Biochem Genet, HDB, NIH, Bethesda, MD USA. Rigshosp, Dept Clin Genet, DK-2100 Copenhagen, Denmark. Sheba Med Ctr, Tel Hashomer, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1458 BP 420 EP 420 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801453 ER PT J AU Gahl, WA Bernardini, I Hermos, CR Kleta, R AF Gahl, WA Bernardini, I Hermos, CR Kleta, R TI Making the diagnosis of cystinosis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, SEct Human Biochem Genet, HDB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1465 BP 421 EP 421 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801462 ER PT J AU Kleta, R Fitzpatrick, DL Rausche, M Lucero, C Hermos, CR Anikster, Y Bernardini, I Gahl, WA AF Kleta, R Fitzpatrick, DL Rausche, M Lucero, C Hermos, CR Anikster, Y Bernardini, I Gahl, WA TI Cystinosis due to a CTNS deletion having breakpoints within Alu repeats. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Sect Human Biochem Genet, DB, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1467 BP 421 EP 421 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801463 ER PT J AU Anderson, PD Huizing, M Lynch, M Gahl, WA AF Anderson, PD Huizing, M Lynch, M Gahl, WA TI Hermansky-Pudlak syndrome type-4 (HPS-4): Clinical and molecular characteristics. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Heritable Disorders Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1479 BP 423 EP 423 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801475 ER PT J AU Rao, DA Veszelovszky, E Plotz, PH Hoffman, EP AF Rao, DA Veszelovszky, E Plotz, PH Hoffman, EP TI Membrane regulation in dysferlin deficiency: Evidence for disrupted membrane signaling and altered remodeling through expression profiling. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Childrens Natl Med Ctr, Med Genet Res Ctr, Washington, DC 20010 USA. NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1502 BP 427 EP 427 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801496 ER PT J AU Hermos, CR Huizing, M Gahl, WA AF Hermos, CR Huizing, M Gahl, WA TI Hermansky-Pudlak syndrome type-1: Screening methods, mutations, and clinical outcomes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Heritable Disorders Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1506 BP 428 EP 428 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801501 ER PT J AU Atwood, LD Heard-Costa, N Cupples, LA Jaquish, CE Wilson, PWF Dagostine, RB AF Atwood, LD Heard-Costa, N Cupples, LA Jaquish, CE Wilson, PWF Dagostine, RB TI Genome-wide linkage analysis of body mass index across 28 years of the Framingham Heart Study. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Boston Univ, Sch Med, Boston, MA 02118 USA. NHLBI, Bethesda, MD 20892 USA. Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1564 BP 438 EP 438 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801561 ER PT J AU Bergen, AW van den Bree, MBM Yeager, M Ganjei, JK Welch, R Haque, K Bacanu, S Grice, DE Berrettini, WH Bulik, C Klump, K Fichter, M Halmi, K Kaplan, A Strober, M Treasure, J Woodside, B Kaye, WH AF Bergen, AW van den Bree, MBM Yeager, M Ganjei, JK Welch, R Haque, K Bacanu, S Grice, DE Berrettini, WH Bulik, C Klump, K Fichter, M Halmi, K Kaplan, A Strober, M Treasure, J Woodside, B Kaye, WH TI HTR1D and OPRD1 SNPs exhibit significant association to anorexia nervosa. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Wales Coll Cardiff, Cardiff CF1 3NS, S Glam, Wales. NCI, Core Genotyping Facil, NIH, Bethesda, MD 20892 USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1567 BP 438 EP 438 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801560 ER PT J AU Justice, CM Miller, NH Marosy, B Zhang, J Wilson, AF AF Justice, CM Miller, NH Marosy, B Zhang, J Wilson, AF TI Identification of loci involved in familial idiopathic scoliosis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Johns Hopkins Univ, CIDR, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Genet, Baltimore, MD USA. Johns Hopkins Univ, Dept Orthopaed Surg, Baltimore, MD USA. NHGRI, Genometr Sect, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1577 BP 440 EP 440 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801571 ER PT J AU Jiao, X Munier, FL Schorderet, DF Rubin, BI Smith, J Hejtmancik, JF AF Jiao, X Munier, FL Schorderet, DF Rubin, BI Smith, J Hejtmancik, JF TI Genetic linkage of Francois-Neetens fleck (mouchetee) corneal dystrophy to chromosome 2q35. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Div Med Genet, Lausanne, Switzerland. NEI, NIH, Bethesda, MD 20892 USA. Jules Gonin Eye Hosp, Oculgenet Unit, Lausanne, Switzerland. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1616 BP 446 EP 446 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801611 ER PT J AU Xu, K Tabuman, J Bau, CHD Virkkunen, M Linnoila, M Ferro, E Astor, W Goldman, D AF Xu, K Tabuman, J Bau, CHD Virkkunen, M Linnoila, M Ferro, E Astor, W Goldman, D TI Haplotype-based association of DRD2 gene to alcoholism with antisocial personality disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. RI Bau, Claiton/C-9980-2013 OI Bau, Claiton/0000-0001-5644-3845 NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1611 BP 446 EP 446 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801606 ER PT J AU Loomer, M Gabriel, SB Platko, J O'Donnell, C Daly, MJ Lander, ES Hirschhorn, JN AF Loomer, M Gabriel, SB Platko, J O'Donnell, C Daly, MJ Lander, ES Hirschhorn, JN TI The efficacy of using haplotypes to assay common variation in genes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Whitehead Inst, Ctr Genome Res, Cambridge, MA 02142 USA. NHLBI, Cardiogen PGA, Bethesda, MD 20892 USA. NHLBI, Framingham Heart Study, Framingham, MA USA. MIT, Cambridge, MA 02139 USA. Harvard Univ, Sch Med, Boston, MA USA. Childrens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1639 BP 450 EP 450 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801638 ER PT J AU Arcos-Burgos, M Konecki, D Pineda, DA Lopera, F Palcio, JD Berg, K Castellanos, X Bailey-Wilson, J Muenke, M AF Arcos-Burgos, M Konecki, D Pineda, DA Lopera, F Palcio, JD Berg, K Castellanos, X Bailey-Wilson, J Muenke, M TI ADHD: DRD4 linkage analysis in extended pedigrees. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NYU, Ctr Child Study, New York, NY USA. Univ Antioquia, Medellin, Colombia. NHGRI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1650 BP 452 EP 452 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801652 ER PT J AU Shatunov, A Jankovic, J Elble, R Sambuughin, N Zhang, Y Dagvadorj, A Ji, J Lee, HS Hallett, M Goldfarb, LG AF Shatunov, A Jankovic, J Elble, R Sambuughin, N Zhang, Y Dagvadorj, A Ji, J Lee, HS Hallett, M Goldfarb, LG TI Chromosomal mapping of essential tremor. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA. Baylor Coll Med, Houston, TX 77030 USA. So Illinois Univ, Sch Med, Springfield, IL USA. Barrow Neurol Inst, Phoenix, AZ 85013 USA. BBI Biotech Res Labs, Gaithersburg, MD USA. RI Shatunov, Aleksey/E-6946-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1666 BP 455 EP 455 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801669 ER PT J AU Elbein, SC Wang, H Chu, W Wolford, JK Hanson, RL Mitchell, BD Shuldiner, AR AF Elbein, SC Wang, H Chu, W Wolford, JK Hanson, RL Mitchell, BD Shuldiner, AR TI Linkage disequilibrium mapping of a type 2 diabetes susceptibility gene on chromosome 1q21-q23 in Utah Caucasians, Pima Indians, and Old Order Amish. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Arkansas Med Sci, Dept Med, Little Rock, AR 72205 USA. Cent Arkansas Vet Healthcare Syst, Little Rock, AR 72205 USA. NIDDK, NIH, Phoenix, AZ USA. Univ Maryland, Dept Med, Baltimore, MD 21201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1690 BP 459 EP 459 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801693 ER PT J AU Ghebranious, N Zhao, C Ott, L David, D Marth, G Sachidanadam, R Weber, JL AF Ghebranious, N Zhao, C Ott, L David, D Marth, G Sachidanadam, R Weber, JL TI Human insertion/deletion (indel) polymorphisms SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Marshfield Med Res Fdn, Ctr Med Genet, Marshfield, WI 54449 USA. NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1703 BP 461 EP 461 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801703 ER PT J AU Prodi, DA Drayna, D Angius, A Forabosco, P Piras, D Palmas, MA Pirastu, M AF Prodi, DA Drayna, D Angius, A Forabosco, P Piras, D Palmas, MA Pirastu, M TI Genetic of bitter taste: identification of a Ch 7q35 locus in a Sardinian genetic isolate. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 CNR, Ist Genet Popolazioni, Alghero, SS, Italy. Natl Inst Deafness & Other Commun Disorders, Rockville, MD USA. Shardna, Cagliari, Italy. RI Angius, Andrea/B-8966-2015; Angius, Andrea/P-9549-2015 OI Angius, Andrea/0000-0003-2596-6461 NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1721 BP 464 EP 464 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801721 ER PT J AU Bei, TA Tilkeridis, C Garatziotis, S Kortesas, E Stratakis, CA AF Bei, TA Tilkeridis, C Garatziotis, S Kortesas, E Stratakis, CA TI COL1A1 polymorphism (a four-base pair insertion polymorphism in 3'UTR) in young male Greek army recruits with lumbar disk disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, Unit Genet & Endocrinol, DEB, NIH, Bethesda, MD 20892 USA. Greek Army Med Ctr, Arta, Greece. Greek Army Med Serv, Dept Def, Athens, Greece. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1739 BP 467 EP 467 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801738 ER PT J AU Ishiguro, H Uhl, G AF Ishiguro, H Uhl, G TI Allelic variation at genes encoding NRCAM and NrCAM ligands and possible associations with substance abuse vulnerability. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDA, NIH, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1755 BP 470 EP 470 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801755 ER PT J AU Uhl, GR Liu, QR Ishiguro, H Gong, JP Zhu, X Drgon, T Draganova, J Zhang, PW Lin, Z Polesskaya, O Walther, D AF Uhl, GR Liu, QR Ishiguro, H Gong, JP Zhu, X Drgon, T Draganova, J Zhang, PW Lin, Z Polesskaya, O Walther, D TI Human substance abuse substance vulnerability loci: identification and initial fine mapping studies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDA, Mol Neurobiol Branch, NIH, IRP, Baltimore, MD 21224 USA. RI Liu, Qing-Rong/A-3059-2012 OI Liu, Qing-Rong/0000-0001-8477-6452 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1768 BP 472 EP 472 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801770 ER PT J AU Singleton, AA Subramony, SH Hernandez, D Smith-Jefferson, S Hussey, J Gwinn-Hardy, K Lynch, T McDaniel, O Hardy, J Farrer, M Singleton, A AF Singleton, AA Subramony, SH Hernandez, D Smith-Jefferson, S Hussey, J Gwinn-Hardy, K Lynch, T McDaniel, O Hardy, J Farrer, M Singleton, A TI Ethnic differences in the expression of neurodegenerative disease: Machado-Joseph disease in Africans and Caucasians. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MD SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NINDS, NIH, Bethesda, MD 20892 USA. NIA, NIH, Bethesda, MD 20892 USA. Univ Mississippi, Med Ctr, Dept Neurol, Jackson, MS 39216 USA. Mayo Clin Jacksonville, Dept Neurosci, Neurogenet Lab, Jacksonville, FL 32224 USA. Univ Mississippi, Med Ctr, Dept Prevent Med, Div Med Genet, Jackson, MS 39216 USA. Columbia Univ, Dept Neurol, New York, NY USA. Mater Misericordiae Univ Hosp, Dept Neurol, Dublin 7, Ireland. UCL Royal Free & UCL Med Sch, Reta Lila Weston Inst Neurol Studies, Dept Neurol, London, England. RI Gwinn, Katrina/C-2508-2009; Singleton, Andrew/C-3010-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1791 BP 476 EP 476 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801791 ER PT J AU Chen, Y Kittles, R Zhou, J Chen, G Panguluri, K Chen, W Amoah, A Acheampong, VO Eghan, B Nyantayi, A Ofoegbu, E Abbiyesuku, F Kuti, M Johnson, T Rufus, T Daniel, H Dunston, G Collins, F Rotimi, C AF Chen, Y Kittles, R Zhou, J Chen, G Panguluri, K Chen, W Amoah, A Acheampong, VO Eghan, B Nyantayi, A Ofoegbu, E Abbiyesuku, F Kuti, M Johnson, T Rufus, T Daniel, H Dunston, G Collins, F Rotimi, C CA AADM Study TI Calpain-10 gene Polymorphisms and type 2 diabetes in West Africans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Howard Univ, Natl Human Genome Ctr, Washington, DC 20059 USA. Univ Ghana, Accra, Ghana. Univ Sci & Technol, Kumasi, Ghana. Univ Nigeria, Enugu, Nigeria. UCH, Ibadan, Nigeria. Univ Lagos, Lagos, Nigeria. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1798 BP 477 EP 477 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801800 ER PT J AU Bektas, A Francomano, CA AF Bektas, A Francomano, CA TI The murine klotho gene coding sequence is completely conserved in laboratoryderived inbred strains. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1827 BP 482 EP 482 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801827 ER PT J AU Luo, X Klempan, TA Lappalainen, J Rosenheck, RA Charney, DS Erdos, J van Kammen, DP Kranzler, HR Kennedy, JL Gelernter, J AF Luo, X Klempan, TA Lappalainen, J Rosenheck, RA Charney, DS Erdos, J van Kammen, DP Kranzler, HR Kennedy, JL Gelernter, J TI NOTCH4 gene haplotypes are associated with schizophrenia in African-Americans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD ID LOCUS C1 Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA. VA CT Healthcare Ctr, West Haven, CT USA. CAMH, Toronto, ON, Canada. NIMH, Bethesda, MD 20892 USA. J&J Pharm R&D, Raritan, NJ USA. Univ Penn, Philadelphia, PA 19104 USA. Univ Connecticut, Sch Med, ARC, Dept Psychiat, Farmington, CT USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1843 BP 485 EP 485 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801844 ER PT J AU Wolford, JK Hanson, RL Gruber, JD Vozarova, B Ossowski, VM Bogardus, C AF Wolford, JK Hanson, RL Gruber, JD Vozarova, B Ossowski, VM Bogardus, C TI A polymorphism in the C-reactive protein (CRP) promoter is associated with increased prevalence of type 2 diabetes mellitus in Pima Indians. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDDK, PECRB, NIH, Phoenix, AZ USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1849 BP 486 EP 486 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801850 ER PT J AU Harold, D Peirce, T Hamshere, M Myers, A Turic, D Lovestone, S Powell, J McIlroy, S Craig, D Passmore, P Hardy, J Goate, A Liddell, M O'Donovan, M Williams, J Owen, MJ Jones, L AF Harold, D Peirce, T Hamshere, M Myers, A Turic, D Lovestone, S Powell, J McIlroy, S Craig, D Passmore, P Hardy, J Goate, A Liddell, M O'Donovan, M Williams, J Owen, MJ Jones, L TI No association of polymorphisms in the cholinergic locus with late-onset Alzheimer's disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 UWCM, Dept Psychol Med, Cardiff, S Glam, Wales. Univ Washington, St Louis, MO USA. Inst Psychiat, London, England. Queens Univ Belfast, Belfast, Antrim, North Ireland. NIA, Bethesda, MD 20892 USA. Dept Psychiat, St Louis, MO USA. RI CRAIG, DAVID/C-6232-2009; Lovestone, Simon/E-8725-2010; Myers, Amanda/B-1796-2010; Powell, John/G-4412-2011 OI Myers, Amanda/0000-0002-3100-9396; Powell, John/0000-0001-6124-439X NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1862 BP 488 EP 488 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801865 ER PT J AU Sell, SM Kekes-Szabo, T Chen, D Song, C Chen, H Baier, L Traurig, M Hanson, R AF Sell, SM Kekes-Szabo, T Chen, D Song, C Chen, H Baier, L Traurig, M Hanson, R TI UABSNP58 on human chromosome 20 associated with insulin resistance. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDDK, Phoenix, AZ USA. Univ Alabama, Dept Nutr Sci, Birmingham, AL 35294 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1902 BP 494 EP 494 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801903 ER PT J AU Hollstein, PE Silander, K Scott, LJ Fingerlin, TE Chines, PS Mohlke, KL Narisu, N Erdos, MR Li, M Valle, TT Bergman, RN Tuomilehto, J Boehnke, M Collins, FS AF Hollstein, PE Silander, K Scott, LJ Fingerlin, TE Chines, PS Mohlke, KL Narisu, N Erdos, MR Li, M Valle, TT Bergman, RN Tuomilehto, J Boehnke, M Collins, FS TI Efficient fine-mapping of a type 2 diabetes locus on chromosome 20 through SNP typing on DNA pools. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ So Calif, Keck Sch Med, Dept Physiol & Biophys, Los Angeles, CA USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1912 BP 496 EP 496 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801914 ER PT J AU Rotimi, C Chen, G Zhou, J Parish-Gause, D Daniel, H Chen, Y Amoah, A Acheampong, J Agyenim-Boateng, K Eghan, B Oli, J Okafor, G Furbert-harris, P Osotimehin, B Abbiyesuku, F Johnson, T Fasimade, O Kittles, R Dunston, G Collins, F AF Rotimi, C Chen, G Zhou, J Parish-Gause, D Daniel, H Chen, Y Amoah, A Acheampong, J Agyenim-Boateng, K Eghan, B Oli, J Okafor, G Furbert-harris, P Osotimehin, B Abbiyesuku, F Johnson, T Fasimade, O Kittles, R Dunston, G Collins, F CA Africa Amer Diabet Mellitus Study TI A genome search for type 2 diabetes susceptibility genes in west Africans. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. Univ Lagos, Lagos, Nigeria. UCH, Ibadan, Nigeria. Univ Nigeria, Enugu, Nigeria. Univ Sci & Technol, Kumasi, Ghana. Univ Ghana, Accra, Ghana. Howard Univ, Natl Human Genome Ctr, Washington, DC 20059 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1923 BP 498 EP 498 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801922 ER PT J AU Scott, LJ Li, C Fingerlan, TE Jackson, AU Mohlke, KL Silander, K Collins, FS Boehnke, M AF Scott, LJ Li, C Fingerlan, TE Jackson, AU Mohlke, KL Silander, K Collins, FS Boehnke, M TI Use of pooled DNA in case-control studies: How precision of allele frequency estimation affects efficiency. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1926 BP 498 EP 498 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801926 ER PT J AU Turic, D Dunstan, M Rice, F McIlroy, S Craig, D Passmore, P Myers, A Lovestone, S Powell, J Hardy, J Goate, A Liddell, M Jones, L O'Donovan, M Owen, MJ Williams, J AF Turic, D Dunstan, M Rice, F McIlroy, S Craig, D Passmore, P Myers, A Lovestone, S Powell, J Hardy, J Goate, A Liddell, M Jones, L O'Donovan, M Owen, MJ Williams, J TI Fine mapping of Alzheimers disease linkage region on chromosome 10 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MD SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. NIA, Bethesda, MD 20892 USA. Inst Psychiat, London, England. Washington Univ, St Louis, MO USA. Queens Univ Belfast, Belfast, Antrim, North Ireland. UWCM, Cardiff, S Glam, Wales. RI CRAIG, DAVID/C-6232-2009; Lovestone, Simon/E-8725-2010; Myers, Amanda/B-1796-2010; Powell, John/G-4412-2011 OI Myers, Amanda/0000-0002-3100-9396; Powell, John/0000-0001-6124-439X NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1922 BP 498 EP 498 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801924 ER PT J AU Zhou, J Chen, G Doumatey, A Furbert-Harris, P Amoah, A Acheampong, J Oli, J Osotimehin, B Johnson, T Agyenim-Boateng, K Okafor, G Abbiyesuku, F Fasimade, O Eghan, B Daniel, H Chen, Y Parish-Gause, D Dunston, G Collins, F Rotimi, C AF Zhou, J Chen, G Doumatey, A Furbert-Harris, P Amoah, A Acheampong, J Oli, J Osotimehin, B Johnson, T Agyenim-Boateng, K Okafor, G Abbiyesuku, F Fasimade, O Eghan, B Daniel, H Chen, Y Parish-Gause, D Dunston, G Collins, F Rotimi, C CA Africa Amer Diabet Mellitus Study TI Genome search for genes underlying susceptibility to insulin resistance syndrome in type 2 diabetes patients from West Africa. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, NIH, Bethesda, MD 20892 USA. Univ Lagos, Lagos, Nigeria. UCH, Ibadan, Nigeria. Univ Nigeria, Enugu, Nigeria. Univ Sci & Technol, Kumasi, Ghana. Howard Univ, Natl Human Geneome Ctr, Washington, DC 20059 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1924 BP 498 EP 498 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801925 ER PT J AU Leib, JR Stolle, C Taylor, JP Caress, JB AF Leib, JR Stolle, C Taylor, JP Caress, JB TI Novel point mutations in two compound heterozygous cases of Friedreich's Ataxia. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wake Forest Univ, Bowman Gray Sch Med, Dept Neurol, Winston Salem, NC 27103 USA. Univ Penn, Sch Med, Genet Diagnost Lab, Philadelphia, PA 19104 USA. NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1949 BP 502 EP 502 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801947 ER PT J AU Yan, J Feng, J Chen, J Craddock, N Jones, I Cook, EH Goldman, D Heston, LL Sommer, SS AF Yan, J Feng, J Chen, J Craddock, N Jones, I Cook, EH Goldman, D Heston, LL Sommer, SS TI Comprehensive mutation scanning of RAR/RXR and Vitamin D receptor genes in patients with schizophrenia and other psychiatric diseases: Three missense mutations at highly conserved residues. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. NIAAA, Dept Psychiat, NIH, Bethesda, MD USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Birmingham, Div Neurosci, Birmingham, W Midlands, England. Dept Mol Genet, Duarte, CA USA. RI Jones, Ian/B-4925-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1951 BP 503 EP 503 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801951 ER PT J AU Hu, X Robin, RW Taubman, J Goldman, D AF Hu, X Robin, RW Taubman, J Goldman, D TI Genotyping of the HTTLPR Ins/Del by dHPLC followed by association/linkage disequilibrium to behavior in a southwest American Indian isolate. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAAA, Neurogenet Lab, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1967 BP 505 EP 505 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801965 ER PT J AU Naz, S Riazuddin, S Riazuddin, S Griffith, AJ Friedman, TB Wilcox, ER AF Naz, S Riazuddin, S Riazuddin, S Griffith, AJ Friedman, TB Wilcox, ER TI A mutation of ESPN causes autosomal recessive nonsyndromic hearing loss, DFNB36. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDCD, Sect Human Genet, LMG, Rockville, MD USA. NIDCD, Sect Gene Struct & Funct, LMG, Rockville, MD USA. Univ Punjab, Natl Ctr Excellence Mol Biol, Lahore, Pakistan. RI naz, sadaf/F-4406-2015 NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 1995 BP 511 EP 511 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025801995 ER PT J AU Hague, SM Evey, C Baptista, M Cookson, M Hardy, J Singleton, A AF Hague, SM Evey, C Baptista, M Cookson, M Hardy, J Singleton, A TI Enzyme activity of GTP cyclohydrolase I mutations and their relevance to dopamine insufficiency. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Bethesda, MD 20892 USA. RI Singleton, Andrew/C-3010-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2010 BP 513 EP 513 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802011 ER PT J AU DeSandre-Giovannoli, A Chaouch, M Kozlov, S Kassouri, N Tazir, M Vandenberghe, A Hammadouche, T Stewart, CL Vallat, JM Grid, D Levy, N AF DeSandre-Giovannoli, A Chaouch, M Kozlov, S Kassouri, N Tazir, M Vandenberghe, A Hammadouche, T Stewart, CL Vallat, JM Grid, D Levy, N TI LMNA founder mutation in autosomal recessive axonal Charcot-Marie-Tooth disease reveals a novel laminopathy. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 INSERM, U491, Marseille, France. CHU Ben Aknoun, Neurol Serv, Algiers, Algeria. NCI, Canc & Dev Biol Lab, Frederick, MD 21701 USA. CHU Mustapha, Serv Neurol, Algiers, Algeria. Neurogenet Lab, Lyon, France. Inst Pasteur, Algiers, Algeria. CHU Dupuytren, Serv Neuropathol, Limoges, France. Genethon III, Evry, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2073 BP 524 EP 524 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802073 ER PT J AU Ahmed, ZM Morell, RJ Riazuddin, S Ahmad, MM Mohiddin, SA Caruso, RC Khan, SN Fananapazir, L Husnain, T Griffith, AJ Riazuddin, S Friedman, TB Wilcox, ER AF Ahmed, ZM Morell, RJ Riazuddin, S Ahmad, MM Mohiddin, SA Caruso, RC Khan, SN Fananapazir, L Husnain, T Griffith, AJ Riazuddin, S Friedman, TB Wilcox, ER TI Genetic mapping and identification of a new autosomal nonsyndromic recessive deafness locus DFNB37. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 LMG, NIDCD, Sect Human Genet, NIH, Rockville, MD USA. Univ Punjab, Natl Ctr Excellence Mol Biol, Lahore, Pakistan. NHLBI, Clin Cardiol Sect, NIH, Bethesda, MD 20892 USA. NEI, Sect Ophthalm Mol Genet, NIH, Bethesda, MD 20892 USA. NIDCD, Sect Gene Struct & Funct, LMG, NIH, Rockville, MD USA. RI Nasim Khan, Shaheen/F-2135-2015; Husnain, Tayyab/G-3805-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2102 BP 528 EP 528 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802102 ER PT J AU Tayebi, N Stubblefield, B Sidransky, E AF Tayebi, N Stubblefield, B Sidransky, E TI A novel homozygous fusion allele in a patient with type 2 Gaucher disease. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIMH, Sect Mol Neurogenet, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2110 BP 530 EP 530 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802112 ER PT J AU Johnston, JJ Turner, J Olivos-Glander, IM Biesecker, LG AF Johnston, JJ Turner, J Olivos-Glander, IM Biesecker, LG TI Mutational spectrum of Pallister-Hall and Greig cephalopolysyndactyly syndromes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NHGRI, GDRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2135 BP 534 EP 534 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802134 ER PT J AU Ben-Yosef, T Ness, SL Madeo, AC Bar-Lev, A Wolfman, JH AHmed, ZM Willner, JP Desnick, RJ Avraham, KB Oster, H Oddoux, C Griffith, AJ Friedman, TB AF Ben-Yosef, T Ness, SL Madeo, AC Bar-Lev, A Wolfman, JH AHmed, ZM Willner, JP Desnick, RJ Avraham, KB Oster, H Oddoux, C Griffith, AJ Friedman, TB TI A prevalent founder mutation among Ashkenazi Jews with Usher syndrome type 1. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIDCD, Genet Mol Lab, NIH, Rockville, MD USA. Mt Sinai Sch Med, Dept Human Genet, New York, NY USA. Tel Aviv Univ, Sackler Sch Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. NYU, Sch Med, Human Genet Program, New York, NY USA. RI Madeo, Anne/K-2880-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2150 BP 536 EP 536 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802150 ER PT J AU Dagvadorj, A Karp, BI Sambuughin, N Shatunov, A Bara, W Hallet, M Goldfarb, LG AF Dagvadorj, A Karp, BI Sambuughin, N Shatunov, A Bara, W Hallet, M Goldfarb, LG TI Epsilon-sarcoglycan mutations in three ethnically diverse families segregating Myoclonus-Dystonia. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NINDS, NIH, Bethesda, MD 20892 USA. Barrow Neurol Inst, Phoenix, AZ 85013 USA. RI Shatunov, Aleksey/E-6946-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2149 BP 536 EP 536 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802147 ER PT J AU Aksentijevich, I Austin, F Balow, J Chae, JJ Remmers, E Watford, WT Hofmann, SR O'Shea, JJ Komarow, H Shoham, N Hoffman, H Goldbach-Mansky, R Kastner, DL AF Aksentijevich, I Austin, F Balow, J Chae, JJ Remmers, E Watford, WT Hofmann, SR O'Shea, JJ Komarow, H Shoham, N Hoffman, H Goldbach-Mansky, R Kastner, DL TI Spontaneous mutations in CIAS1 gene cause neonatal onset multisystem inflammatory disease (NOMID/CINCA). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAMS, Genet & Genom Branch, NIH, Bethesda, MD USA. NIAMS, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD USA. NIAMS, Off Clin Director, NIH, Bethesda, MD USA. Univ Calif San Diego, Div Rheumatol & Allergy & Immunol, La Jolla, CA 92093 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2151 BP 537 EP 537 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802151 ER PT J AU Boespflug-Tanguy, O Fogli, A Eymard-Pierre, E Rodriguez, D Bertini, E Pineda, M Surtees, R Uziel, G Malaspina, E Schiffmann, R AF Boespflug-Tanguy, O Fogli, A Eymard-Pierre, E Rodriguez, D Bertini, E Pineda, M Surtees, R Uziel, G Malaspina, E Schiffmann, R TI Detection of mutations in the translation initiation factor eIF2B in a white matter disorder, the CACH/VWM syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MD SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 INSERM, Fac Med, U384, Clermont Ferrand, France. Hop Trousseau, INSERM, U546, F-75571 Paris, France. Bambino Gesu Pediat Hosp, Dept Neurosci, Rome, Italy. Hosp San Joan Deu, Barcelona, Spain. UCL, Inst Child Hlth, London, England. Carlo Basta Inst, Milan, Italy. Inst Clin Padiatr, Bologna, Italy. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2154 BP 537 EP 537 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802155 ER PT J AU Terry, SF Whittemore, VH Driscoll, CT Johnson, EW Davidson, ME Terry, PF AF Terry, SF Whittemore, VH Driscoll, CT Johnson, EW Davidson, ME Terry, PF TI Lay advocacy owned blood and tissue banks. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Genet Alliance, Sharon, MA USA. PXE Int Washington, Washington, DC USA. NHGRI, Bethesda, MD 20892 USA. Barrow Neurol Inst, Phoenix, AZ 85013 USA. Genomic Hlth, Redwood City, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2162 BP 538 EP 538 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802162 ER PT J AU Lin, T Sandusky, SB Zhang, Z Francomano, CA AF Lin, T Sandusky, SB Zhang, Z Francomano, CA TI Thanatophoric dysplasia type II mice generated using cartilage-specific cre. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2181 BP 542 EP 542 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802181 ER PT J AU Shoham, NG Mansfield, E Centola, M Wood, G Wise, CA Kastner, DL AF Shoham, NG Mansfield, E Centola, M Wood, G Wise, CA Kastner, DL TI The pyrin pathway of inflammation: Arthritis-associated mutations in PSTPIP1 cause hyperphosphorylation and increased binding to pyrin. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIAMS, Genet & Genom, NIH, Bethesda, MD USA. Scottish Rite Hosp, Ctr Musculoskeletal Res, Dallas, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2193 BP 544 EP 544 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802193 ER PT J AU McWilliams, S Nelson, T Cavender, M Goldfarb, L Sivakumar, K Sambuughin, N AF McWilliams, S Nelson, T Cavender, M Goldfarb, L Sivakumar, K Sambuughin, N TI Comprehensive screening of the RYR1 gene by denaturing high-performance liquid chromatography SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Barrow Neurol Inst, Phoenix, AZ 85013 USA. Wake Forest Univ, Winston Salem, NC 27109 USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2212 BP 547 EP 547 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802214 ER PT J AU Devers, PL Wagner, AF Treadwell, MC Romero, R Conoscenti, G Johnson, A AF Devers, PL Wagner, AF Treadwell, MC Romero, R Conoscenti, G Johnson, A TI Klippel-Trenaunay Syndrome presenting as possible Amniotic Band Syndrome SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Wayne State Univ, Dept Obstet Gynecol, Div Reprod Genet, Detroit, MI USA. Wayne State Univ, Hutzel Hosp, Dept Obstet Gynecol, Div Maternal Fetal Med, Detroit, MI USA. NICHD, Perinatal Res Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2285 BP 560 EP 560 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802275 ER PT J AU Kaufman, DJ Buetow, K AF Kaufman, DJ Buetow, K TI Path analysis of protein expression data in cancer-related metabolic pathways. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, Lab Populat Genet, Gaithersburg, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2335 BP 568 EP 568 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802321 ER PT J AU Morris, RW Kaplan, NL AF Morris, RW Kaplan, NL TI Power computations with misclassified and missing genotype data in association studies of nuclear families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NIEHS, Biostat Branch, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2355 BP 572 EP 572 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802343 ER PT J AU Pfeiffer, RM Gail, M Hemminki, K Goldin, LR AF Pfeiffer, RM Gail, M Hemminki, K Goldin, LR TI Methods for testing familial aggregation of-diseases in population-based samples: Application to lymphoproliferative cancers in Swedish registry data. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NCI, DCEG, Biostat Branch, Bethesda, MD 20892 USA. Karolinska Inst, Dept Biostat, Novum, Huddinge, Sweden. NCI, DCEG, Genet Epidemiol Branch, Bethesda, MD 20892 USA. RI Pfeiffer, Ruth /F-4748-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2359 BP 572 EP 572 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802345 ER PT J AU Presciuttini, S Toni, C Tempestini, E Verdiani, S Casarino, L Spinetti, I De Stefano, F Dominici, R Bailey-Wilson, JE AF Presciuttini, S Toni, C Tempestini, E Verdiani, S Casarino, L Spinetti, I De Stefano, F Dominici, R Bailey-Wilson, JE TI Inferring relationships between pairs of individuals from locus heterozygosities. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Univ Pisa, Dept Biomed, I-56100 Pisa, Italy. NHGRI, Baltimore, MD USA. Univ Genoa, Dept Legal Med, I-16126 Genoa, Italy. Univ Cagliari, Ist Med Legale, I-09124 Cagliari, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2395 BP 578 EP 578 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802381 ER PT J AU Shrestha, S Strathdee, SA Beaty, TH Smith, MW AF Shrestha, S Strathdee, SA Beaty, TH Smith, MW TI Likelihood measures and methodology for distinguishing single vs. multiple DNAs using STRs in samples for epidemiologic studies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA. NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA. RI Strathdee, Steffanie/B-9042-2009; Smith, Michael/B-5341-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2394 BP 578 EP 578 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802383 ER PT J AU Martin, JC Letocha, AD Reynolds, J Reing, CM Chernoff, E Troendle, J Hill, S Gerber, L Glorieux, FH AF Martin, JC Letocha, AD Reynolds, J Reing, CM Chernoff, E Troendle, J Hill, S Gerber, L Glorieux, FH TI Controlled trial of pamidronate in children with types III and IV OI SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHD, SCTD, NIH, Bethesda, MD 20892 USA. NICHD, BMSB, NIH, Bethesda, MD 20892 USA. NIH, DRD, CC, Bethesda, MD 20892 USA. INOVA, Dept Ortho, Fairfax, VA USA. Shriners, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2401 BP 579 EP 579 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802389 ER PT J AU Correa-Cerro, LS Krakoviak, PA Wassif, CA Porter, FD AF Correa-Cerro, LS Krakoviak, PA Wassif, CA Porter, FD TI Suppression of mRNA nonsense mediated decay in Smith-Lemli-Optiz Syndrome SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NICHHD, Heritage Disorders Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2424 BP 583 EP 583 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802410 ER PT J AU Schiffmann, R Chen, K Gupta, S Sharabi, Y Brady, RO AF Schiffmann, R Chen, K Gupta, S Sharabi, Y Brady, RO TI Enzyme replacement therapy improves sweat function and renal natural history in Fabry disease SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NINDS, NIH, Dev & Metab Neurol Branch, Bethesda, MD 20892 USA. NINDS, NIH, Clin Neurocardiol Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2420 BP 583 EP 583 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802408 ER PT J AU Markowitz, JA Coovert, DD Schussler, K Burghes, AHM Fischbeck, KHK Taylor, JP AF Markowitz, JA Coovert, DD Schussler, K Burghes, AHM Fischbeck, KHK Taylor, JP TI Valproic acid increases SMN levels in spinal muscular atrophy fibroblasts. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT 52nd Annual Meeting of the American-Society-of-Human-Genetics CY OCT 15-19, 2002 CL BALTIMORE, MARYLAND SP Amer Soc Human Genet, NICHHD, NCI, NIMH, Affymetrix Inc, Gentra Syst, NIDCD C1 NINDS, Neurogenet Branch, Bethesda, MD 20892 USA. Ohio State Univ, Coll Biol Sci, Dept Mol Genet, Columbus, OH 43210 USA. Ohio State Univ, Coll Med, Dept Neurol, Dept Biochem Med, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 SU S MA 2444 BP 587 EP 587 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 594AC UT WOS:000178025802432 ER PT J AU Cullen, M Perfetto, SP Klitz, W Nelson, G Carrington, M AF Cullen, M Perfetto, SP Klitz, W Nelson, G Carrington, M TI High-resolution patterns of meiotic recombination across the human major histocompatibility complex SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CLASS-II REGION; HUMAN PSEUDOAUTOSOMAL REGION; GLOBIN GENE-CLUSTER; LINKAGE DISEQUILIBRIUM; DNA-SEQUENCE; HOT-SPOTS; HOMOLOGOUS RECOMBINATION; HUMAN INSULIN; HUMAN GENOME; HUMAN-CELLS AB Definitive characteristics of meiotic recombination events over large (i.e., >1 Mb) segments of the human genome remain obscure, yet they are essential for establishing the haplotypic structure of the genome and for efficient mapping of complex traits. We present a high-resolution map of recombination at the kilobase level across a 3.3-Mb interval encompassing the major histocompatibility complex (MHC). Genotyping of 20,031 single sperm from 12 individuals resulted in the identification and fine mapping of 325 recombinant chromosomes within genomic intervals as small as 7 kb. Several principal characteristics of recombination in this region were observed: (1) rates of recombination can differ significantly between individuals; (2) intense hot spots of recombination occur at least every 0.8 Mb but are not necessarily evenly spaced; (3) distribution in the location of recombination events can differ significantly among individuals; (4) between hot spots, low levels of recombination occur fairly evenly across 100-kb segments, suggesting the presence of warm spots of recombination; and (5) specific sequence motifs associate significantly with recombination distribution. These data provide a plausible model for recombination patterns of the human genome overall. C1 NCI, Lab Genom Divers, Basin Res Program, SAIC Frederick, Ft Detrick, MD 21702 USA. George Washington Univ, Grad Program Genet, Inst Biomed Sci, Washington, DC USA. NIH, USA Program, Vaccine Res Ctr, Bethesda, MD 20892 USA. Childrens Hosp, Oakland Res Inst, Oakland, CA 94609 USA. Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. RP Carrington, M (reprint author), NCI, Lab Genom Divers, Basin Res Program, SAIC Frederick, POB B, Ft Detrick, MD 21702 USA. FU PHS HHS [N01-C0-12400] NR 76 TC 139 Z9 150 U1 1 U2 6 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 759 EP 776 DI 10.1086/342973 PG 18 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800006 PM 12297984 ER PT J AU Weber, JL David, D Heil, J Fan, Y Zhao, CF Marth, G AF Weber, JL David, D Heil, J Fan, Y Zhao, CF Marth, G TI Human diallelic insertion/deletion polymorphisms SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SINGLE-NUCLEOTIDE POLYMORPHISMS; SEQUENCE VARIATION; GENOME SEQUENCE; GENETIC-DISEASE; MUTAGENESIS; MECHANISMS; DIVERSITY; DISCOVERY; RESOURCE; LOCUS AB We report the identification and characterization of 2,000 human diallelic insertion/deletion polymorphisms (indels) distributed throughout the human genome. Candidate indels were identified by comparison of overlapping genomic or cDNA sequences. Average confirmation rate for indels with a greater than or equal to2-nt allele-length difference was 58%, but the confirmation rate for indels with a 1-nt length difference was only 14%. The vast majority of the human diallelic indels were monomorphic in chimpanzees and gorillas. The ratio of deletion: insertion mutations was 4.1. Allele frequencies for the indels were measured in Europeans, Africans, Japanese, and Native Americans. New alleles were generally lower in frequency than old alleles. This tendency was most pronounced for the Africans, who are likely to be closest among the four groups to the original modern human population. Diallelic indels comprise similar to8% of all human polymorphisms. Their abundance and ease of analysis make them useful for many applications. C1 Marshfield Med Res Fdn, Ctr Med Genet, Marshfield, WI 54449 USA. NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA. RP Weber, JL (reprint author), Marshfield Med Res Fdn, Ctr Med Genet, 1000 N Oak Ave, Marshfield, WI 54449 USA. EM weberj@cmg.mfldclin.edu FU NHLBI NIH HHS [HL62681, HV48141, N01HV48141] NR 27 TC 154 Z9 167 U1 0 U2 7 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2002 VL 71 IS 4 BP 854 EP 862 DI 10.1086/342727 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 604HT UT WOS:000178613800013 PM 12205564 ER PT J AU Berrigan, D AF Berrigan, D TI Respiratory cancer and exposure to man-made vitreous fibers: A systematic review SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE man-made vitreous fibers; man-made mineral fibers; lung cancer; respiratory cancer; meta-analysis; glass wool; glass filament; rock wool ID FIBERGLASS MANUFACTURING FACILITY; HISTORICAL COHORT MORTALITY; PRODUCTION WORKERS; LUNG-CANCER; MINERAL FIBERS; FOLLOW-UP; EPIDEMIOLOGIC EVIDENCE; OCCUPATIONAL EXPOSURES; INSULATION WOOLS; CASE-REFERENT AB Background Man-made vitreousfibers (MMVF's) have some structural features similar to those found in asbestos. This has lead to concern that exposure to MMVF's could increase the risk of respiratory cancer. Methods Bibliographic resources were used to identify, 10 case-control and 10 cohort studies, which analyzed the relationship between exposure to MMVF's and cancer of the respiratory system. Standardized mortality ratio's (SMR's) were extracted from the cohort studies for a meta-analysis. Results A significant increase in SMR was observed for workers exposed to rock and glass wool, but not in workers exposed to glass filament. Meta-analysis of SMR's after stratification by fiber type resulted in aggregate estimates of risk of 1.23 (95% CI = 1.10-1.38), 1.08(95% CI=0.93-1.26), and 1.32 (95% CI = 1.15-1.52) for exposure to glass wool, glassfilament, and rock wool, respectively. Some or all of the increased mortality could be attributed to tobacco use. Conclusions The results highlight the difficulty of assessing small increases in risk of respiratory cancer potentially caused by occupational exposure in populations with high prevalence of tobacco use. Published 2002 Wiley-Liss, Inc. C1 NCI, Canc Prevent Fellowship Program, Div Canc Prevent, Bethesda, MD 20892 USA. RP Berrigan, D (reprint author), NCI, Div Canc Control & Populat Sci, Appl Res Program, Execut Plaza N,MSC 7344,Room 4009A,6130 Execut Bl, Bethesda, MD 20892 USA. NR 62 TC 17 Z9 18 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD OCT PY 2002 VL 42 IS 4 BP 354 EP 362 DI 10.1002/ajim.10111 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 598UG UT WOS:000178294400009 PM 12271483 ER PT J AU Beddhu, S Kaysen, GA Yan, GF Sarnak, M Agodoa, L Ornt, D Cheung, AK AF Beddhu, S Kaysen, GA Yan, GF Sarnak, M Agodoa, L Ornt, D Cheung, AK CA HEMO Study Grp TI Association of serum albumin and atherosclerosis in chronic hemodialysis patients SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE serum albumin; atherosclerosis; hemodialysis (HD); coronary artery disease (CAD) ID CORONARY HEART-DISEASE; C-REACTIVE PROTEIN; STAGE RENAL-DISEASE; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; DIALYSIS PATIENTS; RISK-FACTORS; MORTALITY; INFLAMMATION; DEATH AB Background: Because cardiovascular disease is the leading cause of death and hypoalbuminemia predicts mortality, hypoalbuminemia may be associated with atherosclerosis. Methods: In 1,411 patients enrolled in the HEMO study, associations of albumin with the presence of coronary artery disease (CAD), cerebrovascular disease (CVD), peripheral vascular disease (PVD), and any one of the three conditions at baseline were examined using multivariable logistic regression models. Results: In the two-slope model, when albumin level was 3.6 g/dL (36 g/L) or greater, with each 1-g/dL (10-g/L) increase in albumin level the odds for CAD (odds ratio [OR], 0.32; 95% confidence interval [CI], 0.17 to 0.59), PVD (OR, 0.39; 95% CI, 0.18 to 0.80), CVD (OR, 0.33; 95% CI, 0.15 to 0.73), and any one of the three conditions (OR, 0.23; 95% CI, 0.12 to 0.44) decreased. When albumin level was less than 3.6 g/dL (36 g/L), none of the conditions was statistically significantly associated with each 1-g/dL (10-g/L) increase in albumin level. When normal- and low-albumin groups were compared with each other, patients with albumin levels less than 3.6 g/dL (36 g/L) had a higher association with CAD (OR, 1.32; 95% CI, 1.03 to 1.70) and for any one of the three conditions (OR, 1.38; 95% CI, 1.07 to 1.78). Conclusion: The odds for atherosclerosis linearly decreased as albumin level increased in the normal-albumin group, and a plateau was seen in the low-albumin group; however, the low-albumin group had significantly greater CAD. The nonlinearity of association of albumin level with prevalence of atherosclerosis might be due to the cross-sectional nature of the study of higher mortality with hypoalbuminemia. (C) 2002 by the National Kidney Foundation, Inc. C1 NIDDKD, Bethesda, MD 20892 USA. RP Beddhu, S (reprint author), Univ Utah, Sch Med, 85 N Med Dr,East Rm 201, Salt Lake City, UT 84112 USA. NR 27 TC 56 Z9 59 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 OCT PY 2002 VL 40 IS 4 BP 721 EP 727 DI 10.1053/ajkd.2002.35679 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA 600JC UT WOS:000178386000009 PM 12324906 ER PT J AU van der Knaap, MS Naidu, S Pouwels, PJW Bonavita, S van Coster, R Lagae, L Sperner, J Surtees, R Schiffmann, R Valk, J AF van der Knaap, MS Naidu, S Pouwels, PJW Bonavita, S van Coster, R Lagae, L Sperner, J Surtees, R Schiffmann, R Valk, J TI New syndrome characterized by hypomyelination with atrophy of the basal ganglia and cerebellum SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article ID PELIZAEUS-MERZBACHER-DISEASE; MAGNETIC-RESONANCE SPECTROSCOPY; VANISHING WHITE-MATTER; PROTON MR SPECTROSCOPY; METABOLITE CONCENTRATIONS; YOUNG-ADULTS; LEUKOENCEPHALOPATHY; BRAIN; DISORDERS; CHILDREN AB BACKGROUND AND PURPOSE: Leukoencephalopathies of unknown origin constitute a considerable problem in child neurology. The purpose of our ongoing study of the subject was to define new disease entities among them by using primarily MR imaging pattern recognition. METHODS: We identified seven unrelated patients with a distinct MR imaging pattern consisting of hypomyelination and atrophy of the basal ganglia (neostriatum) and cerebellum (H-ABC). We reviewed the clinical, MR imaging, MR spectroscopic, and laboratory data. RESULTS: Clinically, the patients' diseases were characterized by variably disturbed early development followed by increasing extrapyramidal movement abnormalities, ataxia, and spasticity. Mental capacity was variably affected, but it appeared to be relatively preserved. Parents were not related, and none of their siblings were affected. No metabolic defect was found. Follow-up MR imaging demonstrated atrophy of the cerebral white matter, neostriatum, and cerebellum, which was most pronounced in the most clinically severe cases. Single-voxel proton MR spectroscopic results were normal in the parietal cortex. In the cerebral white matter, myo-inositol and creatine levels were elevated; this finding was compatible with gliosis. Nacetylaspartate and choline levels were normal, suggesting that neither axonal loss nor active demyelination occurred. Proton MR spectroscopic imaging revealed relatively decreased Nacetylaspartate levels in the frontal region. CONCLUSION. The uniform and highly characteristic MR imaging findings, in combination with the similarities in the clinical findings, provide evidence of a distinct nosologic entity. The acronym H-ABC is offered to indicate patients sharing these clinical and MR imaging features. C1 Free Univ Amsterdam, Med Ctr, Dept Child Neurol, NL-1007 MB Amsterdam, Netherlands. Free Univ Amsterdam, Med Ctr, Dept Clin Phys & Informat, NL-1007 MB Amsterdam, Netherlands. Free Univ Amsterdam, Med Ctr, Dept Radiol, NL-1007 MB Amsterdam, Netherlands. Kennedy Krieger Inst, Dept Neurogenet, Baltimore, MD USA. NIH, Neuroimaging Branch, Bethesda, MD 20892 USA. NIH, Dev & Metab Neurol Branch, Bethesda, MD 20892 USA. Univ Ziekenhuis C Hooft, Dept Pediat Neurol, Ghent, Belgium. Univ Ziekenhuis Gasthuisberg, Louvain, Belgium. Univ Klinikum Lubeck, Dept Pediat, Lubeck, Germany. Great Ormond St Hosp Children, Dept Pediat Neurol, London WC1N 3JH, England. RP van der Knaap, MS (reprint author), Free Univ Amsterdam, Med Ctr, Dept Child Neurol, POB 7057, NL-1007 MB Amsterdam, Netherlands. NR 35 TC 71 Z9 72 U1 0 U2 2 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD OCT PY 2002 VL 23 IS 9 BP 1466 EP 1474 PG 9 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 603NB UT WOS:000178565000005 PM 12372733 ER PT J AU Zhang, J Troendle, JF Yancey, MK AF Zhang, J Troendle, JF Yancey, MK TI Reassessing the labor curve in nulliparous women SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 22nd Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY JAN 14-19, 2002 CL NEW ORLEANS, LOUISIANA SP Soc Maternal Fetal Med DE arrest; labor curve; nullipara; protraction; cesarean ID ARREST AB OBJECTIVES: Our purpose was to examine the pattern of labor progression in nulliparous parturients in contemporary obstetric practice. STUDY DESIGN: We extracted detailed labor data from 1329 nulliparous parturients with a term, singleton, vertex fetus of normal birth weight after spontaneous onset of labor, Cesarean deliveries were excluded, We used a repeated-measures regression with a 10th-order polynomial function to discover the average labor curve under contemporary practice. With use of an interval-censored regression with a log normal distribution, we also computed the expected time interval of the cervix to reach the next centimeter, the expected rate of cervical dilation at each phase of labor, and the duration of labor for fetal descent at various stations. RESULTS: Our average labor curve differs markedly from the Friedman curve. The cervix dilated substantially slower in the active phase. It took approximately 5.5 hours from 4 cm to 10 cm, compared with 2.5 hours under the Friedman curve. We observed no deceleration phase. Before 7 cm, no perceivable change in cervical dilation for more than 2 hour was not uncommon. The 5th percentiles of rate of cervical dilation were all below 1 cm per hour. The 95th percentile of time interval for fetal descent from station +1/3 to +2/3 was 3 hours at the second stage. CONCLUSION: Our results suggest that the pattern of labor progression in contemporary practice differs significantly from the Friedman curve. The diagnostic criteria for protraction and arrest disorders of labor may be too stringent in nulliparous women. C1 NICHHD, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD 20892 USA. Tripler Army Med Ctr, Dept Obstet & Gynecol, Honolulu, HI 96859 USA. RP Zhang, J (reprint author), NICHHD, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NIH, Bldg 6100,Room 7B03, Bethesda, MD 20892 USA. NR 20 TC 128 Z9 143 U1 2 U2 10 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD OCT PY 2002 VL 187 IS 4 BP 824 EP 828 DI 10.1067/mob.2002.127142 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 606AJ UT WOS:000178709300002 PM 12388957 ER PT J AU Allen, RH Rosenbaum, TC Ghidini, A Poggi, SH Spong, CY AF Allen, RH Rosenbaum, TC Ghidini, A Poggi, SH Spong, CY TI Correlating head-to-body delivery intervals with neonatal depression in vaginal births that result in permanent brachial plexus injury SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 22nd Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY JAN 14-19, 2002 CL NEW ORLEANS, LOUISIANA SP Soc Maternal Fetal Med DE Apgar score; Erb-Duchennes palsy; maneuvers; neonatal asphyxia; shoulder dystocia; time ID SHOULDER DYSTOCIA; OBJECTIVE DEFINITION; RISK-FACTORS AB OBJECTIVE: The purpose of this study was to evaluate which variables predict neonatal depression in vaginal deliveries that result in permanent brachial plexus injury, STUDY DESIGN: With the use of a data set of litigated vaginal deliveries (n = 103 deliveries) from 1978 through 1999 that resulted in permanent brachial plexus injury, detailed delivery and neonatal and pediatric information was obtained by chart review. Neonatal depression was defined as a 5-minute Apgar score of <7. Data that were extrapolated from neonates with low Apgar scores at 5 minutes were compared with neonates with Apgar scores of greater than or equal to 7 with the use of the Fisher exact test, chi(2) test, or one-way analysis of variance; a two-tailed probability value of <.05 was considered significant. RESULTS: Nine of 89 neonates (10%) had low 5-minute Apgar scores. Head-to-body delivery intervals (available for 36 deliveries) were significantly longer in neonates with 5-minute Apgar scores of <7 vs greater than or equal to7 (294 +/- 68 seconds vs 147 +/- 82 seconds, P <.001). Differences in other clinical variables (ie, maternal weight, gestational age, diabetes mellitus, parity, birth weight, and sex) were not significant. None of the infants in this data set, which includes those infants with neonatal depression) died or had long-term asphyxia-related sequelae in the form of speech impediments, seizures, cerebral palsy, coma, or organ dysfunction. CONCLUSION: The head-to-body delivery interval was the only significant factor in the prediction of 5-minute Apgar score of <7 in a data set of deliveries that resulted in permanent brachial plexus injury. Despite extended times (less than or equal to6 minutes) on the perineum that resulted in a higher reduced Apgar score rate, there was no asphyxia-related morbidity. C1 Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD 21218 USA. NICHD, Pregnancy & Perinatol Branch, Ctr Res Mothers & Children, NIH, Washington, DC USA. Georgetown Univ, Med Ctr, Dept Obstet & Gynecol, Washington, DC 20007 USA. Romualdi Davidson & Associates, Bethesda, MD USA. RP Allen, RH (reprint author), Johns Hopkins Univ, Dept Biomed Engn, Clark Hall,3400 N Charles St, Baltimore, MD 21218 USA. RI Allen, Robert/A-3731-2010 NR 20 TC 16 Z9 16 U1 1 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD OCT PY 2002 VL 187 IS 4 BP 839 EP 842 DI 10.1067/mob.2002.127128 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 606AJ UT WOS:000178709300005 PM 12388960 ER PT J AU Chaiworapongsa, T Gervasi, MT Refuerzo, J Espinoza, J Yoshimatsu, J Berman, S Romero, R AF Chaiworapongsa, T Gervasi, MT Refuerzo, J Espinoza, J Yoshimatsu, J Berman, S Romero, R TI Maternal lymphocyte subpopulations (CD45RA+ and CD45RO+) in preeclampsia SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 22nd Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY JAN 14-19, 2002 CL NEW ORLEANS, LOUISIANA SP Soc Maternal Fetal Med DE precclampsia; memory T cells; CD45; naive T cells; lymphocytes ID T-CELLS; ACTIVATION; INFECTION; ATHEROSCLEROSIS; EXPRESSION; MARKERS; SUBSETS; UCHL1 AB OBJECTIVE: The maternal syndrome of preeclampsia has been attributed to a systemic intravascular inflammatory response and endothelial cell dysfunction. The stimulus responsible for intravascular inflammation in preeclampsia has not been determined, The expression of CD45 isoforms on the surface of human T cells has been used to classify CD4(+) T lymphocytes into naive cells (CD45RA+) and memory T cells (CD45RO+). An increased percentage of CD45RO+ cells has been interpreted as consistent with previous exposure to microbial products or other antigens. The purpose of this study was to determine whether preeclampsia is associated with a change in the proportion of CD45RA+ and CD45RO+. STUDY DESIGN: A prospective study was conducted in patients with preeclampsia (n = 24) and normal pregnancy (n = 75), The percentage of CD45RA+ and CD45RO+ on CD4(+) T lymphocytes in peripheral blood was determined using flow cytometry and monoclonal antibodies. Results were reported as a percentage of CD4(+) lymphocytes. Parametric statistics were used for analysis. A probability value of <.05 was considered statistically significant. RESULTS: Patients with preeclampsia had a significantly higher percentage of CD45RO+ than normal pregnant women (P <.01). A significantly lower percentage of CD45RA+ was found in patients with preeclampsia than in normal pregnant women (P <.01). CONCLUSION: Preeclampsia is associated with an increase in the percentage of CD45RO+ and a decrease in the CD45RA+ lymphocyte subpopulation. Therefore, patients with preeclampsia have evidence of previous antigenic exposure, the nature of which remains to be established. C1 Wayne State Univ, Hutzel Hosp, Perinatol Res Branch, NICHHD, Detroit, MI 48201 USA. Wayne State Univ, Hutzel Hosp, Dept Obstet & Gynecol, Detroit, MI 48201 USA. RP Romero, R (reprint author), Wayne State Univ, Hutzel Hosp, Perinatol Res Branch, NICHD,Dept Obstet & Gynecol, 4707 St Antoine Blvd, Detroit, MI 48201 USA. NR 24 TC 27 Z9 28 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD OCT PY 2002 VL 187 IS 4 BP 889 EP 893 DI 10.1067/mob.2002.127309 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 606AJ UT WOS:000178709300016 PM 12388971 ER PT J AU Poggi, SH Vink, J Goodwin, K Hill, JM Brenneman, DE Pinhasov, A Gozes, I Spong, CY AF Poggi, SH Vink, J Goodwin, K Hill, JM Brenneman, DE Pinhasov, A Gozes, I Spong, CY TI Differential expression of embryonic and maternal activity-dependent neuroprotective protein during mouse development SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 22nd Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY JAN 14-19, 2002 CL NEW ORLEANS, LOUISIANA SP Soc Maternal Fetal Med DE activity-dependent neuroprotective protein vasoactive intestinal peptide; embryonic growth; mouse ID VASOACTIVE-INTESTINAL-PEPTIDE; BINDING-SITES; GROWTH; VIP AB OBJECTIVE: Activity-dependent neuroprotective protein (ADNP) potently enhances the survival of neurons and is regulated by vasoactive intestinal peptide, which also mediates postimplantation mouse embryonic growth. The objective of this study was to characterize ADNP in mouse embryonic tissues throughout development. STUDY DESIGN: Developmental tissues (embryo, decidua, placenta) from timed pregnant C57B16/J mice were harvested on days 6 though 18. To evaluate ADNP expression, RNA was extracted from at least three samples from three different mice per day. Five micrograms of total RNA from each sample was used per reverse transcriptase-polymerase chain reaction. Immunocytochemistry with anti-ADNP-derived peptide immunoglobulin and anti-gammadelta T-cell receptor was performed on 20 mum thick fixed sections of day 9.5 uteri. RESULTS: Embryonic ADNP messenger RNA (mRNA) has a temporal pattern with greater amounts present from gestational days 9 to 16. Placental ADNP mRNA was uniformly expressed on gestational days 11 to 18. Levels of decidual ADNP mRNA were greatest early in gestation and declined until delivery. Within the decidua, ADNP and gammadelta T-cell receptor immunoreactivity was present in the same cells. CONCLUSION: The expression of ADNP during pregnancy supports a developmental role for this protein. These data indicate both embryonic and maternal sources of ADNP during the critical period of organogenesis. C1 Georgetown Univ Hosp, Dept Obstet & Gynecol, Washington, DC USA. NICHHD, Lab Dev Neurobiol, Sec Dev & Mol Pharmacol, NIH, Washington, DC USA. Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. RP Poggi, SH (reprint author), Dept Obstet & Gynecol, 3800 Reservoir Rd, Washington, DC 20007 USA. NR 17 TC 17 Z9 17 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD OCT PY 2002 VL 187 IS 4 BP 973 EP 976 DI 10.1067/mob.2002.127141 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 606AJ UT WOS:000178709300034 PM 12388989 ER PT J AU DePaolo, LV Leppert, PC AF DePaolo, LV Leppert, PC TI Providing research and research training infrastructures for clinical research in the reproductive sciences SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE reproduction; physician-scientist; education; research training AB The Reproductive Sciences Branch of the National Institutes of Child Health and Human Development has created pioneering new research and research training programs that address the impending shortage of physician-scientists in obstetrics, gynecology, and women's health and the need to bolster translational and clinical research, This article provides a brief overview of the Specialized Cooperative Centers Program in Reproduction Research, the National Cooperative Program for Infertility Research, the Reproductive Medicine Network, the Reproductive Scientist Development Program, the Women's Reproductive Health Research Career Development Program, and the Contraception and Infertility Research Loan Repayment Program and describes how these programs collectively create an infrastructure to promote the next generation of physician-scientists and to provide an information exchange between basic and clinical investigators. A key component in increasing the number of clinical investigators is the Contraception and Infertility Research Loan Repayment Program. This program has enabled clinicians to be involved in research without having to be concerned about educational loan debt. Other component programs provide basic/translational, clinical hypothesis-oriented research and clinical trials research infrastructure. The programs created are individually strong and collectively poised to support translational and clinical research efforts and to build a well-trained cadre of physician-scientists. The collective use of these types of programs is proposed as a model for the National Institutes of Health. C1 NICHHD, Reprod Sci Branch, Populat Res Ctr, NIH, Bethesda, MD 20892 USA. RP Leppert, PC (reprint author), NICHHD, Reprod Sci Branch, Populat Res Ctr, NIH, Bldg 61EB,Room 8B01, Bethesda, MD 20892 USA. NR 1 TC 6 Z9 6 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD OCT PY 2002 VL 187 IS 4 BP 1087 EP 1090 DI 10.1067/mob.2002.125896 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 606AJ UT WOS:000178709300055 PM 12389010 ER PT J AU Lopez-Franco, O Suzuki, Y Sanjuan, G Blanco, J Hernandez-Vargas, P Yo, Y Kopp, J Egido, J Gomez-Guerrero, C AF Lopez-Franco, O Suzuki, Y Sanjuan, G Blanco, J Hernandez-Vargas, P Yo, Y Kopp, J Egido, J Gomez-Guerrero, C TI Nuclear factor-kappa B inhibitors as potential novel anti-inflammatory agents for the treatment of immune glomerulonephritis SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HUMAN MESANGIAL CELLS; INTERLEUKIN-8 GENE-EXPRESSION; FC-ALPHA RECEPTORS; TRANSCRIPTION FACTOR; SESQUITERPENE LACTONES; FUNGAL METABOLITE; AP-1 ACTIVATION; RENAL-DISEASE; TNF-ALPHA; GLIOTOXIN AB Nuclear factor (NF)-kappaB regulates several genes implicated in the inflammatory response and represents an interesting therapeutic target. We examined the effects of gliotoxin (a fungal metabolite) and parthenolide (a plant extract), which possess anti-inflammatory activities in vitro, on the progression of experimental glomerulonephritis. in the anti-Thy 1.1 rat model, gliotoxin (75 mug/rat/day, 10 days, n = 18 rats) markedly reduced proteinuria, glomerular lesions, and monocyte infiltration. In anti-mesangial cell nephritis in mice, parthenolide (70 mug/mouse/day, 7 days, n = 17 mice) significantly decreased proteinuria, hematuria, and glomerular proliferation. NF-kappaB activity, localized in glomerular and tubular cells, was attenuated by either gliotoxin or parthenolide, in association with diminished renal expression of monocyte chemoattractant protein-1 and inducible nitric oxide synthase. in cultured mesangial cells and monocytes, gliotoxin and parthenolide inhibited NF-kappaB activation and expression of inflammatory genes induced by lipopolysaccharide and cytokines; by blocking the phosphorylation/degradation of the IkappaBalpha subunit. In summary, gliotoxin and parthenolide prevent proteinuria and renal lesions by inhibiting NF-kappaB activation and expression of regulated genes. This may represent a novel approach for the treatment of immune and inflammatory renal diseases. C1 Univ Autonoma Madrid, Fdn Jimenez Diaz, Renal & Vasc Res Lab, Madrid 28040, Spain. NIH, Kidney Dis Sect, Bethesda, MD 20892 USA. Hosp Clin San Carlos, Madrid, Spain. RP Gomez-Guerrero, C (reprint author), Univ Autonoma Madrid, Fdn Jimenez Diaz, Renal & Vasc Res Lab, Avda Reyes Catolicos 2, Madrid 28040, Spain. NR 48 TC 83 Z9 93 U1 0 U2 6 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 OCT PY 2002 VL 161 IS 4 BP 1497 EP 1505 DI 10.1016/S0002-9440(10)64425-2 PG 9 WC Pathology SC Pathology GA 601NQ UT WOS:000178453000041 PM 12368222 ER PT J AU Pujols, L Mullol, J Roca-Ferrer, J Torrego, A Xaubet, A Cidlowski, JA Picado, C AF Pujols, L Mullol, J Roca-Ferrer, J Torrego, A Xaubet, A Cidlowski, JA Picado, C TI Expression of glucocorticoid receptor alpha- and beta-isoforms in human cells and tissues SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE reverse transcriptase-competitive polymerase chain reaction; Western blotting; healthy human tissues; inflammatory cells ID NF-KAPPA-B; MESSENGER-RNA; EPITHELIAL-CELLS; TRANSCRIPTION FACTORS; GENE-EXPRESSION; NASAL POLYP; DEXAMETHASONE; ASTHMA; RESISTANCE; LOCALIZATION AB Alternative splicing of the human glucocorticoid receptor (GR) primary transcript generates two protein isoforms: GR-alpha and GR-beta. We investigated the expression of both GR isoforms in healthy human cells and tissues. GR-alpha mRNA abundance (x10(6) cDNA copies/mug total RNA) was as follows: brain (3.83 +/- 0.80) > skeletal muscle > macrophages > lung > kidney > liver > heart > eosinophils > peripheral blood mononuclear cells (PBMCs) > nasal mucosa > neutrophils > colon (0.33 +/- 0.04). GR-alpha mRNA was much less expressed than GR-alpha mRNA. Its abundance (x10(3) cDNA copies/mug total RNA) was as follows: eosinophils (1.55 +/- 0.58) > PBMCs > liver > skeletal muscle > kidney > macrophages > lung > neutrophils > brain > nasal mucosa > heart (0.15 +/- 0.08). GR-alpha mRNA was not found in colon. While GR-beta protein was detected in all cells and tissues, GR-beta was not detected in any specimen. Our results suggest that, in physiological conditions, the default splicing pathway is the one leading to GR-alpha. The alternative splicing event leading to GR-beta is minimally activated. C1 Univ Barcelona, Dept Med, Hosp Clin, Inst Invest Biomed August Pi & Sunyer, E-08036 Barcelona, Spain. Univ Barcelona, Dept Med, Hosp Clin, Serv Otorinolaringol, E-08036 Barcelona, Spain. Univ Barcelona, Dept Med, Hosp Clin,Srv Pneumol & Allergia Resp, Inst Clin Pneumol & Cirurgia Torac, E-08036 Barcelona, Spain. NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. RP Picado, C (reprint author), Hosp Clin Barcelona, Serv Pneumol, Villarroel 170, E-08036 Barcelona, Catalonia, Spain. RI Pujols, Laura/G-8920-2015 OI Pujols, Laura/0000-0003-3708-5098 NR 52 TC 95 Z9 105 U1 1 U2 7 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD OCT PY 2002 VL 283 IS 4 BP C1324 EP C1331 DI 10.1152/ajpcell.00363.2001 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA 592UE UT WOS:000177954600031 PM 12225995 ER PT J AU Zhong, Z Froh, M Connor, HD Li, XL Conzelmann, LO Mason, RP Lemasters, JJ Thurman, RG AF Zhong, Z Froh, M Connor, HD Li, XL Conzelmann, LO Mason, RP Lemasters, JJ Thurman, RG TI Prevention of hepatic ischemia-reperfusion injury by green tea extract SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE ischemia; free radicals; liver; nuclear factor-kappaB; cytokines ID NF-KAPPA-B; MULTIPLE-ORGAN-FAILURE; TRANSCRIPTION FACTOR; HYDROGEN-PEROXIDE; RADICAL FORMATION; FATTY-ACIDS; CELL INJURY; BLACK TEA; IN-VIVO; OXYGEN AB These experiments were designed to determine whether green tea extract (GTE), which contains polyphenolic free radical scavengers, prevents ischemia-reperfusion injury to the liver. Rats were fed a powdered diet containing 0-0.3% GTE starting 5 days before hepatic warm ischemia and reperfusion. Free radicals in bile were trapped with the spin-trapping reagent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) and measured using electron spin resonance spectroscopy. Hepatic ischemia-reperfusion increased transaminase release and caused pathological changes including focal necrosis and hepatic leukocyte infiltration in the liver. Transaminase release was diminished by over 85% and pathological changes were almost totally blocked by 0.1% dietary GTE. Ischemia-reperfusion increased 4-POBN/radical adducts in bile nearly twofold, an effect largely blocked by GTE. Epicatechin, one of the major green tea polyphenols, gave similar protection as GTE. In addition, hepatic ischemia-reperfusion activated NF-kappaB and increased TNF-alpha mRNA and protein expression. These effects were all blocked by GTE. Taken together, these results demonstrate that GTE scavenges free radicals in the liver after ischemia-reoxygenation, thus preventing formation of toxic cytokines. Therefore, GTE could prove to be effective in decreasing hepatic injury in disease states where ischemia-reperfusion occurs. C1 Univ N Carolina, Dept Cell & Dev Biol, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RP Zhong, Z (reprint author), Univ N Carolina, Dept Cell & Dev Biol, CB 7090, Chapel Hill, NC 27599 USA. NR 47 TC 58 Z9 59 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD OCT PY 2002 VL 283 IS 4 BP G957 EP G964 DI 10.1152/ajpgi.00216.2001 PG 8 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA 592BJ UT WOS:000177916600016 PM 12223356 ER PT J AU Cross, HR Murphy, E Black, RG Auchampach, J Steenbergen, C AF Cross, HR Murphy, E Black, RG Auchampach, J Steenbergen, C TI Overexpression of A(3) adenosine receptors decreases heart rate, preserves energetics, and protects ischemic hearts SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE cardioprotection; ischemia; nuclear magnetic resonance spectroscopy ID CORONARY ANGIOPLASTY; REPERFUSION INJURY; CONSCIOUS RABBITS; TARGETED DELETION; INFARCTION; METABOLISM; MOUSE; A(1); SUSCEPTIBILITY; ACTIVATION AB To determine whether A(3) adenosine receptor (A(3)AR) signaling modulates myocardial function, energetics, and cardioprotection, hearts from wild-type and A(3)AR-overexpressor mice were subjected to 20-min ischemia and 40-min reperfusion while P-31 NMR spectra were acquired. Basal heart rate and left ventricular developed pressure (LVDP) were lower in A(3)AR-overexpressor hearts than wild-type hearts. Ischemic ATP depletion was delayed and postischemic recoveries of contractile function, ATP, and phosphocreatine were greater in A(3)AR-hearts. To determine the role of depressed heart rate and to confirm A(3)AR-specific signaling, hearts were paced at 480 beats/min with or without 60 nmol/l MRS-1220 (A(3)AR-specific inhibitor) and then subjected to ischemia-reperfusion. LVDP was similar in paced A(3)AR-overexpressor and paced wild-type hearts. Differences in ischemic ATP depletion and postischemic contractile and energetic dysfunction remained in paced A(3)AR-overexpressor hearts versus paced wild-type hearts but were abolished by MRS-1220. In summary, A(3)AR overexpression decreased basal heart rate and contractility, preserved ischemic ATP, and decreased postischemic dysfunction. Pacing abolished the decreased contractility but not the ATP preservation or cardioprotection. Therefore, A(3)AR overexpression results in cardioprotection via a specific A(3)AR effect, possibly involving preservation of ATP during ischemia. C1 Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. NIEHS, Res Triangle Pk, NC 27709 USA. Med Coll Wisconsin, Dept Pharmacol, Milwaukee, WI 53226 USA. RP Cross, HR (reprint author), Duke Univ, Med Ctr, Dept Pathol, Box 3712, Durham, NC 27710 USA. FU NHLBI NIH HHS [R01 HL039752, R01 HL060051, R01 HL060051-03, R01 HL060051-04] NR 32 TC 38 Z9 38 U1 0 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 OCT PY 2002 VL 283 IS 4 BP H1562 EP H1568 DI 10.1152/ajpheart.00335.2002 PG 7 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 594DY UT WOS:000178034500035 PM 12234810 ER PT J AU Piermarini, PM Verlander, JW Royaux, IE Evans, DH AF Piermarini, PM Verlander, JW Royaux, IE Evans, DH TI Pendrin immunoreactivity in the gill epithelium of a euryhaline elasmobranch SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE anion exchanger; vacuolar-proton-adenosinetriphosphatase; sodium-potassium-adenosinetriphosphatase; sodium chloride regulation; acid/base regulation; Dasyatis sabina ID STINGRAY DASYATIS-SABINA; SYNDROME GENE PDS; INTERCALATED CELLS; RAINBOW-TROUT; TRANSPORT PROTEIN; SALMO-GAIRDNERI; NA+/K+-ATPASE; RECTAL GLAND; MARINE FISH; EXCRETION AB Pendrin is an anion exchanger in the cortical collecting duct of the mammalian nephron that appears to mediate apical Cl-/HCO3- exchange in bicarbonate-secreting intercalated cells. The goals of this study were to determine 1) if pendrin immunoreactivity was present in the gills of a euryhaline elasmobranch (Atlantic stingray, Dasyatis sabina), and 2) if branchial pendrin immunoreactivity was influenced by environmental salinity. Immunoblots detected pendrin immunoreactivity in Atlantic stingray gills; pendrin immunoreactivity was greatest in freshwater stingrays compared with freshwater stingrays acclimated to seawater (seawater acclimated) and marine stingrays. Using immunohistochemistry, pendrin-positive cells were detected on both gill lamellae and interlamellar regions of freshwater stingrays but were more restricted to interlamellar regions in seawater-acclimated and marine stingray gills. Pendrin immunolabeling in freshwater stingray gills was more apical, discrete, and intense compared with seawater-acclimated and marine stingrays. Regardless of salinity, pendrin immunoreactivity occurred on the apical region of cells rich with basolateral vacuolar-proton-ATPase, and not in Na+-K+-ATPase- rich cells. We suggest that a pendrin-like transporter may contribute to apical Cl-/HCO3- exchange in gills of Atlantic stingrays from both freshwater and marine environments. C1 Univ Florida, Dept Zool, Gainesville, FL 32611 USA. Univ Florida, Coll Med, Gainesville, FL 32611 USA. NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Piermarini, PM (reprint author), Univ Florida, Dept Zool, 223 Bartram Hall,Box 118525, Gainesville, FL 32611 USA. RI Verlander, Jill/I-5991-2015 NR 36 TC 93 Z9 95 U1 0 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD OCT PY 2002 VL 283 IS 4 BP R983 EP R992 DI 10.1152/ajpregu.00178.2002 PG 10 WC Physiology SC Physiology GA 592WN UT WOS:000177960000023 PM 12228069 ER PT J AU Pritchard, JB AF Pritchard, JB TI Comparative models and biological stress SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article ID HYPOXIC HYPOMETABOLISM; TRACHEMYS-SCRIPTA; EXPRESSION; ANOXIA; TURTLE; HEPATOCYTES; VERTEBRATE; EVOLUTION; RECOVERY C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RP Pritchard, JB (reprint author), NIEHS, Lab Pharmacol & Chem, 110 Alexander Dr,MD F1-03, Res Triangle Pk, NC 27709 USA. NR 31 TC 4 Z9 4 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD OCT PY 2002 VL 283 IS 4 BP R807 EP R809 DI 10.1152/ajpregu.00145.2002 PG 3 WC Physiology SC Physiology GA 592WN UT WOS:000177960000001 PM 12228047 ER PT J AU Cai, Q Michea, L Andrews, P Zhang, Z Rocha, G Dmitrieva, N Burg, MB AF Cai, Q Michea, L Andrews, P Zhang, Z Rocha, G Dmitrieva, N Burg, MB TI Rate of increase of osmolality determines osmotic tolerance of mouse inner medullary epithelial cells SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE cell survival; hyperosmolality; growth factor; extracellular matrix; porous support ID REGULATES APOPTOSIS; MITOCHONDRIA; INTEGRINS; KINASE; DIFFERENTIATION; OSMOLARITY; TRANSPORT; ADHESION; ANOIKIS; INVITRO AB Renal inner medullary cells survive and function despite interstitial osmolality of 600-1,700 mosmol/kgH(2)O or more. In contrast, much smaller changes kill cells in tissue culture. Using mouse inner medullary epithelial cells at passage 2, we defined factors that might account for the difference. Most of the factors that we tested, including addition of hormones (insulin-like growth factor I, epidermal growth factor, or deamino-8-D-arginine vasopressin), growth on porous supports, and presence of matrix proteins (collagen I, collagen IV, fibronectin, laminin, or fibrillar collagen I), have no significant effect. However, the time course of the change makes a major difference. When osmolality is increased from 640 to 1,640 mosmol/kgH(2)O by addition of NaCl and urea in a single step, only 30% of cells survive for 24 h. However, when the same increase is made linearly over 20 h, 89% of the cells remain viable 24 h later. We conclude that gradual changes in osmolality, e. g., in vivo, allow cells to survive much greater changes than do the step changes routinely used in cell culture experiments. C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. Univ Los Andes, Fac Med, Lab Cellular & Mol Physiol, Santiago, Chile. Georgetown Univ, Med Ctr, Dept Cell Biol, Washington, DC 20002 USA. RP Cai, Q (reprint author), NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bldg 10,Rm 6N319, Bethesda, MD 20892 USA. EM caiq@nhlbi.nih.gov RI Dmitrieva, Natalia/A-2924-2013 OI Dmitrieva, Natalia/0000-0001-8074-6950 NR 32 TC 16 Z9 16 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD OCT PY 2002 VL 283 IS 4 BP F792 EP F798 DI 10.1152/ajprenal.00046.2002 PG 7 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA 591HH UT WOS:000177873300023 PM 12217871 ER PT J AU Masilamani, S Wang, XY Kim, GH Brooks, H Nielsen, J Nielsen, S Nakamura, K Stokes, JB Knepper, MA AF Masilamani, S Wang, XY Kim, GH Brooks, H Nielsen, J Nielsen, S Nakamura, K Stokes, JB Knepper, MA TI Time course of renal Na-K-ATPase, NHE3, NKCC2, NCC, and ENaC abundance changes with dietary NaCl restriction SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE aldosterone; distal convoluted tubule; collecting duct; type 3 sodium/hydrogen exchanger; bumetanide-sensitive type 2 sodium potassium-2 chloride cotransporter; thiazide-sensitive sodium-chloride cotransporter; epithelial sodium channel ID THICK ASCENDING LIMB; CHANNEL ALPHA-SUBUNIT; RAT-KIDNEY; ALTERED EXPRESSION; MEDIATED REGULATION; CL COTRANSPORTER; MESSENGER-RNA; HENLES LOOP; ALDOSTERONE; TRANSPORTERS AB We have used peptide- directed antibodies to each major renal Na transporter and channel proteins to screen renal homogenates for changes in Na transporter protein expression after initiation of dietary NaCl restriction. After equilibration on a NaCl- replete diet (2.0 meq.200 g body wt(-1) .day(-1)), rats were switched to a NaCl- deficient diet (0.02 meq . 200 g body wt(-1) . day -(1)). Na excretion fell to 25% of baseline levels on day 1, followed by a further decrease <4% of baseline levels on day 3, of NaCl restriction. The decreased Na excretion at day 1 occurred despite the absence of a significant increase in plasma aldosterone level or in the abundance of any of the major renal Na transporters. However, after a 1- day lag, plasma aldosterone levels increased in association with increases in abundances of three aldosterone- regulated Na transporter proteins: the thiazide-sensitive Na- Cl cotransporter (NCC), the alpha-subunit of the amiloride- sensitive epithelial Na channel (alpha-ENaC), and the 70- kDa form of gamma-ENaC. RNase protection assays of transporter mRNA levels revealed an increase in renal alpha-ENaC mRNA coincident with the increase in alpha- ENaC protein abundance. However, there was no change in NCC mRNA abundance, suggesting that the increase in NCC protein in response to dietary NaCl restriction was not a result of altered gene transcription. These results point to early regulatory processes that decrease renal Na excretion without an increase in the abundance of any Na transporter, followed by a late aldosterone-dependent response associated with upregulation of NCC and ENaC. C1 NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA. Aarhus Univ, Water & Salt Inst, DK-8000 Aarhus C, Denmark. Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA. Vet Affairs Med Ctr, Iowa City, IA 52242 USA. RP Knepper, MA (reprint author), NHLBI, Kidney & Electrolyte Metab Lab, NIH, 10 Ctr Dr,MSC-1603,Bldg 10,Rm 6N260, Bethesda, MD 20892 USA. EM knep@helix.nih.gov FU Intramural NIH HHS [Z01 HL001285-21, Z99 HL999999]; NHLBI NIH HHS [K22-HL-66994, Z01-HL-01282-KE]; NIDDK NIH HHS [DK-52617] NR 39 TC 85 Z9 86 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD OCT PY 2002 VL 283 IS 4 BP F648 EP F657 DI 10.1152/ajprenal.00016.2002 PG 10 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA 591HH UT WOS:000177873300007 PM 12217855 ER PT J AU Swendsen, JD Conway, KP Rounsaville, BJ Merikangas, KR AF Swendsen, JD Conway, KP Rounsaville, BJ Merikangas, KR TI Are personality traits familial risk factors for substance use disorders? Results of a controlled family study SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID TWINS REARED APART; ANXIETY DISORDERS; MMPI CHARACTERISTICS; ALCOHOLICS; ABUSE; COMORBIDITY; DEPENDENCE; COMMUNITY; TELEPHONE; HISTORY AB Objective: The well-documented association between maladaptive personality traits and substance use disorders has given rise to diverse explanatory models. In this investigation the authors examined one such explanation, that certain personality traits are familial risk factors for the development of substance abuse or dependence. Method: Data were collected from a controlled family study using direct diagnostic interviews. The Multidimensional Personality Questionnaire was used to assess the personality traits of 325 probands, 205 of whom had diagnoses of substance abuse or dependence, and 262 of their first-degree relatives. Results: Probands with substance use disorders scored higher on alienation and negative emotionality than did probands without substance use disorders, and they scored lower on control, harm avoidance, and constraint. Relatives with substance use disorders also differed from relatives without these conditions on several of these same dimensions. To examine whether such personality traits could be conceptualized as familial risk factors for substance use disorders, a second set of analyses were limited to relatives without substance use disorders themselves but varying in terms of family history for these conditions. These groups of relatives did not differ significantly from each other on any of the identified personality traits. Conclusions: These findings argue for caution in characterizing the personality correlates of substance use disorders as representing familial or heritable risk factors. C1 NIDA, Div Epidemiol Serv & Prevent Res, Bethesda, MD 20892 USA. Univ Bordeaux, Dept Psychol, Bordeaux, France. Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA. Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA. NIMH, Mood & Aniexty Disorder Program, Bethesda, MD 20892 USA. RP Conway, KP (reprint author), NIDA, Div Epidemiol Serv & Prevent Res, 6001 Execut Blvd, Bethesda, MD 20892 USA. OI Conway, Kevin/0000-0002-7638-339X FU NIAAA NIH HHS [AA 07080, AA 09978]; NIDA NIH HHS [DA 00293, DA 05348, DA 09055]; NIMH NIH HHS [MH 36197, MH 00499] NR 35 TC 33 Z9 34 U1 3 U2 5 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD OCT PY 2002 VL 159 IS 10 BP 1760 EP 1766 DI 10.1176/appi.ajp.159.10.1760 PG 7 WC Psychiatry SC Psychiatry GA 600GR UT WOS:000178382700022 PM 12359684 ER PT J AU Sternberg, EM AF Sternberg, EM TI Walter B. Cannon and " 'voodoo' death": A perspective from 60 years on SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Editorial Material C1 NIMH, NIH, Integrat Neural Immune Program, Bethesda, MD 20892 USA. NIMH, NIH, Sect Neuroendocrine Immunol & Behav, Bethesda, MD 20892 USA. RP Sternberg, EM (reprint author), NIMH, NIH, Integrat Neural Immune Program, Bldg 36,Rm 1A-23,36 Convent Dr,MSC 4020, Bethesda, MD 20892 USA. NR 9 TC 5 Z9 5 U1 0 U2 4 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 OCT PY 2002 VL 92 IS 10 BP 1564 EP 1566 DI 10.2105/AJPH.92.10.1564 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 599YU UT WOS:000178363500005 PM 12356591 ER PT J AU Fee, E Brown, TM Lazarus, J Theerman, P AF Fee, E Brown, TM Lazarus, J Theerman, P TI Exploring acupuncture: Ancient ideas, modern techniques SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article C1 NIH, Hist Med Div, Natl Lib Med, Bethesda, MD 20892 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. NR 6 TC 6 Z9 6 U1 0 U2 0 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 OCT PY 2002 VL 92 IS 10 BP 1592 EP 1592 DI 10.2105/AJPH.92.10.1592 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 599YU UT WOS:000178363500012 PM 12356598 ER PT J AU Brown, TM Fee, E AF Brown, TM Fee, E TI Walter Bradford Cannon - Pioneer physiologist of human emotions SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Biographical-Item C1 Univ Rochester, Dept Hist, Rochester, NY 14627 USA. Univ Rochester, Dept Community & Prevent Med, Rochester, NY 14627 USA. NIH, Hist Med Div, Natl Lib Med, Bethesda, MD 20892 USA. RP Brown, TM (reprint author), Univ Rochester, Dept Hist, 601 Elmwood Ave, Rochester, NY 14627 USA. NR 0 TC 8 Z9 8 U1 2 U2 7 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 OCT PY 2002 VL 92 IS 10 BP 1594 EP 1595 DI 10.2105/AJPH.92.10.1594 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 599YU UT WOS:000178363500014 ER PT J AU Yao, L Thomasson, D AF Yao, L Thomasson, D TI Magnetization transfer contrast in rapid three-dimensional MR imaging using segmented radiofrequency prepulses SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 NIH, Dept Radiol, Bethesda, MD 20892 USA. Siemens Corp, Iselin, NJ 08830 USA. RP Yao, L (reprint author), NIH, Dept Radiol, Bldg 10,Rm 1C-640,10 Ctr Dr,MSC 1182, Bethesda, MD 20892 USA. NR 7 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. PD OCT PY 2002 VL 179 IS 4 BP 863 EP 865 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 595JD UT WOS:000178104700008 PM 12239025 ER PT J AU Avila, NA Brantly, M Premkumar, A Huizing, M Dwyer, A Gahl, WA AF Avila, NA Brantly, M Premkumar, A Huizing, M Dwyer, A Gahl, WA TI Hermansky-Pudlak syndrome: Radiography and CT of the chest compared with pulmonary function tests and genetic studies SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Roentgen-Ray-Society CY MAY, 1999 CL NEW ORLEANS, LOUISIANA SP Amer Roentgen Ray Soc ID VESICLE FORMATION; GRANULOMATOUS COLITIS; LOCUS HETEROGENEITY; HPS GENE; MUTATIONS; FORM; FIBROSIS; MANIFESTATIONS; TRAFFICKING; DUPLICATION AB OBJECTIVE. The objective of our study was to describe the chest radiographic and high-resolution CT findings in patients with Hermansky-Pudlak syndrome and to correlate the radiologic findings with age, causative gene, and pulmonary function. SUBJECTS AND METHODS. Sixty-seven patients with Hermansky-Pudlak syndrome underwent high-resolution CT of the chest. A scoring system based on the extent of pulmonary involvement and specific high-resolution CT findings was used, and the findings were compared with patient age and the results of pulmonary function and genetic studies. Fifty-eight (87%) of the 67 patients also underwent chest radiography. These radiographs were compared with the high-resolution CT scans. RESULTS. High-resolution CT was more sensitive than chest radiography in evaluating the extent of pulmonary disease in patients with Hermansky-Pudlak syndrome. All patients with mild findings on high-resolution CT scans had normal findings on chest radiographs. Common chest radiographic findings included reticulonodular interstitial pattern, perihilar fibrosis, and pleural thickening. High-resolution CT showed septal thickening, ground-glass opacities, and peribronchovascular thickening. For patients with Hermansky-Pudlak syndrome who were 30 years old or younger, high-resolution CT findings were usually minimal. Among patients who were older than 30 years, the 34 patients with HPS1 mutations had a score of 1.38 +/- 0.18 (mean standard error of the mean) on high-resolution CT This score is significantly greater than the score for the 11 patients without HPS1 mutations (0.36 +/- 0.15) (p < 0.001). The score based on high-resolution CT findings inversely correlated with percentage of forced vital capacity and was useful in defining the progression of interstitial disease. CONCLUSION. High-resolution CT provides a good radiologic monitor of disease status and progression in patients with Hermansky-Pudlak syndrome and correlates well with patient age, extent of pulmonary dysfunction, and genetic findings. C1 NIH, Warren G Magnuson Clin Ctr, Dept Diagnost Radiol, Bethesda, MD 20892 USA. Univ Florida, Coll Med, J Hillis Miller Hlth Ctr, Div Pulm Crit Care Med, Gainesville, FL 32610 USA. NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. RP Avila, NA (reprint author), NIH, Warren G Magnuson Clin Ctr, Dept Diagnost Radiol, Bldg 10,Rm 1C-660,10 Ctr Dr,MSC 1182, Bethesda, MD 20892 USA. NR 28 TC 30 Z9 31 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 OCT PY 2002 VL 179 IS 4 AR UNSP 0361-803X/02/1794-887 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 595JD UT WOS:000178104700014 PM 12239031 ER PT J AU Patsalides, AD Wood, LV Atac, GK Sandifer, E Butman, JA Patronas, NJ AF Patsalides, AD Wood, LV Atac, GK Sandifer, E Butman, JA Patronas, NJ TI Cerebrovascular disease in HIV-infected pediatric patients: Neuroimaging findings SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; PROTEIN-S DEFICIENCY; CEREBRAL INFARCTION; VARICELLA-ZOSTER; CHILDHOOD AIDS; CHILDREN; ANEURYSMS; STROKE AB OBJECTIVE. The goal of our study was to report on the prevalence and the neuroradiologic manifestations of cerebrovascular complications in children infected with HIV. We also elucidate the types of vascular involvement, identify their anatomic distribution, and discuss possible causes. MATERIALS AND METHODS. We conducted a retrospective study of 567 patients (age range, 1 month-29 years; median age, 5.47 years) who acquired HIV as children. Of these, 426 patients (75%) were evaluated with neuroinraging studies. We reviewed these studies to identify the cerebrovascular abnormalities and classify them by type, anatomic location, and shape. RESULTS. Eleven children (2.6%) were found to have cerebrovascular lesions. Only one had focal neurologic symptoms at the time of diagnosis. Twenty-six aneurysms were found in seven patients, and 27 infarctions were found in eight patients. In four of the patients with infarctions, fusiform aneurysms of the cerebral arteries were also identified. Most patients had advanced HIV disease. Nine of the 11 patients were infected by a vertical transmission route or during blood transfusion early in the neonatal period. In this group of patients, the diagnosis of cerebrovascular disease was made earlier (mean age at diagnosis, 8.2 years) than in the two patients who were infected later in life (mean age at diagnosis, 14.9 years). CONCLUSION. HIV-infected children have an increased incidence of cerebrovascular disease that is associated with severe immune suppression and with vertically acquired HIV infection or exposure to the virus in the neonatal period. Despite extensive lesions, most children in our study were asymptomatic. Screening with MR imaging should be considered for high-risk children and is advisable when evidence of neurologic symptoms or neurocognitive dysfunction is noted. C1 Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, NIH, Bethesda, MD 20892 USA. NCI, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA. RP Patsalides, AD (reprint author), Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, NIH, 10 Ctr Dr,Bldg 10,Rm 1C-660, Bethesda, MD 20892 USA. RI Butman, John/A-2694-2008; OI Butman, John/0000-0002-1547-9195 NR 29 TC 53 Z9 55 U1 0 U2 2 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 OCT PY 2002 VL 179 IS 4 AR UNSP 0361-803X/02/1794-999 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 595JD UT WOS:000178104700032 PM 12239054 ER PT J AU McKenzie, FE Jeffery, GM Collins, WE AF McKenzie, FE Jeffery, GM Collins, WE TI Plasmodium malariae infection boosts Plasmodium falciparum gametocyte production SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID DYNAMICS; AREA; MOSQUITOS; HUMANS AB We analyzed records of malariotherapy patients sequentially or simultaneously inoculated with Plasmodium falciparum and Plasmodium malariae. Gametocyte production was enhanced in P. falciparum by prior or concurrent P. malariae infection but diminished or unaffected in P. malariae by P. falciparum. Conversely, asexual-form c production was diminished in P. malariae but unaffected in P. falciparum. C1 NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA. Ctr Dis Control & Prevent, Div Parasit Dis, Atlanta, GA 30341 USA. RP McKenzie, FE (reprint author), NIH, Fogarty Int Ctr, Bldg 16, Bethesda, MD 20892 USA. FU Intramural NIH HHS [Z99 TW999999] NR 29 TC 25 Z9 26 U1 0 U2 3 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 OCT PY 2002 VL 67 IS 4 BP 411 EP 414 PG 4 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 613EP UT WOS:000179119400016 PM 12452496 ER PT J AU Quezado, ZMN Veihmeyer, J Schwartz, L Nwokoro, NA Porter, PD AF Quezado, ZMN Veihmeyer, J Schwartz, L Nwokoro, NA Porter, PD TI Anesthesia and airway management of pediatric patients with Smith-Lemli-Opitz syndrome SO ANESTHESIOLOGY LA English DT Article ID DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; MALIGNANT HYPERTHERMIA; PHENOTYPE C1 NICHHD, Dept Anesthesia & Surg Sci, Warren G Magnuson Clin Ctr, NIH, Bethesda, MD 20892 USA. NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. George Washington Univ, Childrens Natl Med Ctr, Dept Anesthesia, Washington, DC USA. RP Quezado, ZMN (reprint author), NICHHD, Dept Anesthesia & Surg Sci, Warren G Magnuson Clin Ctr, NIH, Bldg 10,Room 2C624,10 Ctr Dr, Bethesda, MD 20892 USA. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 15 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 2002 VL 97 IS 4 BP 1015 EP 1019 DI 10.1097/00000542-200210000-00041 PG 5 WC Anesthesiology SC Anesthesiology GA 600UH UT WOS:000178409800040 PM 12357175 ER PT J AU Langholz, B Ebi, KL Thomas, DC Peters, JM London, SJ AF Langholz, B Ebi, KL Thomas, DC Peters, JM London, SJ TI Traffic density and the risk of childhood leukemia in a Los Angeles case-control study SO ANNALS OF EPIDEMIOLOGY LA English DT Article DE traffic density; case-control studies; childhood leukemia; electromagnetic fields; epidemiology ID RESIDENTIAL MAGNETIC-FIELDS; MOTOR-VEHICLE EXHAUST; WIRING CONFIGURATIONS; CANCER; EXPOSURE; CALIFORNIA; MODEL AB PURPOSE: To investigate the relationship between traffic density and the risk of childhood leukemia. METHODS: The study group consisted of 212 cases and 202 controls from the London et al. (1991) study of childhood leukemia conducted in the Los Angeles area during 1978 to 1984. Using GIS methods, traffic counts on all streets within 1500 feet of each subject's residence of longest duration were determined. From these counts, an integrated distance-weighted traffic density measure was calculated for each subject for use as the analytic variable. Additional information, including magnetic fields and wire-code, was obtained from the original case-control study. Association between traffic density and leukemia, and confounding and effect modification by other variables, were assessed using standard matched case-control analyses. RESULTS: Although the unadjusted traffic density-childhood leukemia rate ratios were slightly elevated, this weak association was explained by confounding by wire code. Wire code remained associated with leukemia after controlling for traffic density. There was little evidence of effect modification between traffic density and magnetic fields, wire code or other variables. CONCLUSIONS: There is no evidence of an association of traffic density with childhood leukemia in the Los Angeles case-control study. (C) 2002 Elsevier Science Inc. C1 Univ So Calif, Dept Prevent Med, Los Angeles, CA 90089 USA. Elect Power Res Inst, Palo Alto, CA USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Langholz, B (reprint author), Univ So Calif, Dept Prevent Med, 1540 Alcazar St,Chp 220, Los Angeles, CA 90089 USA. OI London, Stephanie/0000-0003-4911-5290 FU NIEHS NIH HHS [5P30ES07048-05] NR 21 TC 64 Z9 67 U1 0 U2 7 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 OCT PY 2002 VL 12 IS 7 BP 482 EP 487 AR PII S1047-2797(01)00317-9 DI 10.1016/S1047-2797(01)00317-9 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 594GN UT WOS:000178041400007 PM 12377426 ER PT J AU Paulson, HL Garbern, JY Hoban, TF Krajewski, KM Lewis, RA Fischbeck, KH Grossman, RI Lenkinski, R Kamholz, JA Shy, ME AF Paulson, HL Garbern, JY Hoban, TF Krajewski, KM Lewis, RA Fischbeck, KH Grossman, RI Lenkinski, R Kamholz, JA Shy, ME TI Transient central nervous system white matter abnormality in X-linked Charcot-Marie-Tooth disease SO ANNALS OF NEUROLOGY LA English DT Article ID MAGNETIZATION-TRANSFER; HIGH-ALTITUDE; CONNEXIN32; MUTATIONS; OLIGODENDROCYTES; BRAIN AB X-linked Charcot-Marie-Tooth disease (CMTX) is a hereditary demyelinating neuropathy caused by mutations in the connexin 32 (Cx32) gene. Cx32 is widely expressed in brain and peripheral nerve, yet clinical manifestations of CMTX mainly arise from peripheral neuropathy. We have evaluated two male patients with CMTX who on separate occasions developed transient ataxia, dysarthria, and weakness within 3 days of returning from ski trips at altitudes above 8,000 feet. Magnetic resonance imaging studies in both patients showed nonenhancing, confluent, and symmetrical white matter abnormalities that were more pronounced posteriorly and that resolved over several months. Magnetic transfer images in one patient demonstrated increased magnetization transfer ratios distinct from that seen in demyelination or edema. Both patients returned to their normal baseline within 2 to 3 weeks. These cases suggest that CMTX patients are at risk for developing an acute, transient, neurological syndrome when they travel to places at high altitudes and return to sea level. Cx32 mutations may cause central nervous system dysfunction by reducing the number of functioning gap junctions between oligodendrocytes and astrocytes, making both cells more susceptible to abnormalities of intercellular exchange of ions and small molecules in situations of metabolic stress. C1 Wayne State Univ, Sch Med, Dept Neurol, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA. Univ Iowa, Dept Neurol, Iowa City, IA 52242 USA. Univ Michigan, Dept Pediat & Neurol, Ann Arbor, MI 48109 USA. NINDS, Bethesda, MD 20892 USA. NYU, Sch Med, Dept Radiol, New York, NY USA. Harvard Univ, Beth Israel Deaconess Med Ctr, Boston, MA USA. RP Shy, ME (reprint author), Wayne State Univ, Sch Med, Dept Neurol, 421 E Canfield,Elliman Bldg,Room 3206, Detroit, MI 48201 USA. RI Lenkinski, Robert/F-9045-2014; OI Lenkinski, Robert/0000-0001-7371-5048 NR 26 TC 94 Z9 97 U1 3 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 2002 VL 52 IS 4 BP 429 EP 434 DI 10.1002/ana.10305 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 600GG UT WOS:000178381800007 PM 12325071 ER PT J AU Cutler, RG Pedersen, WA Camandola, S Rothstein, JD Mattson, MP AF Cutler, RG Pedersen, WA Camandola, S Rothstein, JD Mattson, MP TI Evidence that accumulation of ceramides and cholesterol esters mediates oxidative stress-induced death of motor neurons in amyotrophic lateral sclerosis SO ANNALS OF NEUROLOGY LA English DT Article ID SERINE PALMITOYLTRANSFERASE; ENDOTHELIAL-CELLS; MASS-SPECTROMETRY; INDUCED APOPTOSIS; IN-VITRO; SUPEROXIDE-DISMUTASE; VITAMIN-E; SPHINGOMYELINASE; MODEL; ATHEROSCLEROSIS AB Amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motor neurons in the spinal cord resulting in progressive paralysis and death. The pathogenic mechanism of ALS is unknown but may involve increased oxidative stress, overactivation of glutamate receptors, and apoptosis. We report abnormalities in sphingolipid and cholesterol metabolism in the spinal cords of ALS patients and in a transgenic mouse model (Cu/ZnSOD mutant mice), which manifest increased levels of sphingomyelin, ceramides, and cholesterol esters; in the Cu/ZnSOD mutant mice, these abnormalities precede the clinical phenotype. In ALS patients and Cu/Zn-SOD mutant mice, increased oxidative stress occurs in association with the lipid alterations, and exposure of cultured motor neurons to oxidative stress increases the accumulation of sphingomyelin, ceramides, and cholesterol esters. Pharmacological inhibition of sphingolipid synthesis prevents accumulation of ceramides, sphingomyelin, and cholesterol esters and protects motor neurons against death induced by oxidative and excitotoxic insults. These findings suggest a pivotal role for altered sphingolipid metabolism in the pathogenesis of ALS. C1 NIA, Gerontol Res Ctr, Neurosci Lab, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. RP Mattson, MP (reprint author), NIA, Gerontol Res Ctr, Neurosci Lab, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Mattson, Mark/F-6038-2012 NR 53 TC 112 Z9 115 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 2002 VL 52 IS 4 BP 448 EP 457 DI 10.1002/ana.10312 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 600GG UT WOS:000178381800010 PM 12325074 ER PT J AU Fogli, A Wong, KD Eymard-Pierre, E Wenger, J Bouffard, JP Goldin, E Black, DN Boespflug-Tanguy, O Schiffmann, R AF Fogli, A Wong, KD Eymard-Pierre, E Wenger, J Bouffard, JP Goldin, E Black, DN Boespflug-Tanguy, O Schiffmann, R TI Cree leukoencephalopathy and CACH/VWM disease are allelic at the EIF2B5 locus SO ANNALS OF NEUROLOGY LA English DT Article ID VANISHING WHITE-MATTER; NERVOUS-SYSTEM HYPOMYELINATION; CHILDHOOD ATAXIA; CHROMOSOME 3Q27; DIFFUSE; PHENOTYPE AB Cree leukoencephalopathy is a rapidly fatal infantile autosomal recessive leukodystrophy of unknown cause observed in the native North American Cree and Chippewayan indigenous population. We found in the brain of affected individuals the typical foamy cells with the oligodendroglial phenotype described in central hypomyelination syndrome/vanishing white matter, a syndrome related to mutations in the genes encoding the five subunits of the eucaryotic translation initiation factor eIF2B. In three patients of two Cree families, we found a homozygous missense mutation resulting in a histidine substitution at arginine 195 of epsilon-eIF2B. C1 Fac Pharm Clermont Ferrand, INSERM UMR 384, F-63001 Clermont Ferrand, France. Armed Forces Inst Pathol, Dept Neuropathol, Washington, DC 20306 USA. NIH, Dev & Metab Neurol Branch, Bethesda, MD 20892 USA. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. RP Fogli, A (reprint author), Fac Pharm Clermont Ferrand, INSERM UMR 384, 28 Pl Henri Dunant,BP 38, F-63001 Clermont Ferrand, France. FU PHS HHS [97-N-0170] NR 16 TC 74 Z9 75 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 2002 VL 52 IS 4 BP 506 EP 510 DI 10.1002/ana.10339 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 600GG UT WOS:000178381800018 PM 12325082 ER PT J AU Jin, SJ Moon, SK Gu, XX Ueyama, S Rhim, JS Lim, DJ AF Jin, SJ Moon, SK Gu, XX Ueyama, S Rhim, JS Lim, DJ TI Immortalization of rat eustachian tube epithelial cells by adenovirus 12-simian virus 40 hybrid virus SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE adenovirus 12-simian virus 40 hybrid virus; cell line; eustachian tube epithelial cell; immortalization; primary culture ID MIDDLE-EAR EPITHELIUM; SURFACTANT PROTEIN-A; MONOCLONAL-ANTIBODIES; CULTURE; TRANSFORMATION; EXPRESSION; AD12-SV40; TRANSPORT; LINE AB The eustachian tube epithelial cells play an important role in the initial pathogenesis of otitis media. In order to study the role of the eustachian tube epithelial cells in the pathogenesis of otitis media, we have established a rat eustachian tube epithelial cell line. The cell line was derived by infecting primary cultures of eustachian tube epithelial cells with the adenovirus 12-simian virus 40 (Ad12-SV40) hybrid virus. The immortalized cells have retained the morphological characteristics of the parental cells and show positive staining with anti-cytokeratin antibodies (a marker for epithelial cells), but not with anti-vimentin antibodies (a fibroblast marker). The cells have been in continuous culture for more than 10 months and have undergone 38 passages. Western blotting and cell staining have confirmed the expression of the SV40 T antigen and p53. Chromosomal analysis indicates that the cell line is aneuploid and derived from male rat epithelial cells. Together, our results suggest that the cell line originated from eustachian tube epithelial cells from a male rat and was successfully immortalized by the Ad12-SV40 virus. C1 Natl Inst Deafness & Other Commun Disorders, Immunol Lab, Bethesda, MD USA. Uniformed Serv Univ Hlth Sci, Ctr Prostate Dis Res, Rockville, MD USA. RP Lim, DJ (reprint author), House Ear Res Inst, Gonda Dept Cell & Mol Biol, 2100 W 3rd St, Los Angeles, CA 90057 USA. NR 28 TC 3 Z9 3 U1 0 U2 2 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 OCT PY 2002 VL 111 IS 10 BP 919 EP 925 PG 7 WC Otorhinolaryngology SC Otorhinolaryngology GA 604GR UT WOS:000178609200011 PM 12389862 ER PT J AU Lans, TE ten Hagen, TLM van Horssen, R Wu, PC van Tiel, ST Libutti, SK Alexander, HR Eggermont, AMM AF Lans, TE ten Hagen, TLM van Horssen, R Wu, PC van Tiel, ST Libutti, SK Alexander, HR Eggermont, AMM TI Improved antitumor response to isolated limb perfusion with tumor necrosis factor after upregulation of endothelial monocyte-activating polypeptide II in soft tissue sarcoma SO ANNALS OF SURGICAL ONCOLOGY LA English DT Article DE limb perfusion; EMAP-II; sarcoma; TNF ID INTERFERON-GAMMA; FACTOR-ALPHA; TNF-ALPHA; GENE-TRANSFER; IN-VIVO; MELPHALAN; MULTICENTER; MODEL; RATS; MELANOMA AB Background: Experiments with tumor necrosis factor alpha (TNF) in rodents have shown that a high dose can lead to hemorrhagic necrosis in tumors. Endothelial monocyte-activating polypeptide Il (EMAP-II) is a novel tumor-derived cytokine, and its expression increases the TNF-1 receptor on tumor endothelium, enhances the induction of tissue factor on tumor endothelial cells, and has an antiangiogenic effect. It has recently been shown that in vivo sensitivity of tumor vasculature to TNF is determined by tumor production of EMAP-II. Methods: We measured the level of EMAP-II in a TNF-resistant soft tissue sarcoma. We subsequently stabile-transfected this cell line with a retroviral construct containing the EMAP gene. In an extremity perfusion model in tumor-bearing rats, we measured response rates to TNF therapy. Results: Functional EMAP-II production was increased after this transfection. Immunostaining of paraffin-embedded tumor tissue sections in rats showed an overexpression of human EMAP-II. Results of the TNF perfusions in rats suggest that this tumor is more sensitive to TNF therapy. Conclusions: EMAP-II is produced in various levels. One can increase the sensitivity of tumor for TNF therapy in vivo by upregulating the EMAP-II production. This result leaves an opportunity for enhanced TNF response of tumors in future settings. C1 Univ Rotterdam Hosp, Dr Daniel Den Hoed Canc Ctr, Dept Surg Oncol, Rotterdam, Netherlands. NCI, Ctr Canc Res, Surg Branch, Bethesda, MD 20892 USA. RP Lans, TE (reprint author), Erasmus Univ, Lab Expt Surg Oncol, Room Ee 110A,POB 1738, NL-3000 DR Rotterdam, Netherlands. NR 18 TC 17 Z9 19 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1068-9265 J9 ANN SURG ONCOL JI Ann. Surg. Oncol. PD OCT PY 2002 VL 9 IS 8 BP 812 EP 819 DI 10.1245/ASO.2001.09.019 PG 8 WC Oncology; Surgery SC Oncology; Surgery GA 601NJ UT WOS:000178452400017 PM 12374666 ER PT J AU Pluymers, W Pais, G Van Maele, B Pannecouque, C Fikkert, V Burke, TR De Clercq, E Witvrouw, M Neamati, N Debyser, Z AF Pluymers, W Pais, G Van Maele, B Pannecouque, C Fikkert, V Burke, TR De Clercq, E Witvrouw, M Neamati, N Debyser, Z TI Inhibition of human immunodeficiency virus type 1 integration by diketo derivatives SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID HIV-1 INTEGRASE; STRAND TRANSFER; PRIMARY TARGET; IN-VITRO; DNA; PROTEIN; CELLS; REPLICATION; GLYCOPROTEIN; GP120 AB A series of diketo derivatives was found to inhibit human immunodeficiency virus type 1 (HIV-1) integrase activity. Only L-708,906 inhibited the replication of HIV-1(III(B)) (50% effective concentration, 12 muM), HIV-1 clinical strains, HIV-1 strains resistant to reverse transcriptase or fusion inhibitors, HIV-2 (ROD strain) and simian immunodeficiency virus (MAC(251)). The combinations of L-708,906 with zidovudine, nevirapine, or nelfinavir proved to be subsynergistic. In cell culture, addition of L-708,906 could be postponed for 7 It after infection, a moment coinciding with HIV integration. Inhibition of integration in cell culture was confirmed by quantitative Alu-PCR. C1 Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium. NCI, Med Chem Lab, Canc Res Ctr, Frederick, MD 21702 USA. Univ So Calif, Sch Pharm, Los Angeles, CA 90089 USA. RP Debyser, Z (reprint author), Katholieke Univ Leuven, Rega Inst Med Res, Minderbroedersstr 10, B-3000 Louvain, Belgium. EM zeger.debyser@uz.kuleuven.ac.be RI Burke, Terrence/N-2601-2014 NR 26 TC 38 Z9 42 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD OCT PY 2002 VL 46 IS 10 BP 3292 EP 3297 DI 10.1128/AAC.46.10.3292-3297.2002 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA 596EG UT WOS:000178150700033 PM 12234864 ER PT J AU Bautista, AP AF Bautista, AP TI Acute ethanol binge followed by withdrawal regulates production of reactive oxygen species and cytokine-induced neutrophil chemoattractant and liver injury during reperfusion after hepatic ischemia SO ANTIOXIDANTS & REDOX SIGNALING LA English DT Article ID NF-KAPPA-B; MACROPHAGE INFLAMMATORY PROTEIN-2; CHRONIC ALCOHOL-INTOXICATION; TUMOR-NECROSIS-FACTOR; KUPFFER CELLS; RAT; ACTIVATION; ENDOTOXIN; INTERLEUKIN-8; HEPATOCYTES AB This work tests the hypothesis that withdrawal from an acute ethanol binge regulates the production of reactive oxygen species (ROS) and chemokines by Kupffer cells, and as a result compromises or protects the liver from injury. Male Sprague-Dawley rats received an intravenous ethanol bolus (1.75 g/kg), followed by an intravenous infusion of 200-300 mg/kg/h for 12 h. At 12 h, ethanol infusion was stopped and replaced by saline. At 18 h, rats were subjected to 45 min of partial hepatic ischemia, followed by 0-24 h of reperfusion (L/R). At specific time points, Kupffer cells were isolated for superoxide anion assay and CINC (cytokine-induced neutrophil chemoattractant) and MIP-2 (macrophage inflammatory protein-2) production in vitro. Alanine transferase (ALT) activity, endotoxin, CINC, and MIP-2 were measured in serum samples taken at appropriate intervals. Results show that at 3 h post reperfusion, serum ALT was significantly elevated in the ethanol-reated group + I/R, compared with the saline + I/R group. ROS production by Kupffer cells at this time was also significantly increased compared with the saline + I/R group. However, ethanol withdrawal + I/R did not significantly alter CINC and MIP-2 production at 3 h of reperfusion. After 24 h, serum ALT was lower in the ethanol + I/R group than in the saline + I/R group. Superoxide anion and MIP-2 releases by Kupffer cells were not statistically significantly different between these two groups at this time. CINC production by Kupffer cells from the ethanol-treated + I/R group was significantly lower than in the saline + I/R group. Concomitantly, CINC and nuclear factor-kappaB (NF-kappaB) mRNAs and NF-kappaB translocation and binding in Kupffer cells in this treatment group were down-regulated. Moreover, the number of polymorphonuclear neutrophils (PMNs) sequestered in the liver was significantly lower in the ethanol + I/R group than in the saline-treated group. ROS and chemokine productions in sham animals with or without ethanol were lower than in the I/R group. These data suggest that acute ethanol binge followed by withdrawal may compromise the liver to injury during the early phase, whereas in the later phase it may be protective. Furthermore, these results support the notion that Kupffer cells are involved in hepatic injury in the early phase, whereas PMNs participate more actively during the later phase of reperfusion. C1 Louisiana State Univ, Hlth Sci Ctr, Dept Physiol, New Orleans, LA USA. Louisiana State Univ, Hlth Sci Ctr, NIAAA, Sponsored Alcohol Res Ctr, New Orleans, LA USA. RP NIH, Ctr Sci Review, 6701 Rockledge Dr, Bethesda, MD 20892 USA. EM abauti123@cs.com FU NIAAA NIH HHS [R01 AA08846-08]; PHS HHS [P50 09803] NR 37 TC 12 Z9 12 U1 0 U2 1 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1523-0864 EI 1557-7716 J9 ANTIOXID REDOX SIGN JI Antioxid. Redox Signal. PD OCT PY 2002 VL 4 IS 5 BP 721 EP 731 DI 10.1089/152308602760598864 PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 607NP UT WOS:000178797900004 PM 12470499 ER PT J AU Kimball, AB Kawamura, T Tejura, K Hancox, AR Vogel, JC Steinberg, SM Turner, ML Blauvelt, A AF Kimball, AB Kawamura, T Tejura, K Hancox, AR Vogel, JC Steinberg, SM Turner, ML Blauvelt, A TI Clinical and immunologic assessment of patients with psoriasis in a randomized, double-blind, placebo-controlled trial using recombinant human interleukin 10 SO ARCHIVES OF DERMATOLOGY LA English DT Article ID T-CELLS; RHEUMATOID-ARTHRITIS; CYTOKINE PRODUCTION; LESION-FREE; IL-10; SKIN; KERATINOCYTE; DISEASE; LYMPHOCYTE; EXPRESSION AB Background: In several open-label studies, recombinant human interleukin 10 (rhIL-10), a type 2 anti-inflammatory cytokine, has been reported to improve psoriasis, a disease characterized by type 1 cytokine inflammation. Objective: To evaluate the safety, efficacy, and immunologic parameters in individuals with psoriasis treated with rhIL-10. Design and Intervention: Patients received rhIL-10 (20 mug/kg) or placebo subcutaneously 3 times weekly for 12 weeks in a randomized, double-blind manner. Setting and Patients: National Institutes of Health Clinical Center in Bethesda. Twenty-eight patients with moderate-to-severe psoriasis as defined by a Psoriasis Area Severity Index (PASI) score of 10 or higher. Main outcome Measure: The primary clinical end point was the mean percentage change in the PASI score comparing baseline and week 12 scores. Intracellular cytokine production by peripheral blood mononuclear cells (PBMCs) was measured by flow cytometry. Results: There was no significant difference in the mean percentage change in the PASI score from baseline to week 12 between the rhIL-10-treated group and control patients (17% vs 13% improvement, respectively; P=.69), although a modest trend toward improvement in patients receiving rhIL-10 was documented at both the 6- and 8-week points. Interestingly, proinflammatory and type I cytokine production by PBMCs progressively declined in the rhIL-10-treated patients during the entire 12-week study period. Conclusions: Treatment with rhIL-10 resulted in only temporary clinical improvement in psoriasis, despite sustained systemic decreases in proinflammatory and type I cytokine production. These data suggest that immunotherapy that decreases the ratio of systemic type 1 and type 2 cytokine production does not necessarily lead to improvement of type 1 cytokine-mediated disease. C1 NCI, Dermatol Branch, Bethesda, MD 20892 USA. NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA. RP Blauvelt, A (reprint author), NCI, Dermatol Branch, Bldg 10,Room 12N238,10 Ctr Dr MSC 1908, Bethesda, MD 20892 USA. NR 24 TC 38 Z9 45 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD OCT PY 2002 VL 138 IS 10 BP 1341 EP 1346 DI 10.1001/archderm.138.10.1341 PG 6 WC Dermatology SC Dermatology GA 603EN UT WOS:000178546000009 PM 12374540 ER PT J AU Kang, DW Chu, K Ko, SB Kwon, SJ Yoon, BW Roh, JK AF Kang, DW Chu, K Ko, SB Kwon, SJ Yoon, BW Roh, JK TI Lesion patterns and mechanism of ischemia in internal carotid artery disease - A diffusion-weighted imaging study SO ARCHIVES OF NEUROLOGY LA English DT Article ID MAJOR CEREBRAL-ARTERIES; VASCULAR TERRITORIES; STROKE PATTERNS; INFARCTION; OCCLUSION; BRAIN; VARIABILITY; PATHOGENESIS; STENOSIS AB Context: Although embolism and low-flow phenomenon are the 2 main mechanisms of stroke in internal carotid artery (ICA) occlusive disease, the mechanism of border-zone infarction remains controversial. Diffusion-weighted imaging (DWI) can more easily detect small or multiple ischemic lesions than conventional imaging. Objectives: To investigate the ischemic lesion patterns on DWI and to discuss the mechanisms of stroke in ICA disease. Design: Case series. Setting: A tertiary referral center. Patients: We enrolled 35 consecutive patients who had an acute ischemic stroke and (greater than or equal to70%) stenosis or an occlusion of the extracranial ICA confirmed by cerebral angiography and an acute relevant stroke lesion on DWI within 1 week of onset, but without cardiac sources of embolism and tandem intracranial arterial disease. Main Outcome Measures: The lesion pattern on DWI was categorized as territorial or border zone. Multiple ischemic lesions were defined as noncontiguous lesions on DWI in more than 1 vascular territory. Results: There were 3 distinctive stroke lesion patterns. (1) A territorial lesion without a border-zone lesion was found in 21 patients: superficial and superficial territorial in 9, superficial and deep territorial in 7, and single in 5. (2) A border-zone lesion with or without a territorial lesion was found in 10 patients: border zone and territorial in 9 and border zone alone in 1. (3) Bilateral hemispheric lesions were found in 4 patients. Multiple ischemic lesions were found in 29 (82.9%) of the 35 patients. No patient had episodes of hemodynamic compromise. Conclusions: An acute ischemic lesion in ICA occlusive disease is mainly multiple. Border-zone infarction was mostly associated with territorial infarction. These results support the fact that embolism is the predominant stroke mechanism in ICA occlusive disease. C1 Seoul Univ, Dept Neurol, Med Res Ctr, Seoul Natl Univ Hosp,Neurosci Res Inst, Seoul 110744, South Korea. Seoul Univ, Clin Res Inst, Med Res Ctr, Seoul Natl Univ Hosp,Neurosci Res Inst, Seoul 110744, South Korea. Natl Inst Neurol Disorders & Stroke, Sect Stroke Diagnost & Therapeut, Bethesda, MD USA. RP Roh, JK (reprint author), Seoul Univ, Dept Neurol, Med Res Ctr, Seoul Natl Univ Hosp,Neurosci Res Inst, 28 Yongon Dong, Seoul 110744, South Korea. RI Roh, Jae Kyu/J-5459-2012; Yoon, Byung Woo/J-5557-2012 NR 38 TC 48 Z9 57 U1 0 U2 2 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 OCT PY 2002 VL 59 IS 10 BP 1577 EP 1582 DI 10.1001/archneur.59.10.1577 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 603LC UT WOS:000178560100008 PM 12374495 ER PT J AU Elghetany, MT Alter, BP AF Elghetany, MT Alter, BP TI p53 protein overexpression in Shwachman-Diamond syndrome - Reply SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Letter ID ANEMIA C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Elghetany, MT (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NR 4 TC 0 Z9 0 U1 0 U2 1 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD OCT PY 2002 VL 126 IS 10 BP 1158 EP 1158 PG 1 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA 603HN UT WOS:000178553400005 ER PT J AU Glied, S Pine, DS AF Glied, S Pine, DS TI Consequences and correlates of adolescent depression SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID STRESSFUL LIFE EVENTS; DSM-III DISORDERS; PSYCHIATRIC-DISORDERS; MAJOR DEPRESSION; CHILDREN; CHILDHOOD; HEALTH; GIRLS; SYMPTOMS; PSYCHOPATHOLOGY AB Objective: To examine the correlates and consequences of high levels of depressive symptoms among adolescents. Design: Secondary analysis of the 1997 Commonwealth Fund Survey of the Health of Adolescent Girls, a survey of a nationally representative sample of 4648 adolescent boys and girls between the ages of 10 and 18 years, inclusive, conducted in school settings. The self-administered questionnaire contains a screening instrument for depression based on the Children's Depression Inventory. Outcome: Days of school missed, performance at grade level, alcohol use, drug use, smoking, and bingeing. Results: After controlling for sociodemographics, life events, sexual abuse, physical abuse, and exposure to violence, relative to other children, children and adolescents with high degrees of depressive symptoms missed about I day more of school in the month preceding the survey (P < .05) and had higher odds of smoking (odds ratio, 1.84; P < .001), bingeing (odds ratio, 2.02; P < .001), and suicidal ideation (odds ratio, 16.59; P < .001). Conclusion: High levels of depressive symptoms are correlated with serious and significant consequences, even after controlling for life circumstances. C1 Columbia Univ, Mailman Sch Publ Hlth, Dept Hlth Policy & Management, New York, NY USA. NIMH, Sect Dev & Affect Neurosci, Mood & Anxiety Disorders Program, Intramural Res Program, Bethesda, MD 20892 USA. RP Glied, S (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Hlth Policy & Management, New York, NY USA. NR 41 TC 69 Z9 79 U1 4 U2 11 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 OCT PY 2002 VL 156 IS 10 BP 1009 EP 1014 PG 6 WC Pediatrics SC Pediatrics GA 602EY UT WOS:000178493900011 PM 12361447 ER PT J AU North, KE MacCluer, JW Devereux, RB Howard, BV Welty, TK Best, LG Lee, ET Fabsitz, RR Roman, MJ AF North, KE MacCluer, JW Devereux, RB Howard, BV Welty, TK Best, LG Lee, ET Fabsitz, RR Roman, MJ TI Heritability of carotid artery structure and function - The Strong Heart Family Study SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE carotid artery structure and function; heritability; American Indians; Strong Heart Family Study ID PRESSURE WAVE-FORM; TRAIT LINKAGE ANALYSIS; WALL THICKNESS; RISK-FACTORS; MYOCARDIAL-INFARCTION; CARDIOVASCULAR RISK; DIABETES-MELLITUS; AMERICAN-INDIANS; AORTIC PRESSURE; DISEASE AB Objective-Alterations in carotid artery structure and function may represent phenotypic measures of vascular disease that contain information beyond that which can be inferred from conventional cardiovascular disease risk assessment. However, apart from their associations with cardiovascular disease risk factors and outcome, the genetic basis of variations in carotid artery structure and function is largely unknown. The purpose of this study was to examine the genetic and environmental contributions to carotid artery structure and function in 3 large groups of American Indians. Methods and Results-Approximately 950 men and women, aged greater than or equal to 18 years, in 32 extended families were examined between 1997 and 1999. By use of a variance component approach and the program Sequential Oligogenic Linkage Analysis Routines, heritabilities for carotid artery structure and function phenotypes were estimated. After accounting for the effects of covariates (sex, age, diabetes, impaired glucose tolerance, smoking, cholesterol, body surface area, and hypertension), we detected significant heritabilities (given as h(2) values) for common carotid artery diastolic diameter (h(2) <0.44), intimal-medial wall thickness (h(2) <0.21), vascular mass (h(2) <0.27), arterial stiffness (h(2) <0.23), and the augmentation index (h(2) < 0.18). Conclusions-These results suggest that the additive effects of genes explain a moderate proportion of the variability of carotid artery structure and function. C1 Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA. SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA. Cornell Univ, Div Cardiol, Weill Med Coll, New York, NY 10021 USA. MedStar Res Inst, Washington, DC USA. Aberdeen Area Tribal Chairmens Hlth Board, Rapid City, SD USA. Missouri Breaks Ind Res Inc, Timber Lake, SD USA. Univ Oklahoma, Ctr Hlth Sci, Ctr Amer Indian Hlth Res, Sch Publ Hlth, Oklahoma City, OK USA. NHLBI, Epidemiol & Biometry Program, Bethesda, MD 20892 USA. RP Roman, MJ (reprint author), Cornell Univ, Div Cardiol, Weill Med Coll, 525 E 68th St, New York, NY 10021 USA. FU NHLBI NIH HHS [U01 HL-41652, U01 HL-41642, U01 HL-41654, U01 HL-65520, U01 HL-65521]; NIMH NIH HHS [U01 MH-59590] NR 41 TC 79 Z9 78 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD OCT PY 2002 VL 22 IS 10 BP 1698 EP 1703 DI 10.1161/01.ATV.0000032656.91352.5E PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 605PR UT WOS:000178686700032 PM 12377752 ER PT J AU Lipsky, PE Felson, DT Maini, RN AF Lipsky, PE Felson, DT Maini, RN TI Blocking tumor necrosis factor inhibits radiographic damage even in patients who show minimal or no clinical improvement: comment on the concise communication by Boers SO ARTHRITIS AND RHEUMATISM LA English DT Letter ID RHEUMATOID-ARTHRITIS; DISEASE-ACTIVITY; CRITERIA C1 NIAMSD, NIH, Bethesda, MD 20892 USA. Boston Univ, Sch Med, Boston, MA 02118 USA. Univ London Imperial Coll Sci Technol & Med, Kennedy Inst, Div Rheumatol, London, England. RP Lipsky, PE (reprint author), NIAMSD, NIH, Bethesda, MD 20892 USA. OI Felson, David/0000-0002-2668-2447 NR 6 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD OCT PY 2002 VL 46 IS 10 BP 2817 EP 2818 DI 10.1002/art.10446 PG 2 WC Rheumatology SC Rheumatology GA 604QX UT WOS:000178633500037 PM 12384946 ER PT J AU Lipsky, PE Maini, RN AF Lipsky, PE Maini, RN TI Blocking tumor necrosis factor inhibits radiographic damage even in patients who show minimal or no clinical improvement: comment on the concise communication by Boers - Comment SO ARTHRITIS AND RHEUMATISM LA English DT Letter C1 NIAMSD, NIH, Bethesda, MD 20892 USA. Univ London Imperial Coll Sci Technol & Med, Kennedy Inst, Div Rheumatol, London, England. RP Lipsky, PE (reprint author), NIAMSD, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD OCT PY 2002 VL 46 IS 10 BP 2820 EP 2821 DI 10.1002/art.10689 PG 2 WC Rheumatology SC Rheumatology GA 604QX UT WOS:000178633500039 ER PT J AU Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS AF Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS TI Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). I. Antigenicity and immunogenicity SO AVIAN PATHOLOGY LA English DT Article ID VP2 HYPERVARIABLE REGION; AMINO-ACID CHANGES; SEGMENT-A; SEQUENCE-ANALYSIS; VIRULENT-STRAINS; VARIABLE REGION; CHICKEN EMBRYOS; SERIAL PASSAGE; LYMPHOCYTES-B; GENE AB In vitro and in ovo virus neutralization assays were conducted to assess the role of different host systems in infectious bursal disease virus (IBDV) antigenic and immunogenic variation. Four different strains, two variant (1084 E and GLS) and two standard (Edgar and STC), were propagated separately in the bursa of Fabricius and embryos, and were compared with cell culture-adapted preparations of the homologous strains. Chicken polyclonal antisera were prepared against each IBDV and neutralizing antibody titres were determined. Normalized IBDV antibody concentrations were used in neutralization assays against homologous and heterologous IBDVs in 10-day-old specific pathogen free embryos. Both antigenic and immunogenic changes occurred in IBDVs evaluated, as evidenced by differences in the ability of normalized antibody to neutralize IBDV propagated in different host systems. Antibody induced by bursal-derived IBDV neutralized all isolates equally well, whereas antibody induced by cell culture-derived virus neutralized bursal-derived IBDV much less effectively. C1 Univ Delaware, Dept Anim & Food Sci, Allen Biotechnol Lab, Newark, DE 19717 USA. RP Rodriguez-Chavez, IR (reprint author), NCI, NIH, Ctr Canc Res, HIV & AIDS Malignancy Branch, 9000 Rockville Pike,Bldg 10,Room 10S255, Bethesda, MD 20892 USA. NR 70 TC 8 Z9 8 U1 0 U2 1 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0307-9457 J9 AVIAN PATHOL JI Avian Pathol. PD OCT PY 2002 VL 31 IS 5 BP 463 EP 471 DI 10.1080/0307945021000005833 PG 9 WC Veterinary Sciences SC Veterinary Sciences GA 599VW UT WOS:000178356700007 PM 12427340 ER PT J AU Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS AF Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS TI Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). II. Antigenicity at the epitope level SO AVIAN PATHOLOGY LA English DT Article ID DOUBLE-STRANDED-RNA; AMINO-ACID CHANGES; GENOME SEGMENT-A; MONOCLONAL-ANTIBODIES; SEQUENCE-ANALYSIS; VARIANT STRAINS; MOLECULAR CHARACTERIZATION; NEUTRALIZING ANTIBODIES; HYPERVARIABLE REGION; VP2 GENE AB Antigenic variation of infectious bursal disease virus (IBDV) due to propagation in different host systems (bursa of Fabricius, embryos, or cell cultures) was determined by enzyme-linked immunosorbent assay (indirect and antigen capture) and western blot analysis. To conduct this study, we used 27 non-neutralizing anti-VP2 monoclonal antibodies, a reference panel of nine neutralizing monoclonal antibodies, and 13 neutralizing anti-IBDV chicken polyclonal antibodies. Changes occurred in neutralizing, cross-reactive, conformation-dependent epitopes on the VP2 protein of IBDV. Interestingly, non-neutralizing, cross-reactive, conformation-dependent and confirmation-independent epitopes also changed on VP2. These epitope changes were directly associated with the method used to propagate IBDV. These results demonstrate that different host systems may play an important role in the antigenicity of IBDV. C1 Univ Delaware, Dept Anim & Food Sci, Allen Biotechnol Lab, Newark, DE 19717 USA. RP Rodriguez-Chavez, IR (reprint author), NCI, NIH, Ctr Canc Res, HIV & AIDS Malignancy Branch, 9000 Rockville Pike,Bldg 10,Room 10S255, Bethesda, MD 20892 USA. NR 71 TC 4 Z9 4 U1 2 U2 2 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0307-9457 J9 AVIAN PATHOL JI Avian Pathol. PD OCT PY 2002 VL 31 IS 5 BP 473 EP 483 DI 10.1080/0307945021000005842 PG 11 WC Veterinary Sciences SC Veterinary Sciences GA 599VW UT WOS:000178356700008 PM 12427341 ER PT J AU Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS Pope, CR AF Rodriguez-Chavez, IR Rosenberger, JK Cloud, SS Pope, CR TI Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). III. Pathogenicity SO AVIAN PATHOLOGY LA English DT Article ID NEWCASTLE-DISEASE; SEROTYPE-I; CHICKENS; STRAINS; VP2; VIRULENT; REPLICATION; ATTENUATION; PHENOTYPE; VACCINES AB Differences in the relative pathogenicity of variant (1084 E and GLS) and standard (Edgar and STC) infectious bursal disease virus (IBDV) strains were observed after propagation in the bursa of Fabricius, embryos, or cell cultures. Bursa-derived IBDV induced the most severe lesions in the bursa of Fabricius when compared with strains propagated in embryos or cell cultures. Embryo-derived IBDV induced moderate gross bursal lesions, whereas cell culture-derived IBDV did not damage the bursa grossly. A high frequency of virus re-isolations was obtained from bursal, spleen, and thymic samples collected from birds inoculated with bursa-derived or embryo-derived IBDV. Virus reisolation occurred much less frequently from birds inoculated with cell culture-adapted IBDV. Serological evaluations demonstrated that bursa-derived IBDV strains induced a higher neutralizing antibody response than did embryo-derived or cell culture-derived strains. These results document that the relative pathogenicity and immunogenicity of IBDV is reduced following propagation in embryos or cell cultures. C1 Univ Delaware, Dept Anim & Food Sci, Allen Biotechnol Lab, Newark, DE 19717 USA. RP Rodriguez-Chavez, IR (reprint author), NCI, NIH, Ctr Canc Res, HIV & AIDS Malignancy Branch, 9000 Rockville Pike,Bldg 10,Room 10S255, Bethesda, MD 20892 USA. NR 52 TC 7 Z9 8 U1 0 U2 0 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0307-9457 J9 AVIAN PATHOL JI Avian Pathol. PD OCT PY 2002 VL 31 IS 5 BP 485 EP 492 DI 10.1080/0307945021000005851 PG 8 WC Veterinary Sciences SC Veterinary Sciences GA 599VW UT WOS:000178356700009 PM 12427342 ER PT J AU Moffat, SD Resnick, SM AF Moffat, SD Resnick, SM TI Effects of age on virtual environment place navigation and allocentric cognitive mapping SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID MORRIS WATER MAZE; SPATIAL MEMORY; TOPOGRAPHICAL DISORIENTATION; ALZHEIMERS-DISEASE; OLD RATS; TASK; PERFORMANCE; HIPPOCAMPUS; DEFICITS; CELLS AB This study assessed age differences in navigational behavior in a virtual Morris water maze (vMWM) and examined the ability of older adults to develop cognitive maps after vMWM experience. Compared with younger participants, older volunteers traversed a longer linear distance to locate the hidden platform. On the probe trial, younger volunteers spent a greater proportion of their total distance traveled in proximity to the platform and had more platform intersections. Analysis of map reproductions demonstrated that older participants used proximal objects to locate the goal but did not use room-geometry cues to aid navigation. These findings demonstrate age-related deficits on a laboratory measure of place learning and suggest that deficiencies in allocentric mapping may contribute to these deficits. C1 NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Moffat, SD (reprint author), Wayne State Univ, Inst Gerontol, 87 E Ferry St, Detroit, MI 48202 USA. NR 45 TC 122 Z9 125 U1 3 U2 17 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD OCT PY 2002 VL 116 IS 5 BP 851 EP 859 DI 10.1037//0735-7044.116.5.851 PG 9 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 598DM UT WOS:000178260100010 PM 12369805 ER PT J AU Schuler, B Kremer, W Kalbitzer, HR Jaenicke, R AF Schuler, B Kremer, W Kalbitzer, HR Jaenicke, R TI Role of entropy in protein thermostability: Folding kinetics of a hyperthermophilic cold shock protein at high temperatures using F-19 NMR SO BIOCHEMISTRY LA English DT Article ID BACTERIUM THERMOTOGA-MARITIMA; N-TERMINAL DOMAIN; ESCHERICHIA-COLI; STABILITY; DENATURANT; DYNAMICS; STATES; ACID; L9 AB We used F-19 NMR to extend the temperature range accessible to detailed kinetic and equilibrium studies of a hyperthermophilic protein. Employing an optimized incorporation strategy, the small cold shock protein from the bacterium Thermotoga maritima (TmCsp) was labeled with 5-fluorotryptophan. Although chaotropically induced unfolding transitions revealed a significant decrease in the stabilization free energy upon fluorine labeling, the protein's kinetic folding mechanism is conserved. Temperature- and guanidinium chloride-dependent equilibrium unfolding transitions monitored by F-19 NMR agree well with the results from optical spectroscopy, and provide a stringent test of the two-state folding character of TmCsp. Folding and unfolding rate constants at high temperatures were determined from the F-19 NMR spectra close to the midpoint of thermal unfolding by global line shape analysis. In combination with results from stopped-flow experiments at lower temperatures, they show that the folding rate constant of TmCsp and its temperature dependence closely resemble those of its mesophilic homologue from Bacillus subtilis, BsCspB. However, the unfolding rate constant of TmCsp is two orders of magnitude lower over the entire temperature range that was investigated. Consequently, the difference in conformational stability between the two proteins is solely due to the unfolding rate constant over a wide temperature range. A thermodynamic analysis points to an important role of entropic factors in the stabilization of TmCsp relative to its mesophilic homologues. C1 Univ Regensburg, Inst Biophys & Phys Biochem, D-93040 Regensburg, Germany. NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Schuler, B (reprint author), Univ Potsdam, D-14476 Golm, Germany. RI Schuler, Benjamin/E-7342-2011 OI Schuler, Benjamin/0000-0002-5970-4251 NR 54 TC 34 Z9 36 U1 0 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 1 PY 2002 VL 41 IS 39 BP 11670 EP 11680 DI 10.1021/bi0262931 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 598DP UT WOS:000178260400015 PM 12269809 ER PT J AU Gao, XG Wen, XL Yu, CA Esser, L Tsao, S Quinn, B Zhang, L Yu, L Xia, D AF Gao, XG Wen, XL Yu, CA Esser, L Tsao, S Quinn, B Zhang, L Yu, L Xia, D TI The crystal structure of mitochondrial cytochrome bc1 in complex with famoxadone: The role of aromatic-aromatic interaction in inhibition SO BIOCHEMISTRY LA English DT Article ID IRON-SULFUR PROTEIN; ELECTRON-DENSITY MAPS; PROTONMOTIVE Q-CYCLE; BC(1) COMPLEX; DOMAIN MOVEMENT; ENERGY TRANSDUCTION; BOVINE HEART; TRANSLOCATION; UBIQUINONE; REGION AB Ubiquinol cytochrome c oxido-reductase (EC. 1.10.2.2, bcl) is an integral membrane protein complex essential to cellular respiration. Structures of the 11-subunit mitochondrial bcl complex were determined with and without the fungicide famoxadone. Specific inhibition by famoxadone is achieved through a coordinated optimization of aromatic-aromatic interactions where conformational rearrangements in famoxadone and in residues lining the inhibitor-binding pocket produce a network of aromatic-aromatic interactions that mimic the crystal lattice of benzene. The profound aromatic-aromatic interactions as supported by prior mutagenesis provide a structural basis for specific protein-ligand interaction in a hydrophobic environment. Dramatic conformational changes, both in cyt. b and ISP subunits in the inhibitor-protein complex, confer experimental evidence for a functional role of cytochrome b in the induced conformational arrest of ISP and allow the identification of a possible intrasubunit signal transduction pathway that controls the movement of ISP. These results support an inhibitory mechanism that is consistent with the requirement for ISP movement in the electron transfer of this complex. C1 NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Oklahoma State Univ, Dept Biochem & Mol Biol, Stillwater, OK 74078 USA. RP Xia, D (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Room 1B22, Bethesda, MD 20892 USA. FU NIGMS NIH HHS [GM 30721] NR 44 TC 85 Z9 99 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 1 PY 2002 VL 41 IS 39 BP 11692 EP 11702 DI 10.1021/bi026252p PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 598DP UT WOS:000178260400017 PM 12269811 ER PT J AU Shen, J Rothman, DL AF Shen, J Rothman, DL TI Magnetic resonance spectroscopic approaches to studying neuronal: Glial interactions SO BIOLOGICAL PSYCHIATRY LA English DT Article DE glucose metabolism; glutamate-glutamine cycle; glutamine synthesis; magnetic resonance spectroscopy; stable isotope labels ID VIVO C-13 NMR; CEREBRAL METABOLIC COMPARTMENTATION; HUMAN BRAIN; GLUTAMINE SYNTHESIS; CYCLE FLUX; RAT-BRAIN; GLUCOSE; CLEARANCE; TURNOVER; INVIVO AB In vivo magnetic resonance spectroscopy (MRS) is a noninvasive technique for the measurement of the concentration and synthesis of metabolites in the brain. Application of the state-of-the-art in vivo C-13 anti N-15 MRS techniques to studying the synthesis of glutamate and glutamine has revealed that the glutamate-glutamine cycle between neurons and glia is a major metabolic flux, with a flux rate of 60%-80% relative to neuronal oxidative glucose metabolism in the resting human cerebral cortex. The MRS studies leading to the quantification of the glutamate-glutamine cycling flux are reviewed here. The advantages and limitations of different strategies are also discussed. (C) 2002 Society of Biological Psychiatry. C1 Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA. Yale Univ, Sch Med, Dept Diagnost Radiol, New Haven, CT 06510 USA. RP Shen, J (reprint author), NIMH, Mol Imaging Branch, Bldg 1,Room B3-10,1 Ctr Dr,MSC 0135, Bethesda, MD 20892 USA. FU NIBIB NIH HHS [R01 EB 00315] NR 33 TC 24 Z9 28 U1 2 U2 3 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 OCT 1 PY 2002 VL 52 IS 7 BP 694 EP 700 AR PII S0006-3223(02)01502-0 DI 10.1016/S0006-3223(02)01502-0 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 601EM UT WOS:000178433600002 PM 12372659 ER PT J AU Hewitt, SC Goulding, EH Eddy, EM Korach, KS AF Hewitt, SC Goulding, EH Eddy, EM Korach, KS TI Studies using the estrogen receptor alpha knockout uterus demonstrate that implantation but not decidualization-associated signaling is estrogen dependent SO BIOLOGY OF REPRODUCTION LA English DT Article DE cytokines; decidua; estradiol receptor; female reproductive tract; uterus ID LEUKEMIA INHIBITORY FACTOR; EMBRYO IMPLANTATION; PROGESTERONE-RECEPTOR; TARGETED DISRUPTION; MOUSE UTERUS; MICE LACKING; FEMALE MICE; CROSS-TALK; GENE; EXPRESSION AB Ovarian hormonal signaling is essential for proper functioning of the uterus in the establishment of pregnancy. Previous studies have demonstrated that decidualization, a stromal transformation that occurs in response to embryo implantation, can be elicited in the uterus of estrogen receptor alpha knockout (alpha-ERKO) mice in the absence of the estrogen dependence normally seen in wild-type (WT) mice for this response. While the alphaERKO stromal compartment demonstrated the necessary decidual response, embryo implantation is a process initiated in the epithelial layer, a uterine component that lacks estrogen responsiveness in the alphaERKO. To determine if the alphaERKO uterus would be competent for implantation, donor embryos were transferred into the uterine lumen of WT and alphaERKO females that had been ovariectomized and treated with exogenous estradiol and progesterone to mimic early pregnancy. No implantation occurred in the alphaERKO, while implantation sites containing live embryos were seen in similarly treated WT uteri, indicating that functional estrogen receptor alpha (ERalpha) is required for implantation. Previous observations of estrogen-independent decidualization in the alphaERKO prompted investigation of the mechanism leading to estrogen independence of this process. The disruption of progesterone receptor (PR), Hoxa10, Cox2, or LIF in transgenic mice results in the loss of decidualization response. Therefore, the expression of these genes was studied in WT and alphaERKO uteri by comparing expression following vehicle, progesterone alone (P), or estradiol priming followed by progesterone with nidatory estradiol (E+Pe) and by comparing expression following the above hormonal manipulations in addition to luminal infusion of oil used previously as decidualization-initiating stimulus. The whole-uterus level of PR and Hoxa10 mRNAs did not vary; however, the PR protein was induced in the stroma 24 h after oil infusion. Interestingly, in the WT, this induction was most apparent in samples receiving E+Pe, while in the alphaERKO samples, the induction occurred independent of any hormone priming. Cox2 protein and mRNA increased in both WT and alphaERKO samples 2 h after oil infusion in all three of the treatment groups. In the WT samples, Cox2 levels remained elevated 24 h after oil infusion only in the E+Pe treatment group; however, the elevated Cox2 was seen in samples taken 24 h after oil infusion in all three alphaERKO treatment groups. The alphaERKO uterine tissue appeared to sustain more extensive damage when examined 24 h after oil infusion. Severe trauma, such as crushing of the uterine tissue, has previously been shown to remove the requirement for nidatory estradiol for deciduomas to develop, indicating that the greater susceptibility of alphaERKO uterine tissue to damage from intraluminal oil infusion is contributing to decidualization in the absence of ERalpha. Leukemia inhibitory factor (LIF) mRNA was also induced following estradiol treatment in the WT, but also following oil infusion in WT samples that were not treated with estradiol. In contrast, estradiol does not induce LIF mRNA in the alphaERKO, but oil infusion leads to a robust increase in LIF in all aERKO sample groups. LIF binds and activates its membrane receptor, which initiates responses including the phosphorylation and nuclear translocation of Stat3 transcription factor. Thus, Stat3 phosphorylation was studied in WT and alphaERKO samples and found to be induced following oil infusion in all samples. Together, these and previous observations illustrate that estrogen is essential for epithelial proliferation and embryo implantation and that estrogen is dispensable for stromal decidualization in the alphaERKO, as the essential genes and signals required for the response are still induced. C1 NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Korach, KS (reprint author), NIEHS, Reprod & Dev Toxicol Lab, NIH, POB 12233,MD B3-02,111TW Alexander Dr, Res Triangle Pk, NC 27709 USA. OI Korach, Kenneth/0000-0002-7765-418X NR 33 TC 49 Z9 49 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 OCT PY 2002 VL 67 IS 4 BP 1268 EP 1277 DI 10.1095/biolreprod.102.002436 PG 10 WC Reproductive Biology SC Reproductive Biology GA 598FX UT WOS:000178266200030 ER PT J AU Jefferson, WN Couse, JF Padilla-Banks, E Korach, KS Newbold, RR AF Jefferson, WN Couse, JF Padilla-Banks, E Korach, KS Newbold, RR TI Neonatal exposure to genistein induces estrogen receptor (ER)alpha expression and multioocyte follicles in the maturing mouse ovary: Evidence for ER beta-mediated and nonestrogenic actions SO BIOLOGY OF REPRODUCTION LA English DT Article DE follicular development; granulosa cells; mechanisms of hormone action; oocyte development; steroid hormone receptors ID MESSENGER-RNA EXPRESSION; POLYOVULAR FOLLICLES; ALPHA GENE; ENVIRONMENTAL ESTROGENS; TISSUE DISTRIBUTION; UTERINE ADENOCARCINOMA; FETAL EXPOSURE; FEMALE MICE; ADULT MICE; RAT OVARY AB Outbred CD-1 mice were treated neonatally on Days 1-5 with the phytoestrogen, genistein (1, 10, or 100 mug per pup per day), and ovaries were collected on Days 5, 12, and 19. Ribonuclease protection assay analysis of ovarian mRNA showed that estrogen receptor 0 (ERR) predominated over ERalpha in controls and increased with age. Genistein treatment did not alter ERR expression, however, ERalpha expression was higher on Days 5 and 12. ERbeta was immunolocalized in granulosa cells, whereas Met was immunolocalized in interstitial and thecal cells. Genistein treatment caused a dramatic increase in Mat in granulosa cells. Genistein-treated ERR knockout mice showed a similar induction of ERalpha, which is seen in CD-1 mice, suggesting that ERR does not mediate this effect. Similar ERalpha induction in granulosa cells was seen in CD-1 mice treated with lavendustin A, a tyrosine kinase inhibitor that has no known estrogenic actions, which suggests that this property of genistein may be responsible. As a functional analysis, genistein-treated mice were superovulated and the number of oocytes was counted. A statistically significant increase in the number of ovulated oocytes was observed with the lowest dose, whereas a decrease was observed with the two higher doses. This increase in ovulatory capacity with the low dose coincided with higher ERalpha expression. Histological evaluations on Day 19 revealed a dose-related increase in multioocyte follicles (MOFs) in genistein-treated mice. Tyrosine kinase inhibition was apparently not responsible for MOFs because they were not present in mice that had been treated with lavendustin; however, ERbeta must play a role, because mice lacking ERR showed no MOFs. These data taken together demonstrate alterations in the ovary following neonatal exposure to genistein. Given that human infants are exposed to high levels of genistein in soy-based foods, this study indicates that the effects of such exposure on the developing reproductive tract warrant further investigation. C1 NIEHS, Lab Mol Toxicol, Environm Toxicol Program, Dev Endocrinol Sect, Res Triangle Pk, NC 27709 USA. NIEHS, Receptor Biol Sect, Lab Reprod & Dev Toxicol, Environm Dis & Med Program, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27605 USA. RP Newbold, RR (reprint author), NIEHS, Lab Mol Toxicol, Environm Toxicol Program, Dev Endocrinol Sect, POB 12233,Mail Drop E4-02,111 Alexander Dr,South, Res Triangle Pk, NC 27709 USA. OI Korach, Kenneth/0000-0002-7765-418X NR 72 TC 156 Z9 167 U1 0 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 OCT PY 2002 VL 67 IS 4 BP 1285 EP 1296 DI 10.1095/biolreprod.102.005371 PG 12 WC Reproductive Biology SC Reproductive Biology GA 598FX UT WOS:000178266200032 PM 12297547 ER PT J AU Hori, H Nagasawa, H Ishibashi, M Uto, Y Hirata, A Saijo, K Ohkura, K Kirk, KL Uehara, Y AF Hori, H Nagasawa, H Ishibashi, M Uto, Y Hirata, A Saijo, K Ohkura, K Kirk, KL Uehara, Y TI TX-1123: An antitumor 2-hydroxyarylidene-4-cyclopentene-1,3-dione as a protein tyrosine kinase inhibitor having low mitochondrial toxicity SO BIOORGANIC & MEDICINAL CHEMISTRY LA English DT Article ID AG17 INDUCES APOPTOSIS; LYMPHOMA CELL-LINE; TYRPHOSTIN AG17; ANTIPROLIFERATIVE AGENTS; SIGNAL TRANSDUCTION; OVEREXPRESSES BCL-2; CDK2 ACTIVITY; EGF RECEPTOR; NUDE-MICE; GROWTH AB A series of 2-hydroxyarylidene-4-cyclopentene-1,3-diones were designed, synthesized, and evaluated with respect to protein tyrosine kinase (PTK) inhibition, mitochondrial toxicity, and antitumor activity. Our results show that the cyclopentene-dione-derived TX-1123 is a more potent antitumor tyrphostin and also shows lower mitochondrial toxicity than the malononitrile-derived AG17, a potent antitumor tyrphostin. The O-methylation product of TX-1123 (TX-1925) retained its tyrphostin-like properties, including mitochondrial toxicity and antitumor activities. However, the methylation product of AG17 (TX-1927) retained its tyrphostin-like antitumor activities, but lost its mitochondrial toxicity. Our comprehensive evaluation of these agents with respect to protein tyrosine kinase inhibition, mitochondrial inhibition, antitumor activity, and hepatotoxicity demonstrates that PTK inhibitors TX-1123 and TX-1925 are more promising candidates for antitumor agents than tyrphostin AG17. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Univ Tokushima, Fac Engn, Dept Biol Sci & Technol, Tokushima 7708506, Japan. NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. Natl Inst Infect Dis, Dept Bioact Mol, Shinjuku Ku, Tokyo 1628640, Japan. RP Hori, H (reprint author), Univ Tokushima, Fac Engn, Dept Biol Sci & Technol, Tokushima 7708506, Japan. NR 39 TC 33 Z9 36 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0968-0896 J9 BIOORGAN MED CHEM JI Bioorg. Med. Chem. PD OCT PY 2002 VL 10 IS 10 BP 3257 EP 3265 AR PII S0968-0896(02)00160-8 DI 10.1016/S0968-0896(02)00160-8 PG 9 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Organic SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA 590QT UT WOS:000177834100018 PM 12150871 ER PT J AU Hashimoto, A Jacobson, AE Rothman, RB Dersch, CM George, C Flippen-Anderson, JL Rice, KC AF Hashimoto, A Jacobson, AE Rothman, RB Dersch, CM George, C Flippen-Anderson, JL Rice, KC TI Probes for narcotic receptor mediated phenomena. Part 28: New opioid antagonists from enantiomeric analogues of 5-(3-hydroxyphenyl)-N-phenylethylmorphan SO BIOORGANIC & MEDICINAL CHEMISTRY LA English DT Article ID BINDING-SITES AB Enantiomeric analogues of 5-(3-hydroxyphenyl)morphan ligands were synthesized and evaluated because of our unexpected finding that opioid antagonists can be obtained in the 5-phenylmorphan series of opioids without sterically hindering the rotation of the phenolic ring. We determined the opioid receptor binding affinity of these new analogues, as well as the efficacy of the more interesting ligands. One of the new compounds [(1R,5S)-(-)-3-[2-(3'-phenylpropyl)-2-azabicyclo[3.3.1] non-5-yl]-phenol, 15] was found to have half of the efficacy of naloxone, a potent opioid antagonist, in the [S-35]GTPgammaS assay, and two others (1R,5S)-(-)-3-[2-(4'-phenylbutyl)-2-azabicyclo[3.3.1]non- 5-yl]-phenol, 17, and (1R,5S,1'S)-(+)-3-[2-(1'-methyl-2'-phenylethyl)-2-azabicyclo[3.3.1]non-5-yl]-phenol, 26, acted as moderately potent opioid antagonists. X-ray crystallographic structure data were obtained on three compounds. Two of them had three chiral centers; 25 [(1R,5S,1'R)-(-)-3-[2-(1'-methyl-2'-phenylethyl)-2-azabicyclo[3.3.1] non-5-yl]-phenol] was determined to have the 1R,5S,1'R configuration, and 26 the 1R,5S,1'S configuration. Since (1S,5R)-(+)-2-bromo-5-[2-(2'-phenylethyl)-2-azabicyclo[3.3.1]non-5-yl]-phenol (32) was a position isomer of (1S,5R)-(+)-4-bromo-3-[2-(2'-phenylethyl)-2-azabicyclo[3.3.1]non-5-yl]-phenol (30), and both showed the same H-1 NMR spectrum, the structure of 32 was unequivocally determined by X-ray structure analysis. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 NIDDKD, Med Chem Lab, NIH, Bethesda, MD 20892 USA. NIDA, Addict Res Ctr, Clin Psychopharmacol Sect, Baltimore, MD 21224 USA. USN, Res Lab, Struct Matter Lab, Washington, DC 20375 USA. RP Rice, KC (reprint author), NIDDKD, Med Chem Lab, NIH, Bldg 8,Room B1-23, Bethesda, MD 20892 USA. NR 20 TC 24 Z9 24 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0968-0896 J9 BIOORGAN MED CHEM JI Bioorg. Med. Chem. PD OCT PY 2002 VL 10 IS 10 BP 3319 EP 3329 AR PII S0968-0896(02)00219-5 DI 10.1016/S0968-0896(02)00219-5 PG 11 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Organic SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA 590QT UT WOS:000177834100026 PM 12150879 ER PT J AU Kawai, T Suzuki, Y Eda, S Kase, T Ohtani, K Sakai, Y Keshi, H Fukuoh, A Sakamoto, T Nozaki, M Copeland, NG Jenkins, NA Wakamiya, N AF Kawai, T Suzuki, Y Eda, S Kase, T Ohtani, K Sakai, Y Keshi, H Fukuoh, A Sakamoto, T Nozaki, M Copeland, NG Jenkins, NA Wakamiya, N TI Molecular cloning of mouse collectin liver 1 SO BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY LA English DT Article DE collectin liver 1; collectin; mouse; cDNA; chromosome ID MANNOSE-BINDING PROTEIN; INFLUENZA-A VIRUSES; CARBOHYDRATE-RECOGNITION DOMAIN; PULMONARY SURFACTANT APOPROTEIN; TRANSFER-RNA SYNTHETASE; CHROMOSOMAL LOCALIZATION; LECTIN; GENE; CONGLUTININ; HOMOLOGY AB Collectins are members of the superfamily of vertebrate C-type lectins that contain a collagen-like region, and are involved in first-line host defense. We earlier cloned and characterized a new kind of collectin, collectin liver 1 (CL-L1). In this study, we isolated the mouse homologue of CL-L1 encoding 277 amino acid residues; its deduced protein sequence was 88% identical with human CL-L1. Mouse CL-L1 mRNA was expressed mainly in the liver and stomach, but was found also in muscles, testes, intestines, and embryos. In mouse embryos, the level of CL-L1 mRNA gradually increased with embryonic age. In 16-day-old mouse embryos, CL-L1 mRNA was expressed in the liver, amnion, and visceral yolk sac. The mouse CL-L1 gene, Cll1 was found on chromosome 15 in a region syntenic with human chromosome 8q. CL-L1 was a highly conserved protein in mammals, birds, and fish. C1 Osaka Prefectural Inst Publ Hlth, Div Food Microbiol, Nagashinari Ku, Osaka 5370025, Japan. Osaka Prefectural Inst Publ Hlth, Div Pathol, Nagashinari Ku, Osaka 5370025, Japan. Osaka Prefectural Inst Publ Hlth, Div Virol, Nagashinari Ku, Osaka 5370025, Japan. Fuso Pharmaceut Ind Ltd, Ctr Res & Dev, Dept Biol Sci Res, Joto Ku, Osaka 5360025, Japan. Asahikawa Med Coll, Dept Microbiol, Asahikawa, Hokkaido 0788510, Japan. Osaka Univ, Res Inst Microbial Dis, Dept Sci, Lab Anim Expt, Suita, Osaka 5650871, Japan. Natl Canc Inst Frederick, Mouse Canc Genet Program, Frederick, MD 21702 USA. RP Kawai, T (reprint author), Osaka Prefectural Inst Publ Hlth, Div Food Microbiol, Nagashinari Ku, 1-3-69 Nakamichi, Osaka 5370025, Japan. EM kawai@iph.pref.osaka.jp RI Suzuki, Yasuhiko/F-6890-2012 NR 46 TC 9 Z9 11 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0916-8451 EI 1347-6947 J9 BIOSCI BIOTECH BIOCH JI Biosci. Biotechnol. Biochem. PD OCT PY 2002 VL 66 IS 10 BP 2134 EP 2145 PG 12 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Chemistry, Applied; Food Science & Technology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Chemistry; Food Science & Technology GA 611DU UT WOS:000179001800016 PM 12450124 ER PT J AU Wiener, MC Richmond, BJ AF Wiener, MC Richmond, BJ TI Model based decoding of spike trains SO BIOSYSTEMS LA English DT Article; Proceedings Paper CT International Workshop on Neuronal Coding CY SEP 09-14, 2001 CL PLYMOUTH, ENGLAND DE Vl; vision; coding ID VISUAL-CORTEX; TEMPORAL PATTERNS; FIRING PATTERNS; FRONTAL-CORTEX; NEURONS; RESPONSES; MONKEY; INFORMATION; PRECISION; CORTICES AB Reliably decoding neuronal responses requires knowing what aspects of neuronal responses are stimulus related, and which aspects act as noise. Recent work shows that spike trains can be viewed as stochastic samples from the rate variation function, as estimated by the time dependent spike density function (or normalized peristimulus time histogram). Such spike trains are exactly described by order statistics, and can be decoded millisecond-by-millisecond by iterative application of order statistics. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA. RP Richmond, BJ (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Rm 1B80, Bethesda, MD 20892 USA. NR 24 TC 6 Z9 6 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0303-2647 J9 BIOSYSTEMS JI Biosystems PD OCT-DEC PY 2002 VL 67 IS 1-3 BP 295 EP 300 AR PII S0303-2647(02)00087-4 DI 10.1016/S0303-2647(02)00087-4 PG 6 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA 627UN UT WOS:000179954700033 PM 12459310 ER PT J AU Abramowitz, M Spring, KR Keller, HE Davidson, MW AF Abramowitz, M Spring, KR Keller, HE Davidson, MW TI Basic principles of microscope objectives SO BIOTECHNIQUES LA English DT Article C1 Florida State Univ, Natl High Magnet Field Lab, Tallahassee, FL 32310 USA. NHLBI, NIH, Bethesda, MD 20892 USA. Carl Zeiss, Thornwood, NY USA. Olympus Amer, Melville, NY USA. RP Davidson, MW (reprint author), Florida State Univ, Natl High Magnet Field Lab, 1800 E Paul Dirac Dr, Tallahassee, FL 32310 USA. NR 7 TC 11 Z9 11 U1 2 U2 10 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD OCT PY 2002 VL 33 IS 4 BP 772 EP + PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 604VN UT WOS:000178641900011 PM 12398185 ER PT J AU Feldman, AL Costouros, NG Wang, E Qian, M Marincola, FM Alexander, HR Libutti, SK AF Feldman, AL Costouros, NG Wang, E Qian, M Marincola, FM Alexander, HR Libutti, SK TI Advantages of mRNA amplification for microarray analysis SO BIOTECHNIQUES LA English DT Article ID GENE-EXPRESSION; RNA AB Expanding applications of cDNA microarrays such as fine needle aspiration biopsy and laser capture microdissection necessitate the ability to perform arrays with minute starting amounts of RNA. While methods for amplifying RNA have been advocated, the fidelity of array results using amplified material has not been fully validated. Here we demonstrate preserved fidelity in arrays using one or two rounds of mRNA amplification, validated by downstream real-time quantitative PCR. In addition, the quality of the array data was superior to that obtained using total RNA. Based on these results, we recommend routine mRNA amplification for all cDNA microaray-based analysis of gene expression. C1 NIH, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. RP Libutti, SK (reprint author), NIH, Bldg 10,Room 3C428, Bethesda, MD 20892 USA. RI Feldman, Andrew/D-5028-2012 NR 13 TC 118 Z9 125 U1 0 U2 5 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD OCT PY 2002 VL 33 IS 4 BP 906 EP + PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 604VN UT WOS:000178641900026 PM 12398200 ER PT J AU Khaled, AR Durum, SK AF Khaled, AR Durum, SK TI The role of cytokines in lymphocyte homeostasis SO BIOTECHNIQUES LA English DT Review ID CD8(+) T-CELLS; SEVERE COMBINED IMMUNODEFICIENCY; RECEPTOR-DEFICIENT MICE; B-CELL; IN-VIVO; NATURAL-KILLER; GAMMA-CHAIN; IL-7 RECEPTOR; CUTTING EDGE; CD4 MEMORY AB The size of lymphocyte populations is regulated by replication and death. Cytokines produced by non-lymphoid cells provide key survival and replication signals for several lymphocyte subpopulations. The availability of these cytokines thus serves as a homeostatic regulatory mechanism by determining the upper limit of the population size. IL-7 is required for survival of naive CD4(+) and CD8(+) cells and memory CD8(+) cells. IL-15 is required for survival of memory CD8(+) cells. IL-12 and IL-4 also promote memory CD8(+) survival BAFF is required for survival of mature B cells. Antigen receptor signals, together with these cytokines signals, are required for survival of mature B cells and naive T cells. The list of extracellular survival signals for lymphocytes remains incomplete, and the intracellular pathways leading to survival are poorly understood. C1 NCI, Sect Cytokines & Immun, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21702 USA. RP Durum, SK (reprint author), NCI, Sect Cytokines & Immun, Mol Immunoregulat Lab, Ctr Canc Res, Bldg 560,Rm 31-71, Frederick, MD 21702 USA. EM durums@mail.ncifcrf.gov NR 76 TC 12 Z9 14 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD OCT PY 2002 SU S BP 40 EP 45 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 606ZG UT WOS:000178765500005 ER PT J AU Ozato, K Tsujimura, H Tamura, T AF Ozato, K Tsujimura, H Tamura, T TI Toll-like receptor signaling and regulation of cytokine gene expression in the immune system SO BIOTECHNIQUES LA English DT Review ID SEQUENCE-BINDING-PROTEIN; NF-KAPPA-B; DOUBLE-STRANDED-RNA; DENDRITIC CELLS; I INTERFERON; TRANSCRIPTION FACTORS; BACTERIAL-DNA; DIFFERENTIAL EXPRESSION; BETA ENHANCEOSOME; IL-12 PRODUCTION AB Dendritic cells, macrophages, and granulocytes are derived from hematopoietic stem cells and provide a first line of defense against infectious pathogens. Toll-like receptors (TLRs) expressed on these cells recognize molecular structures present in the pathogens. Upon binding of a pathogen ligand, TLRs trigger a cascade of signaling pathways that is conserved from insect to plants to humans, which ultimately activates NFkappaB. In mammalian cells, this leads to the induction of cytokine genes and the establishment of innate immunity. For example, TLR signals induce type I inteferons (IFN alpha/beta) in dendrytic cells conferring an antiviral state upon host cells. Moreover, TLR signals stimulate not only pro-inflammatory cytokines such as IFNs, IL-1, TNFalpha, and IL-12 but also anti-inflammatory cytokines such as IL-10 and IL-6. IL-12 and IL-10 are cytokines that bridge early innate responses and the ensuing specific immune responses. TLR signals also enhance an antigen presentation capacity in dendritic cells and macrophages. Recent studies with mouse and human cells indicate that TLRs activate multiple signaling cascades that involve chromatin structure alterations as well as activation of many transcription factors (e.g., IRF-3, IRF-8/ICSBP and PU.1). Together, although the basic backbone is conserved throughout evolution, the TLR signaling system in mammalian species has an added complexity to accommodate a mechanism that links innate and adaptive immunity. RP Ozato, K (reprint author), NICHD, Lab Mol Growth Regulat, NIH, 6 Ctr Dr,MSC-2753, Bethesda, MD 20892 USA. NR 93 TC 49 Z9 56 U1 1 U2 3 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD OCT PY 2002 SU S BP 66 EP + PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 606ZG UT WOS:000178765500008 ER PT J AU Suppes, T Chisholm, KA Dhavale, D Frye, MA Atshuler, LL McElroy, SL Keck, PE Nolen, WA Kupka, R Denicoff, KD Leverich, GS Rush, AJ Post, RM AF Suppes, T Chisholm, KA Dhavale, D Frye, MA Atshuler, LL McElroy, SL Keck, PE Nolen, WA Kupka, R Denicoff, KD Leverich, GS Rush, AJ Post, RM TI Tiagabine in treatment refractory bipolar disorder: a clinical case series SO BIPOLAR DISORDERS LA English DT Article DE anticonvulsants; bipolar disorder; depression; GABAergic activity; mania; seizures; tiagabine ID NONCONVULSIVE STATUS EPILEPTICUS; DEPRESSIVE SYMPTOMATOLOGY IDS; PLACEBO-CONTROLLED TRIAL; MOOD DISORDERS; THERAPY; MANIA; GABAPENTIN; INVENTORY; EPILEPSY; SCALE AB Objectives: Anticonvulsants have provided major treatment advances for patients with bipolar disorder. Many of these drugs, including several with proven efficacy in bipolar mania or depression, enhance the activity of the gamma-amino butyric acid (GABA) neurotransmitter system. A new anticonvulsant, tiagabine, has selective GABAergic activity and is approved for patients with partial epilepsy. Few reports of its potential effectiveness in bipolar disorder, however, have been published. We sought to evaluate the effectiveness of tiagabine added to ongoing medication regimens in patients with bipolar disorder inadequately responsive to or intolerant of usual treatments. Methods: Seventeen treatment-refractory patients participating in the Stanley Foundation Bipolar Network (SFBN) long-term follow-up study were offered open treatment with add-on tiagabine after discussion of the risks, benefits, other treatment options and giving informed consent. Patients' clinical symptoms and somatic complaints were closely monitored with SFBN longitudinal and cross-sectional ratings. Four patients discontinued low-dose tiagabine prior to the second visit and were excluded from data analysis. Results: Thirteen patients received a mean of 38 days of treatment at a mean dose of 8.7 mg/day of tiagabine. On the Clinical Global Impression Scale for Bipolar Disorder Overall category, three (23%) patients showed much or very much improvement and 10 (77%) patients showed no change or worsening. Three significant adverse events were noted, including two presumptive seizures. Conclusions: Open add-on tiagabine for treatment-refractory patients with bipolar disorder demonstrated limited efficacy with the majority of patients showing no change or worsening of clinical symptoms. In addition, patients experienced serious side-effects attributed as likely due to the medication, which resolved without lasting consequence when tiagabine was discontinued. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75390 USA. Univ Calif Los Angeles, Sch Med, Stanley Bipolar Treatment Network, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Dept Psychiat, Los Angeles, CA 90024 USA. Univ Cincinnati, Coll Med, Cincinnati, OH USA. Univ Med Ctr, Utrecht, Netherlands. Altrecht Inst Mental Hlth Care, Utrecht, Netherlands. NIMH, Biol Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Suppes, T (reprint author), Univ Texas, SW Med Ctr, Dept Psychiat, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. RI Nolen, Willem/E-9006-2014; OI Rush, Augustus/0000-0003-2004-2382 NR 35 TC 50 Z9 51 U1 1 U2 2 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1398-5647 J9 BIPOLAR DISORD JI Bipolar Disord. PD OCT PY 2002 VL 4 IS 5 BP 283 EP 289 DI 10.1034/j.1399-5618.2002.01201.x PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 602TL UT WOS:000178520500002 PM 12479659 ER PT J AU Kundu, M Chen, A Anderson, S Kirby, M Xu, LP Castilla, LH Bodine, D Liu, PP AF Kundu, M Chen, A Anderson, S Kirby, M Xu, LP Castilla, LH Bodine, D Liu, PP TI Role of Cbfb in hematopoiesis and perturbations resulting from expression of the leukemogenic fusion gene Cbfb-MYH11 SO BLOOD LA English DT Article ID BINDING-FACTOR-BETA; MYOSIN HEAVY-CHAIN; FETAL LIVER HEMATOPOIESIS; DEFINITIVE HEMATOPOIESIS; CLEIDOCRANIAL DYSPLASIA; DNA-BINDING; LEUKEMIA; DIFFERENTIATION; CBF-ALPHA-2; DISRUPTION AB Core-blinding factor beta (CBFbeta) and CBFalpha2 form a heterodimeric transcription factor that plays an important role in hematopoiesis. The genes encoding either CBFbeta or CBFalpha2 are involved in chromosomal rearrangements In more than 30% of cases of acute myeloid leukemia (AML), suggesting that CBFbeta and CBFalpha2 play important roles in leukemogenesis. Inv(16)(p13; q22) is found in almost all cases of AML M4Eo and results in the fusion of CBFbeta with MYH11, the gene encoding smooth muscle myosin heavy chain. Mouse embryos heterozygous for a Cbfb-MYH11 knock-in gene lack definitive hematopoiesis, a phenotype shared by Cbfb(-/-) embryos. In this study we generated a Cbfb-GFP knock-in mouse model to characterize the normal expression pattern of Cbfbeta in hematopoietic cells. In midgestation embryos, Cbfbeta was expressed in populations enriched for hematopoietic stem cells and progenitors. This population of stem cells and progenitors was not present in mouse embryos heterozygous for the Cbfb-MYH11 knock-in gene. Together, these data suggest that Cbfb-MYH11 blocks embryonic hematopoiesis at the stem-progenitor cell level and that Cbfb is essential for the generation of hematopoietic stem and progenitor cells. In adult mice, Cbfbeta was expressed in stem and progenitor cells, as well as mature myelold and lymphoid cells. Although it was expressed in erythroid progenitors, Cbfbeta was not expressed during the terminal stages of erythropoiesis. Our data indicate that Cbfb is required for myeloid and lymphoid differentiation; but does not play a critical role in erythroid differentiation. 2002 by The American Society of Hematology. C1 NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. Univ Massachusetts, Sch Med, Program Gene Funct & Express, Worcester, MA USA. RP Liu, PP (reprint author), NHGRI, Genet & Mol Biol Branch, NIH, Room 3A18,Bldg 49,49 Convent Dr, Bethesda, MD 20892 USA. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 30 TC 44 Z9 45 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 2002 VL 100 IS 7 BP 2449 EP 2456 DI 10.1182/blood-2002-04-1064 PG 8 WC Hematology SC Hematology GA 598FV UT WOS:000178266000022 PM 12239155 ER PT J AU Sinha, ML Fry, TJ Fowler, DH Miller, G Mackall, CL AF Sinha, ML Fry, TJ Fowler, DH Miller, G Mackall, CL TI Interleukin 7 worsens graft-versus-host disease SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; STEM-CELL TRANSPLANTATION; MATURE T-CELLS; MESSENGER-RNA; IN-VIVO; IMMUNE RECONSTITUTION; CYTOTOXIC LYMPHOCYTES; EPITHELIAL-CELLS; PARENTAL DONORS; GENE-EXPRESSION AB Impaired immune reconstitution has moved to the forefront of clinical problems limiting progress In allogeneic bone marrow transplantation (BMT). The Identification of therapies that can enhance immune reconstitution by increasing thymopoiesis is critical to solving this problem. Interleukin 7 (IL-7) is the most potent thymopoietic cytokine identified thus far. To study the effects of IL-7 on immune reconstitution and graft-versus-host disease (GVHD) following allogeneic BMT, we administered recombinant human IL-7 (rhIL-7) in a murine parent into an F1 model. Results showed that rhIL-7 therapy lowered the "threshold" T-cell dose required to induce both clinical signs of GVHD as well as lethal GVHD. Histologic analysis of GVHD target tissues revealed that rhIL-7 Increased the degree of Inflammation and tissue damage observed at all T-cell doses studied, but did not change the pattern of organs affected or the histologic appearance of the GVHD within target organs. In addition, we evaluated the capacity for rhIL-7 to enhance thymopoiesis In the setting of allogeneic T cell-depleted (TCD) and T-cell-replete BMT. We observed that rhIL-7 therapy enhanced thymic function In TCD allogeneic BM transplant recipients, but not In animals that received even modest doses of T cells presumably due to thymic toxicity of the graft-versus-host reaction. Thus, caution must be exercised as IL-7 is developed clinically as an immunorestorative agent for use In the setting of allogeneic BMT. These results suggest that use of IL-7 should be limited to the setting of TCD BMT to obtain the greatest benefit on Immune competence with the least toxicity. (C) 2002 by The American Society of Hematology. C1 NCI, Pediat Oncol Branch, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA. NIH, Vet Resources Program, Bethesda, MD 20892 USA. RP Mackall, CL (reprint author), Bldg 10,Room 13N240,MSC 1928,10 Ctr Dr, Bethesda, MD 20892 USA. NR 61 TC 80 Z9 82 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 2002 VL 100 IS 7 BP 2642 EP 2649 DI 10.1182/blood-2002-04-1082 PG 8 WC Hematology SC Hematology GA 598FV UT WOS:000178266000047 PM 12239180 ER PT J AU Balkin, TJ Braun, AR Wesensten, NJ Jeffries, K Varga, M Baldwin, P Belenky, G Herscovitch, P AF Balkin, TJ Braun, AR Wesensten, NJ Jeffries, K Varga, M Baldwin, P Belenky, G Herscovitch, P TI The process of awakening: a PET study of regional brain activity patterns mediating the re-establishment of alertness and consciousness SO BRAIN LA English DT Article DE alertness; consciousness; sleep inertia; rCBF; PET ID SLEEP INERTIA; PERFORMANCE; CORTEX AB Awakening from sleep entails rapid re-establishment of consciousness followed by the relatively slow (20-30 min later) re-establishment of alertness-a temporal dissociation that facilitates specification of the physiological underpinnings of each of these facets of the awakening process. (H2O)-O-15 PET was used to assess changes in regional cerebral blood flow (rCBF) upon awakening from stage 2 sleep. Cerebral blood flow (CBF) was most rapidly re-established in centrencephalic regions (e.g. brainstem and thalamus), suggesting that the reactivation of these regions underlies the reestablishment of conscious awareness. Across the ensuing 15 min of wakefulness, further increases in CBF were evident primarily in anterior cortical regions, suggesting that the dissipation of sleep inertia effects (postawakening performance and alertness deficits) is effected by reactivation of these regions. Concomitant shifts in correlation patterns of regional brain activity across the post-awakening period [in particular, a waning negative correlation between prefrontal cortex and mesencephalic reticular formation (RF) activity, and a waxing positive correlation between prefrontal cortex and ventromedial caudate nucleus (CAUD) activity] suggest that the post-awakening reversal of sleep inertia effects may be mediated by more than mere reactivation-it may also involve the functional reorganization of brain activity. Conversely, stable post-awakening correlations-such as those found between the anterior cingulate cortex (ACC) and most other brain regions-may denote the pattern of functional connectivity that underlies consciousness itself. C1 Walter Reed Army Inst Res, Dept Behav Biol, Washington, DC 20307 USA. NIDCD, Language Sect, Voice Speech & Language Branch, NIH, Bethesda, MD USA. NIDCD, PET Imaging Sect, NIH, Bethesda, MD USA. RP Balkin, TJ (reprint author), Walter Reed Army Inst Res, Dept Behav Biol, Washington, DC 20307 USA. NR 20 TC 120 Z9 130 U1 1 U2 16 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD OCT PY 2002 VL 125 BP 2308 EP 2319 DI 10.1093/brain/awf228 PN 10 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 604HR UT WOS:000178613700013 PM 12244087 ER PT J AU Ullman, MT Estabrooke, IV Steinhauer, K Brovetto, C Pancheva, R Ozawa, K Mordecai, K Maki, P AF Ullman, MT Estabrooke, IV Steinhauer, K Brovetto, C Pancheva, R Ozawa, K Mordecai, K Maki, P TI Sex differences in the neurocognition of language SO BRAIN AND LANGUAGE LA English DT Meeting Abstract C1 Georgetown Univ, Dept Neurosci, Washington, DC USA. Georgetown Univ, Dept Linguist, Washington, DC USA. Georgetown Univ, Interdisciplinary Program Neurosci, Washington, DC USA. Univ So Calif, Dept Linguist, Los Angeles, CA 90089 USA. Univ So Calif, Dept Slav, Los Angeles, CA USA. NIA, Baltimore, MD 21224 USA. NR 5 TC 20 Z9 21 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT PY 2002 VL 83 IS 1 BP 141 EP 143 AR PII S0093-934X(02)00110-4 PG 3 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 601EP UT WOS:000178433800054 ER PT J AU Estabrooke, IV Mordecai, K Maki, P Ullman, MT AF Estabrooke, IV Mordecai, K Maki, P Ullman, MT TI The effect of sex hormones on language processing SO BRAIN AND LANGUAGE LA English DT Meeting Abstract ID BRAIN; MODEL C1 Georgetown Univ, Brain & Language Lab, Washington, DC USA. NIA, Baltimore, MD 21224 USA. NR 6 TC 7 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT PY 2002 VL 83 IS 1 BP 143 EP 146 AR PII S0093-934X(02)00111-6 PG 4 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 601EP UT WOS:000178433800055 ER PT J AU Park, GH McNeil, MR Doyle, PJ AF Park, GH McNeil, MR Doyle, PJ TI Effects of increased inter-word intervals following prepositions on auditory sentence comprehension in agrammatic and normal comprehenders SO BRAIN AND LANGUAGE LA English DT Meeting Abstract C1 Univ Pittsburgh, Dept Commun Sci & Disorders, Pittsburgh, PA 15260 USA. VA Pittsburgh Hlth Care Syst, Aphasia Rehabil Res Lab & Clin, Pittsburgh, PA USA. Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT PY 2002 VL 83 IS 1 BP 220 EP 222 AR PII S0093-934X(02)00142-6 PG 3 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 601EP UT WOS:000178433800086 ER PT J AU Neubert, JK Matsuka, Y Maidment, NT Spigelman, I AF Neubert, JK Matsuka, Y Maidment, NT Spigelman, I TI Microdialysis in trigeminal ganglia SO BRAIN RESEARCH PROTOCOLS LA English DT Article DE neurophysiology; microdialysis; trigeminal ganglia; substance P; adenosine triphosphate; guinea pig; in vivo recovery ID DORSAL-ROOT GANGLIA; IN-VIVO; EVOKED RELEASE; SUBSTANCE-P; RAT; NEURONS; INVIVO AB Recent evidence demonstrates that neurons in sensory ganglia contribute to sensory signaling in both physiological and pathological states. In vivo sampling from this site may provide important insights into which substances mediate or modulate sensory transmission. To address this possibility, we have applied the microdialysis technique to the guinea pig trigeminal ganglia (TG). The large size and easy access of the TG in the guinea pig make it an ideal sampling site, while the somatotopic organization allows for specific regions of innervation to be studied at the ganglionic level. This report describes the use of microdialysis probes within the TG and use recovery and analysis of substance P (SP) and adenosine triphosphate (ATP) as case in points. Various physiological and pharmacological manipulations can be made, for example release of peptides from ganglionic neurons can be monitored in the presence or absence of inflammation in the orofacial region. Microdialysis performed in the TG thus provides a valuable site for recovery and measurement of a variety of extracellular substances that may be integral in the processing of trigeminal sensory information. Published by Elsevier Science B.V. C1 Natl Inst Dent & Craniofacial Res, Pain Neurosensory Mech Branch, NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Sch Dent, Div Oral Biol & Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. RP Neubert, JK (reprint author), Natl Inst Dent & Craniofacial Res, Pain Neurosensory Mech Branch, NIH, Bethesda, MD 20892 USA. OI Matsuka, Yoshizo/0000-0003-1069-2605 FU NIDCR NIH HHS [DE00408]; NINDS NIH HHS [NS-05685] NR 11 TC 2 Z9 4 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1385-299X J9 BRAIN RES PROTOC JI Brain Res. Protoc. PD OCT PY 2002 VL 10 IS 2 BP 102 EP 108 AR PII S1385-299X(02)00188-5 DI 10.1016/S1385-299X(02)00188-5 PG 7 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 625LW UT WOS:000179818800007 PM 12431709 ER PT J AU Bonnot, A Whelan, PJ Mentis, GZ O'Donovan, MJ AF Bonnot, A Whelan, PJ Mentis, GZ O'Donovan, MJ TI Locomotor-like activity generated by the neonatal mouse spinal cord SO BRAIN RESEARCH REVIEWS LA English DT Article; Proceedings Paper CT Segerfalk Symposium on Principles of Spinal Cord Function Plasticity and Repair CY SEP 22-25, 2001 CL YSTAD SALTSJOBAD, SWEDEN DE locomotion; spinal networks; motoneurons; calcium imaging ID CENTRAL PATTERN GENERATORS; IN-VITRO; HINDLIMB LOCOMOTION; RHYTHMIC NETWORKS; NEURAL NETWORKS; MOTOR PATTERNS; NEWBORN RAT; LAMPREY; INVITRO; LOCALIZATION AB This report describes locomotor-like activity generated by the neonatal mouse spinal cord in vitro. We demonstrate that locomotor-like activity can be produced either spontaneously or by a train of stimuli applied to the dorsal roots or in the presence of bath-applied drugs. Calcium imaging of the motoneuron activity generated by a train of dorsal root stimuli revealed a rostrocaudally propagating component of the optical signal in the anterior lumbar (L1-L3) and in the caudal segments (S1-S4). We hypothesize that this spatio-temporal pattern arises from a rostrocaudal gradient of excitability in the relevant segments. Our experiments suggest that left/right reciprocal inhibition and NMDA-mediated oscillarions are not essential mechanisms underlying rhythmogenesis in the neonatal mouse cord. Finally, our data are discussed in the context of other models of locomotion in lower and higher vertebrates. Published by Elsevier Science B.V. C1 NINDS, Neural Control Lab, Sect Dev Neurobiol, NIH, Bethesda, MD 20892 USA. RP Bonnot, A (reprint author), NINDS, Neural Control Lab, Sect Dev Neurobiol, NIH, Bethesda, MD 20892 USA. RI o'donovan, michael/A-2357-2015 OI o'donovan, michael/0000-0003-2487-7547 NR 53 TC 53 Z9 53 U1 1 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0173 J9 BRAIN RES REV JI Brain Res. Rev. PD OCT PY 2002 VL 40 IS 1-3 BP 141 EP 151 AR PII S0165-0173(02)00197-2 DI 10.1016/S0165-0173(02)00197-2 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 623RV UT WOS:000179717400014 PM 12589913 ER PT J AU Antman, K Abraido-Lanza, AF Blum, D Brownfield, E Cicatelli, B Debor, MD Emmons, K Fitzgibbon, M Gapstur, SM Gradishar, W Hiatt, RA Hubbell, FA Joe, AK Klassen, AC Lee, NC Linden, HM McMullin, J Mishra, SI Neuhaus, C Olopade, FI Walas, K AF Antman, K Abraido-Lanza, AF Blum, D Brownfield, E Cicatelli, B Debor, MD Emmons, K Fitzgibbon, M Gapstur, SM Gradishar, W Hiatt, RA Hubbell, FA Joe, AK Klassen, AC Lee, NC Linden, HM McMullin, J Mishra, SI Neuhaus, C Olopade, FI Walas, K TI Reducing disparities in breast cancer survival: A Columbia University and Avon Breast Cancer Research and Care Network Symposium SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE breast cancer; disparities; minorities; mortality; survival; underserved ID ETHNIC-DIFFERENCES; BLACK-WOMEN; RACIAL/ETHNIC GROUPS; ESTROGEN-RECEPTOR; AFRICAN-AMERICAN; RISK PERCEPTION; WHITE WOMEN; HEALTH-CARE; FREQUENCY; EDUCATION AB On November 8th, 2001, faculty from Universities, government and non-profit community organizations met to determine how, separately and together, they could address disparities in survival of women with breast cancer in the diverse patient populations served by their institutions. Studies and initiatives directed at increasing access had to date met modest success. The day was divided into three sections, defining the issues, model programs, government initiatives and finally potential collaborations. By publishing these proceedings, interested readers will be aware of the ongoing programs and studies and can contact the investigators for more information. The Avon Foundation funded this symposium to bring together interested investigators to share programmatic experiences, data and innovative approaches to the problem. C1 Columbia Univ, New York, NY 10027 USA. Canc Care Inc, New York, NY USA. Emory Univ, Sch Med, Atlanta, GA 30322 USA. Avon Prod Fdn Inc, Avon Breast Crusade, New York, NY USA. Harvard Univ, Harvard Sch Publ Hlth, Cambridge, MA 02138 USA. DFCI, Boston, MA USA. Northwestern Univ, Sch Med, Evanston, IL 60201 USA. NCI, Div Canc Control, Bethesda, MD 20892 USA. Univ Calif Irvine, Dept Med, Irvine, CA 92717 USA. Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD 21224 USA. Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA 30333 USA. Univ Washington, Seattle, WA 98195 USA. Univ Calif Irvine, Ctr Hlth Policy & Res, Irvine, CA 92717 USA. Johns Hopkins Univ, Johns Hopkins Sch Med, Baltimore, MD 21224 USA. Univ Chicago, Pritzker Sch Med, Ctr Clin Canc Genet, Chicago, IL 60637 USA. RP Antman, K (reprint author), MHB 6N 435,177 Ft Washington Ave, New York, NY 10032 USA. FU NCI NIH HHS [P30-CA13696, R03CA81619] NR 42 TC 6 Z9 7 U1 1 U2 8 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD OCT PY 2002 VL 75 IS 3 BP 269 EP 280 DI 10.1023/A:1019947110236 PG 12 WC Oncology SC Oncology GA 588AF UT WOS:000177676700009 PM 12353816 ER PT J AU Wickerham, L AF Wickerham, L TI Tamoxifen - an update on current data and where it can now be used SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE breast cancer; ductal carcinoma in situ; efficacy; estrogen receptor; prevention; tamoxifen ID SURGICAL-ADJUVANT-BREAST; RECEPTOR-POSITIVE TUMORS; CARCINOMA IN-SITU; BOWEL-PROJECT P-1; CANCER PATIENTS; CLINICAL-TRIAL; CHEMOTHERAPY; PREVENTION; THERAPY AB Over the past 30 years, data from a large number of clinical trials have confirmed the efficacy of tamoxifen in estrogen receptor (ER)-positive breast cancer, both as adjuvant therapy and for advanced disease. The 1995 Early Breast Cancer Trialists' Collaborative Group (EBCTCG) overview of randomized trials of adjuvant tamoxifen versus no tamoxifen showed that during approximately 10 years of follow-up, the proportional reductions in mortality for 1, 2 and similar to5 years of adjuvant tamoxifen were 12, 17 and 26%, respectively. Tamoxifen is also effective for the prevention of breast cancer. In the National Surgical Adjuvant Breast and Bowel Project (NSABP) breast cancer prevention study (P-1), 5 years of tamoxifen therapy reduced the incidence of invasive and non-invasive breast cancers by 49 and 50%, respectively. In a randomized NSABP trial in women with ductal carcinoma in situ (DCIS), tamoxifen brought about a significant 47% reduction in ipsilateral invasive breast cancers and a 15% reduction in non-invasive breast cancers, compared with placebo. In trials performed by the Swedish Breast Cancer Co-operative Group and the NSABP, the optimal duration of adjuvant tamoxifen therapy appears to be 5 years, although this is equivocal and not yet conclusively defined. C1 Natl Surg Adjuvant Breast & Bowel Project, Operat Ctr, Pittsburgh, PA USA. RP Wickerham, L (reprint author), 4 Allegheny Ctr,E Commons Profess Bldg 5th Flo, Pittsburgh, PA 15212 USA. EM larry.wickerham@nsabp.org NR 18 TC 12 Z9 14 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD OCT PY 2002 VL 75 IS 1 SU S BP S7 EP S12 PG 6 WC Oncology SC Oncology GA 588XJ UT WOS:000177727200002 PM 12353826 ER PT J AU Melenhorst, JJ Eniafe, R Follmann, D Nakamura, R Kirby, M Barrett, AJ AF Melenhorst, JJ Eniafe, R Follmann, D Nakamura, R Kirby, M Barrett, AJ TI Molecular and flow cytometric characterization of the CD4 and CD8 T-cell repertoire in patients with myelodysplastic syndrome SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE MDS; TCRBV analysis; autoimmunity; CD57; clonal expansions ID BONE-MARROW TRANSPLANTATION; CHRONIC LYMPHOCYTIC-LEUKEMIA; V-SEGMENT FREQUENCIES; CHRONIC HIV-INFECTION; RECEPTOR REPERTOIRE; MULTIPLE-MYELOMA; IN-VIVO; ANTITHYMOCYTE GLOBULIN; MONOCLONAL GAMMOPATHY; CLONAL POPULATIONS AB We studied 18 patients with myelodysplastic syndrome (MDS), measuring clonality and T-cell receptor Vbeta (TCRBV) expression of CD4 and CD8 T cells by polymerase chain reaction and by flow cytometric analysis of TCRBV families. The CD4 and CD8 T-cell repertoire in most MDS patients is characterized by an abnormal TCRBV-restricted expansion of T cells in CD4 and CD8 cells, and increased expression of the CD8 effector marker CD57 of multiple TCRBV in CD8 cells. Clonality analysis of CD4 and CD8 cells showed that seven of 10 patients analysed had a major clone in the CD8 cells but not in CD4 cells. Furthermore, in one patient we found that both the CD57(-) and CD57(+) fraction contained the clone (which was absent from the TCRBV-negative fraction). These data suggest that, in MDS, multiple T-cell expansions can be found in both helper and cytotoxic T cells, and that, in the CD8 cells, T cells functionally differentiate in vivo from memory to effector T cells. Together, these data support the hypothesis of the involvement of T cells in the pathogenesis of MDS. C1 NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA. RP Melenhorst, JJ (reprint author), NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bldg 10,Room 7c103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 50 TC 35 Z9 36 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD OCT PY 2002 VL 119 IS 1 BP 97 EP 105 DI 10.1046/j.1365-2141.2002.03802.x PG 9 WC Hematology SC Hematology GA 599RB UT WOS:000178348000013 PM 12358908 ER PT J AU Mandelblatt, JS Kerner, JF Hadley, J Hwang, YT Eggert, L Johnson, LE Gold, K AF Mandelblatt, JS Kerner, JF Hadley, J Hwang, YT Eggert, L Johnson, LE Gold, K CA OPTIONS Res Team TI Variations in breast carcinoma treatment in older Medicare beneficiaries - Is it black and white? SO CANCER LA English DT Article DE breast carcinoma; elderly; race; Health Services Research; treatment ID CONSERVING SURGERY; RADIATION-THERAPY; CANCER PATIENTS; RACIAL-DIFFERENCES; CONSERVATION THERAPY; AFRICAN-AMERICAN; UNITED-STATES; FOLLOW-UP; STAGE-I; WOMEN AB BACKGROUND. To evaluate associations between race and breast carcinoma treatment. METHODS. Data from 984 black and 849 white Medicare beneficiaries 67 years or older with local breast carcinoma and a subset of 732 surviving women interviewed 3-4 years posttreatment were used to calculate adjusted odds of treatment, controlling for age, comorbidity, attitudes, region, and area measures of socioeconomic and health care resources. RESULTS. Sixty-seven percent of women received a mastectomy and 33% received breast-conserving surgery. The odds of radiation omission were 48 70 higher (95% confidence interval [CI] 1.01-2.19) for blacks than for whites after considering covariates, but the absolute number of women who failed to receive this modality was small (11%). In race-stratified models, the odds of having radiation omitted were significantly higher among blacks living greater distances from a cancer center (vs. lesser) or living in areas with high poverty (vs, low), but these factors did not affect radiation use among whites. Among those interviewed, blacks reported perceiving more ageism and racism in the health care system than whites (P = 0.001). The independent odds of receiving mastectomy (vs. breast conservation and radiation) were 2.72 times higher (95% CI 1.25-5.92) among women reporting the highest quartile of perceived ageism scores, compared with the lowest, and higher perceived ageism tended to be associated with higher odds of radiation omission (P = 0.06). CONCLUSIONS. Older black women with localized breast carcinoma tray have a different experience obtaining treatment than their white counterparts. The absolute number of women receiving nonstandard care was small and the effects were small to moderate. However, if these patterns persist, it will be important to evaluate whether such experiences contribute to within-stage race mortality disparities. C1 Georgetown Univ, Med Ctr, Dept Oncol, Lombardi Canc Ctr, Washington, DC 20007 USA. Georgetown Univ, Med Ctr, Dept Med, Lombardi Canc Ctr, Washington, DC 20007 USA. NCI, NIH, Washington, DC USA. Urban Inst, Washington, DC 20037 USA. Georgetown Univ, Med Ctr, Dept Stat & Biomath, Washington, DC 20007 USA. RP Mandelblatt, JS (reprint author), Georgetown Univ, Med Ctr, Dept Oncol, Lombardi Canc Ctr, 2233 Wisconsin Ave,Suite 317, Washington, DC 20007 USA. FU AHRQ HHS [R01 HS 08395]; NCI NIH HHS [R01 CA72908] NR 62 TC 91 Z9 91 U1 3 U2 4 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 1 PY 2002 VL 95 IS 7 BP 1401 EP 1414 DI 10.1002/cncr.10025 PG 14 WC Oncology SC Oncology GA 595VE UT WOS:000178128600002 PM 12237908 ER PT J AU Olson, JE Janney, CA Rao, RD Cerhan, JR Kurtin, PJ Schiff, D Kaplan, RS O'Neill, BP AF Olson, JE Janney, CA Rao, RD Cerhan, JR Kurtin, PJ Schiff, D Kaplan, RS O'Neill, BP TI The continuing increase in the incidence of primary central nervous system non-Hodgkin lymphoma - A surveillance, epidemiology, and end results analysis SO CANCER LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 12-15, 2001 CL SAN FRANCISCO, CALIFORNIA SP Amer Soc Clin Oncol DE primary central nervous system lymphoma (PCNSL); epidemiology; brain tumor; Surveillance, Epidemiology, and End Results (SEER) program; lymphoma ID HIGH-DOSE METHOTREXATE; PRIMARY CNS LYMPHOMA; BRAIN LYMPHOMA; SURVIVAL; GLIOMAS; TRENDS AB BACKGROUND. Primary central nervous system lymphoma (PCNSL) is an extranodal form of non-Hodgkin lymphoma arising in the craniospinal axis. The incidence of PCNSL appears to be increasing. METHODS. PCNSL incidence data from 1973-1997 were obtained from the nine Surveillance, Epidemiology and End Results (SEER) registries. To limit the influence of the human immunodeficiency virus on incidence rates, data of never-married males and females and persons of unknown marital status were excluded. As a surrogate for new technology, SEER data were reviewed by dates of diagnosis (surrogate for imaging) and compared with glioma incidence (surrogate for stereotactic neurosurgery and improved diagnostic neuropathology). Age-adjusted incidence rates were estimated and compared for the period prior to computed tomography (CT) (1973-1984) and the magnetic resonance imaging (MRI) period (1985-1997). The estimated annual percent change was calculated based on linear regression analyses using SEER*STAT. RESULTS. The incidence of PCNSL appears to be increasing in all SEER registries examined. All age groups demonstrated an increase over tune. This increase was observed both in the CT era as well as in the MRI era. PCNSL age-adjusted incidence (0.15 to 0.48, a 3-fold increase) outpaced that of systemic lymphoma (14.1 to 18.5, a 33% increase) for the same registries over the same time periods. The rate of increase has begun to slow since 1985; the estimated annual percent change for PCNSL was three-fold higher during the period 1973-1985 compared with 1986-1997. CONCLUSION. The incidence rate of PCNSL continues to rise. The increase is evident in all age groups and in both genders. Data from the current study suggest that improved diagnostic tools, such as CT or MRI, cannot explain this increase. C1 Mayo Clin & Mayo Fdn, Dept Neurol, Rochester, MN 55905 USA. Mayo Clin, Ctr Canc, Rochester, MN USA. Mayo Clin & Mayo Fdn, Dept Oncol, Rochester, MN 55905 USA. Univ Pittsburgh, Med Ctr, Dept Neurosurg, Pittsburgh, PA USA. Pittsburgh Canc Inst, Pittsburgh, PA 15213 USA. NCI, Off Trials Evaluat Program, Rockville, MD USA. Mayo Clin & Mayo Fdn, Dept Neurol, Rochester, MN 55905 USA. RP O'Neill, BP (reprint author), Mayo Clin & Mayo Fdn, Dept Neurol, 200 1St St SW, Rochester, MN 55905 USA. OI Cerhan, James/0000-0002-7482-178X FU NCI NIH HHS [K07 CA64220, P30 CA15030] NR 22 TC 148 Z9 173 U1 1 U2 4 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 1 PY 2002 VL 95 IS 7 BP 1504 EP 1510 DI 10.1002/cncr.10851 PG 7 WC Oncology SC Oncology GA 595VE UT WOS:000178128600013 PM 12237919 ER PT J AU Janne, PA Freidlin, B Saxman, S Johnson, DH Livingston, RB Shepherd, FA Johnson, BE AF Janne, PA Freidlin, B Saxman, S Johnson, DH Livingston, RB Shepherd, FA Johnson, BE TI Twenty-five years of clinical research for patients with limited-stage small cell lung carcinoma in North America - Meaningful improvements in survival SO CANCER LA English DT Article; Proceedings Paper CT 9th Meeting of the International-Association-for-the-Study-of-Lung-Cancer CY SEP 11-15, 2000 CL TOKYO, JAPAN SP Int Assoc Study Lung Canc DE lung neoplasm; small cell lung carcinoma; limited stage; randomized ID SOUTHWEST-ONCOLOGY-GROUP; PROPHYLACTIC CRANIAL IRRADIATION; PHASE-III TRIALS; LEUKEMIA GROUP-B; COMBINED MODALITY TREATMENT; ELECTIVE BRAIN IRRADIATION; CANCER-TREATMENT-GROUP; LONG-TERM SURVIVAL; RANDOMIZED TRIAL; COMBINATION CHEMOTHERAPY AB BACKGROUND. To determine the changes in clinical trials and outcomes of patients with limited-stage small cell lung carcinoma (SCLC) treated on Phase III randomized trials initiated in North America between 1972 and 1992. METHODS. Phase III trials from 1972 to 1992 for patients with limited-stage SCLC were identified. Patients with limited-stage SCLC treated during a similar time interval were also evaluated in the Surveillance, Epidemiology, and End Results (SEER) database. Trends were tested in the number of trials, in the number and gender of patients entered on trial, and in survival duration over time. RESULTS. Thirty trials involving 6564 patients were eligible for analyses. Nineteen trials (61%) involving 3626 patients were initiated within the first half of thus tune period (1972-1981). The median of median survival times of all patients treated on the control arms of the Phase III trials initiated between 1972 and 1981 and between 1982 and 1992 were 12.0 months (range, 10-16 months) and 17.0 months (range, 11-20 months), respectively (P < 0.001). Of 26 studies available for survival analysis, 5 (19%) showed a statistically significant survival prolongation in the experimental arm compared with the control arm with a median prolongation of 3.4 months (range, 1-5.2 months). All five evaluated some aspect of thoracic radiation therapy. Over a similar time period, there was a 6.4-month increase in the median survival of limited-stage SCLC patients listed in the SEER database (P < 0.0001) and a more than doubling of the 5-year survival from 5.2% to 12.1% (P = 0.0001). CONCLUSIONS. Analyses of the patients with limited-stage SCLC treated on Phase III trials in North America initiated between 1972 and 1992 and those listed in the SEER database show significant improvements in median survivals. Furthermore, the 5-year survival of patients with limited-stage SCLC listed in the SEER database has more than doubled over the last 25 years. Further research will be needed to determine the relative contribution of improved therapy, supportive care, and stage migration to this prolongation in survival. C1 Brigham & Womens Hosp, Dept Med, Dana Farber Canc Inst, Dept Adult Oncol,Lowe Ctr Thorac Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. NIH, Biometr Res Branch, Bethesda, MD 20892 USA. NCI, Clin Invest Branch, Bethesda, MD 20892 USA. Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA. Univ Washington, Seattle, WA 98195 USA. Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada. RP Johnson, BE (reprint author), Dana Farber Canc Inst, Lowe Ctr Thorac Oncol, D1234,44 Binney St, Boston, MA 02115 USA. RI Johnson, David/A-7437-2009 NR 70 TC 85 Z9 94 U1 0 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD OCT 1 PY 2002 VL 95 IS 7 BP 1528 EP 1538 DI 10.1002/cncr.10841 PG 11 WC Oncology SC Oncology GA 595VE UT WOS:000178128600016 PM 12237922 ER PT J AU Hill, DA Preston-Martin, S Ross, RK Bernstein, L AF Hill, DA Preston-Martin, S Ross, RK Bernstein, L TI Medical radiation, family history of cancer, and benign breast disease in relation to breast cancer risk in young women, USA SO CANCER CAUSES & CONTROL LA English DT Article DE breast diseases; breast neoplasms; genetic predisposition to disease; radiography ID ATOMIC-BOMB SURVIVORS; CASE-CONTROL INTERVIEW; X-RAYS; INFANCY; BRCA1; RADIOTHERAPY; IRRADIATION; MUTATIONS AB Objective: In previous studies breast cancer risk has been increased among women who received high doses (above 100-200 cGy) of ionizing radiation or those exposed to lower doses prior to age 20. Some evidence suggests that such risk may be distinctly elevated among women with a family history of breast or ovarian cancer (probably only carriers of specific gene mutations) and women with benign breast disease (BBD). Methods: A population-based case-control study in Los Angeles County obtained interview data from 744 women who were aged 40 or younger and diagnosed with breast cancer during 1983-1988, and from 744 matched controls. Women with a positive family history of breast or ovarian cancer reported cancer in a mother, sister, or grandmother. Women with BBD reported a physician diagnosis. Radiation exposure was defined as a history of either radiation therapy or moderate exposure to medical radiography. Results: Breast cancer risk was elevated among women exposed to medical radiation prior to age 20 years (odds ratio (OR) = 1.4, 95% confidence interval (CI) = 1.2-1.8), relative to unexposed women. This increased risk was observed only among women with a history of BBD (OR = 2.4, 95% CI = 1.6-3.7). Overall, risk was not associated with exposure to medical radiation after age 20 years, although among women with a positive family history of breast or ovarian cancer, exposed women had an increased risk (OR = 1.8, 95% CI = 1.0-3.1). Breast cancer risk was not increased among women with a family history of breast/ovarian cancer exposed to medical radiation before age 20 years or those with BBD exposed to medical radiation after age 20 years. Discussion: Study participants may have received radiation doses that are no longer common, hampering study generalizability. Although differences in recall between cases and controls cannot be completely excluded, women with BBD or a family history of breast cancer appear to have greater breast cancer risk following relatively low ionizing radiation exposure than other women in this study. C1 Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA. Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA. RP Hill, DA (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC 7238, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA17054, CA44546] NR 30 TC 25 Z9 25 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD OCT PY 2002 VL 13 IS 8 BP 711 EP 718 DI 10.1023/A:1020201106117 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 594RC UT WOS:000178063700003 PM 12420949 ER PT J AU Palmer, JR Hatch, EE Rosenberg, CL Hartge, P Kaufman, RH Titus-Ernstoff, L Noller, KL Herbst, AL Rao, RS Troisi, R Colton, T Hoover, RN AF Palmer, JR Hatch, EE Rosenberg, CL Hartge, P Kaufman, RH Titus-Ernstoff, L Noller, KL Herbst, AL Rao, RS Troisi, R Colton, T Hoover, RN TI Risk of breast cancer in women exposed to diethylstilbestrol in utero: preliminary results (United States) SO CANCER CAUSES & CONTROL LA English DT Article DE breast carcinoma; diethylstilbestrol; hormones; prenatal factors ID YOUNG-WOMEN; IN-UTERO; MOTHERS; BIRTH; PREGNANCY AB Background: A synthetic estrogen, diethylstilbestrol (DES), was widely prescribed to pregnant women during the 1950s and 1960s but was later discovered to be associated with an increased risk of clear-cell carcinoma of the vagina and cervix in female offspring. DES has not been linked to other cancers in female offspring, but studies of other prenatal factors such as twin gestation and pre-eclampsia have indicated that in-utero estrogen levels may influence breast cancer risk. We evaluated the relation of in-utero DES exposure to the risk of adult breast cancer. Methods: A cohort of 4821 exposed women and 2095 unexposed women, most of whom were first identified in the mid-1970s, were followed by mailed questionnaires for an average of 19 years. Reported cancer outcomes were validated by medical record review. Breast cancer incidence in DES-exposed daughters was compared with cancer incidence in unexposed daughters with use of Poisson regression analysis, adjusting for year of birth, age at menarche, age at first birth, and number of births. Findings: The rate ratio for incidence of invasive breast cancer in exposed versus unexposed women was 1.4 (95% confidence interval (CI) = 0.7-2.6). DES exposure was not associated with an increased risk of breast cancer in women under 40 years, but among women aged 40 and older the rate ratio was 2.5 (95% CI = 1.0-6.3). The rate ratio for the association of DES exposure with estrogen receptor-positive tumors was 1.9 (95% CI = 0.8-4.5). Interpretation: While not statistically significant, the overall 40% excess risk, arising exclusively from the subset of estrogen receptor-positive cases, raises a concern calling for continued investigation. C1 Boston Univ, Sch Med, Slone Epidemiol Unit, Boston, MA 02215 USA. Boston Univ, Sch Med, Sect Hematol & Oncol, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Boston, MA USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Baylor Coll Med, Dept Obstet & Gynecol, Houston, TX 77030 USA. Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Lebanon, NH 03766 USA. Tufts Univ New England Med Ctr, Dept Obstet & Gynecol, Boston, MA 02111 USA. Univ Chicago, Dept Obstet & Gynecol, Chicago, IL 60637 USA. RP Palmer, JR (reprint author), Boston Univ, Sch Med, Slone Epidemiol Unit, 1010 Commonwealth Ave, Boston, MA 02215 USA. FU NCI NIH HHS [N01-CP-21168, N01-CP-51017] NR 27 TC 93 Z9 95 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD OCT PY 2002 VL 13 IS 8 BP 753 EP 758 DI 10.1023/A:1020254711222 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 594RC UT WOS:000178063700008 PM 12420954 ER PT J AU Bosetti, C Negri, E Kolonel, L Ron, E Franceschi, S Preston-Martin, S McTiernan, A Dal Maso, L Mark, SD Mabuchi, K Land, C Jin, F Wingren, G Galanti, MR Hallquist, A Glattre, E Lund, E Levi, F Linos, D La Vecchia, C AF Bosetti, C Negri, E Kolonel, L Ron, E Franceschi, S Preston-Martin, S McTiernan, A Dal Maso, L Mark, SD Mabuchi, K Land, C Jin, F Wingren, G Galanti, MR Hallquist, A Glattre, E Lund, E Levi, F Linos, D La Vecchia, C TI A pooled analysis of case-control studies of thyroid cancer. VII. Cruciferous and other vegetables (International) SO CANCER CAUSES & CONTROL LA English DT Article DE case-control studies; diet; meta-analysis; pooled analysis; thyroid cancer; vegetables ID HISTORY; WOMEN; RISK; DISEASE; CONSUMPTION; PAPILLARY; HAWAII; FRUIT; DIET AB Objective: To investigate the association between cruciferous and other vegetables and thyroid cancer risk we systematically reanalyzed the original data from 11 case-control studies conducted in the US, Asia, and Europe. Methods: A total of 2241 cases (1784 women, 457 men) and 3716 controls (2744 women, 972 men) were included. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated for each study by logistic regression models, conditioned on age and sex, and adjusted for history of goiter, thyroid nodules or adenomas, and radiation. Summary ORs for all studies combined were computed as the weighted average of the estimates from each study. Results: A decreased risk for the highest level of cruciferous vegetable intake, as compared to the lowest, was observed in Los Angeles, Hawaii, Connecticut, southeastern Sweden, Tromso, and Switzerland; the OR were above unity in Japan and Uppsala, whereas no material association was found in northern Sweden, Italy, or Greece. The OR values for all studies combined were 0.87 (95% CI 0.75-1.01) for moderate and 0.94 (95% CI 0.80-1.10) for high cruciferous vegetables intake. The results were similar in studies from iodine-rich areas and endemic goiter areas, and were consistent when the analysis was restricted to papillary carcinomas and women. The summary OR values for vegetables other than cruciferous were 1.04 (0.88-1.22) for moderate and 0.82 (0.69-0.98) for high consumption. Conclusions: This combined analysis indicates that cruciferous vegetables are not positively related to thyroid cancer risk. Their effect does not seem to be substantially different from that of other vegetables, which appear to be protective on this cancer. C1 Mario Negri Inst Pharmacol Res, Lab Gen Epidemiol, I-20157 Milan, Italy. Univ Hawaii Manoa, Canc Res Ctr Hawaii, Honolulu, HI 96813 USA. NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA. Int Agcy Res Canc, Field & Intervent Studies Unit, F-693702 Lyon 08, France. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. Ctr Riferimento Oncol, I-33081 Aviano, PN, Italy. Radiat Effects Res Fdn, Hiroshima 732, Japan. Shanghai Canc Inst, Shanghai, Peoples R China. Linkoping Univ, Fac Hlth Sci, Dept Hlth & Environm, Div Environm & Occupat Med, SE-58185 Linkoping, Sweden. Univ Hosp, Dept Canc Epidemiol, SE-57185 Uppsala, Sweden. Karolinska Inst, Dept Oncol, SE-11235 Stockholm, Sweden. Stockholms Sjukhem, SE-11235 Stockholm, Sweden. Canc Registry Norway, NO-3010 Oslo, Norway. Inst Univ Med Sociale & Prevent, Registre Vaudois Tumeurs, CH-1011 Lausanne, Switzerland. Inst Prevent Med, GR-14561 Kifisia, Greece. Univ Milan, Ist Stat Med & Biometria, I-20133 Milan, Italy. Univ Tromso, Inst Community Med, NO-9037 Tromso, Norway. RP Negri, E (reprint author), Mario Negri Inst Pharmacol Res, Lab Gen Epidemiol, Via Eritrea 62, I-20157 Milan, Italy. RI Negri, Eva/B-7244-2013; OI Negri, Eva/0000-0001-9712-8526; La Vecchia, Carlo/0000-0003-1441-897X NR 36 TC 32 Z9 34 U1 2 U2 7 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD OCT PY 2002 VL 13 IS 8 BP 765 EP 775 DI 10.1023/A:1020243527152 PG 11 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 594RC UT WOS:000178063700010 PM 12420956 ER PT J AU Smith-Warner, SA Ritz, J Hunter, DJ Albanes, D Beeson, WL van den Brandt, PA Colditz, G Folsom, AR Fraser, GE Freudenheim, JL Giovannucci, E Goldbohm, RA Graham, S Kushi, LH Miller, AB Rohan, TE Speizer, FE Virtamo, J Willett, WC AF Smith-Warner, SA Ritz, J Hunter, DJ Albanes, D Beeson, WL van den Brandt, PA Colditz, G Folsom, AR Fraser, GE Freudenheim, JL Giovannucci, E Goldbohm, RA Graham, S Kushi, LH Miller, AB Rohan, TE Speizer, FE Virtamo, J Willett, WC TI Dietary fat and risk of lung cancer in a pooled analysis of prospective studies SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID POSTMENOPAUSAL BREAST-CANCER; FOOD FREQUENCY QUESTIONNAIRE; IOWA-WOMENS-HEALTH; YORK-STATE COHORT; UNITED-STATES; ALCOHOL-CONSUMPTION; CIGARETTE-SMOKING; NUTRIENT INTAKE; CHOLESTEROL; REPRODUCIBILITY AB Lung cancer rates are highest in countries with the greatest fat intakes. In several case-control studies, positive associations have been observed between lung cancer and intakes of total and saturated fat, particularly among nonsmokers. We analyzed the association between fat and cholesterol intakes and lung cancer risk in eight prospective cohort studies that met predefined criteria. Among the 280,419 female and 149,862 male participants who were followed for up to 6-16 years, 3,188 lung cancer cases were documented. Using the Cox proportional hazards model, we calculated study-specific relative risks that were adjusted for smoking history and other potential risk factors. Pooled relative risks were computed using a random effects model. Fat intake was not associated with lung cancer risk. For an increment of 5% of energy from fat, the pooled multivariate relative risks were 1.01 [95% confidence interval (CI), 0.98-1.05] for total, 1.03 (95% CI, 0.96-1.11) for saturated, 1.01 (95% CI, 0.93-1.10) for monounsaturated, and 0.99 (95% CI, 0.90-1.10) for polyunsaturated fat. No associations were observed between intakes of total or specific types of fat and lung cancer risk among never, past, or current smokers. Dietary cholesterol was not associated with lung cancer incidence [for a 100-mg/day increment, the pooled multivariate relative risk was 1.01 (95% CI, 0.97-1.05)]. There was no statistically significant heterogeneity among studies or by sex. These data do not support an important relation between fat or cholesterol intakes and lung cancer risk. The means to prevent this important disease remains avoidance of smoking. C1 Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Ctr Canc Prevent, Boston, MA 02115 USA. NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA 92350 USA. Univ Limburg, Dept Epidemiol, NL-6200 MD Maastricht, Netherlands. Univ Minnesota, Div Epidemiol, Sch Publ Hlth, Minneapolis, MN 55454 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14214 USA. TNO, Nutr & Food Res Inst, Dept Epidemiol, NL-3700 AJ Zeist, Netherlands. Kaiser Permanente, Div Res, Oakland, CA 94612 USA. Deutsch Krebsforschungszentrum, Div Clin Epidemiol, D-69120 Heidelberg, Germany. Yeshiva Univ Albert Einstein Coll Med, Dept Epidemiol & Social Med, Bronx, NY 10461 USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, FIN-00300 Helsinki, Finland. RP Smith-Warner, SA (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA. RI Albanes, Demetrius/B-9749-2015; Colditz, Graham/A-3963-2009; OI Colditz, Graham/0000-0002-7307-0291; Kushi, Lawrence/0000-0001-9136-1175 FU NCI NIH HHS [CA55075, CA78548] NR 59 TC 33 Z9 36 U1 1 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 987 EP 992 PN 1 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RD UT WOS:000178634100005 PM 12376497 ER PT J AU Stern, MC Johnson, LR Bell, DA Taylor, JA AF Stern, MC Johnson, LR Bell, DA Taylor, JA TI XPD codon 751 polymorphism, metabolism genes, smoking, and bladder cancer risk SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID DNA-REPAIR GENES; BASAL-CELL CARCINOMA; XERODERMA-PIGMENTOSUM; LUNG-CANCER; ACETYLATION POLYMORPHISMS; ENVIRONMENT INTERACTION; EXPOSURE; ERCC2; XRCC1; MUTATIONS AB Cigarette smoking is the main risk factor for bladder cancer, accounting for at least 50% of bladder cancer in men. Cigarette smoke is a rich source of arylamines, which are detoxified by the NAT2 enzyme and activated by the NAT1 enzyme to highly reactive species that can form bulky adducts on DNA. DNA damage from such adducts is mainly repaired by the nucleotide excision repair pathway, in which the XPD protein functions in opening the DNA helix. We hypothesized that an XPD codon 751 polymorphism (Lys-to-Gln amino acid change) could affect the repair of smoking-induced DNA damage and could be associated with bladder-cancer risk. We also hypothesized that allelic variants of the NAT1 and NAT2 genes might modify the effect of the XPD codon 751 polymorphism on smoking-associated bladder-cancer risk. We determined the XPD codon 751 genotype for 228 bladder-cancer cases and 210 controls who were frequency-matched to cases by age, sex, and ethnicity, and we used our previously published data on the NAT1 and NAT2 genotypes for these same individuals (J. A. Taylor et al., Cancer Res., 58: 3603-3610, 1998). We found a slight decrease in risk for the XPD codon 751 Gln/Gln genotype (adjusted odds ratio: 0.8; 95% confidence interval: 0.4-1.3) compared with subjects with the Lys/Lys or Lys/Gln genotypes. The analysis with smoking showed that smokers with the Lys/Lys or Lys/Gln genotypes were twice as likely to have bladder cancer than smokers with the Gln/Gln genotype (test of interaction P = 0.03). The combined presence of the NAT1/NAT2 high-risk genotype and the XPD Lys/Lys or Lys/Gln genotypes ignoring smoking had an odds ratio that was only slightly higher than expected, assuming no genotype-genotype interaction (P = 0.52). We found little evidence for a gene-gene-exposure, three-way interaction among the XPD codon 751 genotype, smoking, and the NAT1/NAT2 genotype. C1 NIEHS, Mol & Genet Epidemiol Sect, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Environm Genom Sect, Lab Computat Biol & Risk Anal, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA. RP Taylor, JA (reprint author), NIEHS, Mol & Genet Epidemiol Sect, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 41 TC 75 Z9 82 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1004 EP 1011 PN 1 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RD UT WOS:000178634100008 PM 12376500 ER PT J AU Groves, FD Perez-Perez, G Zhang, L You, WC Lipsitz, SR Gail, MH Fraumeni, JF Blaser, MJ AF Groves, FD Perez-Perez, G Zhang, L You, WC Lipsitz, SR Gail, MH Fraumeni, JF Blaser, MJ TI Serum antibodies to Helicobacter pylori and the CagA antigen do not explain differences in the prevalence of precancerous gastric lesions in two chinese Populations with contrasting gastric cancer rates SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID HIGH-RISK; POSITIVE STRAINS; 2 COUNTIES; INFECTION; STOMACH AB Incidence and mortality rates for gastric cancer in rural People's Republic of China differ greatly over short distances. In Shandong Province, we studied asymptomatic adult subjects from Bei Duan village (n = 196) in Linqu County (a high-risk area for gastric cancer) and from Shi Huang village (n = 192) in Cangshan County (a low-risk area for gastric cancer). The prevalence of advanced precancerous gastric lesions (APGL) was assessed by microscopic examination of endoscopic stomach biopsies. ELISAs were used to detect serum IgG to Helicobacter pylori whole-cell antigen and to the CagA protein. A logistic regression model was used to quantify the role of the two H. pylori seromarkers in explaining the differences in prevalence of APGL between the two villages after adjusting for age and sex. The prevalence of APGL was much greater in Bei Duan than in Shi Huang. Although H. pylori seroprevalence by the whole-cell ELISA was similar in the two populations, seroprevalence of CagA was significantly greater in Bei Duan. Although age, sex, and both H. pylori seromarkers were associated with APGL in the logistic regression model, the effect of village of residence remained strong after adjustment for all four covariates. Only a relatively small proportion of the difference in prevalence of APGL between these two rural Chinese populations can be explained by differences in H. pylori or CagA seroprevalence. C1 Med Univ S Carolina, Dept Biometry & Epidemiol, Charleston, SC 29425 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NYU, Sch Med, Dept Internal Med, New York, NY 10016 USA. Peking Univ, Beijing Inst Canc Res, Beijing 100034, Peoples R China. Peking Univ, Sch Oncol, Beijing 100034, Peoples R China. Vet Adm Med Ctr, New York, NY 10010 USA. RP Groves, FD (reprint author), Med Univ S Carolina, Dept Biometry & Epidemiol, 135 Cannon St,Room 302-H, Charleston, SC 29425 USA. FU NCI NIH HHS [N01-CP-33041]; NIDDK NIH HHS [R01-DK-53707] NR 25 TC 11 Z9 13 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1091 EP 1094 PN 1 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RD UT WOS:000178634100020 PM 12376512 ER PT J AU Limburg, PJ Stolzenberg-Solomon, RZ Colbert, LH Perez-Perez, GI Blaser, MJ Taylor, PR Virtamo, J Albanes, D AF Limburg, PJ Stolzenberg-Solomon, RZ Colbert, LH Perez-Perez, GI Blaser, MJ Taylor, PR Virtamo, J Albanes, D TI Helicobacter pylori seropositivity and colorectal cancer risk: A prospective study of male smokers SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID GASTRIN-CONCENTRATIONS; COLONIC ADENOMAS; INFECTION; ADENOCARCINOMA; SEROPREVALENCE; ANTIBODIES; NEOPLASIA; STRAINS; CAGA AB Because Helicobacter pylori colonization can produce systemic as well as local effects, it may be associated with carcinogenesis in extra gastric target organs. The currently available data regarding a possible link between H. pylori seropositivity and colorectal cancer risk are limited and inconclusive. In this prospective case-control study nested within the Alpha-Tocopherol, Beta-Carotene Study cohort of Finnish male smokers aged 50-69 years, we examined the association between H. pylori seropositivity and incident colorectal adenocarcinoma. Separate risk estimates were derived by colorectal cancer anatomical subsite and by H. pylori CagA seropositivity status. Demographic, dietary, and lifestyle variables were accounted for in the data analyses using information obtained from a prerandomization questionnaire and physical examination. Baseline serum samples from 118 cases and 236 matched controls were assayed for both H. pylori whole cell and H. pylori CagA antibodies. In total, 258 (73%) and 212 (60%) subjects expressed whole cell and CagA antibodies, respectively. H. pylori seropositivity, defined as one or both antibody assays positive, was present in 273 (77%) subjects. None of the seropositivity results were statistically different between cases and controls. Multivariate odds ratio ( 5 confidence interval) estimates for whole cell, cagA, and H. pylori seropositivity were 1.05 (0.63-1.74), 1.17 (0.74-1.84), and 0.91 (0.53-1.55), respectively. Stratification by colorectal cancer subsite yielded similarly unremarkable results. On the basis of these data, H. pylori carriage does not appear to be an important risk factor for colorectal adenocarcinoma. C1 Mayo Clin & Mayo Fdn, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NCI, Div Clin Sci, Bethesda, MD 20892 USA. NYU, Sch Med, Dept Med, New York, NY 10016 USA. Vet Affairs Med Ctr, New York, NY 10016 USA. Natl Publ Hlth Inst, SF-00300 Helsinki, Finland. RP Limburg, PJ (reprint author), Mayo Clin & Mayo Fdn, Div Gastroenterol & Hepatol, 200 1st St SW, Rochester, MN 55905 USA. RI Albanes, Demetrius/B-9749-2015 FU NCI NIH HHS [N01-CN-45035, N01-CN-45165]; NIDDK NIH HHS [R01-DK-53707] NR 25 TC 41 Z9 47 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1095 EP 1099 PN 1 PG 5 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RD UT WOS:000178634100021 PM 12376513 ER PT J AU Terry, MB Gammon, MD Schoenberg, JB Brinton, LA Arber, N Hanina, H AF Terry, MB Gammon, MD Schoenberg, JB Brinton, LA Arber, N Hanina, H TI Oral contraceptive use and cyclin D1 overexpression in breast cancer among young women SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID RISK-FACTORS; GENE-EXPRESSION; PROGRESSION; ESTROGEN; CARCINOMA; CELLS; PHOSPHORYLATION; ADENOCARCINOMAS AB Cyclin D1, an important cell cycle regulator, is overexpressed in several human cancers including breast. Both estrogens and progestins activate the transcription of the gene; antiestrogens have been shown to reduce cyclin D1 protein levels. Cyclin D1 protein overexpression has been strongly associated with well-differentiated, estrogen receptor-positive tumors. Little is known, however, as to whether epidemiological risk factors are related to this molecularly defined subset of tumors. Using a population-based study of young women <45 years in New Jersey, we analyzed whether oral contraceptives (OCs) and other risk factors were associated with the overexpression of cyclin D1 in breast cancer tissue. We measured cyclin D1 status in paraffin-embedded, archived tissue from 78.8% of the breast cancer cases using immunohistochemistry. Cyclin D1 was overexpressed in 33.7% of the cases (123 of 365). We used unordered polytomous logistic regression to estimate the odds ratios (ORs) for two case groups-(a) breast cancer with cyclin D1 overexpression (n = 123) and (b) breast cancer without overexpression (n = 242)-compared with 462 population-based controls. The multivariate-adjusted OR for ever use of OCs was 1.6 [95% confidence interval (CI), 1.0-2.5] for cases that overexpressed cyclin D1 and 1.0 (95% CI, 0.7-1.5) for those with no overexpression. Among women who started using OCs at least 20 years before the reference date, the OR was increased 2-fold for breast cancer with cyclin D1 overexpression (OR, 2.2; 95% CI, 1.2-4.0) but not for breast cancer without cyclin D1 overexpression (OR, 1.1; 95% Cl, 0.7-1.8). If replicated, these findings suggest that early OC use may be associated with the subset of mammary tumors that overexpress cyclin D1. C1 Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY 10032 USA. Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA. Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA. New Jersey State Dept Hlth & Senior Serv, Canc Epidemiol Serv, Trenton, NJ 08625 USA. NCI, Environm Epidemiol Branch, Bethesda, MD 20892 USA. Tel Aviv Sourasky Med Ctr, Dept Gastroenterol, IL-55454 Tel Aviv, Israel. RP Terry, MB (reprint author), Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, 600 W 168th St,PH 18-102, New York, NY 10032 USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 31 TC 16 Z9 17 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1100 EP 1103 PN 1 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RD UT WOS:000178634100022 PM 12376514 ER PT J AU Cracchiolo, BM Heller, DS Wolff, EC Hameed, M Clement, PMJ Park, MH Hanauske-Abel, HM AF Cracchiolo, BM Heller, DS Wolff, EC Hameed, M Clement, PMJ Park, MH Hanauske-Abel, HM TI Eukaryotic translation initiation factor 5A, an emerging target for cytostatic compounds, localizes to proliferative regions in human tissue. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A101 BP 1145S EP 1145S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200001 ER PT J AU Zecevic, M Stancel, GM Barrett, CJ AF Zecevic, M Stancel, GM Barrett, CJ TI Elucidating the mechanism of estrogen and insulin-like growth factor-1 (IGF-1) cross-talk in uterine cancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Univ Texas, Houston, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A117 BP 1148S EP 1148S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200018 ER PT J AU Wang, Y Zhang, ZQ Kastens, E Luber, RA You, M AF Wang, Y Zhang, ZQ Kastens, E Luber, RA You, M TI Chemopreventive effect of budesonide on chemically induced lung tumorigenesis in A/J mice bearing a mutation in the p53 gene and a deletion of the Ink4a/Arf gene. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Ohio State Univ, Ctr Canc, Columbus, OH 43210 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A203 BP 1153S EP 1153S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200043 ER PT J AU Hursting, SD Perkins, SN Colbert, LH Berrigan, DA Davis, BJ Fuchs-Young, R Donehower, LA Barrett, JC AF Hursting, SD Perkins, SN Colbert, LH Berrigan, DA Davis, BJ Fuchs-Young, R Donehower, LA Barrett, JC TI Effects of energy balance modulation on spontaneous mammary tumorigenesis in p53-deficient, Wnt-1 transgenic mice. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NIEHS, Res Triangle Pk, NC 27709 USA. MD Anderson Canc Ctr, Smithville, TX USA. Baylor Coll Med, Houston, TX 77030 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A205 BP 1154S EP 1154S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200045 ER PT J AU Kavanaugh, CJ Calvo, A Shibata, MA Brown, P Lubet, R Green, JE AF Kavanaugh, CJ Calvo, A Shibata, MA Brown, P Lubet, R Green, JE TI Application of the C3(1)SV40-Tag mouse mammary cancer model to chemoprevention research. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Osaka Med Coll, Osaka, Japan. Baylor Coll Med, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A207 BP 1154S EP 1154S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200047 ER PT J AU Yang, K Fan, KH Shinozaki, H Yang, WC Kurihara, N Newmark, H Steele, V Kopelovich, L Edelmann, W Kucherlapati, R Augenlicht, L Lipkin, M AF Yang, K Fan, KH Shinozaki, H Yang, WC Kurihara, N Newmark, H Steele, V Kopelovich, L Edelmann, W Kucherlapati, R Augenlicht, L Lipkin, M TI Increasing dietary calcium and vitamin D in mouse models of intestinal tumorigenesis. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Strang Canc Prevent Ctr, New York, NY USA. Albert Einstein Canc Ctr, Bronx, NY USA. Rutgers State Univ, Piscataway, NJ USA. NCI, Div Canc Prevent, Bethesda, MD 20892 USA. Harvard Med Sch, Boston, MA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A214 BP 1155S EP 1156S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200054 ER PT J AU Herbert, BS Perou, CM Wright, WE Kopelovich, L Shay, JW AF Herbert, BS Perou, CM Wright, WE Kopelovich, L Shay, JW TI Effects of chemopreventive agents on the spontaneous immortalization of breast epithelial cells from individuals predisposed to breast cancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Texas, SW Med Ctr Dallas, Dallas, TX 75235 USA. Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA. NCI, DCP, CADRG, Bethesda, MD 20892 USA. RI Shay, Jerry/F-7878-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A220 BP 1157S EP 1157S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200060 ER PT J AU Loaiza-Perez, AI Kenney, S Hose, C Hollingshead, M Alley, M Ciolino, H Yeh, G Linehan, M Vistica, D Sausville, E AF Loaiza-Perez, AI Kenney, S Hose, C Hollingshead, M Alley, M Ciolino, H Yeh, G Linehan, M Vistica, D Sausville, E TI CYP1A1 and CYP1B1 induction and high covalent binding of metabolites are markers to predict sensitivity to aminoflavone in breast and renal cancer cells. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A224 BP 1158S EP 1158S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200064 ER PT J AU Eng-Wong, J Venzon, D Schmidt, B Perkins, SN Hursting, SD Zujewski, JA AF Eng-Wong, J Venzon, D Schmidt, B Perkins, SN Hursting, SD Zujewski, JA TI The effect of raloxifene on insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3) in premenopausal women at high risk for developing breast cancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A317 BP 1162S EP 1162S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200081 ER PT J AU Seminara, D Beck, JC Hopper, JL John, EM Knight, JA Neuhausen, SL Senie, RT Andrulis, I Anton-Culver, H Buys, S West, D Whittemore, A Daly, MB AF Seminara, D Beck, JC Hopper, JL John, EM Knight, JA Neuhausen, SL Senie, RT Andrulis, I Anton-Culver, H Buys, S West, D Whittemore, A Daly, MB TI The Breast Cancer Family Registry: 1997-2002. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Coriell Inst Med Res, Camden, NJ USA. Univ Melbourne, Melbourne, Vic, Australia. No Calif Canc Ctr, Union City, CA USA. CancCare Ontario, Toronto, ON, Canada. Univ Utah, Salt Lake City, UT USA. Columbia Univ, New York, NY USA. Univ Calif Irvine, Irvine, CA USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NCI, EGRP, DCCPS, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A326 BP 1164S EP 1164S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200090 ER PT J AU Kidd, LCR Paltoo, D Wang, SP Chen, WD Kittles, R AF Kidd, LCR Paltoo, D Wang, SP Chen, WD Kittles, R TI Prevalence of vitamin D receptor (VDR) promoter SNP and its influence on prostate cancer risk. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Canc Prevent Studies Branch, CCR, Bethesda, MD 20892 USA. Howard Univ, Ctr Canc, Natl Human Genome Ctr, Washington, DC 20059 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA A331 BP 1166S EP 1166S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200095 ER PT J AU Moslehi, R Kariminejad, MH Ghaffari, V Narod, S AF Moslehi, R Kariminejad, MH Ghaffari, V Narod, S TI A novel BRCA1 mutation in an Iranian family with hereditary breast and ovarian cancer syndrome. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT 1st Annual Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MA SP Amer Assoc Canc Res C1 NCI, NIH, Rockville, MD USA. Univ Tehran, Tehran, Iran. Womens Coll Hosp, Toronto, ON M5S 1B2, Canada. NR 0 TC 0 Z9 0 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 OCT PY 2002 VL 11 IS 10 MA A332 BP 1166S EP 1166S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200096 ER PT J AU Kelley, MJ Folz, RJ Glaser, EM Herndon, JE Crowell, JA Perloff, M Ferdman, E Gallot, L Becker, R Bergan, RC AF Kelley, MJ Folz, RJ Glaser, EM Herndon, JE Crowell, JA Perloff, M Ferdman, E Gallot, L Becker, R Bergan, RC TI Randomized controlled clinical trial of weekly oltipraz in smokers. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Duke Univ, Med Ctr, Thorac Oncol Program, Durham, NC USA. NCI, DCP, Rockville, MD USA. Northwestern Univ, Dept Med, Div Hematol Oncol, Chicago, IL 60611 USA. Northwestern Univ, Robert H Lurie Canc Ctr, Chicago, IL 60611 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B106 BP 1169S EP 1169S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200108 ER PT J AU Bosland, MC Johnson, WD Luber, RA Steele, VE McCormick, DL AF Bosland, MC Johnson, WD Luber, RA Steele, VE McCormick, DL TI Efficacy testing of chemoprevention agents in the MNU plus testosterone WU rat prostate carcinogenesis model SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NYU, Sch Med, New York, NY USA. IIT, Res Inst, Chicago, IL 60616 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B111 BP 1170S EP 1171S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200113 ER PT J AU Hakim, IA Harris, RB Brown, S Ali, I AF Hakim, IA Harris, RB Brown, S Ali, I TI Effect of a 4-month tea intervention on oxidative DNA damage among heavy smokers. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Arizona, Tucson, AZ USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B125 BP 1174S EP 1174S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200127 ER PT J AU Lawrence, D Shavers, VL Fagan, P AF Lawrence, D Shavers, VL Fagan, P TI Cigarette smoking prevalence among US employment and occupational groups: The Current Population Survey (CPS), 1998-1999. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 2 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B127 BP 1174S EP 1174S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200129 ER PT J AU Hsieh, G Lawrence, D Wewers, ME Hartman, AM AF Hsieh, G Lawrence, D Wewers, ME Hartman, AM TI Prevalence of non-cigarette tobacco product use among adults between 1992-2000. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Rockville, MD USA. Ohio State Univ, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B129 BP 1175S EP 1175S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200131 ER PT J AU Schulte, PA Ward, E Toraason, M Blair, A Brandt-Rauf, P Melnick, R Rothman, N Tennant, R Weston, A Mirer, F Bonassi, S AF Schulte, PA Ward, E Toraason, M Blair, A Brandt-Rauf, P Melnick, R Rothman, N Tennant, R Weston, A Mirer, F Bonassi, S TI Criteria for utilizing high output technologies for occupational cancer research and prevention. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NIOSH, Cincinnati, OH 45226 USA. NCI, Rockville, MD USA. Columbia Univ, New York, NY USA. NIEHS, Res Triangle Pk, NC 27709 USA. NIH, Rockville, MD USA. NIOSH, Morgantown, WV USA. United Auto Workers Union, Detroit, MI USA. Natl Inst Canc Res, Genoa, Italy. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B136 BP 1176S EP 1176S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200138 ER PT J AU Dhar, A Keefer, LK Colburn, NH AF Dhar, A Keefer, LK Colburn, NH TI Nitric oxide prevents tumor promotion and suppresses tumor phenotype. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Frederick, MD 21701 USA. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B207 BP 1179S EP 1179S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200149 ER PT J AU Athar, M Tang, XW Kim, AL Kopelovich, L Epstein, EH Bickers, DR AF Athar, M Tang, XW Kim, AL Kopelovich, L Epstein, EH Bickers, DR TI Cyclopamine as a specific inhibitor of hedgehog signaling and a novel inhibitor of basal cell carcinomas (BCCs) in ptch +/- knockout heterozygous mice. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Columbia Univ, New York, NY USA. NCI, Div Canc Chemoprevent, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B213 BP 1180S EP 1181S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200155 ER PT J AU Hebert, J Athar, M Aszterbaum, M Kopelovich, L Bickers, DR Epstein, EH AF Hebert, J Athar, M Aszterbaum, M Kopelovich, L Bickers, DR Epstein, EH TI Tazarotene chemoprevention of UV-induced basal cell carcinomas in the ptc1+/- mouse. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Calif San Francisco, Sch Med, San Francisco, CA USA. Columbia Univ Coll Phys & Surg, New York, NY 10032 USA. NCI, DCP, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B217 BP 1181S EP 1182S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200159 ER PT J AU Berrigan, D Lavigne, JA Perkins, SN Colbert, L Nagy, TR Barrett, JC Hursting, SD AF Berrigan, D Lavigne, JA Perkins, SN Colbert, L Nagy, TR Barrett, JC Hursting, SD TI Insulin-like growth factor-I addback restores bone mineral density in calorie restricted C57BL/6 mice: Implications for cancer prevention and control. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NIA, Bethesda, MD 20892 USA. Univ Alabama, Dept Nutr Sci, Birmingham, AL 35294 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B301 BP 1183S EP 1184S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200167 ER PT J AU Mai, V Colbert, L Berrigan, D Lavigne, J Pfeiffer, R Perkins, SN Srinivas, P Lanza, E Schatzkin, A Hursting, SD AF Mai, V Colbert, L Berrigan, D Lavigne, J Pfeiffer, R Perkins, SN Srinivas, P Lanza, E Schatzkin, A Hursting, SD TI Effects of calorie restriction and diet composition on intestinal carcinogenesis in ApcMin (Min) mice. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NIA, Bethesda, MD 20892 USA. RI Pfeiffer, Ruth /F-4748-2011 NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B302 BP 1184S EP 1184S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200168 ER PT J AU Rigas, B Williams, JL Chen, J Rayyan, Y Qiao, L del Soldato, P Kopelovich, L Kashfi, K AF Rigas, B Williams, JL Chen, J Rayyan, Y Qiao, L del Soldato, P Kopelovich, L Kashfi, K TI NO-releasing NSAIDs inhibit the growth of human cultured cancer cells: Evidence for a tissue type-independent effect. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Amer Hlth Fdn, Valhalla, NY 10595 USA. New York Med Coll, Valhalla, NY 10595 USA. Univ Iowa, Iowa City, IA USA. Nicox SA, Sophia Antipolis, France. NCI, CADRG, DCP, Bethesda, MD 20892 USA. CUNY, Sch Med, New York, NY 10031 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B303 BP 1184S EP 1184S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200169 ER PT J AU Beenken, SW Manne, U Niwas, S Weiss, H Perloff, M Malone, W Grizzle, W Bland, KI AF Beenken, SW Manne, U Niwas, S Weiss, H Perloff, M Malone, W Grizzle, W Bland, KI TI Surrogate endpoint biomarker modulation in patients with oral dysplastic leukoplakia is dependent on tissue type and histologic response and is confounded by spontaneous resolution. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Alabama, Birmingham, AL USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B318 BP 1187S EP 1188S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200184 ER PT J AU Tao, LH Li, YZ Kramer, PM Wang, W Lubet, RA Steele, VE Pereira, MA AF Tao, LH Li, YZ Kramer, PM Wang, W Lubet, RA Steele, VE Pereira, MA TI Modulation of DNA methylation in colon and lung tumors as a surrogate endpoint biomarker for chemoprevention. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Med Coll Ohio, Toledo, OH 43699 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B319 BP 1188S EP 1188S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200185 ER PT J AU Kramer, PM Li, YZ Gunning, WT Alyaqoub, FS Lubet, RA Steele, VE Tao, LH Pereira, MA AF Kramer, PM Li, YZ Gunning, WT Alyaqoub, FS Lubet, RA Steele, VE Tao, LH Pereira, MA TI Rapid modulation of surrogate endpoint biomarkers by chemopreventive agents in rat colon and mouse lung tumors. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Med Coll Ohio, Toledo, OH 43699 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA B331 BP 1190S EP 1190S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200197 ER PT J AU Grubbs, CJ Steele, VE Eto, I Juliana, MM Lubert, RA AF Grubbs, CJ Steele, VE Eto, I Juliana, MM Lubert, RA TI Chemoprevention by indomethacin of hydroxybutyl(butyl) nitrosamine (OH-BBN) induced urinary bladder cancer: Time of administration and duration of treatment. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Alabama, Birmingham, AL 35294 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C102 BP 1192S EP 1193S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200206 ER PT J AU Lubet, RA Kopelovich, L You, M Grubbs, CJ AF Lubet, RA Kopelovich, L You, M Grubbs, CJ TI Prevention of methylnitrosourea (MNU)-induced hormonally responsive mammary cancers by rosiglitazone, 9-cis-retinoic acid and the RXR agonist targretin. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Rockville, MD USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C106 BP 1193S EP 1193S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200210 ER PT J AU Rodriguez, GC Barnes, J Anderson, K Petitte, J Windham, J Lancaster, J Wenham, R Berchuck, A Kopelovich, L Carver, D AF Rodriguez, GC Barnes, J Anderson, K Petitte, J Windham, J Lancaster, J Wenham, R Berchuck, A Kopelovich, L Carver, D TI Evaluation of ovarian cancer preventive agents in the chicken. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Northwestern Univ, Evanston NW Healthcare, Evanston, IL USA. N Carolina State Univ, Raleigh, NC 27695 USA. Duke Univ, Durham, NC 27710 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C103 BP 1193S EP 1193S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200207 ER PT J AU Elmore, E Siddiqui, S Desai, N Steele, VE Redpath, JL AF Elmore, E Siddiqui, S Desai, N Steele, VE Redpath, JL TI In vitro prediction of chemopreventive agent efficacy and toxicity using cultured normal human epithelial cells: Correlations with in vivo response, clinical trial plasma levels, and adverse events. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Calif Irvine, Irvine, CA USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C110 BP 1194S EP 1194S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200214 ER PT J AU Shavers, VL Harlan, LC Stevens, J AF Shavers, VL Harlan, LC Stevens, J TI Racial/ethnic variation in clinical presentation, treatment and survival among breast cancer patients under age 35. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Informat Management Syst, Silver Spring, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C211 BP 1203S EP 1203S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200253 ER PT J AU Hatch, E Liner, M Inskip, P AF Hatch, E Liner, M Inskip, P TI Reproductive factors and risk of glioma and meningioma. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Boston Univ, Sch Publ Hlth, Boston, MA USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA C215 BP 1204S EP 1204S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200257 ER PT J AU Crowell, JA Mirsalis, J Zeisel, S McCormick, D AF Crowell, JA Mirsalis, J Zeisel, S McCormick, D TI Genotoxicity/oncogenicity evaluations of soy isoflavone formulations containing genistein. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. SRI Int, Menlo Pk, CA 94025 USA. Univ N Carolina, Chapel Hill, NC USA. IITRI Res Inst, Chicago, IL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D103 BP 1213S EP 1214S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200297 ER PT J AU Wang, TTY Milner, MJ Kim, YS AF Wang, TTY Milner, MJ Kim, YS TI Identification of estrogen receptor alpha as a gene down regulated by indole-3-carbinol in human breast cancer cell MCF-7: A DNA microarray approach. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 USDA, Beltsville, MD 20705 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D105 BP 1214S EP 1214S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200299 ER PT J AU Marshall, JR Reid, ME Lillico, A Lieberman, R AF Marshall, JR Reid, ME Lillico, A Lieberman, R TI Update: Clinical trial results of the nutritional prevention of cancer and other selenium-based chemoprevention studies SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85724 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D114 BP 1215S EP 1216S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200307 ER PT J AU Lavigne, JA Baer, DJ Wimbrow, HH Giffin, CA Judd, JT Brown, ED Dorgan, JF Hartman, TJ Campbell, WS Barrett, JC Hursting, SD Taylor, PR AF Lavigne, JA Baer, DJ Wimbrow, HH Giffin, CA Judd, JT Brown, ED Dorgan, JF Hartman, TJ Campbell, WS Barrett, JC Hursting, SD Taylor, PR TI Effect of moderate alcohol intake on serum insulin-like growth factor-I and insulin-like growth factor binding protein-3 in a diet-controlled intervention study in postmenopausal women SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. USDA, Beltsville, MD 20705 USA. SAIC, Frederick, MD USA. Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Penn State Univ, University Pk, PA 16802 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D133 BP 1219S EP 1220S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200326 ER PT J AU Flood, AP Chaterjee, N Peters, U Schairer, C Schatzkin, A AF Flood, AP Chaterjee, N Peters, U Schairer, C Schatzkin, A TI Calcium from diet and from supplements is associated with a reduced risk of colorectal cancer in the BCDDP follow-up cohort SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D134 BP 1220S EP 1220S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200327 ER PT J AU Newcomb, P Haile, R Anton-Culver, H Gallinger, S Hopper, J Jass, J LeMarchand, L Lindor, N Potter, J Seminara, D AF Newcomb, P Haile, R Anton-Culver, H Gallinger, S Hopper, J Jass, J LeMarchand, L Lindor, N Potter, J Seminara, D TI The Colorectal Cancer Family Registry: 1998-2002 SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. USC Norris Canc Ctr, Los Angeles, CA USA. Univ Calif Irvine, Irvine, CA USA. Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada. Univ Melbourne, Carlton, Vic 3053, Australia. McGill Univ, Montreal, PQ, Canada. Canc Res Ctr Hawaii, Honolulu, HI 96813 USA. Mayo Clin, Rochester, MN USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D205 BP 1222S EP 1223S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200338 ER PT J AU Paltoo, DN Flood, A Woodson, K Tangrea, J Schatzkin, A Schoenfeld, P AF Paltoo, DN Flood, A Woodson, K Tangrea, J Schatzkin, A Schoenfeld, P TI IGF-2 gene polymorphisms and polyp status among women SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D207 BP 1223S EP 1223S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200340 ER PT J AU Yang, XH Wacholder, S Xu, ZY Dean, M Clark, V Gold, B Brown, LM Stone, BJ Caporaso, N AF Yang, XH Wacholder, S Xu, ZY Dean, M Clark, V Gold, B Brown, LM Stone, BJ Caporaso, N TI CYP1A1 and other single nucleotide polymorphisms in relation to lung cancer risk: A case-control study of women in north-east China SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, DCEG, NIH, Rockville, MD USA. Liaoning Publ Hlth & Anti Epidem Stn, Shenyang, Peoples R China. NCI, Lab Genet Divers, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D208 BP 1223S EP 1223S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200341 ER PT J AU Berwick, M Mahabir, S Roush, GC Hu, J AF Berwick, M Mahabir, S Roush, GC Hu, J TI ADPRT [poly(ADP-ribose) transferase] affects lung cancer risk SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NCI, Bethesda, MD 20892 USA. NYU, New York, NY USA. Wake Forest Univ, Winston Salem, NC 27109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D210 BP 1224S EP 1224S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200343 ER PT J AU Sturgeon, SR Potischman, N Dorgan, J Daling, J Schairer, C Brinton, L AF Sturgeon, SR Potischman, N Dorgan, J Daling, J Schairer, C Brinton, L TI Serum levels of sex hormones and breast cancer risk in premenopausal women: A case-control study SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Massachusetts, Amherst, MA 01003 USA. NCI, Bethesda, MD 20892 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ Washington, Seattle, WA 98195 USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D218 BP 1226S EP 1226S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200351 ER PT J AU Ciolino, H MacDonald, C Yeh, G AF Ciolino, H MacDonald, C Yeh, G TI The steroid hormone dehydroepiandrosterone inhibits the expression of carcinogen-activating enzymes in vivo SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D315 BP 1230S EP 1230S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200371 ER PT J AU MacDonald, C Ciolino, H Yeh, G AF MacDonald, C Ciolino, H Yeh, G TI Salicylamide functions as an aryl hydrocarbon receptor ligand and inhibits expression of cytochromes P450 1A1, 1A2 and 1B1 SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D316 BP 1230S EP 1230S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200372 ER PT J AU Suh, N Roberts, A Heiss, E Place, A Williams, C Risingsong, R Reffey, S Honda, T Gribble, G Miyazono, K Itoh, S ten Dijke, P Sporn, M AF Suh, N Roberts, A Heiss, E Place, A Williams, C Risingsong, R Reffey, S Honda, T Gribble, G Miyazono, K Itoh, S ten Dijke, P Sporn, M TI Synthetic triterpenoids activate TGF-beta/SMAD signalling SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Dartmouth Coll Sch Med, Hanover, NH USA. NCI, Bethesda, MD 20892 USA. Dartmouth Coll, Hanover, NH 03755 USA. Japanese Fdn Canc Res, Inst Canc, Tokyo 170, Japan. Netherlands Canc Inst, Amsterdam, Netherlands. RI Heiss, Elke/B-6086-2015 OI Heiss, Elke/0000-0001-7618-5505 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D317 BP 1230S EP 1230S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200373 ER PT J AU Rao, CV Simi, B Cooma, I Rigas, B Kopelovich, L Reddy, BS AF Rao, CV Simi, B Cooma, I Rigas, B Kopelovich, L Reddy, BS TI Chemoprevention of colonic aberrant crypt foci by nitric oxide (NO)-releasing NSAIDs SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Amer Hlth Fdn, Valhalla, NY 10595 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D321 BP 1231S EP 1231S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200377 ER PT J AU Bensasson, RV Scurlock, R Rougee, M Zoete, V Steele, VE Boone, CWW Dauzonne, D Rao, CV AF Bensasson, RV Scurlock, R Rougee, M Zoete, V Steele, VE Boone, CWW Dauzonne, D Rao, CV TI Redox regulation of chemoprotection against inflammation and carcinogenesis SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Museum Natl Hist Nat, CNRS, Paris, France. Univ Strasbourg 1, ISIS, Lab Chim Biophys, Strasbourg, France. NCI, Div Canc Prevent, Bethesda, MD 20892 USA. Inst Curie, Lab Pharmacochim, Paris, France. Amer Hlth Fdn, Valhalla, NY 10595 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D325 BP 1232S EP 1232S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200381 ER PT J AU Christov, K Peng, XJ Kim, E You, M Grubbs, C End, D Lubet, R AF Christov, K Peng, XJ Kim, E You, M Grubbs, C End, D Lubet, R TI Early cellular responses of mammary tumors to farnesyl transferase inhibitors (FTIs): Effects on cell proliferation and apoptosis SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Univ Illinois, Chicago, IL USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Alabama, Ctr Prevent, Birmingham, AL USA. NCI, Chemoprevent Drug Dev Grp, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D332 BP 1233S EP 1234S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200388 ER PT J AU Perkins, SN Kim, K Klug, HLP Richie, ER Hursting, SD AF Perkins, SN Kim, K Klug, HLP Richie, ER Hursting, SD TI Mechanisms underlying the anti-lymphoma activity of dehydroepiandrosterone: Studies in murine thymocytes and murine T-cell hybridoma cells SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Univ Texas, MD Anderson Canc Ctr, Smithville, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D331 BP 1233S EP 1233S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200387 ER PT J AU Sharma, S Gao, P Kang, M Rigas, B Steele, VE Kopelovich, L AF Sharma, S Gao, P Kang, M Rigas, B Steele, VE Kopelovich, L TI Differential efficacy response of nonsteroidal anti-inflammatory drugs in an in vivo angiogenesis model SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 ManTech Environm Technol Inc, Res Triangle Pk, NC 27709 USA. Amer Hlth Fdn, Valhalla, NY 10595 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 MA D329 BP 1233S EP 1233S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200385 ER PT J AU Hawk, ET AF Hawk, ET TI Translating prevention science into benefits: Clinical and subclinical SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1237S EP 1237S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200398 ER PT J AU Greene, MH AF Greene, MH TI Risk-reducing surgery in the management of women at increased genetic risk of ovarian, fallopian tube, and endometrial cancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1247S EP 1248S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200478 ER PT J AU Klein, EA Thompson, IM Lippman, SM Goodman, PJ Albanes, D Taylor, PR Coltman, C AF Klein, EA Thompson, IM Lippman, SM Goodman, PJ Albanes, D Taylor, PR Coltman, C TI Prostate cancer prevention: The selenium and vitamin E cancer prevention trial (SELECT). SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 Cleveland Clin, Cleveland, OH 44106 USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Natl Canc Inst, Washington, DC USA. SW Oncol Grp, San Antonio, TX USA. RI Albanes, Demetrius/B-9749-2015 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1253S EP 1254S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200447 ER PT J AU Kelloff, GJ AF Kelloff, GJ TI IEN as the best surrogate endpoint for treatment and prevention of precancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1255S EP 1256S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200454 ER PT J AU Gail, MH AF Gail, MH TI Uses and abuses of the "Gail" model for projecting absolute breast cancer risk. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1257S EP 1257S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200458 ER PT J AU Mccaskill-Stevens, W AF Mccaskill-Stevens, W TI Estrogen receptor negative breast cancer. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1257S EP 1257S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200459 ER PT J AU Price, DK Bennett, CL Thompson, IM Ford, LG Coltman, CA Figg, WD AF Price, DK Bennett, CL Thompson, IM Ford, LG Coltman, CA Figg, WD TI Polymorphisms in the androgen receptor may predispose prostate cancer in African-American men. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. Northwestern Univ, Chicago, IL 60611 USA. UTHSCSA, San Antonio, TX USA. SW Oncol Grp, San Antonio, TX USA. RI Bennett, Charles/C-2050-2008; Figg Sr, William/M-2411-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1257S EP 1258S PN 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200460 ER PT J AU Djordjevic, MV Leischow, SJ AF Djordjevic, MV Leischow, SJ TI Reducing tobacco-related diseases: Are new tobacco potential reduced-exposure products the answer? SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1261S EP 1261S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200472 ER PT J AU Colburn, NH AF Colburn, NH TI Novel molecular targets for cancer prevention: AP-1, NF kappa B, and Pdcd4. SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Meeting Abstract CT Conference on Frontiers in Cancer Prevention Research CY OCT 14-18, 2002 CL BOSTON, MASSACHUSETTS SP Amer Assoc Canc Res C1 NCI, NIH, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD OCT PY 2002 VL 11 IS 10 BP 1262S EP 1262S PN 2 PG 1 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 604RE UT WOS:000178634200475 ER PT J AU Topalian, SL Gonzales, MI Ward, Y Wang, XA Wang, RF AF Topalian, SL Gonzales, MI Ward, Y Wang, XA Wang, RF TI Revelation of a cryptic major histocompatibility complex class II-restricted tumor epitope in a novel RNA-processing enzyme SO CANCER RESEARCH LA English DT Article ID CD4(+) T-CELLS; MELANOMA; ANTIGEN; IDENTIFICATION; PEPTIDES; LYMPHOCYTES; IMMUNITY; PROTEINS AB CD4+ T-cell responses against human tumor antigens are a potentially critical component of the antitumor immune response. Molecular methods have been devised for rapidly identifying MHC class II-restricted tumor antigens and elucidating the recognized epitopes. We describe here the identification of neo-poly(A) polymerase (neo-PAP), a novel RNA processing enzyme overexpressed in a variety of human cancers, by screening a melanoma-derived invariant chain fusion cDNA library with tumorreactive CD4+ T lymphocytes. A cryptic nonmutated HLA-DRbeta1*0701-restricted neo-PAP epitope was processed through the endogenous MHC class 11 pathway. A unique point mutation effected a nonconservative substitution of a leucine for a proline residue at a structurally important site in neo-PAP that was remote from the recognized peptide, revealing a normally silent epitope for immune recognition. Genetic aberrations such as the described point mutation can have unexpected immunological consequences, in this case leading to immune recognition of a distant normal self epitope. C1 NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NCI, Med Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Topalian, SL (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, 10-2B47, Bethesda, MD 20892 USA. NR 14 TC 51 Z9 51 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 2002 VL 62 IS 19 BP 5505 EP 5509 PG 5 WC Oncology SC Oncology GA 600ET UT WOS:000178378200020 PM 12359760 ER PT J AU Shan, L He, M Yu, MS Qiu, CP Lee, NH Liu, ET Snyderwine, EG AF Shan, L He, M Yu, MS Qiu, CP Lee, NH Liu, ET Snyderwine, EG TI cDNA microarray profiling of rat mammary gland carcinomas induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine and 7,12-dimethylbenz[a]anthracene SO CARCINOGENESIS LA English DT Article ID LOW-FAT DIETS; GROWTH-INHIBITING FACTORS; GENE-EXPRESSION PATTERNS; INVASIVE BREAST-CANCER; SPRAGUE-DAWLEY RATS; CYCLIN D1; HA-RAS; MICROSATELLITE INSTABILITY; TUMORS; CARCINOGENESIS AB cDNA microarray analysis was used to examine gene expression profiles in normal female Sprague-Dawley rat mammary gland and in carcinomas induced by the cooked meat-derived carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and the potent experimental carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Nine tubulopapillary carcinomas (five from PhIP-treated rats and four from DMBA-treated rats) and normal mammary gland from virgin, pregnant and lactating rats were examined on a rat 6.9k cDNA microarray. Although histologically identical, PhIP- and DMBA-induced carcinomas could be distinguished by hierarchical clustering and multi-dimensional scaling analyses of cDNA expression. In addition, the expression of 21 clones was statistically different between PhIP- and DMBA-induced carcinomas (F-test, P < 0.05). The data indicate that distinct chemical carcinogens induce unique gene expression patterns in mammary gland carcinomas. The specific chemical carcinogen-associated cDNA array profiles found in carcinomas may ultimately be applicable to better understanding cancer etiology. PhIP- and DMBA-induced carcinomas also shared similarities in cDNA expression profiles. By comparing the expression in carcinomas (PhIP plus DMBA induced) with normal rat mammary gland (at any stage of differentiation), 172 clones were found to be differentially expressed. Genes showing increased expression in carcinomas by cDNA microarray analysis (and further validated by immunohistochemistry and western blot analysis) include cyclin D1, PDGF-A chain, retinol binding protein 1, prohibitin and the transcription factor STAT5A. The similarities in gene expression between PhIP- and DMBA-induced carcinomas raise the possibility that several molecular pathways for rat mammary gland transformation are maintained irrespective of the carcinogenic initiating agent. C1 NCI, Chem Carcinogenesis Sect, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. NCI, Ctr Adv Technol, Ctr Canc Res, NIH, Gaithersburg, MD 20887 USA. Inst Genom Res, Rockville, MD 20852 USA. RP Snyderwine, EG (reprint author), NCI, Chem Carcinogenesis Sect, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. EM elizabeth_snyderwine@nih.gov RI Liu, Edison/C-4141-2008 NR 54 TC 44 Z9 46 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD OCT PY 2002 VL 23 IS 10 BP 1561 EP 1568 DI 10.1093/carcin/23.10.1561 PG 8 WC Oncology SC Oncology GA 607QG UT WOS:000178801800001 PM 12376462 ER PT J AU Perera, FP Mooney, LA Stampfer, M Phillips, DH Bell, DA Rundle, A Cho, S Tsai, WY Ma, J Blackwood, A Tang, DL AF Perera, FP Mooney, LA Stampfer, M Phillips, DH Bell, DA Rundle, A Cho, S Tsai, WY Ma, J Blackwood, A Tang, DL TI Associations between carcinogen-DNA damage, glutathione S-transferase genotypes, and risk of lung cancer in the prospective Physicians' Health Cohort Study SO CARCINOGENESIS LA English DT Article ID POLYCYCLIC AROMATIC-HYDROCARBONS; WHITE BLOOD-CELLS; ADDUCT LEVELS; DIOL EPOXIDES; HEPATOCELLULAR-CARCINOMA; MOLECULAR EPIDEMIOLOGY; CATALYTIC EFFICIENCY; AFLATOXIN EXPOSURE; M1 GSTM1; POLYMORPHISMS AB DNA damage from polycyclic aromatic hydrocarbons (PAH) and other aromatic/hydrophobic compounds has been implicated in case-control studies as a risk factor for lung cancer, as have common polymorphisms in the glutathione S-transferase (GST) genes involved in carcinogen detoxification. However, their joint effects have not been evaluated in prospective studies, leaving open questions about predictive value of these biomarkers. In this matched case-control study nested within the prospective Physicians' Health Study, we evaluated whether biomarkers measured in white blood cells (WBC) significantly predicted risk, alone and in combination, after controlling for level of smoking. The biomarkers reported here are aromatic/hydrophobic-DNA adducts and polymorphisms in genes coding for the GSTM1 and GSTP1 enzymes. Our study population was composed of 89 cases of primary lung cancer and 173 controls, matched in a 1:2 ratio on smoking, age and duration of follow up. Adducts were measured in WBC DNA by the nuclease P1-enhanced P-32-post-labeling method. Genotypes (GSTM1 null versus non-null and GSTP1 Val versus GSTP Ile) were determined by genomic amplification and restriction fragment length polymorphism analysis. Among current smokers, adducts were significant predictors of lung cancer risk (after adjusting for GST genotypes, OR = 3.10, 95% CI 1.07, 9.01). The combined GSTM1 null/GSTP1 Val genotype was associated with lung cancer overall and especially among former smokers, before and after adjusting for adducts (OR for former smokers = 4.21, CI 1.08, 16.41; adjusted OR = 4.68, CI 1.17, 18.71). Among cases only, adducts were significantly higher among current or former smokers with the GSTM1 non-null/GSTP1 Ile genotype. The two risk factors (adducts and genotypes) appear to be independent predictors of risk. The findings underscore the complex and important role of biological susceptibility as a determinant of risk from carcinogens found in tobacco smoke and other environmental compounds. C1 Columbia Univ, Joseph L Mailman Sch Publ Hlth, Div Environm Hlth Sci, New York, NY 10032 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Channing Lab, Boston, MA 02115 USA. Inst Canc Res, Haddow Labs, Sutton SM2 5NG, Surrey, England. NIEHS, Res Triangle Pk, NC 27709 USA. Univ Penn, Sch Med, Ctr Clin Epidemiol & Appl Biostat, Philadelphia, PA 19104 USA. RP Perera, FP (reprint author), Columbia Univ, Joseph L Mailman Sch Publ Hlth, Div Environm Hlth Sci, New York, NY 10032 USA. RI Rundle, Andrew/A-5282-2009; OI Rundle, Andrew/0000-0003-0211-7707; Mooney, LaVerne A./0000-0003-1120-356X FU NCI NIH HHS [5R01 CA 53772] NR 60 TC 77 Z9 79 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD OCT PY 2002 VL 23 IS 10 BP 1641 EP 1646 DI 10.1093/carcin/23.10.1641 PG 6 WC Oncology SC Oncology GA 607QG UT WOS:000178801800011 PM 12376472 ER PT J AU Devereux, TR Holliday, W Anna, C Ress, N Roycroft, J Sills, RC AF Devereux, TR Holliday, W Anna, C Ress, N Roycroft, J Sills, RC TI Map kinase activation correlates with K-ras mutation and loss of heterozygosity on chromosome 6 in alveolar bronchiolar carcinomas from B6C3F1 mice exposed to vanadium pentoxide for 2 years SO CARCINOGENESIS LA English DT Article ID MOUSE LUNG-TUMORS; HIGH-FREQUENCY; EXPRESSION; GENE; CARCINOGENESIS; PROGRESSION AB Previous work showed a correlation between K-ras mutation and loss of heterozygosity (LOH) on chromosome 6 in the region of K-ras in lung carcinomas from B6C3F1 mice. We hypothesized that mitogen-activated protein kinase (MAPK) would be activated only in those lung neoplasms with both K-ras mutation and LOH. As MAPK activity can be correlated directly with signal detection using antibodies to phosphorylated MAPK, we were able to analyze lung carcinomas from B6C3F1 mice for the presence or absence of MAPK activity by western analysis. Vanadium pentoxide-induced mouse lung carcinomas, which had been shown to have a high frequency of K-ras mutations and LOH on chromosome 6 and for which frozen tumor tissue was available, were used for this study. Total MAPK expression levels were similar between normal lung and lung carcinomas. Phospho-MAPK was elevated in five of six lung carcinoma samples examined in which K-ras mutations and chromosome 6 LOH were identified and in four of five carcinomas with K-ras mutations that lacked LOH. Phospho-MAPK was undetectable or weakly expressed in seven carcinomas examined without K-ras mutations and in normal lung. By immunohistochemistry three K-ras positive/LOH negative samples exhibited multifocal areas of nuclear and cytoplasmic staining for phospho-MAPK. Large amounts of non-staining fibroblasts, lymphocytes and macrophages were also observed in these tumors. Two of these lung carcinomas were microdissected and chromosome 6 LOH was detected in regions of phospho-MAPK positive cells. These results suggest that MAPK is activated during vanadium pentoxide-induced B6C3F1 mouse lung tumorigenesis following K-ras mutation and loss of the wild-type K-ras allele. C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Toxicol Operat Branch, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Expt Pathol, NIH, Res Triangle Pk, NC 27709 USA. RP Devereux, TR (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 25 TC 19 Z9 19 U1 2 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD OCT PY 2002 VL 23 IS 10 BP 1737 EP 1743 DI 10.1093/carcin/23.10.1737 PG 7 WC Oncology SC Oncology GA 607QG UT WOS:000178801800023 PM 12376484 ER PT J AU Johnson, F Huff, J AF Johnson, F Huff, J TI Development of a multi-organ rat model for evaluating chemopreventive agents: efficacy of indole-3-carbinol - Certain health supplements may cause both carcinogenic and anticarcinogenic effects SO CARCINOGENESIS LA English DT Letter ID BETA-CAROTENE; LUNG-CANCER; CHEMICALS C1 NIEHS, Res Triangle Pk, NC 27709 USA. RP Johnson, F (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. NR 20 TC 2 Z9 2 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD OCT PY 2002 VL 23 IS 10 BP 1767 EP 1768 DI 10.1093/carcin/23.10.1767 PG 2 WC Oncology SC Oncology GA 607QG UT WOS:000178801800027 PM 12376488 ER PT J AU Yap, GS Sher, A AF Yap, GS Sher, A TI The use of germ line-mutated mice in understanding host-pathogen interactions SO CELLULAR MICROBIOLOGY LA English DT Review ID TOXOPLASMA-GONDII INFECTION; IFN-GAMMA; T-CELLS; INTRACELLULAR PATHOGEN; IMMUNE-RESPONSE; GENE-EXPRESSION; TRANSGENIC MICE; BASIC CONCEPTS; NITRIC-OXIDE; INTERFERON AB Microbial pathogenesis reflects an imbalance between parasite and host factors that favour pathogen multiplication and tissue destruction over those required for microbial elimination and preservation of the integrity of host tissues. In vivo analysis of host-pathogen interactions has been revolutionized by the ability to engineer specific genetic alterations including loss of function mutations and transgenes into the mouse germline. This brief review recapitulates what we have learned about the host response to Toxoplasma gondii infection to illustrate the usefulness of gene-altered mice in microbial pathogenesis research. A consideration of the pitfalls and limitations of experiments in knockout mice and ways of addressing these concerns are discussed. Finally, advances in inducible and tissue-restricted alterations in gene function are presented and their possible applications to microbiology research are considered. C1 Brown Univ, Dept Mol Microbiol & Immunol, Providence, RI 02912 USA. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Yap, GS (reprint author), Brown Univ, Dept Mol Microbiol & Immunol, Providence, RI 02912 USA. FU NCRR NIH HHS [RR-00-003]; NIAID NIH HHS [AI-50618] NR 43 TC 9 Z9 10 U1 0 U2 2 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1462-5814 J9 CELL MICROBIOL JI Cell Microbiol. PD OCT PY 2002 VL 4 IS 10 BP 627 EP 634 DI 10.1046/j.1462-5822.2002.00224.x PG 8 WC Cell Biology; Microbiology SC Cell Biology; Microbiology GA 601ZX UT WOS:000178480600001 PM 12366400 ER PT J AU Shenoy, SR Barrientos, LG Ratner, DM O'Keefe, BR Seeberger, PH Gronenborn, AM Boyd, MR AF Shenoy, SR Barrientos, LG Ratner, DM O'Keefe, BR Seeberger, PH Gronenborn, AM Boyd, MR TI Multisite and multivalent binding between cyanovirin-N and branched oligomannosides: Calorimetric and NMR characterization SO CHEMISTRY & BIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIGH-MANNOSE OLIGOSACCHARIDES; INACTIVATING PROTEIN; STRUCTURAL BASIS; THERMODYNAMIC ANALYSIS; CONCANAVALIN-A; PIG-LIVER; GP120; LECTIN; MAN9-MANNOSIDASE AB Binding of the protein cyanovirin-N to oligomannose-8 and oligomannose-9 of gp120 is crucially involved in its potent virucidal activity against the human immunodeficiency virus (HIV). The interaction between cyanovirin-N and these oligosaccharides has not been thoroughly characterized due to aggregation of the oligosaccharide-protein complexes. Here, cyanovirin-N's interaction with a nonamannoside, a structural analog of oligomannose-9, has been studied by nuclear magnetic resonance and isothermal titration calorimetry. The nonamannoside interacts with cyanovirin-N in a multivalent fashion, resulting in tight complexes with an average 1:1 stoichiometry. Like the nonamannoside, an alpha1-2-linked trimannoside substructure interacts with cyanovirin-N at two distinct protein subsites. The chitobiose and internal core trimannoside substructures of oligomannose-9 are not recognized by cyanovirin-N, and binding of the core hexamannoside occurs at only one of the sites on the protein. This is the first detailed analysis of a biologically relevant interaction between cyanovirin-N and high-mannose oligosaccharides of HIV-1 gp120. C1 NCI, Ctr Canc Res, Mol Targets Discovery Program, Frederick, MD 21702 USA. NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. MIT, Dept Chem, Cambridge, MA 02139 USA. Univ S Alabama, Canc Res Inst, Coll Med, Mobile, AL 36688 USA. RP Boyd, MR (reprint author), NCI, Ctr Canc Res, Mol Targets Discovery Program, Frederick, MD 21702 USA. NR 29 TC 72 Z9 73 U1 0 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-5521 J9 CHEM BIOL JI Chem. Biol. PD OCT PY 2002 VL 9 IS 10 BP 1109 EP 1118 AR PII S1074-5521(02)00237-5 DI 10.1016/S1074-5521(02)00237-5 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 609GL UT WOS:000178895200007 PM 12401495 ER PT J AU Summers, RM Shelhamer, JH Magnuson, WG Sneller, MC Langford, CA AF Summers, RM Shelhamer, JH Magnuson, WG Sneller, MC Langford, CA TI CT virtual bronchoscopy for detecting Wegener granulomatosis SO CHEST LA English DT Letter C1 NIH, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Summers, RM (reprint author), NIH, Warren G Magnuson Clin Ctr, Bldg 10,Rm 1C660,10 Ctr Dr Msc 1183, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA SN 0012-3692 J9 CHEST JI Chest PD OCT PY 2002 VL 122 IS 4 BP 1496 EP 1496 PG 1 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 605PA UT WOS:000178685200070 ER PT J AU Cassiano, NM Cass, QB Degani, ALG Wainer, IW AF Cassiano, NM Cass, QB Degani, ALG Wainer, IW TI Determination of the plasma levels of metyrapone and its enantiomeric metyrapol metabolites by direct plasma injection and multidimensional achiral-chiral chromatography SO CHIRALITY LA English DT Article DE enantioseparation; restricted access media (RAM); polysaccharide chiral phases; Bradford's method; method validation ID PERFORMANCE LIQUID-CHROMATOGRAPHY; RESTRICTED-ACCESS MEDIA; COLUMN; DRUGS; HPLC AB The development and validation of a direct injection high-performance liquid chromatographic (HPLC) method, with column switching, for the determination of metyrapol enantiomers and metyrapone in human plasma is described. The system used in this work was composed of a restricted access media (RAM) bovine serum albumin (BSA) octyl column coupled to an amylose tris(3,5-dimethoxyphenylcarbamate) chiral column. Water was used as eluent for the first 5 min at a flow rate of 1.0 ml/min for the elution of the plasma proteins and then acetonitrile-water (30:70 v/v) for the transfer and analysis of metyrapol enantiomers and metyrapone, which were detected by UV at lambda = 260 nm. The total analysis time was about 32 min. The calibration curves for each enantiomer and for the metyrapone were linear in the ranges 0.075-0.75 mug/ml and 0.150-1.50 mug/ml, respectively. Recoveries, intra- and interday precision and accuracy were determined using three quality controls, one low (0.18 pg/ml), one medium (0.75 mug/ml), and one high (1.35 mug/ml) plasma concentration. Quantitative recoveries and good precision and accuracy were obtained. The limit of quantitation were 0.045 mug/ml for both enantiomers and for the metyrapone. (C) 2002 Wiley-Liss, Inc. C1 Univ Fed Sao Carlos, Dept Quim, BR-13565905 Sao Carlos, SP, Brazil. NIA, Gerontol Res Ctr, Bioanalyt & Drug Discovery Unit, NIH, Baltimore, MD 21224 USA. RP Cass, QB (reprint author), Univ Fed Sao Carlos, Dept Quim, Cx Postal 676, BR-13565905 Sao Carlos, SP, Brazil. RI Cass, Quezia/B-8188-2012; Cassiano, Neila /N-9472-2013 OI Cass, Quezia/0000-0002-6550-1194; NR 15 TC 25 Z9 26 U1 1 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0899-0042 J9 CHIRALITY JI Chirality PD OCT PY 2002 VL 14 IS 9 BP 731 EP 735 DI 10.1002/chir.10133 PG 5 WC Chemistry, Medicinal; Chemistry, Analytical; Chemistry, Organic; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA 598JB UT WOS:000178271600008 PM 12237834 ER PT J AU Leclercq, C Faris, O Tunin, R Johnson, J Kato, R Evans, F Spinelli, J Halperin, H McVeigh, E Kass, DA AF Leclercq, C Faris, O Tunin, R Johnson, J Kato, R Evans, F Spinelli, J Halperin, H McVeigh, E Kass, DA TI Systolic improvement and mechanical resynchronization does not require electrical synchrony in the dilated failing heart with left bundle-branch block SO CIRCULATION LA English DT Article DE heart failure; pacing; electrical stimulation; bundle-branch block; ventricles ID CONDUCTION DELAY; PACED HEART; FAILURE; ACTIVATION; CARDIOMYOPATHY; MRI AB Background-Biventricular (BiV) and left ventricular (LV) pacing similarly augment systolic function in left bundle-branch block (LBBB)-failing hearts despite different electrical activation. We tested whether electrical synchrony is required to achieve mechanical synchronization and functional benefit from pacing. Methods and Results-Epicardial mapping, tagged MRI, and hemodynamics we re obtained in dogs with LBBB-failing hearts during right atrial, LV, and BiV stimulation. BiV and LV both significantly improved chamber hemodynamics (eg, 25% increase in dP/dt(max) and aortic pulse pressure) compared with atrial pacing-LBBB, and this improvement correlated with mechanical resynchronization. Electrical dispersion, however, decreased 13% with BiV but increased 23% with LV pacing (P<0.01). Conclusion-Improved mechanical synchrony and function do not require electrical synchrony. Mechanical coordination plays the dominant role in global systolic improvement with either pacing approach. C1 Johns Hopkins Univ, Dept Med, Div Cardiol, Baltimore, MD USA. NHLBI, Lab Cardiac Energet, NIH, Bethesda, MD 20892 USA. Cardiac Pacemakers Guidant, Minneapolis, MN USA. RP Kass, DA (reprint author), Johns Hopkins Univ Hosp, Halsted 500,600 N Wolfe St, Baltimore, MD 21287 USA. FU NHLBI NIH HHS [P50HL52307, R01 HL45683, R01 HL64795] NR 14 TC 310 Z9 315 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 1 PY 2002 VL 106 IS 14 BP 1760 EP 1763 DI 10.1161/01.CIR.0000035037.11968.5C PG 4 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 600HZ UT WOS:000178385700007 PM 12356626 ER PT J AU Cardillo, C Campia, U Bryant, MB Panza, JA AF Cardillo, C Campia, U Bryant, MB Panza, JA TI Increased activity of endogenous endothelin in patients with type II diabetes mellitus SO CIRCULATION LA English DT Article DE endothelin; diabetes; vasculature; receptors; atherosclerosis ID ESSENTIAL-HYPERTENSION; RECEPTOR ANTAGONIST; PLASMA ENDOTHELIN; VASCULAR TONE; IN-VIVO; INSULIN; CELLS; RATS; SECRETION; POTENT AB Background-Endothelial dysfunction may contribute to the risk of premature atherosclerosis in patients with diabetes. Endothelin (ET-1) may be involved in this process by activating smooth muscle cell mitogenesis and leukocyte adhesion. We sought to assess the activity of endogenous ET-1 in a group of patients with type II diabetes mellitus with the use of antagonists of ET-1 receptors. Methods and Results-Forearm blood flow (171317) responses (strain gauge plethysmography) to intraarterial infusion of a selective blocker of ETA receptors (BQ-123) and, on a different occasion, to ET-1, were measured in 15 patients with diabetes and 12 healthy controls. In addition, 5 patients with diabetes received coinfusion of BQ-123 and BQ-788 (a selective blocker of ETB receptors). In normal subjects, BQ-123 did not significantly. modify FBF from baseline (P=0.16). in contrast, BQ-123 administration resulted in a significant vasodilator response in patients with diabetes (P<0.001). Infusion of exogenous ET-1 resulted in lower vasoconstrictor responses in patients with diabetes than in controls (P=0.001), whereas the vasoconstrictor response to norepinephrine was similar in the 2 groups (P=0.78). In patients with diabetes, the vasodilator response to selective ETA blockade was not significantly modified by nonselective blockade of ET-1 receptors obtained by coinfusion of BQ-123 and BQ-788. Conclusions-The activity of endogenous ET-1 on ETA receptors is enhanced in the resistance vessels of patients with diabetes, whereas their sensitivity to exogenous ET-1 is blunted. This abnormality may participate in the pathophysiology of vascular complications associated with diabetes. C1 NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. RP Panza, JA (reprint author), Washington Hosp Ctr, 110 Irving St,NW,Suite 2A 74, Washington, DC 20010 USA. NR 34 TC 156 Z9 158 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 1 PY 2002 VL 106 IS 14 BP 1783 EP 1787 DI 10.1161/01.CIR.0000032260.01569.64 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 600HZ UT WOS:000178385700011 PM 12356630 ER PT J AU Fabian, CJ Kimler, BF Brady, DA Mayo, MS Chang, CHJ Ferraro, JA Zalles, CM Stanton, AL Masood, S Grizzle, WE Boyd, NF Arneson, DW Johnson, KA AF Fabian, CJ Kimler, BF Brady, DA Mayo, MS Chang, CHJ Ferraro, JA Zalles, CM Stanton, AL Masood, S Grizzle, WE Boyd, NF Arneson, DW Johnson, KA TI A phase II breast cancer chemoprevention trial of oral alpha-difluoromethylornithine: Breast tissue, imaging, and serum and urine biomarkers SO CLINICAL CANCER RESEARCH LA English DT Review ID CELL NUCLEAR ANTIGEN; ORNITHINE DECARBOXYLASE ACTIVITY; FINE-NEEDLE ASPIRATION; CERVICAL INTRAEPITHELIAL NEOPLASIA; PLACEBO-CONTROLLED TRIAL; GROWTH-FACTOR RECEPTOR; MAMMOGRAPHIC DENSITIES; MENSTRUAL-CYCLE; COLON-CANCER; POLYAMINE INVOLVEMENT AB Purpose: A double-blind randomized Phase II chemoprevention trial of alpha-difluoromethylornithine (DFMO) was conducted in a group of women at high risk for development of breast cancer. DFMO is an irreversible inhibitor of ornithine decarboxylase, the limiting enzyme of polyamine synthesis that is often up-regulated in breast cancer. Experimental Design: Study entrants were required to have random periareolar fine-needle aspiration cytology prior to entry that exhibited hyperplasia or hyperplasia with atypia, as well as a mammogram and clinical breast exam judged as not suspicious for breast cancer and no clinical hearing loss. Subjects were randomized to 6 months of oral DFMO (0.5 g/m(2)/day) or placebo, followed by repeat fine-needle aspiration and biomarker assessment. The main study end point was an improvement in cytologic pattern. Results: Of 119 subjects entered, 96% completed the study and were evaluable for the main study end point. A modest reduction (28%) in average total urine polyamines was obtained in the DFMO group, but there was no reduction in the spermidine:spermine ratio. There was no difference in cytologic improvement between DFMO and placebo. Likewise, there was no difference between DFMO and placebo for the secondary end points of breast molecular marker changes (immunocytochemical expression of proliferating cell nuclear antigen, p53, and epidermal growth factor receptor), mammographic breast density, serum insulin-like growth factor 1: insulin-like growth factor binding protein 3 ratio, adverse events, quality of life indices, or subsequent cancer development. Conclusions: DFMO at a dose level of 0.5 g/m(2)/day administered for 6 months does not modulate breast risk biomarkers tested in this study. C1 Univ Kansas, Med Ctr, Kansas City, KS 66160 USA. Hutchinson Hosp Corp, Hutchinson, KS 67502 USA. Univ Kansas, Lawrence, KS 66045 USA. Univ Florida, Hlth Sci Ctr, Jacksonville, FL 32209 USA. Univ Alabama, Birmingham, AL 35294 USA. Princess Margaret Hosp, Ontario Canc Inst, Toronto, ON M5G 2M9, Canada. Midwest Res Inst, Kansas City, MO 64110 USA. NCI, Bethesda, MD 20892 USA. RP Fabian, CJ (reprint author), Univ Kansas, Med Ctr, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. RI Mayo, Matthew/E-3774-2015 FU NCI NIH HHS [N01-CN-65124] NR 120 TC 65 Z9 67 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD OCT PY 2002 VL 8 IS 10 BP 3105 EP 3117 PG 13 WC Oncology SC Oncology GA 603EB UT WOS:000178544900011 PM 12374678 ER PT J AU Rashid, A Ueki, T Gao, YT Houlihan, PS Wallace, C Wang, BS Shen, MC Deng, J Hsing, AW AF Rashid, A Ueki, T Gao, YT Houlihan, PS Wallace, C Wang, BS Shen, MC Deng, J Hsing, AW TI K-ras mutation, p53 overexpression, and microsatellite instability in biliary tract cancers: A population-based study in China SO CLINICAL CANCER RESEARCH LA English DT Article ID POLYMERASE CHAIN-REACTION; EXTRAHEPATIC BILE-DUCT; DNA-REPLICATION ERRORS; NONPOLYPOSIS COLORECTAL-CANCER; I GALLBLADDER CARCINOMA; MISMATCH REPAIR GENES; RECEPTOR-TYPE-II; CODON-12 MUTATIONS; PANCREATIC-CARCINOMA; SOMATIC MUTATIONS AB Purpose: The genetic alterations in biliary tract cancer and clinicopathological associations have not been studied in large population-based studies. Experimental Design: We evaluated genetic alterations such as K-ras mutation, p53 overexpression, microsatellite instability (MSI), and alterations of the polyadenine tract present in the transforming growth factor beta receptor type II (TGFbetaRII) gene in 126 biliary tract cancers: 75 gallbladder cancers, 33 bile duct cancers, and 18 ampullary cancers. These genetic alterations were compared with patient demographics and clinicopathological characteristics of the tumors. Results: Mutation of the K-ras gene was present in 18 of 126 (14.3%) biliary tract cancers. K-ras mutation was present in 11 of 18 (61.1%) ampullary cancers, 5 of 33 (15.2%) bile duct cancers, and 2 of 75 (2.7%) gallbladder cancers (P = 0.000001). The mean survival of patients who had bile duct carcinomas with K-ras mutation was 3.0 +/- 2.2 months compared with 15.5 +/- 12.5 months for those without mutation (P = 0.03) but was not different for other tumor sites. p53 overexpression was present in 34 of 123 (27.6%) cancers. MSI-high (allelic shifts in 40% or more loci or alteration of the TGFbetaRII gene) was present in 4 of 126 (3.2%) biliary tract cancers without hereditary nonpolyposis colorectal cancer. MSI-high was more common in mucinous adenocarcinomas (P = 0.006) and in patients with early age of onset of cancer (P = 0.04). Conclusions: The genetic alterations in biliary tract cancers are dependent on the tumor subsite, histology, and age of onset and are associated with prognosis. C1 Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Ctr Oncol, Baltimore, MD 21205 USA. Shanghai Canc Inst, Shanghai, Peoples R China. Zhongshan Hosp, Dept Gen Surg, Shanghai, Peoples R China. Shanghai Canc Hosp, Dept Pathol, Shanghai, Peoples R China. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Rashid, A (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Box 85,1515 Holcombe Blvd, Houston, TX 77030 USA. NR 57 TC 91 Z9 101 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD OCT PY 2002 VL 8 IS 10 BP 3156 EP 3163 PG 8 WC Oncology SC Oncology GA 603EB UT WOS:000178544900016 PM 12374683 ER PT J AU Rider, LG Schiffenbauer, AS Zito, M Lim, KL Ahmed, A Zemel, LS Rennebohm, RM Passo, MH Summers, RM Hicks, JE Lachenbruch, PA Heyes, MP Miller, FW AF Rider, LG Schiffenbauer, AS Zito, M Lim, KL Ahmed, A Zemel, LS Rennebohm, RM Passo, MH Summers, RM Hicks, JE Lachenbruch, PA Heyes, MP Miller, FW CA Juvenile Dermatomyositis Dis Activ TI Neopterin and quinolinic acid are surrogate measures of disease activity in the juvenile idiopathic inflammatory myopathies SO CLINICAL CHEMISTRY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; MUSCLE-FIBERS; TNF-ALPHA; DERMATOMYOSITIS; DIAGNOSIS; QUANTIFICATION; ENZYMES; CELLS; BLOOD; BRAIN AB Objective: We evaluated the utility of neopterin and quinolinic acid (QUIN) as surrogate measures of disease activity in juvenile idiopathic inflammatory myopathies (IIMS). Methods: Plasma and first morning void urine samples were measured for neopterin and QUIN using commercial ELISA, HPLC, or gas chromatography-mass spectrometry in 45 juvenile IIM patients and 79 healthy controls. Myositis disease activity assessments were obtained. Results: Plasma and urine neopterin and QUIN concentrations were increased in juvenile IIM patients compared with healthy controls (P < 0.017). Urine neopterin and QUIN highly correlated with each other (r(s) = 0.73; P < 0.0001). Urine neopterin and QUIN correlated moderately with myositis disease activity assessments, including physician and parent global activity assessments, muscle strength testing, functional assessments (Childhood Myositis Assessment Scale, Childhood Health Assessment Questionnaire), skin global activity, and edema on magnetic resonance imaging (r(s) = 0.42-0.62; P < 0.05), but generally not with muscle-associated enzymes in serum. Urine neopterin or QUIN, in combination with either serum lactate dehydrogenase (LD) or aspartate aminotransferase (AST), significantly predicted global disease activity (R-2 = 0.40-0.56; P < 0.002), and both were more sensitive to change than these serum enzymes (standardized response means, -0.41 to -0.48). Conclusions: Urinary neopterin and QUIN are candidate measures of disease activity in juvenile IIM patients and add significantly to the prediction of global disease activity in combination with serum LD or AST values. Measurement of these markers in first morning void urine specimens appears to be as good as, or possibly better than, measurements of their concentrations in plasma. (C) 2002 American Association for Clinical Chemistry. C1 NIEHS, Environm Autoimmun Grp, NIH, Bethesda, MD 20892 USA. US FDA, Lab Mol & Dev Immunol, Div Monoclonal Antibodies, CBER, Bethesda, MD 20892 USA. NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. NIMH, Lab Neurotoxicol, NIH, Bethesda, MD 20892 USA. Univ Glasgow, Glasgow Royal Infirm, Dept Med & Rheumatol, Glasgow G31 2ER, Lanark, Scotland. Sherwood Forest Hosp, NHS Trust, Kings Mill Ctr, Nottingham NG17 4JL, England. Specialty Labs, Santa Monica, CA 90404 USA. Univ Connecticut, Connecticut Childrens Med Ctr, Hartford, CT 06106 USA. Ohio State Univ, Columbus Childrens Hosp, Columbus, OH 43205 USA. Univ Cincinnati, Childrens Hosp, Cincinnati, OH 45229 USA. NIH, Dept Radiol, Ctr Clin, Bethesda, MD 20892 USA. NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA. US FDA, Div Biostat, CBER, Rockville, MD 20852 USA. Curagen Inc, Branford, CT 06405 USA. RP Rider, LG (reprint author), NIEHS, Environm Autoimmun Grp, NIH, 9 Mem Dr,Room 1W101,MSC 0958, Bethesda, MD 20892 USA. OI Schiffenbauer, Adam/0000-0001-9964-9966; Rider, Lisa/0000-0002-6912-2458; Miller, Frederick/0000-0003-2831-9593 NR 29 TC 15 Z9 16 U1 0 U2 3 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD OCT PY 2002 VL 48 IS 10 BP 1681 EP 1688 PG 8 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 597UA UT WOS:000178238100007 PM 12324484 ER PT J AU Oyler, JM Cone, EJ Joseph, RE Moolchan, ET Huestis, MA AF Oyler, JM Cone, EJ Joseph, RE Moolchan, ET Huestis, MA TI Duration of detectable methamphetamine and amphetamine excretion in urine after controlled oral administration of methamphetamine to humans SO CLINICAL CHEMISTRY LA English DT Article ID COCAINE; PHARMACOKINETICS; GUIDELINES; STIMULANT; DEATH; ABUSE AB Background: Confirmation of a workplace drug test requires urinary methamphetamine (MAMP) and amphetamine (AMP) concentrations greater than or equal to500 and 200 mug/L, respectively, but cutoffs at half those values (250/100 mug/L) have been proposed. We determined the urinary excretion of MAMP after oral ingestion and examined the effect of using lower cutoffs on detection of exposure. Methods: Volunteers (n = 8) ingested four 10-mg doses of MAMP . HCl daily over 7 days, and five of them ingested four 20-mg doses 4 weeks later. After ingestion, the volunteers collected all urine specimens for 2 weeks. After solid-phase extraction, MAMP and AMP were measured by gas chromatography-positive chemical ionization mass spectrometry with dual silyl derivatization. Results: MAMP and AMP were generally detected in the first or second void (0.7-11.3 h) collected after drug administration, with concentrations of 82-1827 and 12180 mug/L, respectively. Peak MAMP concentrations (1871-6004 mug/L) after single doses occurred within 1.5-60 h. MAMP greater than or equal to500 mug/L was first detected in the first or second void (1-11 h) at 524-1871 mug/L. Lowering the MAMP cutoff to 250 mug/L changed the initial detection time little. AMP greater than or equal to200 mug/L was first detected in the 2nd-13th (7-20 h) post-administration voids. At a cutoff of 100 mug/L, AMP was first confirmed in the second to eighth void (4-13 h). Reducing the cutoff to 250/100 mug/L extended terminal MAMP detection by up to 24 h, increased total detection time by up to 34 h, and increased the total number of positive specimens by 48%. Conclusions: At the lower cutoff, initial detection times are earlier, detection windows are longer, and confirmation rates are increased. Elimination of the AMP requirement would increase detection rates and allow earlier detection. (C) 2002 American Association for Clinical Chemistry. C1 Natl Inst Drug Abuse, Chem & Drug Metab Sect, Intramural Res Program, Baltimore, MD 21224 USA. LLC, ConeChem Res, Severna Pk, MD 21146 USA. Amgen Inc, Thousand Oaks, CA 91320 USA. RP Oyler, JM (reprint author), Natl Inst Drug Abuse, Chem & Drug Metab Sect, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 40 TC 45 Z9 47 U1 0 U2 5 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD OCT PY 2002 VL 48 IS 10 BP 1703 EP 1714 PG 12 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 597UA UT WOS:000178238100010 PM 12324487 ER PT J AU Herzenberg, LA Parks, D Sahaf, B Perez, O Roederer, M Herzenberg, LA AF Herzenberg, LA Parks, D Sahaf, B Perez, O Roederer, M Herzenberg, LA TI The history and future of the fluorescence activated cell sorter and flow cytometry: A view from Stanford SO CLINICAL CHEMISTRY LA English DT Article; Proceedings Paper CT 34th Annual Oak Ridge Conference CY APR 25-26, 2002 CL LA JOLLA, CA ID T-CELLS; IDENTIFICATION; INFECTION; COLOR AB The Fluorescence Activated Cell Sorter (FACS) was invented in the late 1960s by Bonner, Sweet, Hulett, Herzenberg, and others to do flow cytometry and cell sorting of viable cells. Becton Dickinson Immunocytometry Systems introduced the commercial machines in the early 1970s, using the Stanford patent and expertise supplied by the Herzenberg Laboratory and a Becton Dickinson engineering group under Bernie Shoor. Over the years, we have increased the number of measured FACS dimensions (parameters) and the speed of sorting to where we now simultaneously measure 12 fluorescent colors plus 2 scatter parameters. In this history, I illustrate the great utility of this state-of-the-art instrument, which allows us to simultaneously stain, analyze, and then sort cells from small samples of human blood cells from AIDS patients, infants, stern cell transplant patients, and others. I also illustrate analysis and sorting of multiple subpopulations of lymphocytes by use of 8-12 colors. In addition, I review single cell sorting used to clone and analyze hybridomas and discuss other applications of FACS developed over the past 30 years, as well as give our ideas on the future of FACS. These ideas are currently being implemented in new programs using the internet for data storage and analysis as well as developing new fluorochromes, e.g., green fluorescent protein and tandem dyes, with applications in such areas as apoptosis, gene expression, cytokine expression, cell biochemistry, redox regulation, and AIDS. Finally, I describe new FACS methods for measuring activated kinases and phosphatases and redox active enzymes in individual cells simultaneously with cell surface phenotyping. Thus, key functions can be studied in various subsets of cells without the need for prior sorting. (C) 2002 American Association for Clinical Chemistry. C1 Stanford Univ, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Dept Microbiol & Immunol, Baxter Lab, Stanford, CA 94305 USA. NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. RP Herzenberg, LA (reprint author), Stanford Univ, Dept Genet, Stanford, CA 94305 USA. EM lenherz@darwin.stanford.edu RI Roederer, Mario/G-1887-2011 NR 26 TC 231 Z9 245 U1 4 U2 63 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD OCT PY 2002 VL 48 IS 10 BP 1819 EP 1827 PG 9 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 597UA UT WOS:000178238100033 PM 12324512 ER PT J AU Kaltsas, GA Kola, B Borboli, N Morris, DG Gueorguiev, M Swords, FM Czirjak, S Kirschner, LS Stratakis, CA Korbonits, M Grossman, AB AF Kaltsas, GA Kola, B Borboli, N Morris, DG Gueorguiev, M Swords, FM Czirjak, S Kirschner, LS Stratakis, CA Korbonits, M Grossman, AB TI Sequence analysis of the PRKAR1A gene in sporadic somatotroph and other pituitary tumours SO CLINICAL ENDOCRINOLOGY LA English DT Article ID SCHWANNOMAS CARNEY COMPLEX; FAMILIAL CARDIAC MYXOMAS; SPOTTY SKIN PIGMENTATION; ENDOCRINE OVERACTIVITY; REGULATORY SUBUNIT; SUPPRESSOR GENE; TUMORS; MUTATIONS; ADENOMAS; PATHOGENESIS AB OBJECTIVE Carney complex (CNC) is an autosomal dominant multiple neoplasia syndrome featuring cardiac, endocrine, cutaneous and neural tumours, as well as a variety of pigmented lesions of the skin and mucosa. Pituitary GH-secreting tumours are found in approximately 10% of patients with CNC. One of the genes responsible for CNC, the PRKAR1A gene located on human chromosome 17q22-24, has recently been cloned. This represents a putative tumour suppressor gene, coding for the type 1alpha regulatory subunit of protein kinase A (PKA), which is found to be mutated in approximately half of the patients with CNC. However, it is currently unclear as to whether similar mutations occur in sporadic pituitary tumours. We have therefore investigated a series of GH-secreting and other pituitary tumours for sequence abnormalities in the PRKAR1A gene. The mRNA produced by the PRKAR1A undergoes decay if it codes for a truncated protein; we therefore also determined PRKAR1A mRNA levels in the tumours, and compared them with known mutant PRKAR1A-carrying lymphocyte samples. METHODS We extracted RNA from a series of pituitary tumours, reverse transcribed it to cDNA, and directly sequenced the PRKAR1A coding sequence in 17 GH-secreting, three prolactin-secreting, three ACTH-secreting, one FSH-secreting and 10 nonfunctioning pituitary tumours. Lymphocyte and tumour tissue RNA from two patients with CNC was used as positive controls. Using duplex polymerase chain reaction (PCR) with the PRKAR1A and the 'housekeeping' gene GAPDH, we determined the relative expression of the PRKAR1A gene in the unknown as well as in the positive control samples. RESULTS AND CONCLUSION No mutations were found in any of the exons sequenced. Relative mRNA expression was not decreased in any of the sporadic pituitary tumour samples. The present data thus do not suggest a major role for the PRKAR1A tumour suppressor gene in sporadic GH-secreting or other pituitary tumours. C1 St Bartholomews Hosp, Dept Endocrinol, London EC1A 7BE, England. Inst Neurosurg, Budapest, Hungary. NICHHD, Unit Genet & Endocrinol, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Grossman, AB (reprint author), St Bartholomews Hosp, Dept Endocrinol, London EC1A 7BE, England. OI Czirjak, Sandor/0000-0002-8224-3561; Korbonits, Marta/0000-0002-4101-9432 NR 22 TC 49 Z9 51 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD OCT PY 2002 VL 57 IS 4 BP 443 EP 448 DI 10.1046/j.1365-2265.2002.01643.x PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 598KX UT WOS:000178276000003 PM 12354125 ER PT J AU El Sahly, HM Septimus, E Soini, H Septimus, J Wallace, RJ Pan, X Williams-Bouyer, N Musser, JM Graviss, EA AF El Sahly, HM Septimus, E Soini, H Septimus, J Wallace, RJ Pan, X Williams-Bouyer, N Musser, JM Graviss, EA TI Mycobacterium simiae pseudo-outbreak resulting from a contaminated hospital water supply in Houston, Texas SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 39th Annual Meeting of the Infectious-Diseases-Society-of-America CY OCT 25-28, 2001 CL SAN FRANCISCO, CALIFORNIA SP Infect Dis Soc Amer ID AIDS PATIENTS; NONTUBERCULOUS MYCOBACTERIA; AUGMENTATION MAMMAPLASTY; SPECIES ASSIGNMENT; FORTUITUM COMPLEX; INFECTION; AVIUM; INTRACELLULARE; SUSCEPTIBILITY; PSEUDOEPIDEMIC AB Various species of nontuberculous mycobacteria are known to cause nosocomial pseudo-outbreaks, but there have been no detailed reports of nosocomial Mycobacterium simiae pseudo-outbreaks. From April 1997 through February 2001, we recovered 65 M. simiae isolates from 62 patients at a community teaching hospital in Houston, Texas. The organism was grown in various water samples obtained in the hospital building and in professional building 1 but not in professional building 2, which has a separate water supply system. Thirty-one environmental and human outbreak-related M. simiae isolates had indistinguishable or closely related patterns on pulsed-field gel electrophoresis and were considered clonal. M. simiae can be a cause of nosocomial pseudo-outbreaks. The reservoir for this pseudo-outbreak was identified as a contaminated hospital water supply. C1 Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Mem Hermann Hlth Syst, Dept Med, Houston, TX USA. Univ Texas Hlth Ctr, Dept Microbiol, Tyler, TX 75710 USA. NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT USA. RP Graviss, EA (reprint author), Baylor Coll Med, Dept Pathol, Rm 209E,1 Baylor Plaza, Houston, TX 77030 USA. FU NIAID NIH HHS [N01-AO-02738] NR 45 TC 31 Z9 31 U1 0 U2 3 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD OCT 1 PY 2002 VL 35 IS 7 BP 802 EP 807 DI 10.1086/342331 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 594DF UT WOS:000178032900004 PM 12228816 ER PT J AU Bartlett, JG Inglesby, TV Borio, L AF Bartlett, JG Inglesby, TV Borio, L TI Management of anthrax SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID INHALATIONAL ANTHRAX; UNITED-STATES; BIOTERRORISM; PATHOLOGY AB From 3 October 2001 through 16 November 2001, in the United States, there were 18 confirmed cases of inhalational and cutaneous anthrax, an additional 4 suspected cases of cutaneous anthrax, and 5 deaths due to inhalational anthrax. Although the number of cases was relatively small, this experience brought bioterrorism and its potential to sharp focus as thousands of people began receiving prophylactic antibiotics after possible exposure to anthrax spores. These events have resulted in a substantial impact on the health care system, including the rewriting of pneumonia guidelines, new emphasis on identification of microbial etiology, substantial infusion of funds for bioterrorism-related research, and a sudden mandate for regional disaster and public health planning. This article provides clinicians with clinically relevant information about the diagnosis and management of anthrax. C1 Johns Hopkins Univ, Sch Med, Johns Hopkins Univ Ctr Civilian Biodef Strateg, Baltimore, MD 21287 USA. NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD USA. RP Bartlett, JG (reprint author), Johns Hopkins Univ, Sch Med, Johns Hopkins Univ Ctr Civilian Biodef Strateg, 1830 E Monument St,Rm 439, Baltimore, MD 21287 USA. NR 28 TC 59 Z9 62 U1 0 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD OCT 1 PY 2002 VL 35 IS 7 BP 851 EP 858 DI 10.1086/341902 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 594DF UT WOS:000178032900010 PM 12228822 ER PT J AU Garcia, HH Evans, CAW Nash, TE Takayanagui, OM White, AC Botero, D Rajshekhar, V Tsang, VCW Schantz, PM Allan, JC Flisser, A Correa, D Sarti, E Friedland, JS Martinez, SM Gonzalez, AE Gilman, RH Del Brutto, OH AF Garcia, HH Evans, CAW Nash, TE Takayanagui, OM White, AC Botero, D Rajshekhar, V Tsang, VCW Schantz, PM Allan, JC Flisser, A Correa, D Sarti, E Friedland, JS Martinez, SM Gonzalez, AE Gilman, RH Del Brutto, OH TI Current consensus guidelines for treatment of neurocysticercosis SO CLINICAL MICROBIOLOGY REVIEWS LA English DT Review ID TAENIA-SOLIUM CYSTICERCOSIS; SINGLE-DAY PRAZIQUANTEL; GIANT SUBARACHNOID CYSTICERCI; DOUBLE-BLIND TRIAL; SMALL CT LESIONS; CEREBRAL CYSTICERCOSIS; ALBENDAZOLE THERAPY; MEDICAL-TREATMENT; INDIAN PATIENTS; TOMOGRAPHIC LESIONS AB Taenia solium neurocysticercosis is a common cause of epileptic seizures and other neurological morbidity in most developing countries. It is also an increasingly common diagnosis in industrialized countries because of immigration from areas where it is endemic. Its clinical manifestations are highly variable and depend on the number, stage, and size of the lesions and the host's immune response. In pan due to this variability, major discrepancies exist in the treatment of neurocysticercosis. A panel of experts in taeniasis/cysticercosis discussed the evidence on treatment of neurocysticercosis for each clinical presentation, and we present the panel's consensus and areas of disagreement. Overall, four general recommendations were made: (i) individualize therapeutic decisions, including whether to use antiparasitic drugs, based on the number, location, and viability of the parasites within the nervous system; (ii) actively manage growing cysticerci either with antiparasitic drugs or surgical excision; (iii) prioritize the management of intracranial hypertension secondary to neurocysticercosis before considering any other form of therapy; and (iv) manage seizures as done for seizures due to other causes of secondary seizures (remote symptomatic seizures) because they are due to an organic focus that has been present for a long time. C1 Inst Ciencias Neurol, Cysticercosis Unit, Lima 1, Peru. Univ Peruana Cayetano Heredia, Dept Microbiol, Lima, Peru. Univ Peruana Cayetano Heredia, Dept Pathol, Lima, Peru. Univ Nacl Mayor San Marcos, Sch Vet Med, Lima 14, Peru. Univ Cambridge, Sch Clin, Cambridge, England. Imperial Coll Sci Technol & Med, London, England. Univ Salford, Dept Sci Biol, Salford M5 4WT, Lancs, England. Pfizer Inc, Sandwich, Kent, England. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Int Hlth, Sch Hyg & Publ Hlth, Baltimore, MD USA. Univ Sao Paulo, Dept Neurol, Sch Med Ribeirao Preto, BR-14049 Ribeirao Preto, Brazil. Baylor Coll Med, Infect Dis Sect, Dept Med, Houston, TX 77030 USA. Inst Colombiano Med Trop, Medellin, Colombia. Christian Med Coll & Hosp, Dept Neurol Sci, Vellore 632004, Tamil Nadu, India. Ctr Dis Control, Natl Ctr Infect Dis, Div Parasit Dis, Atlanta, GA 30333 USA. Univ Nacl Autonoma Mexico, Sch Med, Mexico City 04510, DF, Mexico. Inst Nacl Pediat, Secretaria Salud, Mexico City, DF, Mexico. Inst Nacl Diagnost & Referencia Epidemiol, Secretaria Salud, Mexico City, DF, Mexico. Hosp Clin Kennedy, Dept Neurol Sci, Guayaquil, Ecuador. RP Garcia, HH (reprint author), Inst Ciencias Neurol, Cysticercosis Unit, Jr Ancash 1271, Lima 1, Peru. RI Takayanagui, Osvaldo/C-8159-2013; OI Takayanagui, Osvaldo/0000-0002-8190-0275; Evans, Carlton/0000-0002-6873-5447; White, A Clinton/0000-0002-9668-4632 NR 111 TC 198 Z9 210 U1 0 U2 6 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0893-8512 J9 CLIN MICROBIOL REV JI Clin. Microbiol. Rev. PD OCT PY 2002 VL 15 IS 4 BP 747 EP + DI 10.1128/CMR.15.4.747-756.2002 PG 11 WC Microbiology SC Microbiology GA 647MT UT WOS:000181097200010 PM 12364377 ER PT J AU Ageyama, N Hanazono, Y Shibata, H Ohto, K Ono, F Nagashima, T Ueda, Y Donahue, RE Hasegawa, M Ozawa, K Yoshikawa, Y Terao, K AF Ageyama, N Hanazono, Y Shibata, H Ohto, K Ono, F Nagashima, T Ueda, Y Donahue, RE Hasegawa, M Ozawa, K Yoshikawa, Y Terao, K TI Safe and efficient methods of autologous hematopoietic stem cell transplantation for biomedical research in cynomolgus monkeys SO COMPARATIVE MEDICINE LA English DT Article ID NONHUMAN PRIMATE MODEL; BLOOD CD34(+) CELLS; PERIPHERAL-BLOOD; MACACA-FASCICULARIS; GENE-TRANSFER; IN-VIVO; HUMAN-DISEASE; MARROW-CELLS; EXPRESSION; MURINE AB We have established safe and efficient methods for autologous hematopoietic stem cell (HSC) transplantation in cynomolgus monkeys (Macaca fascicularis) that include regimens of supportive care to ensure survival during hematopoietic reconstitution following otherwise lethal total body irradiation. Eleven young adult cynomolgus monkeys were studied. Bone marrow was aspirated from the ilium and/or tuber ischiae after administration of recombinant human stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF). Using the immunomagnetic selection method, CD34(+) cells were then isolated (90 to 95% pure) as a fraction containing HSCs. Just prior to transplantation, the animals received myeloablative total body irradiation-500 to 550 cGy daily for two days. The monkeys re-infused with CD34(+) cells developed moderate to severe myelosuppression, with some animals requiring intravenous hyperalimentation, antibiotic administration, and blood transfusion. Hematopoiesis was restored in all animals after transplantation. It took 12 days, on average, until the peripheral white blood cell count reached more than 1,000 cells/mul. Up to two years after transplantation, signs of radiation-induced pneumonitis or other radiation-related disorders were not evident at the aforementioned dose of irradiation. This transplantation model will be useful for testing new approaches using HSCs for therapy of many diseases and will offer unique insights into the biology of these cells. C1 Jichi Med Sch, Div Genet Therapeut, Ctr Mol Med, Minami Kawachi, Tochigi 3290498, Japan. Corp Prod & Res Lab Primates, Tsukuba, Ibaraki 3050843, Japan. Tsukuba Primate Ctr, Natl Inst Infect Dis, Tsukuba, Ibaraki 3050843, Japan. DNAVEC Res Inc, Tsukuba, Ibaraki 3050856, Japan. NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. Univ Tokyo, Dept Biomed Sci, Grad Sch Agr & Life Sci, Tokyo 1138657, Japan. RP Hanazono, Y (reprint author), Jichi Med Sch, Div Genet Therapeut, Ctr Mol Med, Minami Kawachi, Tochigi 3290498, Japan. NR 40 TC 9 Z9 9 U1 0 U2 0 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI MEMPHIS PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA SN 1532-0820 J9 COMPARATIVE MED JI Comparative Med. PD OCT PY 2002 VL 52 IS 5 BP 445 EP 451 PG 7 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA 606VF UT WOS:000178754500010 PM 12405638 ER PT J AU Westphal, H AF Westphal, H TI International stem cell research considerations SO COMPTES RENDUS BIOLOGIES LA English DT Article DE stem cells; human embryos AB Legislative bodies in the international arena and in individual countries are actively engaged in developing policies regarding the establishment, distribution and use of human embryonic stem cells. Present and anticipated policies concerning research on human adult and embryonic stem cells of possible medical importance reflect the wide spectrum of popular views that range from complete rejection to enthusiastic support. Since the public debate concerning the use of human gametes or embryos for research purposes is not likely to abate anytime soon, all the more urgent becomes the quest for alternative approaches toward generating stem cells that are not embryonic and yet are pluripotent. C1 NICHHD, Lab Mammalian Genes & Dev, Natl Inst Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Westphal, H (reprint author), NICHHD, Lab Mammalian Genes & Dev, Natl Inst Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 1631-0691 J9 CR BIOL JI C. R. Biol. PD OCT PY 2002 VL 325 IS 10 BP 1045 EP 1048 DI 10.1016/S1631-0691(02)01523-8 PG 4 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 626GX UT WOS:000179864400009 PM 12494502 ER PT J AU Berger, VW AF Berger, VW TI Improving the information content of categorical clinical trial endpoints SO CONTROLLED CLINICAL TRIALS LA English DT Article DE binary test; composite endpoint; Lancaster decomposition; omnibus test ID RANDOMIZED CONTROLLED TRIAL; TESTS; PREVENTION; THERAPY; CANCER; TABLES AB Because the severity of most diseases can be measured nonuniquely, different medical interventions with different mechanisms of action may be evaluated differently, even in the same patient population. Complicating this further is the fact that even for a given medical intervention, it may not be clear which endpoint, if any, will be most likely to show an intervention effect. For these and other reasons, clinical trials typically involve the evaluation of multiple safety and efficacy endpoints. As information accrues about diseases and patient populations, some endpoints may cease to be useful, but the trend would still likely be toward increasing numbers of potential endpoints. This trend would provide sponsors with increasing numbers of choices for the primary efficacy endpoint. If the endpoint selected as primary is not the optimal one for demonstrating the superiority of the experimental medical intervention, then a safe and effective medical intervention may be mistakenly found to be otherwise. On the other hand, the sponsor may find the endpoint that makes its case and not study other endpoints that would have shown the experimental intervention to be inferior, in some way, to the control intervention. As such, the reliance of medical decisions on narrow primary endpoints can lead to inflation of both the type I and type 11 error rates. To address these concerns, we propose that all endpoints, especially the primary endpoint, be as informative as possible. This could be accomplished by combining some endpoints into composite endpoints. To avoid losing information in this transformation, we define the concept of information-preserving composite endpoints and provide information concerning when this type of composite endpoint would be most useful. Specifically, we define the concept of joint fusibility of a set of endpoints and note that this property confers upon the derived information-preserving composite endpoint the greatest amenability to statistical analysis. We also point out that using composite endpoints allows sponsors the most discretion in selecting their primary between-group statistical analysis. We illustrate these ideas with examples from a variety of therapeutic areas. (C) 2002 Elsevier Science Inc. All rights reserved. C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA. Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA. RP Berger, VW (reprint author), NCI, Biometry Res Grp, Execut Plaza N,Suite 3131,6130 Execut Blvd,MSC 73, Bethesda, MD 20892 USA. NR 38 TC 22 Z9 23 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD OCT PY 2002 VL 23 IS 5 BP 502 EP 514 AR PII S0197-2456(02)00233-7 DI 10.1016/S0197-2456(02)00233-7 PG 13 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 599GR UT WOS:000178326200004 PM 12392864 ER PT J AU Renfroe, EG Heywood, G Foreman, L Schron, E Powell, J Baessler, C Warwick, D Morris, M Hallstrom, A AF Renfroe, EG Heywood, G Foreman, L Schron, E Powell, J Baessler, C Warwick, D Morris, M Hallstrom, A CA AVID Coordinators Investigators TI The end-of-study patient survey: methods influencing response rate in the AVID Trial SO CONTROLLED CLINICAL TRIALS LA English DT Article DE Antiarrhythmics Versus Implantable Defibrillators Trial (AVID); antiarrhythmic drugs (AAD); implantable cardioverter defibrillator (ICD); patient survey; quality of life; randomized clinical trial; trial satisfaction; ventricular arrhythmias ID CLINICAL-TRIAL; PARTICIPATION; SATISFACTION AB Patient surveys are commonly distributed at the end of a multicenter clinical trial. This Antiarrhythmics Versus Implantable Defibrillators (AVID) substudy prospectively explored the relationship between methods used in distributing a survey and the quantity of responses received. AVID was a multicenter, randomized trial comparing survival in arrhythmia patients treated with antiarrhythmic drugs versus implantable defibrillators. At study termination, a patient satisfaction survey was mailed to the 664 surviving participants. Questions included reasons for study participation, study benefits and problems and quality of care. Survey mailings were stratified by four factors in a 2 X 2 X 2 X 2 factorial design: delivery mode (overnight vs. regular mail), certificate of appreciation, timing of administration ("early" vs. "late") and cover letter signed by a physician versus coordinator. Patients were randomly assigned to received one of 16 combinations of these four factors. Clinical characteristics and response rates were evaluated. Patients were more likely to return surveys delivered by overnight mail (75% vs. 68%, p=0.04), with no certificate of appreciation enclosed (75% vs. 68%, p=0.05) and administered close to the time of study closeout (79% vs. 72%, p=0.085). Compared to the 184 nonrespondents, the 456 (71%) respondents were older, Caucasian, lived with others, were high school graduates and less likely to have Medicare/Medicaid or HMO insurance (p<0.03). Physician recommendation was the most common reason cited for trial participation. Main benefits included increased knowledge of their medical condition and improved health. Reported problems included parking, transportation and excess clinic wait time. This randomized study demonstrated that methods of patient survey distribution affect the survey return rate. Additional studies should explore mechanisms for maximizing return rates. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Univ Washington, Seattle, WA 98195 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA. NHLBI, Bethesda, MD 20892 USA. Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA. Baystate Med Ctr, Springfield, MA USA. RP Renfroe, EG (reprint author), AVID CTC, 1107 NE 45th St,Suite 505, Seattle, WA 98105 USA. FU NHLBI NIH HHS [N01 HC-25117] NR 11 TC 14 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD OCT PY 2002 VL 23 IS 5 BP 521 EP 533 AR PII S0197-2456(02)00225-8 DI 10.1016/S0197-2456(02)00225-8 PG 13 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 599GR UT WOS:000178326200006 PM 12392866 ER PT J AU Sumner, CJ Golden, JA Hemphill, JC AF Sumner, CJ Golden, JA Hemphill, JC TI Should thrombolysis be contraindicated in patients with cerebral arteriovenous malformations? SO CRITICAL CARE MEDICINE LA English DT Article DE pulmonary embolus; cerebral arteriovenous malformation; thrombolysis; intracranial hemorrhage ID TISSUE-PLASMINOGEN-ACTIVATOR; ACUTE MYOCARDIAL-INFARCTION; INTRACRANIAL HEMORRHAGE; PULMONARY-EMBOLISM; THERAPY; RISK; FREQUENCY AB Objectives: To report the successful and uncomplicated use of systemic thrombolysis for massive pulmonary embolism in a patient with a known cerebral arteriovenous malformation and to suggest that the presence of an unruptured arteriovenous malformation or aneurysm should not be considered an absolute contraindication to systemic thrombolysis. Design: Case report. Setting: A 16-bed adult neurologic/medical intensive care unit in a university hospital. Patients: A patient developed a massive pulmonary embolism the morning after elective cerebral embolization of a large unruptured cerebral arteriovenous malformation. Intervention. Radial artery catheterization, arterial blood gas measurements, mechanical ventilation, vasopressors, pulmonary perfusion scan, echocardiogram, head computed tomography, heparin therapy, and systemic recombinant tissue plasminogen activator therapy. Measurement and Main Results: The patient required emergent mechanical ventilation and vasopressor support for respiratory and hemodynamic failure. Echocardiogram showed acute right heart failure, and pulmonary perfusion scan demonstrated massive pulmonary embolism. Despite intravenous heparin therapy, the patient had worsening hypotension and acidosis and we therefore treated with recombinant tissue plasminogen activator. Within the next day the patient was weaned from vasopressor support and extubated. Neurologic examination remained normal, and follow-up head computed tomography revealed no evidence of intracranial hemorrhage. Conclusion: Known arteriovenous malformations or aneurysms are considered a contra indication to thrombolysis, although the true risk of thrombolysis-precipitated intracranial hemorrhage is unknown. We believe that this risk is low in the setting of a previously unruptured arteriovenous malformation or aneurysm. The decision to use systemic thrombolysis in a patient with a known vascular malformation should be individualized. C1 NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. RP Sumner, CJ (reprint author), NINDS, Neurogenet Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 15 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD OCT PY 2002 VL 30 IS 10 BP 2359 EP 2362 DI 10.1097/01.CCM.0000025211.61411.59 PG 4 WC Critical Care Medicine SC General & Internal Medicine GA 609GB UT WOS:000178894300028 PM 12394968 ER PT J AU Seftor, EA Meltzer, PS Schatteman, GC Gruman, LM Hess, AR Kirschmann, DA Seftor, REB Hendrix, MJC AF Seftor, EA Meltzer, PS Schatteman, GC Gruman, LM Hess, AR Kirschmann, DA Seftor, REB Hendrix, MJC TI Expression of multiple molecular phenotypes by aggressive melanoma tumor cells: role in vasculogenic mimicry SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY LA English DT Review DE epithelial cell kinase (ECK, EphA2); microarray; vasculogenic mimicry; melanoma; VE-eadherin ID PROTEIN-TYROSINE KINASE; VASCULAR ENDOTHELIAL-CADHERIN; BREAST-CANCER METASTASIS; GENE-EXPRESSION; MALIGNANT-MELANOMA; UP-REGULATION; CDNA CLONING; VE-CADHERIN; ANGIOGENESIS; PROGRESSION AB Cutaneous melanoma has been increasing at an alarming rate over the past two decades, however, there are no acceptable histopathological markers that classify various stages of melanoma progression. Recently, the molecular analysis of cancer has contributed significantly to our understanding of the cellular and molecular underpinnings of tumor progression, The data summarized in this review describe the molecular signature of aggressive cutaneous melanoma cells as that of multiple phenotypes which may be similar to a pluripotent, embryonic-like phenotype. An example of the plasticity of this phenotype is demonstrated by the ability of aggressive melanoma cells to engage in vasculogenic mimiery and neovascularization. A review of t lie current data demonstrating important cellular and molecular determinants of human melanoma vasculogenic mimery is presented. These findings should stimulate additional studies to address the biological relevance of the multiple molecular phenotypes expressed by aggressive melanoma cells which may lead to the development of new diagnostic markers and therapeutic targets for clinical intervention. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved. C1 Univ Iowa, Dept Anat & Cell Biol, Iowa City, IA 52242 USA. Univ Iowa, Holden Comprehens Canc Ctr, Iowa City, IA 52242 USA. NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA. RP Hendrix, MJC (reprint author), Univ Iowa, Dept Anat & Cell Biol, 51 Newton Rd,1-100 BSB, Iowa City, IA 52242 USA. FU NCI NIH HHS [CA59702, CA83137]; NIDDK NIH HHS [DK55965] NR 54 TC 83 Z9 91 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PD OCT PY 2002 VL 44 IS 1 BP 17 EP 27 AR PII S1040-8428(01)00199-8 DI 10.1016/S1040-8428(01)00199-8 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA 613HN UT WOS:000179127000002 PM 12398997 ER PT J AU Parada, LA McQueen, PG Munson, PJ Misteli, T AF Parada, LA McQueen, PG Munson, PJ Misteli, T TI Conservation of relative chromosome positioning in normal and cancer cells SO CURRENT BIOLOGY LA English DT Article ID ATM-DEFICIENT MICE; NUCLEI; ORGANIZATION; CHROMATIN; PROXIMITY; TRANSLOCATIONS; ARRANGEMENTS; LOCALIZATION; ABERRATIONS; RADIATION AB Chromosomes exist in the interphase nucleus as individual chromosome territories. It is unclear to what extent chromosome territories occupy particular positions with respect to each other and how structural rearrangements, such as translocations, affect chromosome organization within the cell nucleus. Here we analyze the relative interphase positioning of chromosomes in mouse lymphoma cells compared to normal splenocytes. We show that in a lymphoma cell line derived from an ATM(-/-) mouse, two translocated chromosomes are preferentially positioned in close proximity to each other. The relative position of the chromosomes involved in these translocations is conserved in normal splenocytes. Relative positioning of chromosomes in normal splenocytes is not due to their random distribution in the interphase nucleus and persists during mitosis. These observations demonstrate that the relative arrangement of chromosomes in the interphase nucleus can be conserved between normal and cancer cells and our data support the notion that physical proximity facilitates rearrangements between chromosomes. C1 NCI, NIH, Bethesda, MD 20892 USA. NIH, Math & Stat Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Misteli, T (reprint author), NCI, NIH, Bethesda, MD 20892 USA. NR 26 TC 130 Z9 134 U1 0 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD OCT 1 PY 2002 VL 12 IS 19 BP 1692 EP 1697 AR PII S0960-9822(02)01166-1 DI 10.1016/S0960-9822(02)01166-1 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 600RC UT WOS:000178404100023 PM 12361574 ER PT J AU Yamada, KM Kemler, R AF Yamada, KM Kemler, R TI Cell-to-cell contact and extracellular matrix - Editorial overview SO CURRENT OPINION IN CELL BIOLOGY LA English DT Editorial Material C1 NIDCR, NIH, Bethesda, MD 20892 USA. Max Planck Inst Immunbiol, D-79108 Freiburg, Germany. RP Yamada, KM (reprint author), NIDCR, NIH, Bldg 30,Room 421,30 Convent Dr,MSC 4370, Bethesda, MD 20892 USA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 0 TC 4 Z9 4 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD OCT PY 2002 VL 14 IS 5 BP 527 EP 530 DI 10.1016/S0955-0674(02)00376-9 PG 4 WC Cell Biology SC Cell Biology GA 590TJ UT WOS:000177837900002 ER PT J AU Cukierman, E Pankov, R Yamada, KM AF Cukierman, E Pankov, R Yamada, KM TI Cell interactions with three-dimensional matrices SO CURRENT OPINION IN CELL BIOLOGY LA English DT Review ID EXTRACELLULAR-MATRIX; COLLAGEN MATRICES; 3-DIMENSIONAL COLLAGEN; FIBROBLAST QUIESCENCE; BASEMENT-MEMBRANE; MUSCLE-CELLS; ADHESION; FIBRONECTIN; INTEGRIN; DIFFERENTIATION AB Signaling and other cellular functions differ in three-dimensional compared with two-dimensional systems. Cell adhesion structures can evolve in vitro towards in-vivo-like adhesions with distinct biological activities. In this review, we examine recent advances in studies of interactions of fibroblasts with collagen gels and fibronectin-containing matrices that mimic in vivo three-dimensional microenvironments. These three-dimensional systems are illuminating mechanisms of cell-matrix interactions in living organisms. C1 NIDCR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. RP Cukierman, E (reprint author), NIDCR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. RI Ladoux, Benoit/A-9879-2013; Pankov, Roumen/B-3284-2014; OI Pankov, Roumen/0000-0002-3157-3659; Yamada, Kenneth/0000-0003-1512-6805 NR 51 TC 541 Z9 559 U1 6 U2 88 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD OCT PY 2002 VL 14 IS 5 BP 633 EP 639 DI 10.1016/S0955-0674(02)00364-2 PG 7 WC Cell Biology SC Cell Biology GA 590TJ UT WOS:000177837900017 PM 12231360 ER PT J AU Kruth, HS AF Kruth, HS TI Sequestration of aggregated low-density lipoproteins by macrophages SO CURRENT OPINION IN LIPIDOLOGY LA English DT Review DE LDL; aggregation; macrophages; patocytosis; phagocytosis; pinocytosis; endocytosis ID SURFACE-CONNECTED COMPARTMENTS; MOUSE PERITONEAL-MACROPHAGES; CHOLESTERYL ESTER; OXIDIZED LDL; BETA-VLDL; METABOLISM; RECEPTOR; ATHEROSCLEROSIS; ACCUMULATION; DEGRADATION AB Purpose of review Evidence suggests that much of the LDL in atherosclerotic plaques is aggregated. Aggregation of LDL could be an important factor that determines how this lipoprotein is metabolized by plaque macrophages and the fate of aggregated LDL cholesterol within plaques. This review discusses a novel endocytic pathway by which macrophages process aggregated LDL. Recent findings Recently, it has been shown that aggregated LDL can be sequestered in macrophage surface-connected compartments and plasma membrane invaginations by a process termed patocytosis. In contrast to rapid degradation of LDL and aggregated LDL taken up by macrophages through pinocytosis and phagocytosis, respectively, aggregated LDL sequestered in macrophages undergoes only limited degradation. Macrophages can disaggregate and release sequestered aggregated LDL by activating plasminogen to plasmin. Plasmin degrades LDL apolipoprotein B sufficiently to disaggregate the aggregated LDL, releasing it from the macrophage surface-connected compartments. In contrast, activating macrophages with phorbol-myristate-acetate stimulates degradation of aggregated LDL and inhibits plasminogen-mediated release of the aggregated lipoprotein from macrophage surface-connected compartments. Summary Macrophage sequestration of aggregated LDL is a unique endocytic pathway relevant not only to the processing of aggregated LDL in atherosclerotic plaques but also for the processing of other materials, such as hydrophobic particles that trigger this endocytic pathway. Macrophage sequestration of aggregated LDL can result in different fates for the aggregated LDL, depending on the state of macrophage activation and the functioning of the plasminogen-based fibrinolytic system. Patocytosis of aggregated LDL should be considered in addition to phagocytosis as a possible uptake pathway in studies of macrophage processing of aggregated LDL. C1 NHLBI, Sect Expt Atherosclerosis, NIH, Bethesda, MD 20892 USA. RP Kruth, HS (reprint author), NHLBI, Sect Expt Atherosclerosis, NIH, Bldg 10,Room 5N113,10 Ctr Dr MSC-1422, Bethesda, MD 20892 USA. NR 38 TC 59 Z9 62 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0957-9672 J9 CURR OPIN LIPIDOL JI Curr. Opin. Lipidology PD OCT PY 2002 VL 13 IS 5 BP 483 EP 488 DI 10.1097/00041433-200210000-00003 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Peripheral Vascular Disease SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Cardiovascular System & Cardiology GA 601FL UT WOS:000178435800003 PM 12352011 ER PT J AU Tisdale, JF Wilson, DR AF Tisdale, JF Wilson, DR TI Clinical aspects of gene therapy SO CURRENT OPINION IN MOLECULAR THERAPEUTICS LA English DT Editorial Material ID CELLS; LYMPHOCYTES; DISEASE; MARROW C1 NIDDK, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA. Introgen Therapeut Inc, Houston, TX 77030 USA. RP Tisdale, JF (reprint author), NIDDK, Mol & Clin Hematol Branch, NIH, Bldg 10,Room 9N116,9000 Rockville Pike, Bethesda, MD 20892 USA. EM JohnTis@intra.niddk.nih.gov; d.wilson@introgen.com NR 15 TC 0 Z9 0 U1 0 U2 0 PU THOMSON REUTERS (SCIENTIFIC) LTD PI LONDON PA 77 HATTON GARDEN, LONDON, EC1N 8JS, ENGLAND SN 1464-8431 J9 CURR OPIN MOL THER JI Curr. Opin. Mol. Ther. PD OCT PY 2002 VL 4 IS 5 BP 417 EP 418 PG 2 WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Research & Experimental Medicine GA 667XM UT WOS:000182260200001 PM 12435041 ER PT J AU Hu, J Dunbar, CE AF Hu, J Dunbar, CE TI Update on hematopoietic stem cell gene transfer using non-human primate models SO CURRENT OPINION IN MOLECULAR THERAPEUTICS LA English DT Article DE foamy virus; gene therapy; hematopoietic stem cell; lentivirus; non-human primate; retrovirus ID BONE-MARROW CELLS; IN-VIVO SELECTION; NOD/SCID-REPOPULATING CELLS; FOAMY VIRUS VECTORS; SEVERE COMBINED IMMUNODEFICIENCY; PSEUDOTYPED RETROVIRAL VECTORS; FIBRONECTIN FRAGMENT CH-296; RHESUS PERIPHERAL-BLOOD; APE LEUKEMIA-VIRUS; HUMAN MDR1 GENE AB Gene transfer into hematopoietic stem cells (HSCs) using integrating vectors is an attractive treatment strategy for many genetic and hematological diseases. The preclinical testing of gene transfer approaches in non-human primates and other large animal models will be invaluable in order to assess toxicity and efficacy, as their HSC biology is much more closely related to humans than murine models. Gene transfer studies targeting HSCs in non-human primates have focused on optimizing gene transfer efficiency, and significant advances have been achieved using standard retroviral vectors. Utilization of lentiviral and other alternative vector systems are still very preliminary in large animal models. Further development of post-transduction selection and/or expansion strategies using drug-resistance or amplifier genes will most likely be necessary for clinical applications. C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Dunbar, CE (reprint author), NHLBI, Hematol Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 84 TC 14 Z9 14 U1 0 U2 0 PU CURRENT DRUGS LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1P 6LB, ENGLAND SN 1464-8431 J9 CURR OPIN MOL THER JI Curr. Opin. Mol. Ther. PD OCT PY 2002 VL 4 IS 5 BP 482 EP 490 PG 9 WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Research & Experimental Medicine GA 667XM UT WOS:000182260200010 PM 12435050 ER PT J AU Allende, ML Proia, RL AF Allende, ML Proia, RL TI Lubricating cell signaling pathways with gangliosides SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Review ID MYELIN-ASSOCIATED GLYCOPROTEIN; GROWTH-FACTOR RECEPTOR; ADHESION MOLECULE TAG-1; COMPLEX GANGLIOSIDES; LIPID RAFTS; GLYCOSPHINGOLIPID SYNTHESIS; SUBSTRATE DEPRIVATION; GOLGI-APPARATUS; MICE; GM3 AB Gangliosides - glycosphingolipids that contain sialic acid - are concentrated in plasma membrane lipid domains that are specialized for cell signaling. Recent evidence indicates that gangliosides have two different roles in cell signaling. They can act in cis to modulate tyrosine kinase receptor function and in trans as ligands for receptors that facilitate communication between cells. These signaling functions of gangliosides may be potential therapeutic targets in cancer, diabetes and nerve regeneration. C1 NIDDKD, NIH, Genet Dev & Dis Branch, Bethesda, MD 20892 USA. RP Allende, ML (reprint author), NIDDKD, NIH, Genet Dev & Dis Branch, Bethesda, MD 20892 USA. RI Proia, Richard/A-7908-2012 NR 56 TC 112 Z9 116 U1 0 U2 3 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0959-440X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD OCT PY 2002 VL 12 IS 5 BP 587 EP 592 DI 10.1016/S0959-440X(02)00376-7 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 604PP UT WOS:000178630500004 PM 12464309 ER PT J AU Dauter, Z AF Dauter, Z TI New approaches to high-throughput phasing SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Review ID PROTEIN-STRUCTURE DETERMINATION; HEAVY-ATOM DERIVATIVES; QUICK-SOAK METHOD; SOFT X-RAYS; ANOMALOUS-SCATTERING; MOLECULAR REPLACEMENT; MAXIMUM-LIKELIHOOD; S-ATOMS; MACROMOLECULAR CRYSTALLOGRAPHY; DENSITY MODIFICATION AB Recent progress in macromolecular phasing, in part stimulated by the high-throughput structural biology initiatives, has made this crucial stage of the elucidation of crystal structures easier and more automatic. A quick soak in various salts leads to the rapid incorporation of the anomalously scattering ions, suitable for phasing by MAD (multiwavelength anomalous dispersion), SAD (single-wavelength anomalous dispersion) or MIR (multiple isomorphous replacement) methods. The availability of stable synchrotron beam lines equipped with elaborate hardware control and sophisticated data processing programs makes it possible to collect very accurate diffraction data and to solve structures from the very weak anomalous signal of such atoms as sulfur or phosphorus, inherently present in macromolecules. The current progress in phasing, coupled with the parallel advances in protein crystallization, diffraction data collection and so on, suggests that, in the near future, the process of macromolecular crystal structure elucidation may become fully automatic. C1 NCI, Brookhaven Natl Lab, Synchrotron Radiat Res Sect, Upton, NY 11973 USA. RP Dauter, Z (reprint author), NCI, Brookhaven Natl Lab, Synchrotron Radiat Res Sect, Bldg 725A-X9, Upton, NY 11973 USA. EM dauter@bnl.gov NR 47 TC 35 Z9 36 U1 1 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0959-440X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD OCT PY 2002 VL 12 IS 5 BP 674 EP 678 DI 10.1016/S0959-440X(02)00372-X PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 604PP UT WOS:000178630500017 PM 12464322 ER PT J AU Krtolica, A de Solorzano, CO Lockett, S Campisi, J AF Krtolica, A de Solorzano, CO Lockett, S Campisi, J TI Quantification of epithelial cells in coculture with fibroblasts by fluorescence image analysis SO CYTOMETRY LA English DT Article DE cell quantification; coculture; image analysis; epithelial-stromal interactions; cell proliferation; green fluorescent protein; 4,6-diamidino-2-phenylindole; fluorescence microscopy ID TUMOR-STROMAL INTERACTIONS; CYTOMETRY AB Background: To demonstrate that senescent fibroblasts stimulate the proliferation and neoplastic transformation of premalignant epithelial cells (Krtolica et al.: Proc Natl Acad Sci USA 98:12072-12077, 2001), we developed methods to quantify the proliferation of epithelial cells cocultured with fibroblasts. Methods: We stained epithelial-fibroblast cocultures with the fluorescent DNA-intercalating dye 4,6-diamidino2-phenyhndole (DAPI), or expressed green fluorescent protein (GFP) in the epithelial cells, and then cultured them with fibroblasts. The cocultures were photographed under an inverted microscope with appropriate filters, and the fluorescent images were captured with a digital camera. We modified an image analysis program to selectively recognize the smaller, more intensely fluorescent epithelial cell nuclei in DAPI-stained cultures and used the program to quantify areas with DAPI fluorescence generated by epithelial nuclei or GFP fluorescence generated by epithelial cells in each field. Results: Analysis of the image areas with DAPI and GFP fluorescences produced nearly identical quantification of epithelial cells in coculture with fibroblasts. We confinned these results by manual counting. In addition, GFP labeling permitted kinetic studies of the same coculture over multiple time points. Conclusions: The image analysis-based quantification method we describe here is an easy and reliable way to monitor cells in coculture and should be useful for a variety of cell biological studies. (C) 2002 Wiley-Liss, Inc. C1 Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA. NCI, Frederick, MD 21701 USA. RP Campisi, J (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, 1 Cyclotron Rd,MS 84-171, Berkeley, CA 94720 USA. RI Ortiz de Solorzano, Carlos/G-3278-2010 OI Ortiz de Solorzano, Carlos/0000-0001-8720-0205 FU NIA NIH HHS [AG09909]; PHS HHS [N01-C0-56000] NR 21 TC 18 Z9 18 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0196-4763 J9 CYTOMETRY JI Cytometry PD OCT 1 PY 2002 VL 49 IS 2 BP 73 EP 82 DI 10.1002/cyto.10149 PG 10 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 601MY UT WOS:000178451400005 PM 12357463 ER PT J AU Orlic, D AF Orlic, D TI Adult BM stem cells regenerate mouse myocardium SO CYTOTHERAPY LA English DT Article ID COLONY-STIMULATING FACTOR; BONE-MARROW; HEMATOPOIETIC STEM; MYOBLAST TRANSPLANTATION; HEART; PROGENITORS; MIGRATION; MUSCLE C1 NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. RP Orlic, D (reprint author), NHGRI, Genet & Mol Biol Branch, NIH, 49 Convent Dr, Bethesda, MD 20892 USA. NR 26 TC 9 Z9 9 U1 0 U2 1 PU TAYLOR & FRANCIS AS PI OSLO PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PD OCT 1 PY 2002 VL 4 IS 6 BP 521 EP 525 DI 10.1080/146532402761624674 PG 5 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 626JX UT WOS:000179869100007 PM 12568987 ER PT J AU Hill, JM Lederman, RJ AF Hill, JM Lederman, RJ TI Mesenchymal 'stem cell rescue' for myocardial disease SO CYTOTHERAPY LA English DT Article C1 NHLBI, Cardiovasc Branch, Div Intramural Res,Lab Mol Biol, NIH, Bethesda, MD 20892 USA. RP Hill, JM (reprint author), NHLBI, Cardiovasc Branch, Div Intramural Res,Lab Mol Biol, NIH, Room 6N240,Bldg 10, Bethesda, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS AS PI OSLO PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PD OCT 1 PY 2002 VL 4 IS 6 BP 527 EP 529 DI 10.1080/146532402761624683 PG 3 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 626JX UT WOS:000179869100008 PM 12568988 ER PT J AU Khuu, HM Cowley, H David-Ocampo, V Carter, CS Kasten-Sportes, C Wayne, AS Solomon, SR Bishop, MR Childs, RM Read, EJ AF Khuu, HM Cowley, H David-Ocampo, V Carter, CS Kasten-Sportes, C Wayne, AS Solomon, SR Bishop, MR Childs, RM Read, EJ TI Catastrophic failures of freezing bags for cellular therapy products: description, cause, and consequences SO CYTOTHERAPY LA English DT Article DE cryopreservation; cellular therapy product; aseptic methods; plastic bags; bacterial contamination ID PERIPHERAL-BLOOD; BONE-MARROW; BACTERIAL-CONTAMINATION; MICROBIOLOGIC CONTAMINATION; CLINICAL-SIGNIFICANCE; TRANSPLANTATION AB Background Container integrity is critical for maintaining sterility of cryopreserved cellular therapy products. We investigated a series of catastrophic bag failures, first noticed in early 2001. Methods Process records were reviewed for all PBPC and lymphocyte products cryopreserved in bags from January 2000 through April 2002. Patient charts were also reviewed. Results One thousand two hundred and four bags were removed from storage for infusion to 261 patients. All products had been cryopreserved in Cryocyte poly( ethylene co-vinyl acetate) (EVA) bags in either 10% DMSO or 5% DMSO and 6% pentastarch. Product volumes were 25-75 mL, and bags were stored with overwrap bags in a liquid nitrogen tank. From January 2000 to April 2001, failure occurred in 10 of 599 (1.7%) bags. From May 2001 to April 2002, 58 of 605 (9.6%) bags failed, typically with extensive fractures that were visible before thaw. Of the 58 that failed, 24 were salvaged by aseptic methods and infused to patients under antibiotic coverage; 10 of those 24 (42%) had positive bacterial cultures. Bag failures were not related to product type, cryoprotectant solution, liquid versus vapor storage, or freezer location. Failures were linked to use of four Cryocyte bag lots manufactured in 2000 and 2001. After replacing these lots with a 1999 Cryocyte lot and with KryoSafe polyfluoroethylene polyfluoropropylene (FEP) bags, no more failures occurred in 75 and 102 bags, respectively, thawed through April 2002. Discussion High rates of bag failure were associated with four Cryocyte bag lots. No serious adverse patient effects occurred, but bag failures led to microbial contamination, increased product preparation time, increased antibiotic use, and increased resource expenditure to replace products. C1 NCI, Dept Transfus Med, Warren G Magnuson Clin Ctr, Ctr Clin,NIH, Bethesda, MD 20892 USA. NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Khuu, HM (reprint author), NCI, Dept Transfus Med, Warren G Magnuson Clin Ctr, Ctr Clin,NIH, Bldg 10,Rm 1C711,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 19 TC 22 Z9 23 U1 0 U2 0 PU TAYLOR & FRANCIS AS PI OSLO PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PD OCT 1 PY 2002 VL 4 IS 6 BP 539 EP 549 DI 10.1080/146532402761624700 PG 11 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 626JX UT WOS:000179869100010 PM 12568990 ER PT J AU Kim, SH Shin, J Park, HC Yeo, SY Hong, SK Han, ST Rhee, M Kim, CH Chitnis, AB Huh, TL AF Kim, SH Shin, J Park, HC Yeo, SY Hong, SK Han, ST Rhee, M Kim, CH Chitnis, AB Huh, TL TI Specification of an anterior neuroectoderm patterning by Frizzled8a-mediated Wnt8b signalling during late gastrulation in zebrafish SO DEVELOPMENT LA English DT Article DE Fz8a; Wnt8b; anterior neuroectoderm; brain patterning; eye primordia; diencephalon; midbrain; zebrafish ID WINGLESS MORPHOGEN GRADIENT; DI-MESENCEPHALIC BOUNDARY; LONG-RANGE ACTION; XENOPUS EMBRYOS; SPEMANN ORGANIZER; MOLECULAR MECHANISM; SIGNALING PATHWAY; HOMEOBOX GENES; HEAD INDUCTION; AXIS AB Wnts have been shown to provide a posteriorizing signal that has to be repressed in the anterior neuroectoderm for normal anteroposterior (AP) patterning. We have previously identified a zebrafish frizzled8a (fz8a) gene expressed in the presumptive anterior neuroectoderm as well as prechordal plate at the late gastrula stage. We have investigated the role of Fz8a-mediated Wnt8b signalling in anterior brain patterning in zebrafish. We show that in zebrafish embryos: (1) Wnt signalling has at least two different stage-specific posteriorizing activities in the anterior neuroectoderm, one before mid-gastrulation and the other at late gastrulation; (2) Fz8a plays an important role in mediating anterior brain patterning; (3) Wnt8b and Fz8a can functionally interact to transmit posteriorizing signals that determine the fate of the posterior diencephalon and midbrain in late gastrula embryos; and (4) Wnt8b can suppress fz8a expression in the anterior neuroectoderm and potentially affect the level and/or range of Wnt signalling. In conclusion, we suggest that a gradient of Fz8a-mediated Wnt8b signalling may play crucial role in patterning the posterior diencephalon and midbrain regions in the late gastrula. C1 Kyungpook Natl Univ, Dept Genet Engn, Taegu 702701, South Korea. Kyungpook Natl Univ, TG Biotech, Taegu 702701, South Korea. Chungnam Natl Univ, Dept Biol, Taejon 305764, South Korea. NICHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. RP Huh, TL (reprint author), Kyungpook Natl Univ, Dept Genet Engn, Taegu 702701, South Korea. NR 54 TC 63 Z9 65 U1 1 U2 10 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0950-1991 J9 DEVELOPMENT JI Development PD OCT PY 2002 VL 129 IS 19 BP 4443 EP 4455 PG 13 WC Developmental Biology SC Developmental Biology GA 604UU UT WOS:000178640100007 PM 12223403 ER PT J AU David, NB Saint-Etienne, L Tsang, M Schilling, TF Rosa, FM AF David, NB Saint-Etienne, L Tsang, M Schilling, TF Rosa, FM TI Requirement for endoderm and FGF3 in ventral head skeleton formation SO DEVELOPMENT LA English DT Article DE neural crest; fate; cartilage; endoderm; patterning; casanova ID CRANIAL NEURAL CREST; PHARYNGEAL ARCH DEVELOPMENT; GROWTH-FACTOR RECEPTOR; ZEBRAFISH EMBRYO; BRANCHIAL ARCH; RETINOIC ACID; VERTEBRATE DEVELOPMENT; CARDIOVASCULAR-SYSTEM; TISSUE INTERACTIONS; CELL-INTERACTIONS AB The vertebrate head skeleton is derived in part from neural crest cells, which physically interact with head ectoderm, mesoderm and endoderm to shape the pharyngeal arches. The cellular and molecular nature of these interactions is poorly understood, and we explore here the function of endoderm in this process. By genetic ablation and reintroduction of endoderm in zebrafish, we show that it is required for the development of chondrogenic neural crest cells, including their identity, survival and differentiation into arch cartilages. Using a genetic interference approach, we further identify Fgf3 as a critical component of endodermal function that allows the development of posterior arch cartilages. Together, our results reveal for the first time that the endoderm provides differential cues along the anteroposterior axis to control ventral head skeleton development and demonstrate that this function is mediated in part by Fgf3. C1 ENS, INSERM, U368, F-75230 Paris 05, France. NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. Univ Calif Irvine, Irvine, CA 92697 USA. RP Rosa, FM (reprint author), ENS, INSERM, U368, 46 Rue Ulm, F-75230 Paris 05, France. RI David, Nicolas/A-1699-2008; TSANG, Michael/E-2758-2013; Tsang, Michael/I-9305-2014 OI David, Nicolas/0000-0003-1166-6732; TSANG, Michael/0000-0001-6384-2422; Tsang, Michael/0000-0001-7123-0063 FU NIDCR NIH HHS [R01 DE013828, DE 13828]; NINDS NIH HHS [NS 41353] NR 68 TC 113 Z9 114 U1 0 U2 2 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0950-1991 J9 DEVELOPMENT JI Development PD OCT PY 2002 VL 129 IS 19 BP 4457 EP 4468 PG 12 WC Developmental Biology SC Developmental Biology GA 604UU UT WOS:000178640100008 PM 12223404 ER PT J AU Iraha, F Saito, Y Yoshida, K Kawakami, M Izutsu, Y Daar, IO Maeno, M AF Iraha, F Saito, Y Yoshida, K Kawakami, M Izutsu, Y Daar, IO Maeno, M TI Common and distinct signals specify the distribution of blood and vascular cell lineages in Xenopus laevis embryos SO DEVELOPMENT GROWTH & DIFFERENTIATION LA English DT Article DE angiopoiesis; bone morphogenetic protein (BMP)-4; fibroblast growth factor; hemopoiesis; tie-2; ventral blood island ID RECEPTOR TYROSINE KINASE; HEMATOPOIETIC STEM-CELLS; FIBROBLAST-GROWTH-FACTOR; ANIMAL POLE TISSUE; ENDOTHELIAL-CELLS; DEFINITIVE HEMATOPOIESIS; VENTRAL MESODERM; AVIAN EMBRYO; MONOCLONAL-ANTIBODY; VASCULOGENESIS AB In an effort to elucidate the regulatory mechanisms that determine the fate of blood cells and vascular cells in the ventral blood island mesoderm, the embryonic expression of Xtie-2, a Xenopus homolog of the tie-2 receptor tyrosine kinase, was examined. Whole-mount in situ hybridization analysis revealed that Xtie-2 mRNA is expressed at the late tailbud stage within the regions where endothelial precursor cells exist. On the ventral side of embryos, Xtie-2-positive cells are predominantly present just outside the boundary of alpha-globin-positive cells, thus the expression pattern of these two markers seems mutually exclusive. Further experiments revealed that there is a consistent and strong correlation between the induction of Xtie-2 and alpha-globin expression in embryos and explant tissues. First, these two markers displayed overlapping expression in embryos ventralized by the removal of a 'dorsal determinant' from the vegetal cytoplasm at the 1-cell stage. Second, expression of both Xtie-2 and alpha-globin were markedly induced in ectodermal explants (animal caps) from embryos co-injected with activin and bone morphogenetic protein (BMP)-4 RNA. Furthermore, both Xtie-2 and alpha-globin messages were strongly positive in dorsal marginal zone explants that had been injected with BMP-4 RNA. In contrast, however, there was a clear distinction in the localization of these two transcripts in embryos dorsalized by LiCl treatment. Distinct localization was also found in the ventral marginal zone (VMZ) explants. Using the VMZ explant system, we demonstrate a role of fibroblast growth factor (FGF) signaling in enhancing the vascular cell marker and reducing the blood cell marker. The present study suggests that the early steps of blood and vascular cell differentiation are regulated by a common BMP-4-dependent signaling; however, distinct factor(s) such as FGF are involved in different distribution of these two cell lineages. C1 Niigata Univ, Fac Sci, Dept Biol, Niigata 9502181, Japan. Niigata Univ, Grad Sch Sci & Technol, Niigata 9502181, Japan. Natl Canc Inst, Regulat Cell Growth Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. RP Maeno, M (reprint author), Niigata Univ, Fac Sci, Dept Biol, 8050 Ikarashi-2, Niigata 9502181, Japan. OI Daar, Ira/0000-0003-2657-526X NR 68 TC 20 Z9 20 U1 0 U2 4 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 0012-1592 J9 DEV GROWTH DIFFER JI Dev. Growth Diff. PD OCT PY 2002 VL 44 IS 5 BP 395 EP 407 PG 13 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 607UU UT WOS:000178809800005 PM 12392573 ER PT J AU Kim, L Harwood, A Kimmel, AR AF Kim, L Harwood, A Kimmel, AR TI Receptor-dependent and tyrosine phosphatase-mediated inhibition of GSK3 regulates cell fate choice SO DEVELOPMENTAL CELL LA English DT Article ID GLYCOGEN-SYNTHASE KINASE-3; DICTYOSTELIUM-DISCOIDEUM; XENOPUS EMBRYOS; AXIS FORMATION; BETA-CATENIN; DIFFERENTIATION; PHOSPHORYLATION; LITHIUM; 3-BETA; CANCER AB Asymmetric body axis formation is central to metazoan development. Dictyostelium establishes an anterior/posterior axis utilizing seven-transmembrane cAMP morphogen receptors (CARs) and GSK3-mediated signal transductions that has a parallel with metazoan Wnt/Frizzled-GSK3 pathways. In Dictyostelium, GSK3 promotes posterior cell patterning but inhibits anterior cell differentiation. Tyrosine kinase ZAK1 mediates GSK3 activation. We now show that CAR4 regulates a tyrosine phosphatase that inhibits GSK3 activity. We have also identified essential phosphotyrosines in GSK3, confirmed their role in activated/deactivated regulation and cell fate decisions, and relate them to the predicted 3D structure of GSK3beta. CARs differentially regulate GSK3 activity by selectively activating a tyrosine phosphatase or kinase for pattern formation. The findings may provide a comparative understanding of CAR-GSK3 and Wnt/Frizzled-GSK3 pathways. C1 NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. UCL, Dept Biol, London WC1E 6BT, England. UCL, MRC, Mol Cell Biol Lab, London WC1E 6BT, England. RP Kimmel, AR (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, Bldg 50-3351, Bethesda, MD 20892 USA. EM ark1@helix.nih.gov RI Harwood, Adrian/A-4350-2010 NR 34 TC 34 Z9 38 U1 2 U2 6 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD OCT PY 2002 VL 3 IS 4 BP 523 EP 532 DI 10.1016/S1534-5807(02)00269-1 PG 10 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 604PB UT WOS:000178629300010 PM 12408804 ER PT J AU Yoon, SS Hennigan, RF Hilliard, GM Ochsner, UA Parvatiyar, K Kamani, MC Allen, HL DeKievit, TR Gardner, PR Schwab, U Rowe, JJ Iglewski, BH McDermott, TR Mason, RP Wozniak, DJ Hancock, REW Parsek, MR Noah, TL Boucher, RC Hassett, DJ AF Yoon, SS Hennigan, RF Hilliard, GM Ochsner, UA Parvatiyar, K Kamani, MC Allen, HL DeKievit, TR Gardner, PR Schwab, U Rowe, JJ Iglewski, BH McDermott, TR Mason, RP Wozniak, DJ Hancock, REW Parsek, MR Noah, TL Boucher, RC Hassett, DJ TI Pseudomonas aeruginosa anaerobic respiration in biofilms: Relationships to cystic fibrosis pathogenesis SO DEVELOPMENTAL CELL LA English DT Article ID MEMBRANE PROTEIN OPRF; NITRIC-OXIDE; ESCHERICHIA-COLI; INFECTION; ALGINATE; SIGNALS; ROLES AB Recent data indicate that cystic fibrosis (CF) airway mucus is anaerobic. This suggests that Pseudomonas aeruginosa infection in CF reflects biofilm formation and persistence in an anaerobic environment. P. aeruginosa formed robust anaerobic biofilms, the viability of which requires rhl quorum sensing and nitric oxide (NO) reductase to modulate or prevent accumulation of toxic NO, a byproduct of anaerobic respiration. Proteomic analyses identified an outer membrane protein, OprF, that was upregulated similar to40-fold under anaerobic versus aerobic conditions. Further, OprF exists in CF mucus, and CIF patients raise antisera to OprF. An oprF mutant formed poor anaerobic biofilms, due, in part, to defects in anaerobic respiration. Thus, future investigations of CF pathogenesis and therapy should include a better understanding of anaerobic metabolism and biofilm development by P. aeruginosa. C1 Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Cell Biol, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Cellular & Mol Physiol, Cincinnati, OH 45267 USA. Univ Colorado Hlth Sci, Dept Microbiol, Denver, CO 80262 USA. Univ Manitoba, Dept Microbiol & Immunol, Winnipeg, MB R3T 2N2, Canada. Childrens Hosp, Med Ctr, Div Crit Care Med, Cincinnati, OH 45229 USA. Univ N Carolina, Dept Pulm Biol, Chapel Hill, NC 27599 USA. Univ Dayton, Dept Biol, Dayton, OH 45469 USA. Univ Rochester, Dept Microbiol & Immunol, Rochester, NY 14642 USA. Montana State Univ, Dept Land Resources, Bozeman, MT 59717 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. Wake Forest Univ, Sch Med, Dept Microbiol & Immunol, Winston Salem, NC 27157 USA. Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC VT6 1Z3, Canada. Northwestern Univ, Dept Civil Engn, Evanston, IL 60208 USA. RP Hassett, DJ (reprint author), Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA. RI Hancock, Robert/E-1145-2013 FU NIAID NIH HHS [AI-40541] NR 27 TC 331 Z9 336 U1 6 U2 46 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD OCT PY 2002 VL 3 IS 4 BP 593 EP 603 DI 10.1016/S1534-5807(02)00295-2 PG 11 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 604PB UT WOS:000178629300016 PM 12408810 ER PT J AU Flugel-Koch, C Ohlmann, A Platigorsky, J Tamm, ER AF Flugel-Koch, C Ohlmann, A Platigorsky, J Tamm, ER TI Disruption of anterior segment development by TGF-beta 1 overexpression in the eyes of transgenic mice SO DEVELOPMENTAL DYNAMICS LA English DT Article DE cornea; neural crest; TGF-beta; differentiation; lens; eye development ID GROWTH-FACTOR-BETA; LENS-SPECIFIC EXPRESSION; A-CRYSTALLIN PROMOTER; CRANIAL NEURAL CREST; SMOOTH MUSCLE-ACTIN; CORNEAL STROMAL FIBROBLASTS; TGF-BETA; EXTRACELLULAR-MATRIX; RABBIT CORNEA; MYOFIBROBLAST TRANSFORMATION AB Previous experiments showed that transgenic mice expressing a secreted self-activating transforming growth factor (TGF)-beta1 did not show a phenotype in the lens and cornea until postnatal day 21, when anterior subcapsular cataracts, sporadic thickening of the corneal stroma, and thinning of the corneal epithelium were noted (Srinivasan et al., 1998). To examine the effects of higher concentrations of TGF-beta1 on the lens and cornea, we constructed transgenic mice harboring the strong, lens-specific chicken betaB1-crystallin promoter driving an activated porcine TGF-beta1 gene. In contrast to the earlier study, the transgenic mice had microphthalmic eyes with closed eyelids. Already at embryonic day (E) 13.5, the future cornea of the transgenic mice was threefold thicker than that of wild-type littermates due to increased proliferation of corneal stromal mesenchyme cells. Staining of fibronectin and thrombospondin-1 was increased in periocular mesenchyme. At E17.5, the thickened transgenic corneal stroma was vascularized and densely populated by abundant star-shaped, neural cell adhesion molecule-positive cells of mesenchymal appearance surrounded by irregular swirls of collagen and extracellular matrix. The corneal endothelium, anterior chamber, and stroma of iris/ciliary body did not develop, and the transgenic cornea was opaque. Fibronectin, perlecan, and thrombospondin-1 were elevated, whereas type VI collagen decreased in the transgenic corneal stroma. Stromal mesenchyme cells expressed alpha-smooth muscle actin as did lens epithelial. cells and cells of the retinal pigmented epithelium. By E17.5, lens fiber cells underwent apoptotic cell death that was followed by apoptosis of the entire anterior lens epithelium between E18.5 and birth. Posteriorly, the vitreous humor was essentially absent; however, the retina appeared relatively normal. Thus, excess TGF-beta1, a mitogen for embryonic corneal mesenchyme, severely disrupts corneal and lens differentiation. Our findings profoundly contrast with the mild eye phenotype observed with presumably lower levels of ectopic TGF-beta and illustrate the complexity of TGF-beta utilization and the importance of dose when assessing the effects of this growth factor. (C) 2002 Wiley-Liss, Inc. C1 Univ Erlangen Nurnberg, Dept Anat Mol Anat & Embryol, D-91054 Erlangen, Germany. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RP Tamm, ER (reprint author), Univ Erlangen Nurnberg, Dept Anat Mol Anat & Embryol, Univ Str 19, D-91054 Erlangen, Germany. OI Tamm, Ernst/0000-0002-6679-8743 NR 72 TC 42 Z9 44 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD OCT PY 2002 VL 225 IS 2 BP 111 EP 125 DI 10.1002/dvdy.10144 PG 15 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 599TZ UT WOS:000178352400001 PM 12242711 ER PT J AU Delise, AM Tuan, RS AF Delise, AM Tuan, RS TI Analysis of N-cadherin function in limb mesenchymal chondrogenesis in vitro SO DEVELOPMENTAL DYNAMICS LA English DT Article DE mesenchymal chondrogenesis; N-cadherin; cell adhesion; condensation; cartilage; limb development ID GAP JUNCTIONAL COMMUNICATION; MEMBRANE-PROXIMAL REGION; CELL-CELL ADHESION; CYTOPLASMIC DOMAIN; SKELETAL DEVELOPMENT; IN-VITRO; COLORIMETRIC ASSAY; XENOPUS EMBRYOS; LECTIN BINDING; EXPRESSION AB During embryonic limb development, cartilage formation is presaged by a crucial mesenchymal cell condensation phase. N-Cadherin, a Ca2+-dependent cell-cell adhesion molecule, is expressed in embryonic chick limb buds in a spatiotemporal pattern suggestive. of its involvement during cellular condensation; functional blocking of N-cadherin homotypic binding, by using a neutralizing monoclonal antibody, results in perturbed chondrogenesis in vitro and in vivo. In high-density micromass cultures of embryonic limb mesenchymal cells, N-cadherin expression level is high during days 1 and 2, coincident with active cellular condensation, and decreases upon overt chondrogenic differentiation from day 3 on. In this study, we have used a transfection approach to evaluate the effects of gain- and loss-of-function expression of N-cadherin constructs on mesenchymal condensation and chondrogenesis in vitro. Chick limb mesenchymal cells were transfected by electroporation with recombinant expression plasmids encoding wild-type or two mutant extracellular/cytoplasmic deletion forms of N-cadherin. Expression of the transfected N-cadherin forms showed a transient profile, being high on days 1-2 of culture, and decreasing by day 3, fortuitously coincident with the temporal profile of endogenous N-cadherin gene expression. Examined by means of peanut agglutinin (PNA) staining for condensing precartilage mesenchymal cells, cultures overexpressing wild-type N-cadherin showed enhanced cellular condensation on culture days 2 and 3, whereas expression of the deletion mutant forms (extracellular/cytoplasmic) of N-cadherin resulted in a decrease in PNA staining, suggesting that a complete N-cadherin protein is required for normal cellular condensation to occur. Subsequent chondrogenesis was also affected. Cultures overexpressing the wildtype N-cadherin protein showed enhanced chondrogenesis, indicated by increased production of cartilage matrix (sulfated proteoglycans, collagen type II, and cartilage proteoglycan link protein), as well as increased cartilage nodule number and size of individual nodules, compared with control cultures and cultures transfected with either of the two mutant N-cadherin constructs. These results demonstrate that complete N-cadherin function, at the levels of both extracellular homotypic binding and cytoplasmic linkage to the cytoskeleton by means of the catenin complex, is required for chondrogenesis by mediating functional mesenchymal cell condensation. Published 2002 Wiley-Liss, Inc.(dagger). C1 NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Bethesda, MD 20892 USA. Thomas Jefferson Univ, Dept Orthopaed Surg, Philadelphia, PA 19107 USA. RP Tuan, RS (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, 50 South Dr,Bldg 50,Room 1503, Bethesda, MD 20892 USA. FU NIAMS NIH HHS [AR42887, AR45181]; NIDCR NIH HHS [DE16864]; NIEHS NIH HHS [ES07282, ES07005, T32ES07282] NR 59 TC 87 Z9 88 U1 0 U2 12 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD OCT PY 2002 VL 225 IS 2 BP 195 EP 204 DI 10.1002/dvdy.10151 PG 10 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 599TZ UT WOS:000178352400009 PM 12242719 ER PT J AU Zhang, HH Halbleib, M Ahmad, F Manganiello, VC Greenberg, AS AF Zhang, HH Halbleib, M Ahmad, F Manganiello, VC Greenberg, AS TI Tumor necrosis factor-alpha stimulates lipolysis in differentiated human Adipocytes through activation of extracellular signal-related kinase and elevation of intracellular cAMP SO DIABETES LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Diabetes-Association CY JUN 22-26, 2001 CL PHILADELPHIA, PENNSYLVANIA SP Amer Diabetes Assoc ID HORMONE-SENSITIVE LIPASE; BETA-ADRENERGIC STIMULATION; INSULIN-RESISTANCE; 3T3-L1 ADIPOCYTES; ADIPOSE-TISSUE; PERILIPIN-A; LIPOPROTEIN-LIPASE; METABOLIC RESPONSE; LIPID DROPLETS; HUMAN OBESITY AB Tumor necrosis factor-alpha (TNF-alpha) stimulates lipolysis in human adipocytes. However, the mechanisms regulating this process are largely unknown. We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP similar to1.7-fold, and the increase was abrogated by PD98059. Furthermore, H89, a specific. PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 313 (PDE3B) by similar to50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. Cotreatment with PD98059 restored PDE3B expression. These studies suggest that in human adipocytes, TNF-alpha stimulates lipolysis through activation of MEK-ERK and subsequent increase in intracellular cAMP. C1 Tufts Univ, USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA. NHLBI, Sect Biochem Physiol Pulm Crit Care Med, NIH, Bethesda, MD 20892 USA. RP Greenberg, AS (reprint author), Tufts Univ, USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA. NR 43 TC 218 Z9 233 U1 0 U2 9 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 2002 VL 51 IS 10 BP 2929 EP 2935 DI 10.2337/diabetes.51.10.2929 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 599LT UT WOS:000178336600008 PM 12351429 ER PT J AU Vozarova, B Stefan, N Lindsay, RS Krakoff, J Knowler, WC Funahashi, T Matsuzawa, Y Stumvoll, M Weyer, C Tataranni, PA AF Vozarova, B Stefan, N Lindsay, RS Krakoff, J Knowler, WC Funahashi, T Matsuzawa, Y Stumvoll, M Weyer, C Tataranni, PA TI Low plasma adiponectin concentrations do not predict weight gain in humans SO DIABETES LA English DT Article ID ADIPOSE-SPECIFIC PROTEIN; PIMA-INDIANS; OBESITY AB Low concentrations of plasma adiponectin, the most abundant adipose-specific protein, are observed in obese individuals and predict the development of type 2 diabetes. Administration of adiponectin to rodents prevented diet-induced weight gain, suggesting a potential etiologic role of hypoadiponectinemia in the development of obesity. Our aim was to prospectively examine whether low plasma adiponectin concentrations predict future weight gain in Pima Indians, explaining the predictive effect of adiponectin on the development of type 2 diabetes. We measured plasma adiponectin concentrations in 219 nondiabetic Pima Indians (112 111107 F, age 31 +/- 9 years, body weight 96 +/- 20 kg [mean +/- SD]) in whom body weight and height were measured and BMI calculated at baseline and follow-up. Cross-sectionally, plasma adiponectin concentrations were negatively associated with body weight (r = -0.28, P = 0.0001). Prospectively, plasma adiponectin concentrations at baseline were not associated with change in weight or BMI before or after adjustment for time of follow-up or after additional adjustment for age at follow-up and sex (all P > 0.3). Our data suggest that low plasma adiponectin concentrations do not play an etiologic role in development of obesity in Pima Indians. Therefore, the predictive effect of low plasma adiponectin concentrations on the development of type 2 diabetes seems to be mediated by factors other than increased adiposity. C1 NIDDKD, NIH, Phoenix, AZ USA. Osaka Univ, Grad Sch Med, Dept Internal Med & Mol Med, Osaka, Japan. RP Vozarova, B (reprint author), NIH, Clin Diabet & Nutr Sect, 4212 N 16Th St,Rm 5-41, Phoenix, AZ 85016 USA. OI de Courten, Barbora/0000-0001-8760-2511 NR 18 TC 42 Z9 42 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 2002 VL 51 IS 10 BP 2964 EP 2967 DI 10.2337/diabetes.51.10.2964 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 599LT UT WOS:000178336600013 PM 12351434 ER PT J AU Golden, SH Folsom, AR Coresh, J Sharrett, AR Szklo, M Brancati, F AF Golden, SH Folsom, AR Coresh, J Sharrett, AR Szklo, M Brancati, F TI Risk factor groupings related to insulin resistance and their synergistic effects on subclinical atherosclerosis - The Atherosclerosis Risk in Communities Study SO DIABETES LA English DT Article ID CORONARY HEART-DISEASE; INTIMA-MEDIA THICKNESS; JAPANESE-AMERICAN MEN; CARDIOVASCULAR-DISEASE; DIABETES-MELLITUS; SYNDROME PREDICTS; FASTING INSULIN; WALL THICKNESS; ARTERIAL-WALL; PLASMA AB The extent to which groupings of insulin resistance-related cardiovascular risk factors synergize to produce atherosclerosis beyond what is expected from their additive effects is uncertain. The objective of this study was to measure interactions among groupings of the features of the insulin resistance syndrome (IRS) on carotid intimal-medial thickness (IMT). This crosssectional study used baseline data from the Atherosclerosis Risk in Communities Study on 11,790 adults aged 45-64 years without diagnosed diabetes, treated dyslipidemia, or coronary heart disease. The main outcome was carotid IMT, assessed using B-mode ultrasound. The excess carotid IMT attributable to each IRS grouping was determined using multiple linear regression models. There were 57 possible combinations of six IRS components (hypertension, hyperinsulinemia, obesity, hypertriglyceridemia, low HDL cholesterol, and hyperglycemia). In multivariate analysis, 29 of the 57 groupings were associated with excess carotid IMT. Individuals with all six IRS components had the greatest excess IMT compared with those without this grouping (71 mum; 95% Cl 40-102 mum). The groupings most strongly associated with excess carotid IMT included hypertension and hypertriglyceridemia. Interventions aimed at ameliorating the IRS may produce reductions in atherosclerotic risk beyond that predicted by treatment of individual IRS-related risk factors. C1 Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Epidemiol, Baltimore, MD 21205 USA. NHLBI, Bethesda, MD 20892 USA. RP Brancati, F (reprint author), Welch Ctr Prevent Epidemiol & Clin Res, 2024 E Monument St,Suite 2-600, Baltimore, MD 21205 USA. FU NHLBI NIH HHS [N01 HC55020, N01 HC55021, N01 HC55015, N01 HC55022, N01 HC55016, N01 HC55018, N01 HC55019, T32HL07024] NR 42 TC 113 Z9 125 U1 1 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 2002 VL 51 IS 10 BP 3069 EP 3076 DI 10.2337/diabetes.51.10.3069 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 599LT UT WOS:000178336600028 PM 12351449 ER PT J AU Hanson, RL Imperatore, G Bennett, PH Knowler, WC AF Hanson, RL Imperatore, G Bennett, PH Knowler, WC TI Components of the "metabolic syndrome" and incidence of type 2 diabetes SO DIABETES LA English DT Article; Proceedings Paper CT 59th Scientific Session of the American-Diabetes-Association CY JUN 18-22, 1999 CL SAN DIEGO, CALIFORNIA SP Amer Diabet Assoc ID INSULIN-RESISTANCE SYNDROME; CORONARY HEART-DISEASE; CARDIOVASCULAR RISK-FACTORS; SYNDROME PREDICTS; SYNDROME-X; PIMA INDIANS; MEN; OBESITY; HYPERTENSION; MELLITUS AB The combination of insulin resistance, dyslipidemia, hypertension, and obesity has been described as a metabolic syndrome" that is A strong determinant of type 2 diabetes. Factor analysis was used to identify components of this syndrome in 1,918 Pima Indians. Prospective analyses were conducted to evaluate associations of identified factors with incidence of diabetes. Factor analysis identified 4 factors that accounted for 79% of the variance in the original 10, variables. Each of these factors reflected a proposed component of the metabolic syndrome: insulinemia, body size, blood pressure, and lipid metabolism. Among 890 originally nondiabetic participants with follow-up data, 144 developed. diabetes in a median follow-up of 4.1 years. The insulinemia factor was strongly associated with diabetes incidence (incidence rate ratio [IRR] for a 1-SD) difference in factor scores = 1.81, P < 0.01). The body size and lipids factors also significantly predicted diabetes (IRR 1.52 and 1.37, respectively, P < 0.01 for both), whereas the blood pressure factor did not (IRR 1.11, P = 0.20). Identification of four unique factors with different associations with incidence of diabetes suggests that the correlations among these variables reflect distinct metabolic processes, about which substantial information may be lost in the attempt to combine them into a single entity. C1 NIDDKD, Diabet & Arthrit Epidemiol Sect, Phoenix, AZ 85014 USA. RP Hanson, RL (reprint author), NIDDKD, Diabet & Arthrit Epidemiol Sect, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA. RI Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 NR 44 TC 315 Z9 339 U1 0 U2 10 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 2002 VL 51 IS 10 BP 3120 EP 3127 DI 10.2337/diabetes.51.10.3120 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 599LT UT WOS:000178336600036 PM 12351457 ER PT J AU Lindsay, RS Prochazka, M Baier, LJ Knowler, WC Bogardus, C Hanson, RL AF Lindsay, RS Prochazka, M Baier, LJ Knowler, WC Bogardus, C Hanson, RL TI Currently identified genes affecting insulin resistance are not associated with birth weight in the Pima population SO DIABETIC MEDICINE LA English DT Letter ID FETAL C1 NIDDKD, NIH, Phoenix, AZ 85016 USA. RP Lindsay, RS (reprint author), NIDDKD, NIH, Phoenix, AZ 85016 USA. RI Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 NR 9 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0742-3071 J9 DIABETIC MED JI Diabetic Med. PD OCT PY 2002 VL 19 IS 10 BP 882 EP 884 DI 10.1046/j.1464-5491.2002.07602.x PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 599PW UT WOS:000178345200018 PM 12358881 ER PT J AU Martiniuk, F Chen, A Mack, A Donnabella, V Slonim, A Bulone, L Arvanitopoulos, E Raben, N Plotz, P Rom, WN AF Martiniuk, F Chen, A Mack, A Donnabella, V Slonim, A Bulone, L Arvanitopoulos, E Raben, N Plotz, P Rom, WN TI Helios gene gun particle delivery for therapy of acid maltase deficiency SO DNA AND CELL BIOLOGY LA English DT Article ID GLYCOGEN-STORAGE-DISEASE; ADENOVIRUS-MEDIATED TRANSFER; ALPHA-GLUCOSIDASE GENE; SKELETAL-MUSCLE; FOREIGN GENES; MESSENGER-RNA; WOUND REPAIR; EXPRESSION; MICE; DNA AB Autosomal recessive deficiency of lysosomal acid maltase (GAA) or glycogen storage disease type II (GSDII) results in a spectrum of phenotypes including a rapidly fatal infantile disorder (Pompe's), juvenile, and a late-onset adult myopathy. The infantile onset form presents as hypotonia with massive accumulation of glycogen in skeletal and heart muscle, with death due to cardiorespiratory failure. Adult patients with the slowly progressive form develop severe skeletal muscle weakness and respiratory failure. Particle bombardment is a safe, efficient physical method in which high-density, subcellular-sized particles are accelerated to high velocity to carry DNA into cells. Because it does not depend on a specific ligand, receptor, or biochemical features on cell surfaces, particle-mediated gene transfer can be readily applied to a variety of systems. We evaluated particle bombardment as a delivery system for therapy of GSDII. We utilized a vector carrying the CMV promoter linked to the human GAA cDNA. Human GSDII cell lines (fibroblasts and lymphoid) as well as ex vivo with adult-onset peripheral blood cells (lymphocytes and monocytes) were transiently transfected by bombardment with a Helios gene gun delivering gold particles coated with the GAA expression plasmid. All cell types showed an increase in human GAA activity greater than 50% of normal activity. Subsequently, GAA(-/-) mice were treated every 2 weeks for 4 months by particle bombardment to the epidermis of the lower back and hind limbs. Muscle weakness in the hind and forelimbs was reversed. These data suggest that particle delivery of the GAA cDNA by the Helios gene gun may be a safe, effective treatment for GSDII. C1 NYU, Sch Med, Dept Med, Div Pulm & Crit Care, New York, NY USA. N Shore Univ Hosp, Manhasset, NY USA. NIAMS, Arthrit & Rheumatism Branch, NIH, Bethesda, MD USA. RP Martiniuk, F (reprint author), NYU, Sch Med, Dept Med, Div Pulm & Crit Care Med, New Bellevue 6N5-8,550 1st Ave, New York, NY 10010 USA. FU PHS HHS [M0100096] NR 48 TC 6 Z9 6 U1 1 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD OCT PY 2002 VL 21 IS 10 BP 717 EP 725 DI 10.1089/104454902760599690 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA 609BJ UT WOS:000178882500003 PM 12443541 ER PT J AU Chan, FKM Lenardo, MJ AF Chan, FKM Lenardo, MJ TI Tumor necrosis factor family ligands and receptors in the immune system: Targets for future pharmaceuticals SO DRUG NEWS & PERSPECTIVES LA English DT Article ID PERIPHERAL LYMPHOID ORGANS; AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; ANTIGEN-INDUCED APOPTOSIS; AUTOSOMAL RECESSIVE FORM; MATURE T-LYMPHOCYTES; TNF RECEPTOR; CRYSTAL-STRUCTURE; MICE DEFICIENT; FACTOR-ALPHA; HYPER-IGM AB Members of the superfamily of ligands related to tumor necrosis factor (TNF) as well as the superfamily of receptors that recognize these ligands play critical roles in various aspects of mammalian lymphocyte development and immune function. Many of the receptors and their cognate ligands have well-known roles in the regulation of cell-cell interactions as well as in the proper development of lymphoid organs, skin and other systems. Disruption of the ligand-receptor interactions within this superfamily of molecules often leads to pathological conditions. Consequently, these are two of the most widely studied and pharmacologically interesting gene families in biology and medicine. The roles of TNF and TNF receptor-like molecules in the immune system are discussed. (C) 2002 Prous Science. All rights reserved. C1 Univ Massachusetts, Sch Med, Dept Pathol, Amherst, MA 01003 USA. NIAID, NIH, Bethesda, MD 20892 USA. RI Chan, Francis/E-9647-2014; Chan, Francis K. L./F-4851-2010 OI Chan, Francis/0000-0002-4803-8353; Chan, Francis K. L./0000-0001-7388-2436 NR 80 TC 1 Z9 2 U1 0 U2 2 PU PROUS SCIENCE, SA PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0214-0934 J9 DRUG NEWS PERSPECT JI Drug News Perspect. PD OCT PY 2002 VL 15 IS 8 BP 483 EP 490 DI 10.1358/dnp.2002.15.8.840068 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 619JY UT WOS:000179473900002 ER PT J AU Fojo, T AF Fojo, T TI p53 as a therapeutic target: unresolved issues on the road to cancer therapy targeting mutant p53 SO DRUG RESISTANCE UPDATES LA English DT Review DE p53; apoptosis; chemotherapy; drug targets ID CELL LUNG-CANCER; P53-DEPENDENT APOPTOSIS; P53-INDUCED APOPTOSIS; POTENTIAL MEDIATOR; TUMOR SUPPRESSION; COLORECTAL-CANCER; ANTICANCER AGENTS; GENE-THERAPY; WILD-TYPE; PROTEIN AB As a tumor suppressor, p53 has a central role in oncogenesis: it inhibits the growth of abnormal cells and thus prevents cancer development. The frequent occurrence of p53 mutations in human cancer and its role as "guardian of the genome" has led to numerous investigations evaluating its role as a potential therapeutic target in terms of restoring wild type (wt) p53 and thereby either reverting the malignant phenotype or enhancing drug sensitivity. A critical evaluation of the available data suggests that following the restoration of wt p53 growth inhibition is an attainable goal, although induction of apoptosis would be more desirable. As for attempts to enhance drug sensitivity, the evidence suggest that this too can be accomplished, but how best to accomplish it remains to be explored. To properly evaluate these strategies, one must consider the known and putative roles of p53. Research conducted in the last decade has firmly established the importance of p53 in mediating the cell cycle arrest that occurs following DNA damage. However, during this same time, the role of p53 in mediating apoptosis has become increasingly less clear, even as the number of putative pro-apoptotic proteins transactivated by p53 has increased. Similarly unclear is how p53 makes a choice between cell cycle arrest or apoptosis, raising the possibility that p53 alone is not responsible for this crucial decision. Despite the existence of several crucial unresolved issues, strategies attempting to enhance the expression of the wt p53 phenotype in cancer cells deserve further investigation. Although the importance of p53 in maintaining an established malignant phenotype as well as its role in apoptosis and chemotherapy-induced cytotoxicity are far from settled, a subset of cancers may respond to these strategies. (C) 2002 Published by Elsevier Science Ltd. C1 NCI, Canc Res Ctr, Med Branch, Bethesda, MD 20892 USA. RP Fojo, T (reprint author), NCI, Canc Res Ctr, Med Branch, Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 58 TC 26 Z9 27 U1 0 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PD OCT PY 2002 VL 5 IS 5 BP 209 EP 216 AR PII S1368-7646(02)00119-X DI 10.1016/S1368-7646(02)00119-X PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 626NN UT WOS:000179879400004 PM 12450786 ER PT J AU Takai, H Naka, K Okada, Y Watanabe, M Harada, N Saito, S Anderson, CW Appella, E Nakanishi, M Suzuki, H Nagashima, K Sawa, H Ikeda, K Motoyama, N AF Takai, H Naka, K Okada, Y Watanabe, M Harada, N Saito, S Anderson, CW Appella, E Nakanishi, M Suzuki, H Nagashima, K Sawa, H Ikeda, K Motoyama, N TI Chk2-deficient mice exhibit radioresistance and defective p53-mediated transcription SO EMBO JOURNAL LA English DT Article DE ataxia-telangiectasia mutated (ATM); cell cycle checkpoint; DNA damage; phosphorylation; transcriptional activation ID ATM-DEPENDENT PHOSPHORYLATION; CELL-CYCLE CHECKPOINT; DNA-DAMAGE CHECKPOINT; ATAXIA-TELANGIECTASIA; IONIZING-RADIATION; GENOTOXIC STRESS; DEFICIENT MICE; NERVOUS-SYSTEM; HUMAN P53; KINASE AB The mammalian Chk2 kinase is thought to mediate ATM-dependent signaling in response to DNA damage. The physiological role of mammalian Chk2 has now been investigated by the generation of Chk2-deficient mice. Although Chk2(-/-) mice appeared normal, they were resistant to ionizing radiation (IR) as a result of the preservation of splenic lymphocytes. Thymocytes and neurons of the developing brain were also resistant to IR-induced apoptosis. The IR-induced G(1)/S cell cycle checkpoint, but not the G(2)/M or S phase checkpoints, was impaired in embryonic fibroblasts derived from Chk2(-/-) mice. IR-induced stabilization of p53 in Chk2(-/-) cells was 50-70% of that in wild-type cells. Caffeine further reduced p53 accumulation, suggesting the existence of an ATM/ ATR-dependent but Chk2-independent pathway for p53 stabilization. In spite of p53 protein stabilization and phosphorylation of Ser23, p53-dependent transcriptional induction of target genes, such as p21 and Noxa, was not observed in Chk2(-/-) cells. Our results show that Chk2 plays a critical role in p53 function in response to IR by regulating its transcriptional activity as well as its stability. C1 Natl Inst Longev Sci, Dept Geriatr Res, Aichi 4748522, Japan. Hokkaido Univ, Grad SchMed, Lab Mol & Cellular Pathol, Sapporo, Hokkaido 0608638, Japan. JST, CREST, Sapporo, Hokkaido 0608638, Japan. Chugai Pharmaceut Co Ltd, Res Labs, Shizuoka 4128513, Japan. Nagoya City Univ, Sch Med, Dept Biochem, Nagoya, Aichi 4678601, Japan. NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA. RP Motoyama, N (reprint author), Natl Inst Longev Sci, Dept Geriatr Res, Aichi 4748522, Japan. RI Takai, Hiroyuki/B-8352-2011; Sawa, Hirofumi/F-6954-2012 NR 53 TC 300 Z9 303 U1 0 U2 10 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 1 PY 2002 VL 21 IS 19 BP 5195 EP 5205 DI 10.1093/emboj/cdf506 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 602JR UT WOS:000178502600019 PM 12356735 ER PT J AU Spence, JM Critcher, R Ebersole, TA Valdivia, MM Earnshaw, WC Fukagawa, T Farr, CJ AF Spence, JM Critcher, R Ebersole, TA Valdivia, MM Earnshaw, WC Fukagawa, T Farr, CJ TI Co-localization of centromere activity, proteins and topoisomerase II within a subdomain of the major human X alpha-satellite array SO EMBO JOURNAL LA English DT Article DE alpha-satellite; centromere; DT40; DXZ1; topoisomerase II alpha ID SISTER-CHROMATID COHESION; MITOTIC CHROMOSOME STRUCTURE; INNER KINETOCHORE PLATE; CENP-C; Y-CHROMOSOME; ARTIFICIAL CHROMOSOMES; MAMMALIAN-CELLS; DNA-REPLICATION; TELOMERE; FRAGMENTATION AB Dissection of human centromeres is difficult because of the lack of landmarks within highly repeated DNA. We have systematically manipulated a single human X centromere generating a large series of deletion derivatives, which have been examined at four levels: linear DNA structure; the distribution of constitutive centromere proteins; topoisomerase IIalpha cleavage activity; and mitotic stability. We have determined that the human X major alpha-satellite locus, DXZ1, is asymmetrically organized with an active subdomain anchored similar to150 kb in from the Xp-edge. We demonstrate a major site of topoisomerase II cleavage within this domain that can shift if juxtaposed with a telomere, suggesting that this enzyme recognizes an epigenetic determinant within the DXZ1 chromatin. The observation that the only part of the DXZ1 locus shared by all deletion derivatives is a highly restricted region of <50 kb, which coincides with the topoisomerase II cleavage site, together with the high levels of cleavage detected, identify topoisomerase II as a major player in centromere biology. C1 Univ Cambridge, Dept Genet, Cambridge CB2 3EH, England. Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. NCI, Lab Biosyst, NIH, Bethesda, MD 20892 USA. NCI, Canc Genome Struct & Funct Sect, NIH, Bethesda, MD 20892 USA. Univ Cadiz, Dept Biochem & Mol Biol, Cadiz 11510, Spain. Natl Inst Genet, PRESTO, Japan Sci & Technol Corp, Shizuoka 4118540, Japan. Grad Univ Adv Studies, Shizuoka 4118540, Japan. RP Farr, CJ (reprint author), Univ Cambridge, Dept Genet, Downing St, Cambridge CB2 3EH, England. OI Martinez Valdivia, Manuel Jesus/0000-0002-2888-849X FU Wellcome Trust [073915] NR 56 TC 77 Z9 79 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 1 PY 2002 VL 21 IS 19 BP 5269 EP 5280 DI 10.1093/emboj/cdf511 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 602JR UT WOS:000178502600027 PM 12356743 ER PT J AU Morens, DM AF Morens, DM TI Epidemic anthrax in the eighteenth century, the Americas SO EMERGING INFECTIOUS DISEASES LA English DT Article AB Anthrax has been described as a veterinary disease of minor importance to clinical medicine, causing occasional occupational infections in single cases or clusters. Its potential for rapid and widespread epidemic transmission under natural circumstances has not been widely appreciated. A little-known 1770 epidemic that killed 15,000 people in Saint-Domingue (modern Haiti) was probably intestinal anthrax. The epidemic spread rapidly throughout the colony in association with consumption of uncooked beef. Large-scale, highly fatal epidemics of anthrax may occur under unusual but natural circumstances. Historical information may not only provide important clues about epidemic development but may also raise awareness about bioterrorism potential. C1 NIAID, NIH, Bethesda, MD 20892 USA. RP Morens, DM (reprint author), NIAID, NIH, 6700-B Rockledge Dr,Room 3149, Bethesda, MD 20892 USA. NR 18 TC 6 Z9 6 U1 0 U2 2 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 USA SN 1080-6040 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD OCT PY 2002 VL 8 IS 10 BP 1160 EP 1162 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 605AL UT WOS:000178653200027 PM 12396933 ER PT J AU Strott, CA AF Strott, CA TI Sulfonation and molecular action SO ENDOCRINE REVIEWS LA English DT Review ID ASPARAGINE-LINKED OLIGOSACCHARIDES; ADENOSINE 5'-PHOSPHOSULFATE KINASE; HUMAN PHENOL SULFOTRANSFERASE; SULFATE-TRANSPORTER GENE; D-GLUCOSAMINYL 3-O-SULFOTRANSFERASE; HUMAN CYTOSOLIC SULFOTRANSFERASES; PITUITARY GLYCOPROTEIN HORMONES; CHOLECYSTOKININ-A RECEPTOR; FIBROBLAST-GROWTH-FACTOR; HUMAN HYDROXYSTEROID SULFOTRANSFERASE AB The sulfonation of endogenous molecules is a pervasive biological phenomenon that is not always easily understood, and although it is increasingly recognized as a function of fundamental importance, there remain areas in which significant cognizance is still lacking or at most minimal. This is particularly true in the field of endocrinology, in which the sulfoconjugation of hormones is a widespread occurrence that is only partially, if at all, appreciated. In the realm of steroid/sterol sulfoconjugation, the discovery of a novel gene that utilizes an alternative exon 1 to encode for two sulfotransferase isoforms, one of which sulfonates cholesterol and the other pregnenolone, has been an important advance. This is significant because cholesterol sulfate plays a crucial role in physiological systems such as keratinocyte differentiation and development of the skin barrier, arid pregnenolone sulfate is now acknowledged as an important neurosteroid. The sulfonation of thyroglobulin and thyroid hormones has been extensively investigated and, although this transformation is better understood, there remain areas of incomplete comprehension. The sulfonation of catecholamines is a prevalent modification that has been extensively studied but, unfortunately, remains poorly understood. The sulfonation of pituitary glycoprotein hormones, especially LH and TSH, does not affect binding to their cognate receptors; however, sulfonation does play an important role in their plasma clearance, which indirectly has a significant effect on biological activity. On the other hand, the sulfonation of distinct neuroendocrine peptides does have a profound influence on receptor binding and, thus, a direct effect on biological activity. The sulfonation of specific extracellular structures plays an essential role in the binding and signaling of a large family of extracellular growth factors. In summary, sulfonation is a ubiquitous posttranslational modification of hormones and extracellular components that can lead to dramatic structural changes in affected molecules, the biological significance of which is now beginning to be appreciated. C1 NICHHD, Sect Steroid Regulat, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. RP Strott, CA (reprint author), NICHHD, Sect Steroid Regulat, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. NR 387 TC 250 Z9 255 U1 3 U2 19 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA SN 0163-769X J9 ENDOCR REV JI Endocr. Rev. PD OCT PY 2002 VL 23 IS 5 BP 703 EP 732 DI 10.1210/er.2001.0040 PG 30 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 602ZQ UT WOS:000178534700006 PM 12372849 ER PT J AU Costa, M Zoroddu, MA Suk, WA Thompson, C Rossman, T AF Costa, M Zoroddu, MA Suk, WA Thompson, C Rossman, T TI Preface - Third International Meeting on the Molecular Mechanisms of Metal Toxicity and Carcinogenicity SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 NYU, Sch Med, New York, NY USA. Univ Sassari, I-07100 Sassari, Italy. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Costa, M (reprint author), NYU, Sch Med, Dept Environm Med, 57 Old Forge Rd, Tuxedo Pk, NY 10987 USA. RI costa, max/H-1754-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 SU 5 BP 687 EP 687 PG 1 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 612FQ UT WOS:000179064200001 ER PT J AU Trouba, KJ Geisenhoffer, KM Germolec, DR AF Trouba, KJ Geisenhoffer, KM Germolec, DR TI Sodium arsenite-induced stress-related gene expression in normal human epidermal, HaCaT, and HEL30 keratinocytes SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT 3rd International Meeting on the Molecular Mechanisms of Metal Toxicity and Carcinogenicity CY SEP 02-06, 2001 CL STINTINO, ITALY DE arsenite; glutathione; keratinocyte; redox; toxicity ID NF-KAPPA-B; INDUCED MALIGNANT TRANSFORMATION; OXIDOREDUCTASE(1) DT-DIAPHORASE; AORTIC ENDOTHELIAL-CELLS; OXIDATIVE DNA-DAMAGE; C-FOS TRANSCRIPTION; HUMAN-FIBROBLASTS; REACTIVE OXYGEN; OXIDANT STRESS; GROWTH-FACTORS C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. RP Germolec, DR (reprint author), NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. NR 72 TC 15 Z9 15 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 SU 5 BP 761 EP 766 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 612FQ UT WOS:000179064200017 PM 12426128 ER PT J AU Salnikow, K Davidson, T Costa, M AF Salnikow, K Davidson, T Costa, M TI The role of hypoxia-inducible signaling pathway in nickel carcinogenesis SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT 3rd International Meeting on the Molecular Mechanisms of Metal Toxicity and Carcinogenicity CY SEP 02-06, 2001 CL STINTINO, ITALY DE gene chip; HIF knockout; hypoxia; transcription factors ID MAMMALIAN-CELLS; GENE-EXPRESSION; P53; PROTEIN; ACTIVATION; CHECKPOINT; SUBSULFIDE; FACTOR-1; STRESS; HIF-1 AB Using human and rodent cells in vitro, we characterized a hypoxia-inducible signaling pathway as one of the pathways affected by carcinogenic nickel compounds. Acute exposure to nickel activates hypoxia-inducible transcription factor-1 (HIF-1), which strongly induces hypoxia-inducible genes, including the recently discovered tumor marker Cap43. This gene has been cloned based on its nickel inducibility and was found to be highly inducible by hypoxia. To identify other HIF-1-dependent/independent nickel-inducible genes, we used cells obtained from HIF-1alpha null mouse embryos and analyzed gene expression changes using the microarray technique. We found that genes coding for glycolytic enzymes, known to be regulated by HIF-1, were also induced in nickel-exposed cells. In addition, we identified a number of new genes highly induced by nickel in an HIF-dependent manner. Elevated HIT-1 activity after acute nickel exposure might be selectively advantageous because nickel-transformed rodent and human cells possess increased HIT-1 transcriptional activity. Hypoxia plays an important role in tumor progression. It selects for cells with enhanced glycolytic activity, causing production of large amounts of lactic acid, one of the most common features of tumor cells (Warburg effect). Here, we hypothesize that exposure to nickel activates the hypoxia-inducible pathway and facilitates selection of cells with increased transcriptional activity of hypoxia-inducible genes, which may be important in the nickel-induced carcinogenic process. C1 NIEHS, Dept Environm Med, New York, NY 10016 USA. NYU, Sch Med, Kaplan Comprehens Canc Ctr, New York, NY 10016 USA. NIEHS Ctr, Nelson Inst Environm Med, New York, NY USA. RP Salnikow, K (reprint author), NIEHS, Dept Environm Med, 550 1st Ave, New York, NY 10016 USA. RI costa, max/H-1754-2012 FU NCI NIH HHS [CA 16087]; NIEHS NIH HHS [ES 00260, ES 05512, ES 10344] NR 29 TC 45 Z9 46 U1 0 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 SU 5 BP 831 EP 834 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 612FQ UT WOS:000179064200031 PM 12426141 ER PT J AU Centeno, JA Mullick, FG Martinez, L Page, NP Gibb, H Longfellow, D Thompson, C Ladich, ER AF Centeno, JA Mullick, FG Martinez, L Page, NP Gibb, H Longfellow, D Thompson, C Ladich, ER TI Pathology related to chronic arsenic exposure SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT 3rd International Meeting on the Molecular Mechanisms of Metal Toxicity and Carcinogenicity CY SEP 02-06, 2001 CL STINTINO, ITALY DE angiosarcoma; arsenic; Bowen disease; hepatocellular carcinoma; hepatoportal sclerosis; hyperkeratosis; liver; noncirrhotic portal fibrosis; squamous cell carcinoma ID IDIOPATHIC PORTAL-HYPERTENSION; DRINKING-WATER; WELL WATER; MORTALITY; ANGIOSARCOMA; PREVALENCE; ARGENTINA; DISEASES AB Millions now suffer the effects of chronic arseniasis related to environmental arsenic exposure. The biological mechanisms responsible for arsenic-induced toxicity and especially chronic effects, including cancer, are not well known. The U.S. Armed Forces Institute of Pathology (AFIP) is participating in an international research effort to improve this understanding by the development of the International Tissue and Tumor Repository for Chronic Arsenosis (ITTRCA). The ITTRCA obtains, archives, and makes available for research purposes, tissues from subjects exposed to arsenic. We provide here a short overview of arsenic-induced pathology, briefly describe arsenic-induced lesions in the skin and liver, and present five case reports from the ITTRCA. Arsenic-induced skin pathology includes hyperkeratosis, pigmentation changes, Bowen disease, squamous cell carcinoma, and basal cell carcinomas. A unique spectrum of skin lesions, known as arsenical keratosis, is rather characteristic of chronic arseniasis. Bowen disease, or squamous cell carcinoma in situ of the skin, has been well documented as a consequence of arsenical exposure. A spectrum of liver lesions has also been attributed to chronic arseniasis. Of these, hepatocellular carcinoma, angiosarcoma, cirrhosis, and hepatoportal sclerosis have been associated with arsenic exposure. We present case reports that relate to these health conditions, namely, squamous cell carcinoma, basal cell carcinoma, and Bowen disease of the skin and hepatocellular carcinoma and angiosarcoma of the liver. Four patients had been treated with arsenical medications for such conditions as asthma, psoriasis, and syphilis, and one case occurred in a boy chronically exposed to arsenic in drinking water. C1 Armed Forces Inst Pathol, Div Biophys Toxicol, Washington, DC 20306 USA. US EPA, Washington, DC 20460 USA. Natl Canc Inst, Bethesda, MD USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Centeno, JA (reprint author), Armed Forces Inst Pathol, Div Biophys Toxicol, Washington, DC 20306 USA. NR 26 TC 132 Z9 137 U1 6 U2 9 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 SU 5 BP 883 EP 886 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 612FQ UT WOS:000179064200042 PM 12426152 ER PT J AU Gemmel, A Tavares, M Alperin, S Soncini, J Daniel, D Dunn, J Crawford, S Braveman, N Clarkson, TW McKinlay, S Bellinger, DC AF Gemmel, A Tavares, M Alperin, S Soncini, J Daniel, D Dunn, J Crawford, S Braveman, N Clarkson, TW McKinlay, S Bellinger, DC TI Blood lead level and dental caries in school-age children SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE blood lead; dental caries; epidemiology; tooth; toxicology ID NON-EXPOSED POPULATION; SOUTHERN BAVARIA FRG; HUMAN BONES; NHANES-III; TOOTH; SALIVA; ASSOCIATION; CHILDHOOD; DISEASE; HEALTH AB The association between blood lead level and dental caries was evaluated in cross-sectional analyses of baseline data for 543 children 6-10 years old screened for enrollment in the Children's Amalgam Trial, a study designed to assess potential health effects of mercury in silver fillings. Approximately half of the children were recruited from an urban setting (Boston/Cambridge, MA, USA) and approximately half from a rural setting (Farmington, ME, USA). Mean blood lead level was significantly greater among the urban subgroup, as was the mean number of carious tooth surfaces. Blood lead level was positively associated with number of caries among urban children, even with adjustment for demographic and maternal factors and child dental practices. This association was stronger in primary than in permanent dentition and stronger for occlusal, lingual, and buccal tooth surfaces than for mesial or distal surfaces. In general, blood lead was not associated with caries in the rural subgroup. The difference between the strength of the associations in the urban and rural settings might reflect the presence of residual confounding in the former setting, the presence of greater variability in the latter setting in terms of important caries risk factors (e.g., fluoride exposure), or greater exposure misclassification in the rural setting. These findings add to the evidence supporting a weak association between children's lead exposure and caries prevalence. A biologic mechanism for lead cariogenicity has not been identified, however. Our data are also consistent with residual confounding by factors associated with both elevated lead exposure and dental caries. C1 Childrens Hosp Boston, Boston, MA 02115 USA. New England Res Inst, Watertown, MA 02172 USA. Forsyth Inst, Boston, MA USA. Univ Maine, Farmington, ME USA. Natl Inst Dent & Craniofacial Res, Bethesda, MD USA. Univ Rochester, Sch Med & Dent, Rochester, NY USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Bellinger, DC (reprint author), Childrens Hosp Boston, Farley Basement Box 127,300 Longwood Ave, Boston, MA 02115 USA. FU NIDCR NIH HHS [U01 DE11886] NR 42 TC 22 Z9 22 U1 2 U2 3 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 IS 10 BP A625 EP A630 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 600VE UT WOS:000178411800044 PM 12361944 ER PT J AU Jacobs, DE Clickner, RP Zhou, JY Viet, SM Marker, DA Rogers, JW Zeldin, DC Broene, P Friedman, W AF Jacobs, DE Clickner, RP Zhou, JY Viet, SM Marker, DA Rogers, JW Zeldin, DC Broene, P Friedman, W TI The prevalence of lead-based paint hazards in US housing SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE childhood lead poisoning; housing; housing survey; lead; lead-based paint; lead paint; lead poisoning prevention ID EXPOSURE; CHILDREN AB In this study we estimated the number of housing units in the United States with lead-based paint and lead-based paint hazards. We included measurements of lead in intact and deteriorated paint, interior dust, and bare soil. A nationally representative, random sample of 831 housing units was evaluated in a survey between 1998 and 2000; the units and their occupants did not differ significantly from nationwide characteristics. Results indicate that 38 million housing units had lead-based paint, down from the 1990 estimate of 64 million. Twenty-four million had significant lead-based paint hazards. Of those with hazards, 1.2 million units housed low-income families (< $30,000/year) with children under 6 years of age. Although 17% of government-supported, low-income housing had hazards, 35% of all low-income housing had hazards. For households with incomes greater than or equal to $30,000/year, 19% had hazards. Fourteen percent of all houses had significantly deteriorated lead-based paint, and 16% and 7%, respectively, had dust lead and soil lead levels above current standards of the U.S. Department of Housing and Urban Development and the U.S. Environmental Protection Agency. The prevalence of lead-based paint and hazards increases with age of housing, but most painted surfaces, even in older housing, do not have lead-based paint. Between 2% and 25% of painted building components were coated with lead-based paint. Housing in the Northeast and Midwest had about twice the prevalence of hazards compared with housing in the South and West. The greatest risk occurs in older units with lead-based paint hazards that either will be or are currently occupied by families with children under 6 years of age and are low-income and/or are undergoing renovation or maintenance that disturbs lead-based paint. This study also confirms projections made in 2000 by the President's Task Force on Environmental Health Risks and Safety Risks to Children of the number of houses with lead-based paint hazards. Public- and private-sector resources should be directed to units posing the greatest risk if future lead poisoning is to be prevented. C1 US Dept Housing & Urban Dev, Off Healthy Homes & Lead Hazard Control, Washington, DC 20410 USA. Westat Corp, Rockville, MD USA. Natl Inst Environm Hlth Sci, Div Intramural Res, Res Triangle Pk, NC USA. RP Jacobs, DE (reprint author), US Dept Housing & Urban Dev, Off Healthy Homes & Lead Hazard Control, P-3202,451 17th St,SW, Washington, DC 20410 USA. NR 41 TC 139 Z9 141 U1 4 U2 28 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 IS 10 BP A599 EP A606 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 600VE UT WOS:000178411800041 PM 12361941 ER PT J AU Olden, K Goehl, TJ AF Olden, K Goehl, TJ TI EHP appoints children's health editors SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 NIEHS, Res Triangle Pk, NC 27709 USA. RP Olden, K (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD OCT PY 2002 VL 110 IS 10 BP A558 EP A558 DI 10.1289/ehp.110-a558 PG 1 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 600VE UT WOS:000178411800002 ER PT J AU Libe, R Dall'Asta, C Barbetta, L Baccarelli, A Beck-Peccoz, P Ambrosi, B AF Libe, R Dall'Asta, C Barbetta, L Baccarelli, A Beck-Peccoz, P Ambrosi, B TI Long-term follow-up study of patients with adrenal incidentalomas SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID SUBCLINICAL CUSHINGS-SYNDROME; MASSES; TUMORS; ABNORMALITIES; MANAGEMENT; ACTH AB Background: The incidence of adrenal incidentalomas has sharply increased in recent decades and concurrent subtle endocrine abnormalities, or even subclinical conditions, have been identified. Nonetheless, data concerning possible changes in adrenal size and/or hormonal pattern during follow-up are still inadequate. Objective: To evaluate long-term morphological and functional evolution of adrenal incidentalomas after initial diagnosis and to identify possible risk factors for hormonal hyperactivity and mass enlargement. Patients: Sixty-four patients (34-79 years) were followed-up for 12-120 months (median 25.5 months). Initial computerized tomography scan showed a unilateral mass in 51 patients and bilateral lesions in 13 patients. Average mass diameter at diagnosis was 2.5+/-0.1 cm (range 1.0-4.0). Twelve patients had subclinical Cushing's syndrome, 41 had mild hormonal alterations, and 11 had normal adrenal function at baseline. All patients were investigated by morphological and functional evaluation 6 and 12 months after diagnosis, and then at 1-year intervals. Results: During follow-up, a mass size increase greater than or equal to 1 cm was observed in 13 patients, and 18 developed further subtle endocrine alterations. Cumulative risk of developing endocrine abnormalities was 17% at 1 year, 29% at 2 years, and 47% at 5 years. The risk was higher in the first 2 years of follow-up if the initial tumor diameter was greater than or equal to 3 cm. Overall, cumulative risk of mass enlargement was 6% at 1 year, 14% at 2 years, and 29% at 5 years, and it was greater in patients with normal adrenal function than in those with subtle hormonal abnormalities (P < 0.05). One female subject showed a mass enlargement after 6 months of follow-up and was eventually diagnosed with non-Hodgkin's lymphoma. Conclusions: Patients with an adrenal incidentaloma are at risk for tumor growth and development of hormonal alterations. The risk of adrenal malignancy, although not elevated, also indicates the need for long-term follow-up. C1 Ist Policlin San Donato, Div Endocrinol & Diabetol, I-20097 San Donato Milanese, Milan, Italy. Univ Milan, Osped Maggiore, IRCCS, Inst Endocrine Sci, Milan, Italy. NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. RP Ambrosi, B (reprint author), Ist Policlin San Donato, Div Endocrinol & Diabetol, Via Morandi 30, I-20097 San Donato Milanese, Milan, Italy. NR 21 TC 95 Z9 105 U1 0 U2 0 PU BIO SCIENTIFICA LTD PI BRISTOL PA 16 THE COURTYARD, WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4NQ, ENGLAND SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD OCT PY 2002 VL 147 IS 4 BP 489 EP 494 DI 10.1530/eje.0.1470489 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 606QE UT WOS:000178744000009 PM 12370111 ER PT J AU Manzotti, CN Tipping, H Perry, LCA Mead, KI Blair, PJ Zheng, Y Sansom, DM AF Manzotti, CN Tipping, H Perry, LCA Mead, KI Blair, PJ Zheng, Y Sansom, DM TI Inhibition of human T cell proliferation by CTLA-4 utilizes CD80 and requires CD25(+) regulatory T cells SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE CTLA-4; CD80; regulatory cell; tolerance ID IMMUNOLOGICAL SELF-TOLERANCE; LYMPHOCYTE-ASSOCIATED ANTIGEN-4; CYTOKINE PRODUCTION; AUTOIMMUNE-DISEASE; B7 COSTIMULATION; DENDRITIC CELLS; IN-VITRO; ACTIVATION; CD28; INDUCTION AB CD28 and CTLA-4 are opposing regulators of T cell activation, triggered by the two ligands CD80 and CD86. How these ligands promote either T cell activation via CD28 or inhibition via CTLA-4 is not understood. Using CD80 and CD86 molecules expressed on transfected cells, we have identified a major difference between these ligands in that CD80 transfectants have the ability to inhibit activation of resting human peripheral blood T cells via interaction with CTLA-4 whereas CD86 transfectants do not. Rather, CTLA-4-CD86 interactions appear to contribute towards T cell proliferation. We also observed that CTLA-4 function is strongly influenced by TCR stimulation, effects being observed only at relatively low levels of TCR stimulation. The kinetics of CD80-CTLA-4 interactions revealed that CTLA-4 inhibition took place within the first 8 h of T cell stimulation, despite there being little measurable CTLA-4 expression on the majority T cells. However, significant amounts of CTLA-4 were observed in the CD25(+) CD4(+) subset of T cells which, when removed from the cultures, accounted for the CTLA-4 inhibition observed. Overall, these data provide evidence that CD80 and CD86 differ in their interactions with CTLA-4 and that CD80 appears to be the preferential inhibitory ligand for CTLA-4 working via a population of CD4(+) CD25(+) CTLA-4(+) regulatory T cells. C1 Univ Birmingham, Sch Med, MRC, Ctr Immune Regulat, Birmingham B15 2TT, W Midlands, England. NIDDK, NAVY Transplantat & Autoimmun Branch, Bethesda, MD USA. RP Sansom, DM (reprint author), Univ Birmingham, Sch Med, MRC, Ctr Immune Regulat, Vincent Dr, Birmingham B15 2TT, W Midlands, England. NR 45 TC 96 Z9 100 U1 1 U2 4 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD OCT PY 2002 VL 32 IS 10 BP 2888 EP 2896 DI 10.1002/1521-4141(2002010)32:10<2888::AID-IMMU2888>3.0.CO;2-F PG 9 WC Immunology SC Immunology GA 606RH UT WOS:000178746600021 PM 12355442 ER PT J AU Dimmock, JR Padmanilyam, MP Zello, GA Quail, JW Oloo, EO Prisciak, JS Kraatz, HB Cherkasov, A Lee, JS Allen, TM Santos, CL Manavathu, EK De Clercq, E Balzarini, J Stables, JP AF Dimmock, JR Padmanilyam, MP Zello, GA Quail, JW Oloo, EO Prisciak, JS Kraatz, HB Cherkasov, A Lee, JS Allen, TM Santos, CL Manavathu, EK De Clercq, E Balzarini, J Stables, JP TI Cytotoxic 1,3-diarylidene-2-tetralones and related compounds SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE 2-tetralones; cytotoxicity; murine toxicity; redox potentials ID MANNICH-BASES; DRUG DESIGN AB A number of 1,3-arylidene-2-tetralones 1, 2 and 4 were synthesised and demonstrated cytotoxic activity towards murine P388 and L 12 10 cells as well as human Molt 4/C8 and CEM T-lymphocytes. In general, the related 1-arylidene-2-tetralones 3 possessed lower potencies in these screens than the compounds in series 1 and 4. Approximately, half of the compounds were evaluated against a panel of human tumour cell lines. In this screen, most of the enones were more cytotoxic than the established anticancer agent melphalan and some demonstrated selective toxicity towards leukemic and colon cancer cells. The modes of action of representative compounds include interfering with the biosyntheses of nucleic acids and proteins as well as altering redox potentials. The compounds were well tolerated when administered intraperiteonally to mice. Thus these novel enones are promising prototypic molecules due to their potent cytotoxic properties and lack of significant murine toxicity. (C) 2002 Published by Editions scientifiques et medicales Elsevier SAS. C1 Univ Saskatchewan, Coll Pharm & Nutr, Saskatoon, SK S7N 5C9, Canada. Univ Saskatchewan, Dept Chem, Saskatoon, SK S7N 5C9, Canada. Univ Saskatchewan, Dept Biochem, Saskatoon, SK S7N 5E5, Canada. Univ Alberta, Dept Pharmacol, Edmonton, AB T6G 2H7, Canada. Wayne State Univ, Dept Med, Detroit, MI 48201 USA. Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium. NINCDS, NIH, Bethesda, MD 20892 USA. RP Dimmock, JR (reprint author), Univ Saskatchewan, Coll Pharm & Nutr, 110 Sci Pl, Saskatoon, SK S7N 5C9, Canada. EM dimmock@skyway.usask.ca RI Cherkasov, Artem/A-2134-2012; Kraatz, Heinz-Bernhard/D-2246-2014 OI Kraatz, Heinz-Bernhard/0000-0002-7149-0110 NR 36 TC 27 Z9 27 U1 0 U2 3 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD OCT PY 2002 VL 37 IS 10 BP 813 EP 824 AR PII S0223-5234(02)01402-2 DI 10.1016/S0223-5234(02)01402-2 PG 12 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 613XA UT WOS:000179155700004 PM 12446039 ER PT J AU Tambeli, CH Parada, CA Levine, JD Gear, RW AF Tambeli, CH Parada, CA Levine, JD Gear, RW TI Inhibition of tonic spinal glutamatergic activity induces antinociception in the rat SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE antinociception; AMPA; kainate; NK1; mGluR1; NMDA; excitatory; nucleus accumbens; glutamate ID JAW-OPENING REFLEX; ENKEPHALIN-LIKE MATERIAL; VENTROLATERAL ORBITAL CORTEX; PERIAQUEDUCTAL GRAY-MATTER; ANTERIOR PRETECTAL NUCLEUS; DORSAL HORN NEURONS; RECEPTOR ANTAGONISTS; CA2+ CHANNELS; N-TYPE; P-TYPE AB Inhibition of tonic activity in spino-supraspinal projection neurons induces heterosegmental antinociception that is mediated by opioid receptors in nucleus accumbens. To investigate the origin of this tonic activity, we evaluated the ability of inhibiting neurotransmission in the spinal cord to produce heterosegmental antinociception in the trigeminal nociceptive jaw-opening reflex (JOR) in the rat. Spinal intrathecal administration of calcium channel blockers attenuated the JOR, suggesting that the tonic spinal activity depends on synaptic input. To identify the excitatory neurotransmitter receptors involved, selective antagonists for AMPA/kainate, mGluR(1), NMDA or NK1 receptors were administered intrathecally to the spinal cord. The AMPA/kainate and mGluR(1) receptor antagonists, but not the NMDA or NK1 receptor antagonists, induced antinociception, which was antagonized by intra-accumbens administration of the selective mu-opioid receptor antagonist CTOP. Thus, inhibition of tonic spinal glutamatergic activity resulted in supraspinally mediated antinociception. As this antinociception occurred in the absence of interventions that would produce a facilitated nociceptive state, this tonic glutamatergic activity is important in setting nociceptive threshold. C1 Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA. Univ Calif San Francisco, NIH, Pain Ctr, San Francisco, CA 94143 USA. Univ Campinas, Fac Dent Piracicaba, Campinas, SP, Brazil. RP Gear, RW (reprint author), Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA. RI Parada, Carlos Amilcar/C-3974-2012; Tambeli, Claudia/D-4356-2012 NR 64 TC 26 Z9 26 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD OCT PY 2002 VL 16 IS 8 BP 1547 EP 1553 DI 10.1046/j.1460-9568.2002.02204.x PG 7 WC Neurosciences SC Neurosciences & Neurology GA 609UL UT WOS:000178922900017 PM 12405969 ER PT J AU Dreher, JC Grafman, J AF Dreher, JC Grafman, J TI The roles of the cerebellum and basal ganglia in timing and error prediction SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE attention; fMRI; predictability; striatum; switching ID EVENT-RELATED FMRI; FRONTAL-LOBE DAMAGE; PARKINSONS-DISEASE; MOTOR CONTROL; PREFRONTAL CORTEX; WORKING-MEMORY; FUNCTIONAL NEUROANATOMY; SHIFTING ATTENTION; COGNITIVE FUNCTION; TASK-PERFORMANCE AB Recent evidence that the cerebellum and the basal ganglia are activated during the performance of cognitive and attention tasks challenges the prevailing view of their primary function in motor control. The specific roles of the basal ganglia and the cerebellum in cognition, however, have been difficult to identify. At least three functional hypotheses regarding their roles have been proposed. The first hypothesis suggests that their main function is to switch attentional set. The second hypothesis states that they provide error signals regarding stimuli or rewards. The third hypothesis is that they operate as an internal timing system, providing a precise representation of temporal information. Using functional magnetic resonance imaging, we tested these three hypotheses using a task-switching experiment with a 2 x 2 factorial design varying timing (random relative to fixed) and task order (unpredictable relative to predictable). This design allowed us to test whether switching between tasks, timing irregularity and/or task order unpredictability activate the basal ganglia and/or the cerebellum. We show that the cerebellum is primarily activated with timing irregularity while the anterior striatum is activated with task order unpredictability, supporting their distinctive roles in two forms of readjustment. Task order unpredictability alone, independent of reward delivery, is sufficient to induce striatal activation. In addition, activation of the cerebellum and basal ganglia were not specific to switching attention because these regions were both activated during switching between tasks and during the simultaneous maintenance of two tasks without switching between them. C1 Natl Inst Neurol Disorder & Stroke, Cognit Neurosci Sect, Bethesda, MD 20892 USA. RP Grafman, J (reprint author), Natl Inst Neurol Disorder & Stroke, Cognit Neurosci Sect, Bldg 10,Room 5C205,MSC 1440, Bethesda, MD 20892 USA. OI Grafman, Jordan H./0000-0001-8645-4457 NR 77 TC 91 Z9 95 U1 3 U2 9 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD OCT PY 2002 VL 16 IS 8 BP 1609 EP 1619 DI 10.1046/j.1460-9568.2002.02212.x PG 11 WC Neurosciences SC Neurosciences & Neurology GA 609UL UT WOS:000178922900023 PM 12405975 ER PT J AU Chou, JY Zingone, A Pan, CJ AF Chou, JY Zingone, A Pan, CJ TI Adenovirus-mediated gene therapy in a mouse model of glycogen storage disease type 1a SO EUROPEAN JOURNAL OF PEDIATRICS LA English DT Article DE gene therapy; GSD-1a mouse model; glucose-6-phosphatase; glycogen storage disease; recombinant adenovirus ID GLUCOSE-6-PHOSPHATASE SYSTEM; MURINE GLUCOSE-6-PHOSPHATASE; ENZYME-DEFICIENT; TRANSPORT; VECTORS AB Glycogen storage disease type 1a (GSD-1a), characterized by growth retardation, hypoglycemia, hepatomegaly, kidney enlargement, hyperlipidemia, hyperuricemia, and renal dysfunction, is caused by deficiencies in glucose-6-phosphatase (G6Pase), a key enzyme in glucose homeostasis. Over the last 20 years, dietary therapies have greatly improved the prognosis of GSD-1a patients. However, the underlying pathological process remains uncorrected and the efficacy of dietary treatment is frequently limited by poor compliance. Therefore, long-term complications still develop in adult patients. To develop future therapeutic approaches for GSD-1a, we have generated G6Pase-deficient (G6Pase(-/-)) mice that mimic the pathophysiology of human GSD-1a patients. To evaluate the feasibility of gene replacement therapy for this disorder, we have infused recombinant adenovirus containing murine G6Pase gene (Ad-mG6Pase) into G6Pase(-/-) mice. While only 15% of G6Pase(-/-) mice under glucose therapy survived weaning, a 100% survival rate was achieved when G6Pase(-/-) mice were infused with Ad-mG6Pase and 90% of which lived to 3 months of age. Hepatic G6Pase activity in Ad-mG6Pase-infused mice was restored to 19% of that in G6Pase(+/+) mice at 7 through 14 post-infusion days. Ad-mG6Pase infusion also greatly improved growth of G6Pase(-/-) mice and normalized plasma glucose, cholesterol, triglyceride, and uric acid profiles. Further, liver and kidney enlargement were less pronounced with near normal levels of glycogen depositions in both organs. Conclusion: our data demonstrate that a single administration of a recombinant adenovirus vector can alleviate the clinical manifestations of glycogen storage, disease type 1a in mice, suggesting that this disorder in humans can potentially be corrected by gene therapy. C1 NICHHD, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. RP Chou, JY (reprint author), NICHHD, Heritable Disorders Branch, NIH, Bldg 10,Room 9S241, Bethesda, MD 20892 USA. NR 22 TC 8 Z9 11 U1 1 U2 1 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-6199 J9 EUR J PEDIATR JI Eur. J. Pediatr. PD OCT PY 2002 VL 161 SU 1 BP S56 EP S61 DI 10.1007/s00431-002-1005-x PG 6 WC Pediatrics SC Pediatrics GA 609LJ UT WOS:000178904800010 PM 12373573 ER PT J AU Baker, R Tohen, M Brown, E Schuh, L Zarate, C Suppes, T AF Baker, R Tohen, M Brown, E Schuh, L Zarate, C Suppes, T TI Olanzapine versus divalproex sodium for bipolar mania in rapid cyclers SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Lilly Res Labs, Indianapolis, IN USA. Harvard Univ, Sch Med, Belmont, MA 02178 USA. NIMH, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, Dallas, TX USA. NR 2 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S256 EP S256 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000335 ER PT J AU Gozes, I Furman, S Vulih, I Segal-Ruder, Y Fridkin, M Brenneman, DE AF Gozes, I Furman, S Vulih, I Segal-Ruder, Y Fridkin, M Brenneman, DE TI VIP, novel proteins and peptide-mediated neuronal survival SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Tel Aviv Univ, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. Weizmann Inst Sci, IL-76100 Rehovot, Israel. NICHD, LDN, SDMP, NIH, Bethesda, MD USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S145 EP S146 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000093 ER PT J AU Kalali, A Bech, P Williams, J Kobak, K Lipsitz, J Engelhardt, N Evans, K Olin, J Pearson, J Rothman, M AF Kalali, A Bech, P Williams, J Kobak, K Lipsitz, J Engelhardt, N Evans, K Olin, J Pearson, J Rothman, M TI The new GRID-HAM-D - Results from field trials SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Univ Calif San Diego, San Diego, CA 92103 USA. Frederiksborg Cent Cty Hosp, Inst Psychiat Res, Frederiksberg, Denmark. Columbia Univ, New York, NY USA. Eli Lilly & Co, Neurosci, Indianapolis, IN 46285 USA. Boehringer Ingelheim, Burlington, ON, Canada. NIMH, Washington, DC USA. Merck Res Labs, Epidemiol, W Point, PA USA. Johnson & Johnson Consumer Prod Inc, Raritan, NJ USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S239 EP S239 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000295 ER PT J AU Konstantinidis, A Heiden, A Stastny, J Baecker, C Letmaier, M Winkler, D Neumeister, A Kasper, S AF Konstantinidis, A Heiden, A Stastny, J Baecker, C Letmaier, M Winkler, D Neumeister, A Kasper, S TI Rapid transcranial magnetic stimulation (r-TMS): A novel treatment option for seasonal affective disorder (SAD)? SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Univ Vienna, Hosp Psychiat, Dept Gen Psychiat, Vienna, Austria. NIMH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S252 EP S252 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000325 ER PT J AU Manji, HK Zhou, R Moore, GJ Gray, N Du, J Chen, G AF Manji, HK Zhou, R Moore, GJ Gray, N Du, J Chen, G TI Genomic studies identify novel targets for the long term actions of mood stabilizers SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract ID BRAIN C1 NIMH, Mol Pathophysiol Lab, Bethesda, MD 20892 USA. RI Moore, Gregory/E-7184-2010; Chen, Guang/A-2570-2017 OI Moore, Gregory/0000-0001-8541-3194; NR 5 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S132 EP S133 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000076 ER PT J AU Nemes, Z Sarvari, M Steinert, PM Fesus, L VanBeeumen, J Devreese, B AF Nemes, Z Sarvari, M Steinert, PM Fesus, L VanBeeumen, J Devreese, B TI Isopeptide cross-links in Alzheimer's neurofibrillary tangles SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Univ Debrecen, H-4012 Debrecen, Hungary. NIAMS, LSB, NIH, Bethesda, MD USA. Univ Ghent, B-9000 Ghent, Belgium. RI Devreese, Bart/B-2011-2009 OI Devreese, Bart/0000-0002-9764-2581 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 0924-977X EI 1873-7862 J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S369 EP S369 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000599 ER PT J AU Willeit, M Praschak-Rieder, N Zill, P Neumeister, A Ackenheil, M Kasper, S Bondy, B AF Willeit, M Praschak-Rieder, N Zill, P Neumeister, A Ackenheil, M Kasper, S Bondy, B TI C825T polymorphism in the G protein beta3-subunit gene is associated with seasonal affective disorder SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 Univ Klin Psychiat, Vienna, Austria. LMU Munich, Dept Neurochem, Munich, Germany. NIMH, Mood & Anxiety Disorders Program, 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 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD OCT PY 2002 VL 12 SU 3 BP S252 EP S253 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 609LL UT WOS:000178905000326 ER PT J AU Jonsson, S Vidarsson, G Valdimarsson, H Schiffman, G Schneerson, R Jonsdottir, I AF Jonsson, S Vidarsson, G Valdimarsson, H Schiffman, G Schneerson, R Jonsdottir, I TI Vaccination of COPD patients with a pneumococcus type 6B tetanus toxoid conjugate vaccine SO EUROPEAN RESPIRATORY JOURNAL LA English DT Article DE antibodies; chronic obstructive pulmonary disease; opsonophagocytosis; pneumococcus; vaccination ID INFLUENZAE TYPE-B; POLYSACCHARIDE VACCINE; LUNG-DISEASE; ANTIBODIES; EFFICACY; PREVENTION; BACTEREMIA; RESPONSES; PNEUMONIA; ADULTS AB This paper examines how pneumococcal type 6B polysaccharide conjugated to tetanus toxoid (Pn6B-TT) compares to a 23 valent pneumococcal vaccine (pneumococcal polysaccharide (PPS)-23) with respect to immunogenicity and serum opsonic activity in patients with chronic obstructive pulmonary disease (COPD). Patients with COPD aged 55-75 yrs, were vaccinated with Pn6B-TT (n=10) or with PPS-23 (n=9). Healthy young adults (HA) were vaccinated with Pn6B-TT as controls. Total antibodies to serotype 6B polysaccharide were measured by radioimmunoassay and immunoglobulin (Ig)G antibodies by enzyme-linked immunosorbent assay. Opsonic activity was measured by a phagocytosis assay using human neutrophils as effector cells. The patient groups were comparable by age, smoking history, lung function and use of steroids. COPD patients vaccinated with Pn6B-TT or PPS-23 showed an increase in IgG antibodies and a nonsignificant increase in opsonic activity. This was similar to the increase in IgG and opsonic activity seen in HA. There was a significant correlation between antibody levels and opsonic activity in COPD patients vaccinated both with Pn6B-TT and PPS-23. Pneumococcal antibodies have been shown to confer protection from infection. The results of the present study indicate that protective immunity can be expected in elderly chronic obstructive pulmonary disease patients vaccinated with conjugate vaccines. C1 Univ Hosp, Dept Immunol, Landspitali, IS-101 Reykjavik, Iceland. Univ Hosp, Dept Med, Landspitali, IS-101 Reykjavik, Iceland. UMCU, Dept Immunol, Utrecht, Netherlands. SUNY Sci Ctr, Dept Microbiol & Immunol, Brooklyn, NY USA. NICHHD, Lab Dev & Mol Immunol, Bethesda, MD 20892 USA. RP Jonsdottir, I (reprint author), Univ Hosp, Dept Immunol, Landspitali, IS-101 Reykjavik, Iceland. RI Vidarsson, Gestur/A-9909-2009 OI Vidarsson, Gestur/0000-0001-5621-003X NR 30 TC 16 Z9 16 U1 0 U2 0 PU EUROPEAN RESPIRATORY SOC JOURNALS LTD PI SHEFFIELD PA 146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND SN 0903-1936 J9 EUR RESPIR J JI Eur. Resp. J. PD OCT PY 2002 VL 20 IS 4 BP 813 EP 818 DI 10.1183/09031936.02.00289702 PG 6 WC Respiratory System SC Respiratory System GA 606BF UT WOS:000178712200006 PM 12412669 ER PT J AU Whitfield, KE Harris, JR AF Whitfield, KE Harris, JR TI Untitled - Preface SO EXPERIMENTAL AGING RESEARCH LA English DT Editorial Material C1 Penn State Univ, Dept Biobehav Hlth, University Pk, PA 16802 USA. NIA, Bethesda, MD 20892 USA. RP Whitfield, KE (reprint author), Penn State Univ, Dept Biobehav Hlth, University Pk, PA 16802 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD OCT-DEC PY 2002 VL 28 IS 4 BP 345 EP 345 DI 10.1080/03610730290080371 PG 1 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA 590JR UT WOS:000177820200001 ER PT J AU Thiagarajan, G Chandani, S Rao, SH Samuni, AM Chandrasekaran, K Balasubramanian, D AF Thiagarajan, G Chandani, S Rao, SH Samuni, AM Chandrasekaran, K Balasubramanian, D TI Molecular and cellular assessment of Ginkgo biloba extract as a possible ophthalmic drug SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE Ginkgo biloba; EGb761; antioxidant; antiapoptotic agent; cytoprotective agent; potential anticataract agent ID RAT RETINA; SUPEROXIDE-DISMUTASE; SELENITE CATARACT; LENS; CONSTITUENTS; INHIBITION; DAMAGE; CELLS; REPERFUSION; APOPTOSIS AB We have investigated the biochemical and cell biological basis of the reported beneficiary effects of the leaf extracts of the plant Ginkgo biloba, which has been used as a possible ophthalmic drug. The antioxidant, antimicrobial, anti-apoptotic and cytoprotective properties of the standardized extract called EGb761 were assayed. Chemical stresses were induced in cells using alloxan or dexamethasone, and the effect of EGb761 on them was studied using the MTT and TUNEL assays. Its ability to modulate the activities of some antioxidant enzymes was tested in vitro. In addition, cataract was induced in rats through selenite injection, and the effect of EGb761 administration on the progression of cataract was studied using slit lamp examination. Ginkgo biloba was found to be an excellent antioxidant. It readily scavenges reactive oxygen and nitrogen radicals and inhibits oxidative modifications that occur to proteins in vitro. It enters intact cells and protects them from alloxan-mediated and light-mediated stress, and the nuclear DNA from single strand breaks. It also effectively inhibits chemically induced apoptosis. It does not modulate the activities of endogenous antioxidant enzymes, nor does it have any significant antimicrobial activity. Unlike some other plant extracts, it is not phototoxic. In experiments wherein selenite cataract was induced in laboratory rats, treatment with the extract significantly retards the progression of lens opacification in vivo. Ginkgo biloba's inherent antioxidant, antiapoptotic and cytoprotective action and potential anticataract ability appear to be some of the factors responsible for its beneficial effects. (C) 2002 Elsevier Science Ltd. C1 LV Prasad Eye Inst, Brien Holden Eye Res Ctr, Hyderabad Eye Res Fdn, Hyderabad 500034, Andhra Pradesh, India. Boston Univ, Boston, MA 02215 USA. Ctr Cellular & Mol Biol, Hyderabad 500007, Andhra Pradesh, India. NCI, Div Radiat Oncol, NIH, Bethesda, MD 20892 USA. Univ Maryland, Sch Med, Dept Anesthesiol, Baltimore, MD 21201 USA. RP Balasubramanian, D (reprint author), LV Prasad Eye Inst, Brien Holden Eye Res Ctr, Hyderabad Eye Res Fdn, Banjara Hills, Hyderabad 500034, Andhra Pradesh, India. EM dbala@lvpeye.stph.net NR 50 TC 33 Z9 42 U1 0 U2 4 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD OCT PY 2002 VL 75 IS 4 BP 421 EP 430 DI 10.1006/exer.2002.2035 PG 10 WC Ophthalmology SC Ophthalmology GA 612QL UT WOS:000179086900006 PM 12387790 ER PT J AU Stevnsner, T Thorslund, T de Souza-Pinto, NC Bohr, VA AF Stevnsner, T Thorslund, T de Souza-Pinto, NC Bohr, VA TI Mitochondrial repair of 8-oxoguanine and changes with aging SO EXPERIMENTAL GERONTOLOGY LA English DT Article; Proceedings Paper CT 2nd Euroconference on Biological Ageing CY MAY 18-22, 2002 CL SPETSES ISL, GREECE DE mitochondria; base excision repair; 8-oxoG; aging ID HAMSTER OVARY CELLS; TRANSCRIPTION-COUPLED REPAIR; OXIDATIVE BASE DAMAGE; DNA-DAMAGE; COCKAYNE-SYNDROME; RAT-LIVER; MAMMALIAN MITOCHONDRIA; FINE-STRUCTURE; RINR-38 CELLS; DHFR GENE AB Reactive oxygen species (ROS) are formed in all living organisms as a by-product of normal metabolism (endogenous sources) and:as a consequence of exposure to environmental compounds (exogenous sources). Endogenous ROS are largely formed during oxidative phosphorylation in the mitochondria and, therefore, mitochondrial DNA (mtDNA) is at particularly high risk of ROS-induced damage. Mitochondria are essential for cell viability, and oxidative damage to mtDNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. One of the most common oxidative DNA lesions is 7,8-dihydro-8-oxoguanine (8-oxoG) which can introduce G/C to T/A transversions after DNA replication. Oxidative DNA base lesions, including 8-oxoG, are repaired primarily by the base excision repair (BER) pathway. While we know much about how this pathway functions in processing the nuclear DNA lesions, little is yet known about BER in mitochondria. We have used a number of different approaches to explore the mechanisms of DNA damage processing in the mtDNA. We have been able to demonstrate that mammalian mitochondria efficiently remove 8-oxoG from their genome, and that the efficiency of 8-oxoG incision increases with age in rats and mice. Yet 8-oxoG accumulates in mtDNA during aging. Changes in mitochondrial function with age have been observed in several organisms and accumulation of DNA lesions in mtDNA with age may be an underlying cause for numerous age-associated diseases including cancer. (C) 2002 Elsevier Science Inc. All rights reserved. C1 Danish Ctr Mol Gerontol, Dept Mol Biol, DK-8000 Aarhus, Denmark. NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. RP Stevnsner, T (reprint author), Danish Ctr Mol Gerontol, Dept Mol Biol, CF Mollers Alle Bldg 130, DK-8000 Aarhus, Denmark. RI Souza-Pinto, Nadja/C-3462-2013 OI Souza-Pinto, Nadja/0000-0003-4206-964X NR 46 TC 51 Z9 51 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD OCT-NOV PY 2002 VL 37 IS 10-11 BP 1189 EP 1196 AR PII S0531-5565(02)00142-0 DI 10.1016/S0531-5565(02)00142-0 PG 8 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 623UW UT WOS:000179722100007 PM 12470830 ER PT J AU Han, SSW Kang, DY Mujtaba, T Rao, MS Fischer, I AF Han, SSW Kang, DY Mujtaba, T Rao, MS Fischer, I TI Grafted lineage-restricted precursors differentiate exclusively into neurons in the adult spinal cord SO EXPERIMENTAL NEUROLOGY LA English DT Article DE neuronal precursors; glial precursors; spinal cord; stem cells; neuronal differentiation; transplantation; transgenic rats; neurogenesis; neuronal replacement ID CENTRAL-NERVOUS-SYSTEM; NEURAL STEM-CELLS; HIPPOCAMPAL-NEURONS; PROGENITOR CELLS; GROWTH-FACTOR; WHITE-MATTER; IN-VIVO; RAT; TRANSPLANTATION; PROLIFERATION AB Multipotent neural stem cells (NSCs) have the potential to differentiate into neuronal and glial cells and are therefore candidates for cell replacement after CNS injury. Their phenotypic fate in vivo is dependent on the engraftment site, suggesting that the environment exerts differential effects on neuronal and glial lineages.. In particular, when grafted into the adult spinal cord, NSCs are restricted to the glial lineage, indicating that the host spinal cord environment is not permissive for neuronal differentiation. To identify the stage at which neuronal differentiation is inhibited we examined the survival, differentiation, and integration of neuronal restricted precursor (NRP) cells, derived from the embryonic spinal cord of transgenic alkaline phosphatase rats, after transplantation into the adult spinal cord. We found that grafted NRP cells differentiate into mature neurons, survive for at least 1 month, appear to integrate within the host spinal cord, and extend processes in both the gray and white matter. Conversely, grafted glial restricted precursor cells did not differentiate into neurons. We did not observe glial differentiation from the grafted NRP cells, indicating that they retained their neuronal restricted properties in vivo. We conclude that the adult nonneurogenic CNS environment does not support the transition of multipotential NSCs to the neuronal commitment stage, but does allow the survival, maturation, and integration of NRP cells. (C) 2002 Elsevier Science (USA) . C1 Drexel Univ Coll, Dept Neurobiol & Anat, MD PHD Program, Philadelphia, PA 19129 USA. NIA, Neurosci Lab, GRC, Baltimore, MD 21224 USA. RP Fischer, I (reprint author), Drexel Univ Coll, Dept Neurobiol & Anat, MD PHD Program, 2900 Queen Lane, Philadelphia, PA 19129 USA. OI Fischer, Itzhak/0000-0003-3187-8740 NR 59 TC 106 Z9 112 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 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD OCT PY 2002 VL 177 IS 2 BP 360 EP 375 DI 10.1006/exnr.2002.7995 PG 16 WC Neurosciences SC Neurosciences & Neurology GA 612PW UT WOS:000179085500002 PM 12429183 ER PT J AU Oh, JD Bibbiani, F Chaset, TN AF Oh, JD Bibbiani, F Chaset, TN TI Quetiapine attenuates levodopa-induced motor complications in rodent and primate parkinsonian models SO EXPERIMENTAL NEUROLOGY LA English DT Article DE AMPA receptor; dopamine; D1 receptor; D2 receptor; dyskinesia; glutamate; Parkinson's disease; quetiapine; striatum ID PHOTON-EMISSION-TOMOGRAPHY; DOPA-INDUCED DYSKINESIAS; RECEPTOR BLOCKADE; IN-VIVO; ANTIPSYCHOTIC AGENTS; GLUTAMATERGIC TRANSMISSION; TARDIVE-DYSKINESIA; 5HT(2A) RECEPTORS; STRIATAL DOPAMINE; 5-HT1A AGONIST AB The contribution of serotoninergic mechanisms to motor dysfunction in Parkinson's disease (PD) has yet to be fully elucidated. Recent clinical observations increasingly suggest that drugs able to block serotonin 5HT2A/C receptors can benefit patients with certain extrapyramidal movement disorders. To further explore the roles of these and other neurotransmitter receptors in the pathogenesis of parkinsonian signs and levodopa-induced dyskinesias; we evaluated the effects of quetiapine, an atypical antipsychotic with 5HT2A/C and D2/3 antagonistic activity, on motor behavior in 6-hydroxydopamine-lesioned rats and MPTP-lesioned nonhuman primates. In hemiparkinsonian rats, quetiapine (5 mg/kg, po) reversed the shortened motor response to levodopa challenge produced by 3 weeks of twice-daily levodopa treatment (P < 0.01). Quetiapine (5 mg(kg po) also normalized the shortened response to the acute injection of either a dopamine D1 receptor agonist (SKF 38392) or a D2 agonist (quinpirole) in rats that had received chronic levodopa treatment. Quetiapine had no effect on parkinsonian dysfunction when given alone or with levodopa to parkinsonian rats and monkeys. Quetiapine (4 mg/kg, po) did, however, substantially reduce levodopa-induced dyskinesias when coadministered with levodopa (P < 0.05). These results suggest that quetiapine could confer therapeutic benefits to patients with levodopa-induced motor complications. Moreover, our findings may indicate that 5HT2A/C receptor-mediated mechanisms, alone or in combination with other mechanisms, contribute to the pathogenesis of the altered motor responses associated with the treatment of PD. Published by Elsevier Science (USA). C1 Cent Michigan Univ, Dept Psychol, Mt Pleasant, MI 48859 USA. Natl Inst Neurol Disorders & Stroke, Expt Therapeut Branch, Bethesda, MD 20892 USA. RP Oh, JD (reprint author), Cent Michigan Univ, Dept Psychol, Sloan 224, Mt Pleasant, MI 48859 USA. NR 64 TC 56 Z9 59 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD OCT PY 2002 VL 177 IS 2 BP 557 EP 564 DI 10.1006/exnr.2002.8009 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 612PW UT WOS:000179085500020 PM 12429201 ER PT J AU Stratton, P Winkel, CA Sinaii, N Merino, MJ Zimmer, C Nieman, LK AF Stratton, P Winkel, CA Sinaii, N Merino, MJ Zimmer, C Nieman, LK TI Location, color, size, depth, and volume may predict endometriosis in lesions resected at surgery SO FERTILITY AND STERILITY LA English DT Article; Proceedings Paper CT 8th World Congress on Endometriosis CY FEB, 2002 CL SAN DIEGO, CALIFORNIA DE endometriosis; color; surgery; histology ID CHRONIC PELVIC PAIN; PERITONEAL ENDOMETRIOSIS; CONTROLLED TRIAL; INFERTILE WOMEN; LAPAROSCOPY; ENDOSALPINGIOSIS; LOCALIZATION; STAGE AB Objective: To correlate the diagnosis of endometriosis in lesions excised at laparoscopy with pathologic diagnosis. , Design: Prospective study. Setting: U.S. government research hospital. Patient(s): Women with chronic pelvic pain thought to be due to endometriosis. Intervention(s): Excision of lesions suspicious for endometriosis. Main Outcome Measure(s): Histologic examination of lesions for color, width, depth, and location of endometriosis. Lesion colors were grouped as black, red, white, mixed color, or endometriomas. Result(s): Sixty-five women with a surgical diagnosis of endometriosis had minimal (n = 22), mild (n = 25), moderate (n = 9), or severe disease (n = 9) according to the revised American Fertility Society classification. Endometriosis was confirmed in all but seven patients with minimal and one with severe disease. Twelve other patients did not have endometriosis, Of 314 lesions excised, 189 (61%) were endometriotic. Black or red lesions were less often histologically confirmed to be endometriosis than were white lesions, mixed-color lesions or endometriomas. Lesions > 5 mm wide or deep were more likely to be endometriosis than were narrower or shallower implants. Endometriomas deeper than 1 cm were histologically confirmed to be endometriosis, and 50% of peritoneal windows contained endometriosis. Conclusion(s): White lesions, mixed-color lesions, endometriomas, and larger lesions by depth or width were more likely to be histologically confirmed endometriosis than were smaller, black, or red lesions. C1 NIH, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. Georgetown Univ, Dept Obstet & Gynecol, Washington, DC USA. RP Stratton, P (reprint author), NICHHD, Pediat & Endocrinol Branch, Bldg 10,Room 9D42, Bethesda, MD 20892 USA. NR 20 TC 32 Z9 33 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD OCT PY 2002 VL 78 IS 4 BP 743 EP 749 AR PII S0015-0282(02)03337-X DI 10.1016/S0015-0282(02)03337-X PG 7 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 603PA UT WOS:000178567200013 PM 12372450 ER PT J AU Snyderwine, EG Yu, M Schut, HAJ Knight-Jones, L Kimura, S AF Snyderwine, EG Yu, M Schut, HAJ Knight-Jones, L Kimura, S TI Effect of CYP1A2 deficiency on heterocyclic amine DNA adduct levels in mice SO FOOD AND CHEMICAL TOXICOLOGY LA English DT Article DE CYP1A2; cytochrome P450; null mice; DNA adducts; postlabelling ID HUMAN-LIVER-MICROSOMES; 2-AMINO-1-METHYL-6-PHENYLIMIDAZO<4,5-B>PYRIDINE PHIP; 2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE IQ; MUTAGENIC ACTIVATION; CARCINOGENIC ARYLAMINES; METABOLIC-ACTIVATION; AROMATIC-AMINES; COOKED FOOD; IN-VITRO; CYTOCHROME-P-450 AB The contribution of CYPIA2 to the formation of DNA adducts of the cooked meat-derived heterocyclic amines (HCAs) 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was examined in CYP1A2-null (knock-out, KO) and wild-type (WT) mice. IQ (25 mg and 75 mg/kg) and PhIP (150 mg/kg) were administered by gavage to mice and DNA adduct levels in liver, kidney, mammary gland and colon were examined by the P-32-postlabeling assay. Three hours after either dose of IQ, adducts levels in liver and kidney of KO mice were 20-30% of the levels in WT mice, a difference that was statistically significant (Student's t-test, P<0.05). In the colon, adduct levels in KO mice were significantly lower than in the WT mice only at the lowest dose of IQ (1.6+/-0.6 vs 4.6+/-0.7, respectively, relative adduct labeling (RAL) x 10(8), mean-+/-S.E.M., n = 3-5 mice). In the mammary gland, however, there was no difference in IQ-DNA adduct levels in KO and WT mice at either dose of IQ. Three hours after dosing with PhIP, PhIP-DNA adduct levels were statistically significantly lower in KO mice than in WT mice in all tissues examined. PhIP-DNA adducts in liver and kidney of WT mice were 9.9+/-1.1 and 22.5+/-6.9, respectively, whereas no PhIP-DNA adducts were detected in either organ of KO mice (limit of detection, 1.4+/-2.8 x 10(9)). PhIP-DNA adduct levels in mammary gland and colon of WT mice were 47.1+/-9.5 and 58.0+/-21.7, respectively, but accordingly only 3.8+/-0.7 and 5.4+/-0.9 in KO mice. The findings indicate that CYPIA2, responsible for IQ and PhIP N-hydroxylation, the first step in the metabolic action, significantly effects DNA adduct formation in vivo. However, the data raise the possibility that other cytochromes P450 as well as other pathways of activation potentially contribute to DNA adduct formation in specific organs, depending on the HCA substrate. Published by Elsevier Science Ltd. C1 NCI, Ctr Canc Res, Chem Carcinogenesis Sect, Lab Expt Carcinogenesis, Bethesda, MD 20892 USA. NCI, Ctr Canc Res, Lab Metab, Bethesda, MD 20892 USA. Med Coll Ohio, Dept Pathol, Toledo, OH 43614 USA. RP Snyderwine, EG (reprint author), NCI, Ctr Canc Res, Chem Carcinogenesis Sect, Lab Expt Carcinogenesis, Bldg 37,Room 3C28,37 Convent Dr,MSC-4258, Bethesda, MD 20892 USA. NR 40 TC 28 Z9 30 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0278-6915 J9 FOOD CHEM TOXICOL JI Food Chem. Toxicol. PD OCT PY 2002 VL 40 IS 10 BP 1529 EP 1533 AR PII S0278-6915(02)00110-2 DI 10.1016/S0278-6915(02)00110-2 PG 5 WC Food Science & Technology; Toxicology SC Food Science & Technology; Toxicology GA 580CZ UT WOS:000177218200024 PM 12387319 ER PT J AU Bilski, P Belanger, AG Chignell, CF AF Bilski, P Belanger, AG Chignell, CF TI Photosensitized oxidation of 2 ',7 '-dichlorofluorescin: Singlet oxygen does not contribute to the formation of fluorescent oxidation product 2 ',7 '-dichlorofluorescein SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE free radicals; singlet oxygen; quenching; photosensitization; fluoroscein; photo-oxidation ID ROSE-BENGAL; STRESS MEASUREMENTS; 2'-7'-DICHLOROFLUORESCEIN; PHOTOOXIDATION; PHOTOREDUCTION; CELLS AB 2',7'-Dichlorofluoresein (DCFH) is often employed to assess oxidative stress in cells by monitoring the appearance of 2',7'-dichlorofluorescein (DCF), its highly fluorescent oxidation product. We have investigated the photosensitized oxidation of DCFH in solution and elucidated the role played by singlet molecular oxygen (O-1(2)) in this reaction. We used rose bengal (RB), protoporphyrin, and DCF as photosensitizers. Irradiation (550 nm) of RB (20 muM) in 50 mM phosphate (pH 7.4) in the presence of DCFH (50 muM) resulted in the rapid formation of DCF, measured as an increase in its characteristic absorbance and fluorescence. The oxidation rate was faster in deoxygenated solution, did not increase in D2O, and even increased in the presence of sodium azide. The presence of antioxidants that react with O-1(2), thus removing oxygen, accelerated DCF formation. Such results eliminate any potential direct involvement of O-1(2) in DCF formation, even though DCFH is an efficient (physical) quencher of O-1(2) (k(q) = 1.4 X 10(8) M-1 s(-1) in methanol). DCF is also a moderate photosensitizer of O-1(2) with a quantum yield of circa phi = 0.06 in D2O and phi = 0.08 in propylene carbonate, which unequivocally indicates that DCF can exist in a triplet state upon excitation with UV and visible light. This triplet can initiate photo-oxidization of DCFH via redox-and-radical mechanism(s) similar to those involving RB (vide supra). Our results show that, upon illumination, DCF can function as a moderate photosensitizer initiating DCFH oxidation, which may prime and accelerate the formation of DCF. We have also shown that, while O-1(2) does not contribute directly to DCF production, it can do so indirectly via reaction with cellular substrates yielding peroxy products and peroxyl radicals, which are able to oxidize DCFH in subsequent dark reactions. These findings Suggest that DCFH should not be regarded as a probe sensitive to singlet molecular oxygen, and that care must be taken when using DCFH to measure oxidative stress in cells as a result of both visible and UV light exposure. Published by Elsevier Science, Inc. C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. RP Bilski, P (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. RI Strid, Ake/E-5309-2012 OI Strid, Ake/0000-0003-3315-8835 NR 14 TC 78 Z9 79 U1 0 U2 14 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD OCT 1 PY 2002 VL 33 IS 7 BP 938 EP 946 AR PII S0891-5849(02)00982-6 DI 10.1016/S0891-5849(02)00982-6 PG 9 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 598NN UT WOS:000178282700006 PM 12361804 ER PT J AU Qian, SY Tomer, KB Yue, GH Guo, Q Kadiiska, MB Mason, RP AF Qian, SY Tomer, KB Yue, GH Guo, Q Kadiiska, MB Mason, RP TI Characterization of the initial carbon-centered pentadienyl radical and subsequent radicals in lipid peroxidation: Identification via on-line high performance liquid chromatography/electron spin resonance and mass spectrometry SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE lipid-derived radicals; POBN adducts of linoleic-derived radicals; on-line LC/ESR separation; ESI and tandem mass spectrometries; soybean lipoxygenase-dependant lipid peroxidation; free radicals ID MURINE LEUKEMIA-CELLS; FAST-ATOM-BOMBARDMENT; IN-VIVO EVIDENCE; SOYBEAN LIPOXYGENASE; LINOLEIC-ACID; PHOTOFRIN PHOTOSENSITIZATION; FATTY-ACIDS; DISEASE; ESR; GENERATION AB The previously reported combination of an on-line high-performance liquid chromatography (LC)/electron spin resonance (ESR) system with mass spectrometric analysis (MS) created a unique technique to identify a variety of lipid-derived radicals (L-.(d)) formed from in vitro lipid peroxidation (Iwahashi et al. [20]). To improve the sensitivity, resolution, and reliability of this method for in vitro and in vivo studies, we have investigated the effects of mobile phase pH, modifiers, and columns on the chromatographic separation of linoleic acid-derived radical adducts. Using tetrahydrofuran (THE) and 0.1% glacial acetic acid (HOAc) in an H2O/acetonitrile (ACN) mobile phase greatly increased the resolution and retention reproducibility of lipid radical adducts in LC/ESR. In addition, these modifications allowed the elimination of an ESR tuning problem and the synchronization of UV and ESR detection of radical adducts in on-line LC/ESR, neither of which had been possible previously. Analyte purity was therefore increased, thus increasing the reliability of radical detection via on-line LC/ESR as well as radical identification via MS analysis. For the first time, POBN adducts of linoleic carbon-centered pentadienyl radicals (L-.) were detected and identified. The optimization of chromatography in the LC/ESR and MS combination provided a reliable and sensitive way for the detection and identification of expected radical adducts in vitro and in vivo. Published by Elsevier Science Inc. C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Qian, SY (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. RI Tomer, Kenneth/E-8018-2013 NR 36 TC 35 Z9 38 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD OCT 1 PY 2002 VL 33 IS 7 BP 998 EP 1009 DI 10.1016/S0891-5849(02)00992-9 PG 12 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 598NN UT WOS:000178282700011 ER PT J AU Sandrini, F Matyakhina, L Sarlis, NJ Kirschner, LS Farmakidis, C Gimm, O Stratakis, CA AF Sandrini, F Matyakhina, L Sarlis, NJ Kirschner, LS Farmakidis, C Gimm, O Stratakis, CA TI Regulatory subunit type I-alpha of protein kinase A (PRKAR1A): A tumor-suppressor gene for sporadic thyroid cancer SO GENES CHROMOSOMES & CANCER LA English DT Article ID SPOTTY SKIN PIGMENTATION; SCHWANNOMAS CARNEY-COMPLEX; THYROTROPIN RECEPTOR GENE; ENDOCRINE OVERACTIVITY; SOMATIC MUTATIONS; TRANSFORMING SEQUENCE; PITUITARY-TUMORS; CELL-LINES; CARCINOMAS; PAPILLARY AB The tumor-suppressor gene encoding the cyclic AMP-dependent protein kinase A type I-a regulatory subunit PRKAR1A has been mapped to chromosome 17 (17q22-24) and is mutated in Carney complex, a familial neoplasia syndrome that is associated with thyroid tumors. Other genes implicated in cyclic nucleotide-dependent signaling have been investigated in thyroid tumorigenesis. We studied protein kinase A (PKA) activity in noninherited follicular thyroid adenomas and follicular, papillary, and undifferentiated (anaplastic) thyroid carcinomas. We then examined these and additional thyroid tumors for losses of the 17q22-24 PRKAR1A region, mutations of the PRKAR1A gene, and expression of its peptide product. Total PKA activity was markedly increased in carcinomas over that in adenomas, whereas the ratio of free vs. total PKA activity was decreased in cancer. Consistent with these findings, the 17q22-24 region was frequently lost in cancer but not in benign adenomas. A novel inactivating mutation of the PRKAR1A gene (leading to premature termination of the predicted protein) was found in an aggressive thyroid cancer. The tumor with PRKAR1A gene mutation, as well as the tumors with 17q allelic losses, showed decreased PRKAR1A expression by immunostaining. We conclude that PRKAR1A, the most abundant regulatory subunit of protein kinase A and a principal cyclic AMP-signaling modulator, acts as a tumor-suppressor gene in sporadic thyroid cancer. Published 2002 Wiley-Liss, Inc.(dagger). C1 NICHD, Unit Genet & Endocrinol, DEB, NIH, Bethesda, MD 20892 USA. Russian Acad Sci, Inst Cytol & Genet, Siberian Dept, Novosibirsk 630090, Russia. NIDDKD, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Ohio State Univ, Ctr Comprehens Canc, Human Canc Genet Program, Columbus, OH 43210 USA. RP Stratakis, CA (reprint author), NICHD, Unit Genet & Endocrinol, DEB, NIH, Bldg 10,Room 10N262,10 Ctr Dr MSC1862, Bethesda, MD 20892 USA. NR 59 TC 54 Z9 55 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD OCT PY 2002 VL 35 IS 2 BP 182 EP 192 DI 10.1002/gcc.10112 PG 11 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 584WH UT WOS:000177491400011 PM 12203783 ER PT J AU Olave, I Wang, WD Xue, YT Kuo, A Crabtree, GR AF Olave, I Wang, WD Xue, YT Kuo, A Crabtree, GR TI Identification of a polymorphic, neuron-specific chromatin remodeling complex SO GENES & DEVELOPMENT LA English DT Article DE chromatin remodeling; bBAF complexes; BAF53b; neuron development ID MAMMALIAN SWI/SNF COMPLEXES; HISTONE DEACETYLASE RPD3; NERVOUS-SYSTEM; TRANSCRIPTION; YEAST; DROSOPHILA; FATE; EXPRESSION; PROTEIN; BINDING AB A variety of chromatin remodeling complexes are thought to assist sequence-specific transcription factors. The complexes described to date are expressed ubiquitously, suggesting that they have general transcriptional functions. We show that vertebrate neurons have a specialized chromatin remodeling complex, bBAF, specifically containing the actin-related protein, BAF53b, which is first expressed in postmitotic neurons at about murine embryonic day 12.5 (E12.5). BAF53b is combinatorially assembled into polymorphic complexes with ubiquitous subunits including the two ATPases BRG1 and BRM. We speculate that bBAF complexes create neuronal-specific patterns of chromatin accessibility, thereby imparting new regulatory characteristics to ubiquitous sequence-specific transcription factors in neurons. C1 Stanford Univ, Howard Hughes Med Inst, Dept Dev Biol, Stanford, CA 94305 USA. Stanford Univ, Howard Hughes Med Inst, Dept Pathol, Stanford, CA 94305 USA. NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. RP Crabtree, GR (reprint author), Stanford Univ, Howard Hughes Med Inst, Dept Dev Biol, Stanford, CA 94305 USA. FU NCI NIH HHS [CA39612] NR 41 TC 80 Z9 84 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT 1 PY 2002 VL 16 IS 19 BP 2509 EP 2517 DI 10.1101/gad.992102 PG 9 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA 601UZ UT WOS:000178468000007 PM 12368262 ER PT J AU Morris, RW Kaplan, NL AF Morris, RW Kaplan, NL TI On the advantage of haplotype analysis in the presence of multiple disease susceptibility alleles SO GENETIC EPIDEMIOLOGY LA English DT Article DE statistical power; likelihood ratio test; case-control design; single-nucleotide polymorphisms; linkage disequilibrium; complex genetic disease ID LINKAGE DISEQUILIBRIUM TESTS; POPULATIONS; FREQUENCIES; SELECTION; POWER AB We investigated the effect of multiple susceptibility alleles at a single disease locus on the statistical power of a likelihood ratio test to detect association between alleles at a marker locus and a disease phenotype in a case-control design. Using simplifying assumptions to obtain the joint frequency distribution of marker and disease locus alleles, we present numerical results that illustrate the impact of historical variation of initial associations between marker alleles and susceptibility alleles on the power of a likelihood ratio test for association. Our results show that an increase in the number of susceptibility alleles produces a decrease in power of the likelihood ratio test. The decrease in power in the presence of multiple susceptibility alleles, however, is less for markers with multiple alleles than for markers with two alleles. We investigate the implications of this observation for tests of association based on haplotypes made up of tightly linked single-nucleotide polymorphisms (SNPs). Our results suggest that an analysis based on haplotypes can be advantageous over an analysis based on individual SNPs in the presence of multiple susceptibility alleles, particularly when linkage disequilibria between SNPs is weak. The results provide motivation for further development of statistical methods based on haplotypes for assessing the potential for association methods to identify and locate complex disease genes. (C) 2002 Wiley-Liss, Inc. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. RP Morris, RW (reprint author), NIEHS, Biostat Branch, Mail Drop A3-03,POB 12233, Res Triangle Pk, NC 27709 USA. EM morrisr@niehs.nih.gov NR 19 TC 244 Z9 265 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PD OCT PY 2002 VL 23 IS 3 BP 221 EP 233 DI 10.1002/gepi.10200 PG 13 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 602RG UT WOS:000178517800005 PM 12384975 ER PT J AU Zhao, Y Kumar, RA Baser, ME Evans, DGR Wallace, A Kluwe, L Mautner, VF Parry, DM Rouleau, GA Joe, H Friedman, JM AF Zhao, Y Kumar, RA Baser, ME Evans, DGR Wallace, A Kluwe, L Mautner, VF Parry, DM Rouleau, GA Joe, H Friedman, JM TI Intrafamilial correlation of clinical manifestations in neurofibromatosis 2 (NF2) SO GENETIC EPIDEMIOLOGY LA English DT Article DE intrafamilial correlation; random effects model; right censoring; negative-binomial gamma mixture model; neurofibromatosis 2 ID GERM-LINE MUTATIONS; TYPE-2 NEUROFIBROMATOSIS; PHENOTYPIC VARIABILITY; EXTENDED PEDIGREE; TUMOR-SUPPRESSOR; UNITED-KINGDOM; SPLICE-SITE; GENE; MILD; DNA AB Measuring correlation in clinical traits among relatives is important to our understanding of the causes of variable expressivity in Mendelian diseases. Random effects models are widely used to estimate intrafamilial correlations, but such models have limitations. We incorporated survival techniques into a random effects model so that it can be used to estimate intrafamilial correlations in continuous variables with right censoring, such as age at onset. We also describe a negative-binomial gamma mixture model to determine intrafamilial correlations of discrete (e.g., count) data. We demonstrate the utility of these methods by analyzing intrafamilial correlations among patients with neurofibromatosis 2 (NF2), an autosomal-dominant disease caused by mutations of the NF2 tumor-suppressor gene. We estimated intrafamilial correlations in age at first symptom of NF2, age at onset of hearing loss, and number of intracranial meningiomas in 390 NF2 nonprobands from 153 unrelated families. A significant intrafamilial correlation was observed for each of the three features: age at onset (0.35; 95% confidence interval (CI) 0.23-0.47), age at onset of hearing loss (0.51; 95% Cl, 0.35-0.64), and number of meninginomas (0.29; 95% Cl, 0.15-0.43). Significant correlations were also observed for age at first symptom within NF2 families with truncating mutations (0.41; 95% CI, 0.06-0.68) or splice-site mutations (0.29; 95% CI, 0.03-0.51), for age at onset of hearing loss within families with missense mutations (0.67; 95% CI, 0.18-0.89), and for number of meningiomas within families with splice-site mutations (0.39; 95% CI, 0.13-0.66). Our findings are consistent with effects of both allelic and nonallelic familial factors on the clinical variability of NF2. (C) 2002 Wiley-Liss, Inc. C1 Univ British Columbia, Dept Med Genet, Vancouver, BC V6T 1Z3, Canada. Univ British Columbia, Dept Stat, Vancouver, BC V6T 1Z3, Canada. St Marys Hosp, Dept Med Genet, Manchester M13 0JH, Lancs, England. Klinikum Nord Ochsenzoll, Dept Neurol, Hamburg, Germany. Univ Hamburg, Hosp Eppendorf, Dept Neurosurg, D-20246 Hamburg, Germany. NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. McGill Univ, Ctr Res Neurosci, Montreal, PQ H3A 2T5, Canada. RP Friedman, JM (reprint author), Univ British Columbia, Dept Med Genet, 6174 Univ Blvd,Room 300H, Vancouver, BC V6T 1Z3, Canada. RI Zhao, Yinshan/K-4789-2014; OI Zhao, Yinshan/0000-0001-5433-4637; Evans, Gareth/0000-0002-8482-5784 NR 48 TC 12 Z9 14 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PD OCT PY 2002 VL 23 IS 3 BP 245 EP 259 DI 10.1002/gepi.10181 PG 15 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 602RG UT WOS:000178517800007 PM 12384977 ER PT J AU Singh, G War, AJS AF Singh, G War, AJS TI The 2.1-kb inverted repeat DNA sequences flank the mat2,3 silent region in two species of Schizosaccharomyces and are involved in epigenetic silencing in Schizosaccharomyces pombe SO GENETICS LA English DT Article ID MATING-TYPE REGION; DE-NOVO METHYLATION; SWITCHING GENE SWI6; FISSION YEAST; CHROMATIN STRUCTURE; MEIOTIC RECOMBINATION; REPRESS TRANSCRIPTION; TRANSGENE REPEATS; LOCI; EXPRESSION AB The mat2,3 region of the fission yeast Schizosaccharomyces pombe exhibits a phenomenon of transcriptional silencing. This region is flanked by two identical DNA sequence elements, 2.1 kb in length, present in inverted orientation: IRL on the left and IRR on the right of the silent region. The repeats do not encode any ORE The inverted repeat DNA region is also present in a newly identified related species, which we named S. kambucha. Interestingly, the left and right repeats share perfect identity within a species, but show similar to2% bases interspecies variation. Deletion of IRL results in variegated expression of markers inserted in the silent region, while deletion of the IRR causes their derepression. When deletions of these repeats were genetically combined with mutations in different trans-acting genes previously shown to cause a partial defect in silencing, only mutations in clr1 and clr3 showed additive defects in silencing with the deletion of IRL. The rate of mat1 switching is also affected by deletion of repeats. The IRL or IRR deletion did not cause significant derepression of the matt or mat3 loci. These results implicate repeats for maintaining full repression of the mat2,3 region, for efficient mat1 switching, and further support the notion that multiple pathways cooperate to silence the mat2,3 domain. C1 NCI, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. RP NCI, Gene Regulat & Chromosome Biol Lab, POB B, Frederick, MD 21702 USA. EM klar@ncifcrf.gov NR 74 TC 14 Z9 14 U1 0 U2 0 PU GENETICS SOCIETY AMERICA PI BETHESDA PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA SN 0016-6731 EI 1943-2631 J9 GENETICS JI Genetics PD OCT PY 2002 VL 162 IS 2 BP 591 EP 602 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 612CZ UT WOS:000179058100007 PM 12399374 ER PT J AU Geer, LY Domrachev, M Lipman, DJ Bryant, SH AF Geer, LY Domrachev, M Lipman, DJ Bryant, SH TI CDART: Protein homology by domain architecture SO GENOME RESEARCH LA English DT Article ID DATABASE AB The Conserved Domain Architecture Retrieval Tool (CDART) performs similarity searches of the NCBl Entrez Protein Database based on domain architecture, defined as the sequential order of conserved domains in proteins. The algorithm finds protein similarities across significant evolutionary distances using sensitive protein domain profiles rather than by direct sequence similarity. Proteins similar to a query protein are grouped and scored by architecture. Relying on domain profiles allows CDART to be fast, and, because it relies on annotated functional domains, informative. Domain profiles are derived from several collections of domain definitions that include functional annotation. Searches can be further refined by taxonomy and by selecting domains of interest. CDART is available at http://www.ncbi.nlm.nih.gov/Structure/lexington/lexington.cgi. C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. RP Geer, LY (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. RI Geer, Lewis/H-2714-2014 NR 10 TC 347 Z9 361 U1 3 U2 20 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD OCT PY 2002 VL 12 IS 10 BP 1619 EP 1623 DI 10.1101/gr.278202 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 600ND UT WOS:000178396400018 PM 12368255 ER PT J AU Roth, G DeAngelis, H Ingram, D Lane, M Black, A AF Roth, G DeAngelis, H Ingram, D Lane, M Black, A TI Altered metabolic responsiveness to dietary caloric restriction (CR) with increased age in monkeys SO GERONTOLOGIST LA English DT Meeting Abstract C1 NIA, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD OCT PY 2002 VL 42 SI 1 BP 6 EP 6 PG 1 WC Gerontology SC Geriatrics & Gerontology GA 620PH UT WOS:000179541400022 ER PT J AU Hodes, R Warner, H Hadley, E Suzman, R Morrison-Bogorad, M Barr, R AF Hodes, R Warner, H Hadley, E Suzman, R Morrison-Bogorad, M Barr, R TI NIA symposium: Research initiatives, funding and training opportunities at the national institute on aging SO GERONTOLOGIST LA English DT Meeting Abstract C1 NIA, Bethesda, MD 20892 USA. NIA, Biol Aging Program, Bethesda, MD USA. NIA, Geriatr Program, Bethesda, MD USA. NIA, Behav & Social Res Program, Bethesda, MD USA. Neurosci & Neuropsychol Aging Program, Bethesda, MD USA. NIA, Off Extramural Affairs, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD OCT PY 2002 VL 42 SI 1 BP 27 EP 27 PG 1 WC Gerontology SC Geriatrics & Gerontology GA 620PH UT WOS:000179541400110 ER PT J AU Newman, A Tylavsky, F Goodpaster, B Visser, M Harris, T AF Newman, A Tylavsky, F Goodpaster, B Visser, M Harris, T TI Sarcopenia: Insights from the health, aging and body composition study SO GERONTOLOGIST LA English DT Meeting Abstract C1 Univ Pittsburgh, Div Geriatr Med, Pittsburgh, PA 15213 USA. Univ Tennessee, Memphis, TN USA. Univ Pittsburgh, Pittsburgh, PA USA. Vrije Univ Amsterdam, Amsterdam, Netherlands. NIA, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD OCT PY 2002 VL 42 SI 1 BP 27 EP 28 PG 2 WC Gerontology SC Geriatrics & Gerontology GA 620PH UT WOS:000179541400111 ER PT J AU Leibson, C Kritchevsky, S Petersen, R Penninx, B Newman, A Pahor, M Harris, T AF Leibson, C Kritchevsky, S Petersen, R Penninx, B Newman, A Pahor, M Harris, T TI The problems and promise of subclinical disease in older adults: Symposium of the epidemiology of aging interest group SO GERONTOLOGIST LA English DT Meeting Abstract C1 Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Univ Tennessee, Memphis, TN 38163 USA. Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC 27157 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA. NIA, Bethesda, MD 20892 USA. RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 NR 0 TC 0 Z9 0 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD OCT PY 2002 VL 42 SI 1 BP 81 EP 81 PG 1 WC Gerontology SC Geriatrics & Gerontology GA 620PH UT WOS:000179541400278 ER EF