FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Li, CY
Liu, QR
Zhang, PW
Li, XM
Wei, LP
Uhl, GR
AF Li, Chuan-Yun
Liu, Qing-Rong
Zhang, Ping-Wu
Li, Xiao-Mo
Wei, Liping
Uhl, George R.
TI OKCAM: an ontology-based, human-centered knowledgebase for cell adhesion
molecules
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID PATHWAY IDENTIFICATION; INTERACTION NETWORK; ALCOHOL DEPENDENCE; HUMAN
GENOME; COPY-NUMBER; 2008 UPDATE; DATABASE; PROTEIN; ASSOCIATION;
EXPRESSION
AB 'Cell adhesion molecules' (CAMs) are essential elements of cell/cell communication that are important for proper development and plasticity of a variety of organs and tissues. In the brain, appropriate assembly and tuning of neuronal connections is likely to require appropriate function of many cell adhesion processes. Genetic studies have linked and/or associated CAM variants with psychiatric, neurologic, neoplastic, immunologic and developmental phenotypes. However, despite increasing recognition of their functional and pathological significance, no systematic study has enumerated CAMs or documented their global features. We now report compilation of 496 human CAM genes in six gene families based on manual curation of protein domain structures, Gene Ontology annotations, and 1487 NCBI Entrez annotations. We map these genes onto a cell adhesion molecule ontology that contains 850 terms, up to seven levels of depth and provides a hierarchical description of these molecules and their functions. We develop OKCAM, a CAM knowledgebase that provides ready access to these data and ontologic system at http://okcam.cbi.pku.edu.cn. We identify global CAM properties that include: (i) functional enrichment, (ii) over-represented regulation modes and expression patterns and (iii) relationships to human Mendelian and complex diseases, and discuss the strengths and limitations of these data.
C1 [Li, Chuan-Yun; Liu, Qing-Rong; Zhang, Ping-Wu; Uhl, George R.] NIDA, Mol Neurobiol Branch, NIH, IRP, Baltimore, MD 21224 USA.
[Li, Chuan-Yun; Li, Xiao-Mo; Wei, Liping] Peking Univ, Coll Life Sci, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Beijing 100871, Peoples R China.
RP Uhl, GR (reprint author), NIDA, Mol Neurobiol Branch, NIH, IRP, Baltimore, MD 21224 USA.
EM guhl@intra.nida.nih.gov
RI Liu, Qing-Rong/A-3059-2012
OI Liu, Qing-Rong/0000-0001-8477-6452
FU National Institutes of Health Intramural Research Program (NIDA); NIH
[P50CA/DA84718]; China Scholarship Council (C.Y.L.); China National
High-tech 863 Programs [2006AA02A312, 2006AA02Z334]; 973 Programs
[2007CB946904]; NIDA/IRP [P50CA/DA84718]
FX National Institutes of Health Intramural Research Program (NIDA), NIH
grants P50CA/DA84718; China Scholarship Council (C.Y.L.); China National
High-tech 863 Programs (2006AA02A312, 2006AA02Z334); 973 Programs
(2007CB946904). Funding for open access charge: NIDA/IRP grants
P50CA/DA84718.
NR 48
TC 7
Z9 7
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D251
EP D260
DI 10.1093/nar/gkn568
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200046
PM 18790807
ER
PT J
AU Marchler-Bauer, A
Anderson, JB
Chitsaz, F
Derbyshire, MK
DeWeese-Scott, C
Fong, JH
Geer, LY
Geer, RC
Gonzales, NR
Gwadz, M
He, S
Hurwitz, DI
Jackson, JD
Ke, Z
Lanczycki, CJ
Liebert, CA
Liu, C
Lu, F
Lu, S
Marchler, GH
Mullokandov, M
Song, JS
Tasneem, A
Thanki, N
Yamashita, RA
Zhang, D
Zhang, N
Bryant, SH
AF Marchler-Bauer, Aron
Anderson, John B.
Chitsaz, Farideh
Derbyshire, Myra K.
DeWeese-Scott, Carol
Fong, Jessica H.
Geer, Lewis Y.
Geer, Renata C.
Gonzales, Noreen R.
Gwadz, Marc
He, Siqian
Hurwitz, David I.
Jackson, John D.
Ke, Zhaoxi
Lanczycki, Christopher J.
Liebert, Cynthia A.
Liu, Chunlei
Lu, Fu
Lu, Shennan
Marchler, Gabriele H.
Mullokandov, Mikhail
Song, James S.
Tasneem, Asba
Thanki, Narmada
Yamashita, Roxanne A.
Zhang, Dachuan
Zhang, Naigong
Bryant, Stephen H.
TI CDD: specific functional annotation with the Conserved Domain Database
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ALIGNMENTS
AB NCBI's Conserved Domain Database (CDD) is a collection of multiple sequence alignments and derived database search models, which represent protein domains conserved in molecular evolution. The collection can be accessed at http://www.ncbi.nlm.nih.gov/Structure/cdd/cdd.shtml, and is also part of NCBI's Entrez query and retrieval system, crosslinked to numerous other resources. CDD provides annotation of domain footprints and conserved functional sites on protein sequences. Precalculated domain annotation can be retrieved for protein sequences tracked in NCBI's Entrez system, and CDD's collection of models can be queried with novel protein sequences via the CD-Search service at http://www.ncbi.nlm.nih.gov/Structure/cdd/wrpsb.cgi. Starting with the latest version of CDD, v2.14, information from redundant and homologous domain models is summarized at a superfamily level, and domain annotation on proteins is flagged as either 'specific' ( identifying molecular function with high confidence) or as 'non-specific' (identifying superfamily membership only).
C1 [Marchler-Bauer, Aron; Anderson, John B.; Chitsaz, Farideh; Derbyshire, Myra K.; DeWeese-Scott, Carol; Fong, Jessica H.; Geer, Lewis Y.; Geer, Renata C.; Gonzales, Noreen R.; Gwadz, Marc; He, Siqian; Hurwitz, David I.; Jackson, John D.; Ke, Zhaoxi; Lanczycki, Christopher J.; Liebert, Cynthia A.; Liu, Chunlei; Lu, Fu; Lu, Shennan; Marchler, Gabriele H.; Mullokandov, Mikhail; Song, James S.; Tasneem, Asba; Thanki, Narmada; Yamashita, Roxanne A.; Zhang, Dachuan; Zhang, Naigong; Bryant, Stephen H.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Marchler-Bauer, A (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bldg 38 A,Room 8N805,8600 Rockville Pike, Bethesda, MD 20894 USA.
EM bauer@ncbi.nlm.nih.gov
RI Marchler-Bauer, Aron/A-9681-2009; Sincan, Murat /A-3794-2010; Geer,
Lewis/H-2714-2014;
OI Marchler-Bauer, Aron/0000-0003-1516-0712
FU Intramural Research Program of the National Library of Medicine at the
National Institutes of Health/DHHS
FX Intramural Research Program of the National Library of Medicine at
National Institutes of Health/DHHS. Funding for open access charge:
Intramural Research Program of the National Library of Medicine at the
National Institutes of Health/DHHS.
NR 13
TC 664
Z9 684
U1 2
U2 38
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D205
EP D210
DI 10.1093/nar/gkn845
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200038
PM 18984618
ER
PT J
AU Novichkov, PS
Ratnere, I
Wolf, YI
Koonin, EV
Dubchak, I
AF Novichkov, Pavel S.
Ratnere, Igor
Wolf, Yuri I.
Koonin, Eugene V.
Dubchak, Inna
TI ATGC: a database of orthologous genes from closely related prokaryotic
genomes and a research platform for microevolution of prokaryotes
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID EVOLUTIONARY GENOMICS; HIGH-THROUGHPUT; ALIGNMENT; BACTERIA; ARCHAEA;
TOOL
AB The database of Alignable Tight Genomic Clusters (ATGCs) consists of closely related genomes of archaea and bacteria, and is a resource for research into prokaryotic microevolution. Construction of a data set with appropriate characteristics is a major hurdle for this type of studies. With the current rate of genome sequencing, it is difficult to follow the progress of the field and to determine which of the available genome sets meet the requirements of a given research project, in particular, with respect to the minimum and maximum levels of similarity between the included genomes. Additionally, extraction of specific content, such as genomic alignments or families of orthologs, from a selected set of genomes is a complicated and time-consuming process. The database addresses these problems by providing an intuitive and efficient web interface to browse precomputed ATGCs, select appropriate ones and access ATGC-derived data such as multiple alignments of orthologous proteins, matrices of pairwise intergenomic distances based on genome-wide analysis of synonymous and nonsynonymous substitution rates and others. The ATGC database will be regularly updated following new releases of the NCBI RefSeq. The database is hosted by the Genomics Division at Lawrence Berkeley National laboratory and is publicly available at http://atgc.lbl.gov
C1 [Novichkov, Pavel S.; Dubchak, Inna] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA.
[Ratnere, Igor; Dubchak, Inna] Joint Genome Inst, Dept Energy, Walnut Creek, CA 94598 USA.
[Wolf, Yuri I.; Koonin, Eugene V.] Natl Ctr Biotechnol Informat, Natl Lib Med, NIH, Bethesda, MD 20894 USA.
RP Novichkov, PS (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, 1 Cyclotron Rd, Berkeley, CA 94720 USA.
EM psnovichkov@lbl.gov
FU US Department of Energy [DE-AC02-05CH11231]; Department of Energy Joint
Genome Institute; US Department of Health and Human Services
FX US Department of Energy (DE-AC02-05CH11231); Department of Energy Joint
Genome Institute (to I. R.); the intramural research program of the US
Department of Health and Human Services (National Library of Medicine,
NIH to Y.I.W. and E.V.K.).
NR 26
TC 30
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U1 1
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D448
EP D454
DI 10.1093/nar/gkn684
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200081
PM 18845571
ER
PT J
AU Papadopoulos, GL
Reczko, M
Simossis, VA
Sethupathy, P
Hatzigeorgiou, AG
AF Papadopoulos, Giorgos L.
Reczko, Martin
Simossis, Victor A.
Sethupathy, Praveen
Hatzigeorgiou, Artemis G.
TI The database of experimentally supported targets: a functional update of
TarBase
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CAENORHABDITIS-ELEGANS; MICRORNA TARGETS; RNAS; IDENTIFICATION; RESOURCE
AB TarBase5.0 is a database which houses a manually curated collection of experimentally supported microRNA (miRNA) targets in several animal species of central scientific interest, plants and viruses. MiRNAs are small non-coding RNA molecules that exhibit an inhibitory effect on gene expression, interfering with the stability and translational efficiency of the targeted mature messenger RNAs. Even though several computational programs exist to predict miRNA targets, there is a need for a comprehensive collection and description of miRNA targets with experimental support. Here we introduce a substantially extended version of this resource. The current version includes more than 1300 experimentally supported targets. Each target site is described by the miRNA that binds it, the gene in which it occurs, the nature of the experiments that were conducted to test it, the sufficiency of the site to induce translational repression and/or cleavage, and the paper from which all these data were extracted. Additionally, the database is functionally linked to several other relevant and useful databases such as Ensembl, Hugo, UCSC and SwissProt. The TarBase5.0 database can be queried or downloaded from http://microrna.gr/tarbase.
C1 [Papadopoulos, Giorgos L.; Reczko, Martin; Simossis, Victor A.; Hatzigeorgiou, Artemis G.] Biomed Sci Res Ctr Alexander Fleming, Inst Mol Oncol, Varkiza 16672, Greece.
[Reczko, Martin] Synaptic Ltd, Iraklion 71110, Greece.
[Sethupathy, Praveen] NHGRI, Bethesda, MD 20892 USA.
[Hatzigeorgiou, Artemis G.] Univ Penn, Philadelphia, PA 19104 USA.
RP Papadopoulos, GL (reprint author), Biomed Sci Res Ctr Alexander Fleming, Inst Mol Oncol, Varkiza 16672, Greece.
EM gipapado@fleming.gr; hatzigeorgiou@fleming.gr
OI Reczko, Martin/0000-0002-0005-8718
FU Aristeia Award from General Secretary Research and Technology, Greece
FX Funding for open access charge: Aristeia Award from General Secretary
Research and Technology, Greece.
NR 19
TC 236
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U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D155
EP D158
DI 10.1093/nar/gkn809
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200028
PM 18957447
ER
PT J
AU Pruitt, KD
Tatusova, T
Klimke, W
Maglott, DR
AF Pruitt, Kim D.
Tatusova, Tatiana
Klimke, William
Maglott, Donna R.
TI NCBI Reference Sequences: current status, policy and new initiatives
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ALIGNMENT; DATABASE; ENTREZ
AB NCBI's Reference Sequence (RefSeq) database (http://www.ncbi.nlm.nih.gov/RefSeq/) is a curated non-redundant collection of sequences representing genomes, transcripts and proteins. RefSeq records integrate information from multiple sources and represent a current description of the sequence, the gene and sequence features. The database includes over 5300 organisms spanning prokaryotes, eukaryotes and viruses, with records for more than 5.5 x 10(6) proteins (RefSeq release 30). Feature annotation is applied by a combination of curation, collaboration, propagation from other sources and computation. We report here on the recent growth of the database, recent changes to feature annotations and record types for eukaryotic (primarily vertebrate) species and policies regarding species inclusion and genome annotation. In addition, we introduce RefSeqGene, a new initiative to support reporting variation data on a stable genomic coordinate system.
C1 [Pruitt, Kim D.; Tatusova, Tatiana; Klimke, William; Maglott, Donna R.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Pruitt, KD (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Rm 4As 47B,45 Ctr Dr, Bethesda, MD 20892 USA.
EM pruitt@ncbi.nlm.nih.gov
RI Sincan, Murat /A-3794-2010
FU Intramural Research Program of the National Institute of Health;
National Library of Medicine
FX Intramural Research Program of the National Institute of Health;
National Library of Medicine. Funding for open access charge: Intramural
Research Program of the NIH, National Library of Medicine.
NR 13
TC 435
Z9 441
U1 1
U2 20
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D32
EP D36
DI 10.1093/nar/gkn721
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200006
PM 18927115
ER
PT J
AU Sayers, EW
Barrett, T
Benson, DA
Bryant, SH
Canese, K
Chetvernin, V
Church, DM
DiCuccio, M
Edgar, R
Federhen, S
Feolo, M
Geer, LY
Helmberg, W
Kapustin, Y
Landsman, D
Lipman, DJ
Madden, TL
Maglott, DR
Miller, V
Mizrachi, I
Ostell, J
Pruitt, KD
Schuler, GD
Sequeira, E
Sherry, ST
Shumway, M
Sirotkin, K
Souvorov, A
Starchenko, G
Tatusova, TA
Wagner, L
Yaschenko, E
Ye, J
AF Sayers, Eric W.
Barrett, Tanya
Benson, Dennis A.
Bryant, Stephen H.
Canese, Kathi
Chetvernin, Vyacheslav
Church, Deanna M.
DiCuccio, Michael
Edgar, Ron
Federhen, Scott
Feolo, Michael
Geer, Lewis Y.
Helmberg, Wolfgang
Kapustin, Yuri
Landsman, David
Lipman, David J.
Madden, Thomas L.
Maglott, Donna R.
Miller, Vadim
Mizrachi, Ilene
Ostell, James
Pruitt, Kim D.
Schuler, Gregory D.
Sequeira, Edwin
Sherry, Stephen T.
Shumway, Martin
Sirotkin, Karl
Souvorov, Alexandre
Starchenko, Grigory
Tatusova, Tatiana A.
Wagner, Lukas
Yaschenko, Eugene
Ye, Jian
TI Database resources of the National Center for Biotechnology Information
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID GENE; PROTEIN; SEARCH; ENTREZ; SEQUENCES; SYSTEM; BLAST; NCBI; TOOL;
SIMILARITIES
AB In addition to maintaining the GenBank (R) nucleic acid sequence database, the National Center for Biotechnology Information (NCBI) provides analysis and retrieval resources for the data in GenBank and other biological data made available through the NCBI web site. NCBI resources include Entrez, the Entrez Programming Utilities, MyNCBI, PubMed, PubMed Central, Entrez Gene, the NCBI Taxonomy Browser, BLAST, BLAST Link (BLink), Electronic PCR, OrfFinder, Spidey, Splign, RefSeq, UniGene, HomoloGene, ProtEST, dbMHC, dbSNP, Cancer Chromosomes, Entrez Genomes and related tools, the Map Viewer, Model Maker, Evidence Viewer, Clusters of Orthologous Groups (COGs), Retroviral Genotyping Tools, HIV-1/Human Protein Interaction Database, Gene Expression Omnibus (GEO), Entrez Probe, GENSAT, Online Mendelian Inheritance in Man (OMIM), Online Mendelian Inheritance in Animals (OMIA), the Molecular Modeling Database (MMDB), the Conserved Domain Database (CDD), the Conserved Domain Architecture Retrieval Tool (CDART) and the PubChem suite of small molecule databases. Augmenting many of the web applications is custom implementation of the BLAST program optimized to search specialized data sets. All of the resources can be accessed through the NCBI home page at www.ncbi.nlm.nih.gov.
C1 [Sayers, Eric W.; Barrett, Tanya; Benson, Dennis A.; Bryant, Stephen H.; Canese, Kathi; Chetvernin, Vyacheslav; Church, Deanna M.; DiCuccio, Michael; Edgar, Ron; Federhen, Scott; Feolo, Michael; Geer, Lewis Y.; Helmberg, Wolfgang; Kapustin, Yuri; Landsman, David; Lipman, David J.; Madden, Thomas L.; Maglott, Donna R.; Miller, Vadim; Mizrachi, Ilene; Ostell, James; Pruitt, Kim D.; Schuler, Gregory D.; Sequeira, Edwin; Sherry, Stephen T.; Shumway, Martin; Sirotkin, Karl; Souvorov, Alexandre; Starchenko, Grigory; Tatusova, Tatiana A.; Wagner, Lukas; Yaschenko, Eugene; Ye, Jian] Natl Inst Hlth, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Sayers, EW (reprint author), Natl Inst Hlth, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 38A,8600 Rockville Pike, Bethesda, MD 20894 USA.
EM sayers@ncbi.nlm.nih.gov
RI Landsman, David/C-5923-2009; Geer, Lewis/H-2714-2014;
OI Landsman, David/0000-0002-9819-6675
FU Intramural Research Program of the National Institutes of Health;
National Library of Medicine
FX Funding for open access charge: Intramural Research Program of the
National Institutes of Health; National Library of Medicine.
NR 41
TC 444
Z9 456
U1 1
U2 25
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D5
EP D15
DI 10.1093/nar/gkn741
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200002
PM 18940862
ER
PT J
AU Schaefer, CF
Anthony, K
Krupa, S
Buchoff, J
Day, M
Hannay, T
Buetow, KH
AF Schaefer, Carl F.
Anthony, Kira
Krupa, Shiva
Buchoff, Jeffrey
Day, Matthew
Hannay, Timo
Buetow, Kenneth H.
TI PID: the Pathway Interaction Database
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID MOLECULAR INTERACTION DATABASE; INFRASTRUCTURE; GENOMES
AB The Pathway Interaction Database (PID,http://pid.nci.nih.gov) is a freely available collection of curated and peer-reviewed pathways composed of human molecular signaling and regulatory events and key cellular processes. Created in a collaboration between the US National Cancer Institute and Nature Publishing Group, the database serves as a research tool for the cancer research community and others interested in cellular pathways, such as neuroscientists, developmental biologists and immunologists. PID offers a range of search features to facilitate pathway exploration. Users can browse the predefined set of pathways or create interaction network maps centered on a single molecule or cellular process of interest. In addition, the batch query tool allows users to upload long list(s) of molecules, such as those derived from microarray experiments, and either overlay these molecules onto predefined pathways or visualize the complete molecular connectivity map. Users can also download molecule lists, citation lists and complete database content in extensible markup language (XML) and Biological Pathways Exchange (BioPAX) Level 2 format. The database is updated with new pathway content every month and supplemented by specially commissioned articles on the practical uses of other relevant online tools.
C1 [Schaefer, Carl F.; Buetow, Kenneth H.] Ctr Biomed Informat & Informat Technol, Natl Canc Inst, Rockville, MD USA.
[Anthony, Kira] Nat Publishing Grp, Boston, MA USA.
[Krupa, Shiva] Novartis Knowledge Ctr, Cambridge, MA USA.
[Buchoff, Jeffrey] SRA Int Inc, Hlth Res & Informat, Fairfax, VA USA.
[Day, Matthew; Hannay, Timo] Nat Publishing Grp, London, England.
RP Schaefer, CF (reprint author), Ctr Biomed Informat & Informat Technol, Natl Canc Inst, Rockville, MD USA.
EM schaefec@mail.nih.gov
FU National Cancer Institute
FX The National Cancer Institute. Funding for open access charge: National
Cancer Institute.
NR 15
TC 480
Z9 489
U1 4
U2 24
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2009
VL 37
BP D674
EP D679
DI 10.1093/nar/gkn653
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386TT
UT WOS:000261906200120
PM 18832364
ER
PT J
AU Kumar, V
Malhotra, SV
AF Kumar, Vineet
Malhotra, Sanjay V.
TI IONIC LIQUID MEDIATED SYNTHESIS OF 5-HALOURACIL NUCLEOSIDES: KEY
PRECURSORS FOR POTENTIAL ANTIVIRAL DRUGS
SO NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS
LA English
DT Article
DE Ionic liquids; antiviral; Idoxuridine; 5-halouracil nucleosides
ID 5-SUBSTITUTED 2'-DEOXYURIDINES; PYRIMIDINE NUCLEOSIDES; SELECTIVE
BENZOYLATION; URACIL NUCLEOSIDES; ANALOGS; DERIVATIVES; EFFICIENT;
NUCLEOTIDES; METHODOLOGY; IODINATION
AB Synthesis of antiviral 5-halouracil nucleosides, also used as key precursors for the synthesis of other potential antiviral drugs, has been demonstrated using ionic liquids as convenient and efficient reaction medium.
C1 [Kumar, Vineet; Malhotra, Sanjay V.] NCI Frederick, SAIC Frederick, Lab Synthet Chem, Frederick, MD 21702 USA.
RP Malhotra, SV (reprint author), NCI Frederick, SAIC Frederick, Lab Synthet Chem, 1050 Boyles St, Frederick, MD 21702 USA.
EM malhotrasa@mail.nih.gov
FU National Cancer Institute, National Institutes of Health [N01-CO-12400]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
NR 35
TC 7
Z9 7
U1 0
U2 6
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1525-7770
J9 NUCLEOS NUCLEOT NUCL
JI Nucleosides Nucleotides Nucleic Acids
PY 2009
VL 28
IS 9
BP 821
EP 834
DI 10.1080/15257770903170252
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 500KQ
UT WOS:000270298400003
PM 20183621
ER
PT B
AU Ross, SA
AF Ross, Sharon A.
BE Choi, SW
Friso, S
TI Nutrition, epigenetics, and cancer
SO NUTRIENTS AND EPIGENETICS
LA English
DT Article; Book Chapter
ID ASSISTED REPRODUCTIVE TECHNOLOGY; HISTONE DEACETYLASE INHIBITORS;
DIETARY METHYL DEFICIENCY; TUMOR-SUPPRESSOR GENES; DIALLYL DISULFIDE;
CELL-LINES; DNA METHYLATION; PROSTATE-CANCER; RAT-LIVER; IN-VIVO
AB Compelling evidence suggests that diet and dietary factors are important in cancer etiology by inhibiting or enhancing the cancer process. Because diet may contribute significantly to the causation of many human cancers, it is important to uncover the molecular mechanisms of action of dietary bioactive factors in cancer prevention, as well as those stimulating neoplastic cell transformations. The role of epigenetic mechanisms in the etiology of disease, including cancer development and progression, has been increasingly recognized in recent years. The importance of epigenetic mechanisms is highlighted by their influence on gene expression and chromatin stability, which thereby impact the regulation of cell cycle control, DNA damage, apoptosis, differentiation, and other cancer-related processes. Evidence suggests that environmental factors, such as diet, may be significant regulators of epigenetic events, including DNA methylation and histone posttranslational modulation. For example, it has long been known that folate participates in the generation of S-adenosylmethionine, which acts as a methyl donor in the methylation of cytosines in DNA and participates in posttranslational methylation of histones. A classic example for the role of diet in epigenetics and cancer is the finding that dietary methyl deficiency (folate, choline, and methionine) in a rat model has been shown to alter hepatic DNA methylation patterns and induce hepatocarcinogenesis in the absence of a carcinogen. Several other bioactive food components (BFCs), including genistein, epigallocatechin gallate, diallyl disulfide, and sulforaphane have been suggested to impact epigenetic mechanisms. Many of these examples will be presented, as well as the next steps in diet, epigenetic events, and cancer prevention research.
C1 NCI, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Ross, SA (reprint author), NCI, NIH, US Dept HHS, Bethesda, MD 20892 USA.
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TC 2
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U1 2
U2 4
PU CRC PRESS-TAYLOR & FRANCIS GROUP
PI BOCA RATON
PA 6000 BROKEN SOUND PARKWAY NW, STE 300, BOCA RATON, FL 33487-2742 USA
BN 978-1-4200-6354-7
PY 2009
BP 207
EP 227
D2 10.1201/9781420063561
PG 21
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA BKK18
UT WOS:000268359800009
ER
PT J
AU Reynolds, MA
Dawson, DR
Novak, KF
Ebersole, JL
Gunsolley, JC
Branch-Mays, GL
Holt, SC
Mattison, JA
Ingram, DK
Novak, MJ
AF Reynolds, Mark A.
Dawson, Dolphus R.
Novak, Karen F.
Ebersole, Jeffrey L.
Gunsolley, John C.
Branch-Mays, Grishondra L.
Holt, Stanley C.
Mattison, Julie A.
Ingram, Donald K.
Novak, M. John
TI Effects of caloric restriction on inflammatory periodontal disease
SO NUTRITION
LA English
DT Article
DE Monkey; Caloric restriction; Inflammation; Periodontal disease; Sex
ID REAL-TIME PCR; POLYMERASE-CHAIN-REACTION; RHESUS-MONKEYS;
CARDIOVASCULAR-DISEASE; DIETARY RESTRICTION;
ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; NONHUMAN-PRIMATES; BACTERIA;
ADULTS; RISK
AB Objective: Dietary caloric restriction (CR) has been found to reduce systemic markers of inflammation and may attenuate the effects of chronic inflammatory conditions. The purpose of this study was to examine the effects of long-term CR on naturally occurring chronic inflammatory periodontal disease in a nonhuman primate model.
Methods: The effects of long-term CR on extent and severity of naturally occurring chronic periodontal disease, local inflammatory and immune responses, and periodontal microbiology, were evaluated in a cohort of 81 (35 female and 46 male; 13-40 y of age) rhesus monkeys (Macaca mulatta) with no previous exposure to routine oral hygiene. CR monkeys had been subjected to 30% CR for 13-17 y relative to control-fed (CON) animals starting at 3-5 y of age.
Results: Same sex CR and CON monkeys exhibited similar levels of plaque, calculus, and bleeding on probing. Among CON animals, males showed significantly greater periodontal breakdown, as reflected by higher mean clinical attachment level and periodontal probing depth scores, than females. CR males exhibited significantly less periodontal pocketing, lower IgG antibody response, and lower IL-8 and beta-glucuronidase levels compared to CON males, whereas CR females showed a lower IgG antibody response but comparable clinical parameters and inflammatory marker levels relative to CON females. Long-term CR had no demonstrable effect on the periodontal microbiota.
Conclusion: Males demonstrated greater risk for naturally occurring periodontal disease than females. Long-term CR may differentially reduce the production of local inflammatory mediators and risk for inflammatory periodontal disease among males but not females. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Reynolds, Mark A.; Branch-Mays, Grishondra L.] Univ Maryland, Sch Dent, Dept Periodont, Baltimore, MD 21201 USA.
[Dawson, Dolphus R.; Novak, Karen F.; Ebersole, Jeffrey L.; Novak, M. John] Univ Kentucky, Coll Dent, Ctr Oral Hlth Res, Lexington, KY USA.
[Gunsolley, John C.] Virginia Commonwealth Univ, Sch Dent, Richmond, VA USA.
[Holt, Stanley C.] Forsyth Inst, Boston, MA USA.
[Mattison, Julie A.] NIA, Lab Expt Gerontol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Ingram, Donald K.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Nutr Neurosci & Aging Lab, Baton Rouge, LA USA.
RP Reynolds, MA (reprint author), Univ Maryland, Sch Dent, Dept Periodont, Baltimore, MD 21201 USA.
EM mreynolds@umaryland.edu
FU USPHS; National Institute of Aging [U01 AG-021406]
FX This work was supported by USPHS grant U01 AG-021406 from the National
Institute of Aging and by funds from the Intramural Research Program of
the National Institute on Aging and the Veterinary Research Program of
the Division of Research Resources of the National Institutes of Health.
NR 64
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0899-9007
J9 NUTRITION
JI Nutrition
PD JAN
PY 2009
VL 25
IS 1
BP 88
EP 97
DI 10.1016/j.nut.2008.07.003
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 383AH
UT WOS:000261646000016
PM 18929461
ER
PT J
AU Islami, F
Malekshah, AF
Kimiagar, M
Pourshams, A
Wakefield, J
Goglani, G
Rakhshani, N
Nasrollahzadeh, D
Salahi, R
Semnani, S
Saadatian-Elahi, M
Abnet, CC
Kamangar, F
Dawsey, SM
Brennan, P
Boffetta, P
Malekzadeh, R
AF Islami, Farhad
Malekshah, Akbar Fazeltabar
Kimiagar, Masoud
Pourshams, Akram
Wakefield, Jon
Goglani, Goharshad
Rakhshani, Nasser
Nasrollahzadeh, Dariush
Salahi, Rasoul
Semnani, Shahryar
Saadatian-Elahi, Mitra
Abnet, Christian C.
Kamangar, Farin
Dawsey, Sanford M.
Brennan, Paul
Boffetta, Paolo
Malekzadeh, Reza
TI Patterns of Food and Nutrient Consumption in Northern Iran, a High-Risk
Area for Esophageal Cancer
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID NORTHEASTERN IRAN; GOLESTAN COHORT; DIET
AB Our objectives were to investigate patterns of food and nutrient consumption in Golestan province, a high-incidence area for esophageal cancer (EC) in northern Iran. Twelve 24-h dietary recalls were administered during a 1-yr period to 131 healthy participants in a pilot cohort study. We compare here nutrient intake in Golestan with recommended daily allowances (RDAs) and lowest threshold intakes (LTIs). We also compare the intake of 27 food groups and nutrients among several population subgroups using mean values from the 12 recalls. Rural women had a very low level of vitamin intake, which was even lower than LTIs (P < 0.01). Daily intake of vitamins A and C was lower than LTI in 67% and 73% of rural women, respectively. Among rural men, the vitamin intakes were not significantly different from LTIs. Among urban women, the vitamin intakes were significantly lower than RDAs but were significantly higher than LTIs. Among urban men, the intakes were not significantly different from RDAs. Compared to urban dwellers, intake of most food groups and nutrients, including vitamins, was significantly lower among rural dwellers. In terms of vitamin intake, no significant difference was observed between Turkmen and non-Turkmen ethnics. The severe deficiency in vitamin intake among women and rural dwellers and marked differences in nutrient intake between rural and urban dwellers may contribute to the observed epidemiological pattern of EC in Golestan, with high incidence rates among women and people with low socioeconomic status and the highest incidence rate among rural women.
C1 [Islami, Farhad; Brennan, Paul; Boffetta, Paolo] Int Agcy Res Canc, F-69008 Lyon, France.
[Islami, Farhad; Malekshah, Akbar Fazeltabar; Kimiagar, Masoud; Pourshams, Akram; Goglani, Goharshad; Rakhshani, Nasser; Nasrollahzadeh, Dariush; Malekzadeh, Reza] Univ Tehran Med Sci, Shariati Hosp, Digest Dis Res Ctr, Tehran, Iran.
[Abnet, Christian C.; Kamangar, Farin; Dawsey, Sanford M.] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Saadatian-Elahi, Mitra] Univ Lyon 1, F-69365 Lyon, France.
[Salahi, Rasoul; Semnani, Shahryar] Golestan Univ Med Sci, Golestan Res Ctr Gastroenterol & Hepatol, Gorgan, Iran.
[Islami, Farhad] Kings Coll London, Thames Canc Registry, London WC2R 2LS, England.
[Malekshah, Akbar Fazeltabar; Kimiagar, Masoud] Shahid Beheshti Univ, Tehran, Iran.
[Wakefield, Jon] Univ Washington, Dept Stat, Seattle, WA 98195 USA.
[Wakefield, Jon] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Boffetta, P (reprint author), Int Agcy Res Canc, 150 Cours Albert Thomas, F-69008 Lyon, France.
EM boffetta@iarc.fr
RI Abnet, Christian/C-4111-2015; Semnani, Shahryar/N-2270-2016;
OI Abnet, Christian/0000-0002-3008-7843; Semnani,
Shahryar/0000-0002-8768-6142; Malekzadeh, Reza/0000-0003-1043-3814
FU DDRC, Iran; IARC, France; NCI, United States
FX This research was supported by funds from DDRC, Iran, IARC, France, and
the Intramural Research Program of the NCI, United States. We thank Dr.
Hajiamin Marjani, Dr. Omid Mozaffari, and Dr. Elham Jafari for their
logistic assistance. We sincerely thank our interviewers: Ailar Jamali,
Anita Ramiar, Azin Kor, AkramMohamadi, Afsane Mosadegh, Halime Pourghaz,
Aijamal Gorgani, Fahime Igder, Saiideh Valaee, Homeira Davoodpour and
Hesam Amanbaee. We also enjoyed the close collaboration of Golestan
health deputy Dr. Mohamad Naemi, Dr. Ali Aghapor, Mr. J Kabir, and Dr.
Jalil Pestei, Chief of Gonbad Health District. We specially thank and
appreciate Mrs Yoosefi and Mr Maramaie (local health workers of Behvarz)
in the study areas. We also express appreciations to all the kind people
of Gonbad for their collaboration in this study. We are deeply grateful
to Dr. Nadia Slimani from IARC for her valuable comments. The authors
have contributed to the manuscript by planning the study (DDRC, IARC,
NNFRI), collecting data (DDRC, NNFRI, GRCGH), calculating the
nutritional components (DDRC, NNFRI), analysis of data (DDRC, IARC,
NCI), and preparation and revision of the manuscript (all authors).
NR 23
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U2 5
PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS
PI PHILADELPHIA
PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 2009
VL 61
IS 4
BP 475
EP 483
DI 10.1080/01635580902803735
PG 9
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA 480LW
UT WOS:000268737300007
PM 19838919
ER
PT J
AU Carpenter, CL
Yu, MC
London, SJ
AF Carpenter, Catherine L.
Yu, Mimi C.
London, Stephanie J.
TI Dietary Isothiocyanates, Glutathione S-Transferase M1 (GSTM1), and Lung
Cancer Risk in African Americans and Caucasians from Los Angeles County,
California
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID CRUCIFEROUS VEGETABLES; NEW-JERSEY; GENETIC-POLYMORPHISM;
N-ACETYLCYSTEINE; VITAMIN-A; WHITE MEN; SMOKING; FRUITS; POPULATION;
WOMEN
AB Isothiocyanates, found in cruciferous vegetables, are anticarcinogenic. Racial differences in smoking do not fully account for the African-American excess lung cancer incidence. African Americans consume more cruciferous vegetables than U. S. Whites. Impact on lung cancer risk is unknown. The glutathione S transferase M1 (GSTM1) gene promotes urinary isothiocyanate excretion. We evaluated dietary isothiocyanates and lung cancer using a population-based case-control study of 933 African Americans and Caucasians (non-Hispanic U. S. White) from Los Angeles County, California (311 cases; 622 controls). Broccoli, cauliflower, greens, and cabbage food-frequency variables represented isothiocyanates. Isothiocyanates were protective for lung cancer risk. Adjusted odds ratio (OR) for the uppermost quartile > 80 mu mol isothiocyanates/wk, compared to lowest, was 0.65 [95% confidence interval (CI) = 0.41-1.00, trend P = 0.02]. Association was stronger among subjects with homozygous deletion of GSTM1 (OR = 0.52, 95% CI = 0.31-0.86) than subjects with at least one GSTM1 copy (OR = 0.77, 95% CI = 0.49-1.21). The difference was not statistically significant (P= 0.16). Despite African Americans consuming more cruciferous vegetables, the isothiocyanate association did not vary by race (P = 0.52). Reduced lung cancer risk with higher isothiocyanate intake may be slightly stronger among subjects with deletion of GSTM1.
C1 [Carpenter, Catherine L.] Univ Calif Los Angeles, David Geffen Sch Med, Ctr Human Nutr, Los Angeles, CA 90095 USA.
[Yu, Mimi C.] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
[London, Stephanie J.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Carpenter, CL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Ctr Human Nutr, Box 951742,12-217 Warren Hall, Los Angeles, CA 90095 USA.
EM ccarpenter@mednet.ucla.edu
OI London, Stephanie/0000-0003-4911-5290
FU California Tobacco Related Disease Research Program (TRDRP) [1RT-140,
3RT-403, 11IT-0082]; NCI [P01-CA42710]; National Institute of
Environmental Health Sciences; National Institute of Health [ZO1
ES49017]; California Department of Health Services; National Cancer
Institute's Surveillance, Epidemiology and End Results Program
[N01-PC-35136]; Northern California Cancer Center [N01-PC-35139];
University of Southern California, [N02-PC-15105]; Centers for Disease
Control and Prevention's National Program of Cancer Registries
[CCR921930-02]
FX Conduct of the case-control study performed at the University of
Southern California was funded by the California Tobacco Related Disease
Research Program (TRDRP) grants, 1RT-140 and 3RT-403, to Dr. London.
Data analysis performed at the University of California at Los Angeles
was supported by TRDRP grant 11IT-0082 to Dr. Carpenter. Dr. Carpenter
was supported by NCI P01-CA42710. Dr. London is supported by the
Division of Intramural Research, National Institute of Environmental
Health Sciences, National Institute of Health (ZO1 ES49017). The
collection of cancer incidence data used in this study was supported by
the California Department of Health Services as part of the statewide
cancer reporting program mandated by California Health and Safety Code
Section 103885; the National Cancer Institute's Surveillance,
Epidemiology and End Results Program under contract N01-PC-35136 awarded
to the Northern California Cancer Center, contract N01-PC-35139 awarded
to the University of Southern California, and contract N02-PC-15105
awarded to the Public Health Institute; and the Centers for Disease
Control and Prevention's National Program of Cancer Registries under
agreement # U55/ CCR921930-02 awarded to the Public Health Institute.
The ideas and opinions expressed herein are those of the author( s), and
endorsement by the State of California, Department of Health Services,
the National Cancer Institute, and the Centers for Disease Control and
Prevention or their contractors and subcontractors is not intended nor
should be inferred.
NR 49
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U1 0
U2 4
PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS
PI PHILADELPHIA
PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 2009
VL 61
IS 4
BP 492
EP 499
DI 10.1080/01635580902752270
PG 8
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA 480LW
UT WOS:000268737300009
PM 19838921
ER
PT J
AU Volkow, ND
Wang, GJ
Telang, F
Fowler, JS
Goldstein, RZ
Alia-Klein, N
Logan, J
Wong, C
Thanos, PK
Ma, Y
Pradhan, K
AF Volkow, Nora D.
Wang, Gene-Jack
Telang, Frank
Fowler, Joanna S.
Goldstein, Rita Z.
Alia-Klein, Nelly
Logan, Jean
Wong, Christopher
Thanos, Panayotis K.
Ma, Yemine
Pradhan, Kith
TI Inverse Association Between BMI and Prefrontal Metabolic Activity in
Healthy Adults
SO OBESITY
LA English
DT Article
ID BODY-MASS INDEX; BRAIN DOPAMINE ACTIVITY; WORKING-MEMORY; FOLLOW-UP;
IN-VIVO; OBESITY; IMPAIRMENT; DECLINE; MODEL; INDIVIDUALS
AB Obesity has been associated with a higher risk for impaired cognitive function, which most likely reflects associated medical complications (i.e., cerebrovascular pathology). However, there is also evidence that in healthy individuals excess weight may adversely affect cognition (executive function, attention, and memory). Here, we measured regional brain glucose metabolism (using positron emission tomography (PET) and 2-deoxy-2[(18)F] fluoro-D-glucose (FDG)) to assess the relationship between BMI and brain metabolism (marker of brain function) in 21 healthy controls (BMI range 19-37 kg/m(2)) studied during baseline (no stimulation) and during cognitive stimulation (numerical calculations). Statistical parametric mapping (SPM) revealed a significant negative correlation between BMI and metabolic activity in prefrontal cortex (Brodmann areas 8, 9, 10, 11, 44) and cingulate gyrus (Brodmann area 32) but not in other regions. Moreover, baseline metabolism in these prefrontal regions was positively associated with performance on tests of memory (California Verbal Learning Test) and executive function (Stroop Interference and Symbol Digit Modality tests). In contrast, the regional brain changes during cognitive stimulation were not associated with BMI nor with neuropsychological performance. The observed association between higher BMI and lower baseline prefrontal metabolism may underlie the impaired performance reported in healthy obese individuals on some cognitive tests of executive function. On the other hand, the lack of an association between BMI and brain metabolic activation during cognitive stimulation indicates that BMI does not influence brain glucose utilization during cognitive performance. These results further highlight the urgency to institute public health interventions to prevent obesity.
C1 [Volkow, Nora D.] NIDA, Bethesda, MD 20892 USA.
[Volkow, Nora D.; Telang, Frank; Thanos, Panayotis K.; Ma, Yemine] NIAAA, Bethesda, MD USA.
[Wang, Gene-Jack; Fowler, Joanna S.; Goldstein, Rita Z.; Alia-Klein, Nelly; Logan, Jean; Wong, Christopher; Pradhan, Kith] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
RP Volkow, ND (reprint author), NIDA, Bethesda, MD 20892 USA.
EM nvolkow@nida.nih.gov
OI Logan, Jean/0000-0002-6993-9994
FU NIH's Intramural Research Program (NIAAA); DOE [DE-AC01-76CH00016]; NIDA
[DA06278-15]
FX We thank David Schlyer, David Alexoff, Paul Vaska, Millard Jayne,
Colleen Shea, Youwen Xu, Lisa Muench, Pauline Carter, Karen Apelskog,
Barbara Hubbard, Thomas Maloney, Patricia Woicik, and Linda Thomas for
their contributions. Research supported by NIH's Intramural Research
Program (NIAAA), by DOE (DE-AC01-76CH00016), and NIDA (DA06278-15).
NR 37
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U1 5
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD JAN
PY 2009
VL 17
IS 1
BP 60
EP 65
DI 10.1038/oby.2008.469
PG 6
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 389QQ
UT WOS:000262110000009
PM 18948965
ER
PT J
AU Myslobodsky, M
AF Myslobodsky, Michael
TI The 'Tyranny of Choices' in the Ingestion-Controlling Network
SO OBESITY FACTS
LA English
DT Article
DE Ingestion control; Obesity; Networks; Motifs; Maximal motifs;
Polypharmacy
ID COMPLEX NETWORKS; SYNAPTIC PLASTICITY; DISCOVERY; MOTIFS; PROMISCUITY;
PANDEMONIUM; EXPRESSION; BIOLOGY; BINDING; OBESITY
AB Background: Currently used antiobesity remedies offer only a modest weight reduction, and have untoward effects that can complicate treatment efforts. Motivated by the needs of the pharmacotherapy of obesity, the study explored the role of neuropeptide Y, leptin, and corticotrophin-releasing hormone. Method: The study used Ingenuity Pathway Analysis which is a tool for automated discovery and visualization of molecular interactions. Results: In ingestion-controlling networks, neuropeptide Y, leptin, and corticotrophin-releasing hormone molecules are commonly combined into the units designated as 'maximal motifs'. The analysis of this triad allowed suggesting that maximal motifs are not more than a compendium of admission rules and transmission alternatives of their nodes catalogued in the dataset. Nonetheless, these options seem to endow them with the flexibility needed to respond dynamically as a functional unit to changing internal (metabolic) conditions or environmental challenges. Conclusion: Thus far, each peptide represents a separate target for pharmaceutical interventions (as judged by US patents scanned). The study concludes with predictions regarding designs of 'multitargeted' antiobesity agents since only by hitting a combination of targets can an appropriate therapeutic effect be achieved.
C1 [Myslobodsky, Michael] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Myslobodsky, Michael] Howard Univ, Grad Sch, Washington, DC 20059 USA.
RP Myslobodsky, M (reprint author), NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
EM myslobom@mail.nih.gov
FU National Institutes of Health/NIMH (CBDB)
FX The author gratefully acknowledges the helpful suggestions by J.
Deschenes, Ph.D. (Ingenuity Systems, CA, USA) and S. Goodman, Ph.D.
(University of Pennsylvania, USA). The constructive comments of the
anonymous referees and Professor Matthias Bluher helped in reshaping the
arguments. This work was supported in part by the Intramural Research
Program of the National Institutes of Health/NIMH (CBDB).
NR 59
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U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-4025
J9 OBESITY FACTS
JI Obes. Facts
PY 2009
VL 2
IS 6
BP 374
EP 382
DI 10.1159/000260906
PG 9
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 545PB
UT WOS:000273745600008
PM 20090389
ER
PT J
AU Myslobodsky, M
Ingraham, LJ
AF Myslobodsky, Michael
Ingraham, Loring J.
TI Managing the Pandemic of Obesity: Siding with the Fox or the Hedgehog?
SO OBESITY FACTS
LA English
DT Review
DE Obesity; Treatment; Prevention; Public health; Cognitive therapy
ID CLOCK MUTANT MICE; BODY-MASS INDEX; METABOLIC SYNDROME; EPIGENETIC
MECHANISMS; DEVELOPMENTAL ORIGINS; ADIPOSE-TISSUE; ENERGY-INTAKE;
FOOD-INTAKE; IMPULSIVITY; WOMEN
AB Obesity is a major public health problem of pandemic proportion. Despite its high prevalence and widespread distribution (consistent with a common underlying etiology), clinical psychologists and primary care physicians routinely approach the problem with individualized but often ineffective treatments like psychotherapy and pharmacotherapy, or propose alterations to specific components of the 'toxic environment', cultural influences, and psychosocial factors purported to cause overeating. This paper presents an alternative perspective and proposes a potential framework for assisting health professionals in developing rational approaches to education about and preventive treatment of obesity based on the role of factors in early life that contribute to personality and behavior and which over time lead to obesity and its maintenance.
C1 [Ingraham, Loring J.] George Washington Univ, Profess Psychol Program, Washington, DC 20052 USA.
[Myslobodsky, Michael] Howard Univ, Grad Sch, Washington, DC 20059 USA.
[Myslobodsky, Michael] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
RP Ingraham, LJ (reprint author), George Washington Univ, Profess Psychol Program, 1922 F St NW, Washington, DC 20052 USA.
EM ingraham@gwu.edu
NR 104
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U1 0
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-4025
J9 OBESITY FACTS
JI Obes. Facts
PY 2009
VL 2
IS 6
BP 384
EP 392
DI 10.1159/000261422
PG 9
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 545PB
UT WOS:000273745600009
PM 20090390
ER
PT J
AU Castle, PE
Schiffinan, M
Eeler, CM
Solomon, D
AF Castle, Philip E.
Schiffinan, Mark
Eeler, Cosette M.
Solomon, Diane
TI Evidence for Frequent Regression of Cervical Intraepithelial
Neoplasia-Grade 2
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID 2006 CONSENSUS GUIDELINES; MILDLY ABNORMAL-CYTOLOGY; ATYPICAL
SQUAMOUS-CELLS; CANCER SCREENING-TESTS; DNA-POSITIVE WOMEN; ASCUS-LSIL
TRIAGE; RANDOMIZED-TRIAL; P16(INK4A) IMMUNOHISTOCHEMISTRY; UNDETERMINED
SIGNIFICANCE; HUMAN PAPILLOMAVIRUSES
AB OBJECTIVE: To estimate the fraction of cervical intraepithelial neoplasia 2 (CIN 2) that might regress if untreated using data from the Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesions Triage Study (ALTS).
METHODS: We compared the cumulative occurrence of CIN 2 (n=397) and CIN 3 or more severe (n=542) diagnosed by the Pathology Quality Control Group in three trial arms-immediate colposcopy, human papillomavirus (HPV) triage, and conservative management-over the 2-year duration of the ALTS trial. A nonparametric test of trend was used to test for differences in the number of CIN 2 cases relative to number of CIN 3 or more severe cases across study arms with an increasing percentage of women referred to colposcopy at baseline.
RESULTS: There were no significant differences in the cumulative 2-year cumulative CIN 3 or more severe diagnoses by study arm (10.9%, conservative management; 10.3%, HPV; 10.9%, immediate colposcopy) (P(trend)=.8), but there was a significant increase in CIN 2 diagnoses (5.8%, conservative management; 7.8%, HPV triage; 9.9%, immediate colposcopy) (P(trend)<.001) in the study arms, with increasing number of women referred to colposcopy at baseline. The relative differences in cumulative CIN 2 by study arm among women who tested HPV-16 positive at baseline were less pronounced (P(trend)=.1) than women who tested positive for other high-risk-HPV genotypes (P(trend)=.01).
CONCLUSION: There was evidence that approximately 40% of undiagnosed CIN 2 will regress over 2 years, but CIN 2 caused by HPV-16 may be less likely to regress than CIN 2 caused by other high-risk-HPV genotypes.
C1 [Castle, Philip E.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
Univ New Mexico, Hlth Sci Ctr, Dept Mol Genet & Microbiol, Sch Med, Albuquerque, NM 87131 USA.
Univ New Mexico, Hlth Sci Ctr, Dept Obstet & Gynecol, Sch Med, Albuquerque, NM 87131 USA.
RP Castle, PE (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,Room 5030,EPS MSC 7234, Bethesda, MD 20892 USA.
EM castlep@mail.nih.gov
FU National Cancer Institute; National Institutes of Health Department of
Health [CN-55153, CN-55154, CN-55155, CN-55156, CN-55157, CN-55158,
CN-55159, CN-55105]
FX The Atypical Squamous Cells of Undetermined Significance/Low-Grade
Squamous Intraepithelial Lesions Triage Study (ALTS) Group was supported
by the National Cancer Institute, National Institutes of Health
Department of Health and Human Services contracts CN-55153, CN-55154,
CN-55155, CN-55156, CN-55157, CN-55158, CN-55159, and CN-55105. This
research was supported in part by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute. Some of the
equipment and supplies used in these studies Were donated or provided at
reduced cost by Qiagen Corporation, Gaithersburg, MD; Cytyc Corporation,
Marlborough, MA; National Testing Laboratories, Fenton, MO; Den Vu,
Tucson, AZ; TriPath Imaging, Inc., Burlington, NC; and Roche Molecular
Systems Inc. Alameda, CA.
NR 28
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U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD JAN
PY 2009
VL 113
IS 1
BP 18
EP 25
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 388KG
UT WOS:000262018100005
PM 19104355
ER
PT J
AU Schenk, M
Purdue, MP
Colt, JS
Hartge, P
Blair, A
Stewart, P
Cerhan, JR
De Roos, AJ
Cozen, W
Severson, RK
AF Schenk, M.
Purdue, M. P.
Colt, J. S.
Hartge, P.
Blair, A.
Stewart, P.
Cerhan, J. R.
De Roos, A. J.
Cozen, W.
Severson, R. K.
TI Occupation/industry and risk of non-Hodgkin's lymphoma in the United
States
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID EPIDEMIOLOGY CONSORTIUM INTERLYMPH; MULTICENTER CASE-CONTROL; POOLED
ANALYSIS; CANCER MORTALITY; FAMILY-HISTORY; EXPOSURE; WORKERS;
CHEMICALS; INDUSTRY; MALIGNANCIES
AB Aims: To identify occupations and industries associated with non-Hodgkin's lymphoma (NHL) in a large population-based, case-control study in the USA.
Methods: Cases (n = 1189) of histologically confirmed malignant NHL ages 20-74 were prospectively identified in four geographic areas covered by the National Cancer Institute SEER Program. Controls (n = 982) were selected from the general population by random digit dialling (, 65 years of age) and from residents listed in Medicare files (65-74 years of age). Odds ratios and 95% confidence intervals for occupations and industries were calculated by unconditional logistic regression analyses, adjusting for age, gender, ethnicity and study centre. Further analyses stratified for gender and histological subtype were also performed.
Results: Risk of NHL was increased for a few occupations and industries. Several white collar occupations, with no obvious hazardous exposures, had elevated risks, including purchasing agents and buyers, religious workers, physical therapists and information clerks. Occupations with excesses that may have exposures of interest include launderers and ironers, service occupations, food/beverage preparation supervisors, hand packers and packagers, roofing and siding, leather and leather products, transportation by air, nursing and personal care facilities, and specialty outpatient clinics. Significantly decreased risks of NHL were found for a number of occupations and industries including post-secondary teachers and chemical and allied products.
Conclusions: The results of this study suggest that several occupations and industries may alter the risk of NHL. Our results support previously reported increased risks among farmers, printers, medical professionals, electronic workers and leather workers. These findings should be evaluated further in larger studies that have the power to focus on specific exposures and histological subtypes of NHL.
C1 [Schenk, M.; Severson, R. K.] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI 48201 USA.
[Schenk, M.; Severson, R. K.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48201 USA.
[Purdue, M. P.; Colt, J. S.; Hartge, P.; Blair, A.; Stewart, P.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Cerhan, J. R.] Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN USA.
[De Roos, A. J.] Univ Washington, Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98195 USA.
[De Roos, A. J.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Cozen, W.] Univ So Calif, Sch Med, Dept Prevent Med, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
RP Schenk, M (reprint author), Wayne State Univ, Dept Family Med & Publ Hlth Sci, 101 E Alexandrine, Detroit, MI 48201 USA.
EM mschenk@med.wayne.edu
RI Purdue, Mark/C-9228-2016;
OI Purdue, Mark/0000-0003-1177-3108; Cerhan, James/0000-0002-7482-178X
FU NIH (Division of Cancer Epidemiology and Genetics of the National Cancer
Institute); National Cancer Institute [N01-PC-65064, N01-PC-67009,
N01-CN-67008, N01-CN-67010]
FX We thank Carol Haines (Westat, Rockville, Maryland) for study
coordination; Laura Capece and Irish Lonn (Information Management
Services, Inc., Silver Spring, Maryland) for computer support; and
Barbara Rusin (Karmanos Cancer Institute), Jeanne DeWall (University of
Iowa), Susan Roberts (University of Southern California), Theresa
Taggart (Fred Hutchinson Cancer Research Center) for study coordination
and management. Supported in part by the Intramural Research Program of
the NIH (Division of Cancer Epidemiology and Genetics of the National
Cancer Institute) and by National Cancer Institute SEER Contracts
N01-PC-65064 (Detroit), N01-PC-67009 (Seattle), N01-CN-67008 (Iowa) and
N01-CN-67010 (Los Angeles).
NR 50
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U1 2
U2 4
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
EI 1470-7926
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD JAN
PY 2009
VL 66
IS 1
BP 23
EP 31
DI 10.1136/oem.2007.036723
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 385SH
UT WOS:000261833400006
PM 18805886
ER
PT J
AU Yong, LC
Sigurdson, AJ
Ward, EM
Waters, MA
Whelan, EA
Petersen, MR
Bhatti, P
Ramsey, MJ
Ron, E
Tucker, JD
AF Yong, L. C.
Sigurdson, A. J.
Ward, E. M.
Waters, M. A.
Whelan, E. A.
Petersen, M. R.
Bhatti, P.
Ramsey, M. J.
Ron, E.
Tucker, J. D.
TI Increased frequency of chromosome translocations in airline pilots with
long-term flying experience
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID COSMIC-RADIATION EXPOSURE; AIR CREW MEMBERS; IONIZING-RADIATION;
CANCER-RISK; ABERRATION ANALYSIS; LYMPHOCYTES; WORKERS; DAMAGE; FISH;
BIODOSIMETRY
AB Background: Chromosome translocations are an established biomarker of cumulative exposure to external ionising radiation. Airline pilots are exposed to cosmic ionising radiation, but few flight crew studies have examined translocations in relation to flight experience.
Methods: We determined the frequency of translocations in the peripheral blood lymphocytes of 83 airline pilots and 50 comparison subjects (mean age 47 and 46 years, respectively). Translocations were scored in an average of 1039 cell equivalents (CE) per subject using fluorescence in situ hybridisation (FISH) whole chromosome painting and expressed per 100 CE. Negative binomial regression models were used to assess the relationship between translocation frequency and exposure status and flight years, adjusting for age, diagnostic x ray procedures, and military flying.
Results: There was no significant difference in the adjusted mean translocation frequency of pilots and comparison subjects (0.37 (SE 0.04) vs 0.38 (SE 0.06) translocations/100 CE, respectively). However, among pilots, the adjusted translocation frequency was significantly associated with flight years (p = 0.01) with rate ratios of 1.06 (95% CI 1.01 to 1.11) and 1.81 (95% CI 1.16 to 2.82) for a 1- and 10-year incremental increase in flight years, respectively. The adjusted rate ratio for pilots in the highest compared to the lowest quartile of flight years was 2.59 (95% CI 1.26 to 5.33).
Conclusions: Our data suggests that pilots with long-term flying experience may be exposed to biologically significant doses of ionising radiation. Epidemiological studies with longer follow-up of larger cohorts of pilots with a wide range of radiation exposure levels are needed to clarify the relationship between cosmic radiation exposure and cancer risk.
C1 [Yong, L. C.; Waters, M. A.; Whelan, E. A.; Petersen, M. R.] NIOSH, Industrywide Studies Branch, Div Surveillance Hazard Evaluat & Field Studies, Cincinnati, OH 45226 USA.
[Sigurdson, A. J.; Bhatti, P.; Ron, E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Ward, E. M.] Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA.
[Ramsey, M. J.] Lawrence Livermore Natl Lab, Livermore, CA USA.
[Tucker, J. D.] Wayne State Univ, Dept Biol Sci, Detroit, MI 48202 USA.
RP Yong, LC (reprint author), NIOSH, Industrywide Studies Branch, Div Surveillance Hazard Evaluat & Field Studies, 4676 Columbia Pkwy,R-15, Cincinnati, OH 45226 USA.
EM LAY7@CDC.GOV
RI Waters, Martha/B-7441-2011
FU National Institute for Occupational Safety and Health and the National
Cancer Institute [Y1CP802904]; Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute
FX This research was supported in part by an interagency agreement between
the National Institute for Occupational Safety and Health and the
National Cancer Institute contract Y1CP802904 and by the Intramural
Research Program of the Division of Cancer Epidemiology and Genetics,
National Cancer Institute. Work was performed in part under the auspices
of the U. S. DOE by the Lawrence Livermore National Laboratory under
contract no. W-7405-ENG-48.
NR 40
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U1 2
U2 13
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD JAN
PY 2009
VL 66
IS 1
BP 56
EP 62
DI 10.1136/oem.2008.038901
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 385SH
UT WOS:000261833400011
PM 19074211
ER
PT J
AU Koutros, S
Baris, D
Bell, E
Zheng, T
Zhang, Y
Holford, TR
Leaderer, BP
Landgren, O
Zahm, SH
AF Koutros, S.
Baris, D.
Bell, E.
Zheng, T.
Zhang, Y.
Holford, T. R.
Leaderer, B. P.
Landgren, O.
Zahm, S. Hoar
TI Use of hair colouring products and risk of multiple myeloma among US
women
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID DYE USE; UNITED-STATES; CONNECTICUT; LEUKEMIA; LYMPHOMA; CANCERS
AB Objective: To evaluate the association between personal hair dye use and risk of multiple myeloma among women.
Methods: A population-based case-control study of 175 cases of multiple myeloma and 679 controls. Cases and controls were interviewed regarding the type and colour of hair colouring product used, age at first use, age use stopped, duration, and the frequency of use per year. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using unconditional logistic regression to compare never users with four exposure groups: all users, ever semi-permanent dye users, ever permanent dye users and dark permanent dye users (most frequent use).
Results: No association was found between ever reporting hair colouring product use and myeloma risk among all users (OR 0.8; 95% CI 0.5 to 1.1), semipermanent dye users (OR 0.7; 95% CI 0.4 to 1.2), permanent dye users (OR 0.8; 95% CI 0.5 to 1.1) or dark permanent dye users (OR 0.8; 95% CI 0.5 to 1.3). There were no significant associations among women who used hair dyes before 30 years of age, started use before 1980, had >= 240 lifetime applications, or had used dark permanent dye for 28 or more years.
Conclusion: No evidence of an association between hair colouring product use and myeloma risk was found. However, given the conflicting body of literature on hair colouring product use and risk of multiple myeloma, this question should be further evaluated in larger studies or consortia, and in high risk groups.
C1 [Koutros, S.; Baris, D.; Landgren, O.; Zahm, S. Hoar] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
[Bell, E.] SUNY Albany, Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
[Zheng, T.; Zhang, Y.; Holford, T. R.; Leaderer, B. P.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
RP Koutros, S (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS 8122, Rockville, MD 20852 USA.
EM Koutross@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (National Cancer Institute, Division of
Cancer Epidemiology and Genetics). Certain data used in the study were
obtained from the Connecticut Tumor Registry, Connecticut Department of
Public Health. The authors thank the institutions that allowed access to
diagnostic materials and pathology reports, including the following
hospitals: Charlotte Hungerford Hospital, Danbury Hospital, Greenwich
Hospital, Griffin Hospital, Hartford Hospital, Johnson Memorial
Hospital, Middlesex Hospital, Lawrence and Memorial Hospital, New
Britain General Hospital, Bradley Memorial Hospital, Norwalk Hospital,
St. Francis Hospital and Medical Center, St. Mary's Hospital, Hospital
of St. Raphael, St. Vincent's Medical Center, Stamford Hospital, William
W. Backus Hospital, Waterbury Hospital, Yale-New Haven Hospital,
Manchester Memorial Hospital, Rockville General Hospital, Bridgeport
Hospital, Windham Hospital, Sharon Hospital, Milford Hospital, New
Milford Hospital, Bristol Hospital, MidState Medical Center and
Day-Kimball Hospital.
NR 17
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PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD JAN
PY 2009
VL 66
IS 1
BP 68
EP 70
DI 10.1136/oem.2008.041053
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 385SH
UT WOS:000261833400013
PM 18805876
ER
PT J
AU Levy-Clarke, G
Goodglick, T
Ding, XY
Byrnes, G
Gangaputra, S
Nussenblatt, R
Chan, CC
Yeh, S
AF Levy-Clarke, Grace
Goodglick, Todd
Ding, Xiaoyan
Byrnes, Gordon
Gangaputra, Sapna
Nussenblatt, Robert
Chan, Chi-Chao
Yeh, Steven
TI Recalcitrant Granulomatous Sclerouveitis in a Patient with Granulomatous
ANCA-associated Vasculitis
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE ANCA-associated granulomatous vasculitis; necrotizing scleritis;
sclero-choroiditis; Wegener granulomatosis
ID WEGENERS-GRANULOMATOSIS
AB Purpose: To report an unusual case of granulomatous sclerochoroiditis. Design: Interventional case report. Methods: A patient with ANCA-associated granulomatous vasculitis presented with nodular necrotizing scleritis, which was recalcitrant to multiple systemic immunosuppressive therapies and progressed to a blind painful eye, which was enucleated. Results: Histopathology revealed extensive occlusive vasculitis, diffuse T- and B- cellular infiltration, and lymphoid granulomatous formation. Enhanced MHC class II antigens, adhesion molecules, and Fas (CD95) and FasL (CD95L) were detected in the lesion. Conclusion: Granulomatous sclerochoroiditis with aggressive immune reaction can be a complication of ANCA-associated granulomatous vasculitis.
C1 [Levy-Clarke, Grace] St Lukes Cataract & Laser Ctr, St Petersburg, FL 33702 USA.
[Goodglick, Todd] Washington Eye Physicians, Chevy Chase, MD USA.
[Ding, Xiaoyan; Nussenblatt, Robert; Chan, Chi-Chao; Yeh, Steven] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Byrnes, Gordon] Retina Grp Washington, Chevy Chase, MD USA.
[Gangaputra, Sapna] Univ Wisconsin, Fundus Photograph Reading Ctr, Madison, WI USA.
RP Levy-Clarke, G (reprint author), St Lukes Cataract & Laser Ctr, St Petersburg, FL 33702 USA.
EM gclarke@stlukeseye.com
FU Intramural NIH HHS [Z01 EY000222-22]
NR 5
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Z9 5
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PY 2009
VL 17
IS 2
BP 83
EP 87
AR PII 910915887
DI 10.1080/09273940802596500
PG 5
WC Ophthalmology
SC Ophthalmology
GA 439WO
UT WOS:000265658500004
PM 19412867
ER
PT J
AU Sen, HN
Bodaghi, B
Le Hoang, P
Nussenblatt, R
AF Sen, H. Nida
Bodaghi, Bahram
Le Hoang, Phuc
Nussenblatt, Robert
TI Primary Intraocular Lymphoma: Diagnosis and Differential Diagnosis
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE intraocular lymphoma; diagnosis; cytology; cytokines;
immunohistochemistry
ID RETICULUM-CELL SARCOMA; NERVOUS-SYSTEM LYMPHOMA;
POLYMERASE-CHAIN-REACTION; CLINICAL-FEATURES; POSTERIOR UVEITIS; OCULAR
LYMPHOMA; FLOW-CYTOMETRY; VITREOUS CELLS; BIOPSY; VITRECTOMY
AB Diagnosis of PIOL can be challenging. It requires a high degree of clinical suspicion and differential diagnosis includes infectious and non-infectious etiologies particularly the common masquaraders sarcoidosis, tuberculosis, viral retinitis and syphilis. The definitive diagnosis depends on demonstration of malignant lymphoma cells in ocular specimens or CSF. Ocular specimen could include vitreous, aqueous or chorioretinal biopsy. Ocular pathologist should be consulted prior to the diagnostic procedure to help handle and process the specimen appropriately. In addition to cytology, flow cytometry, immunohistochemistry, molecular analysis and cytokines may be used as adjuncts in facilitating the diagnosis.
C1 [Sen, H. Nida; Nussenblatt, Robert] NEI, NIH, Bethesda, MD 20892 USA.
[Bodaghi, Bahram; Le Hoang, Phuc] Univ Paris 06, Dept Ophthalmol, Pitie Salpetriere Hosp, Paris, France.
RP Sen, HN (reprint author), NEI, NIH, 10 Ctr Dr Bldg 10 Rm 10N112, Bethesda, MD 20892 USA.
EM senh@nei.nih.gov
FU Intramural NIH HHS [Z99 EY999999]
NR 56
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U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PY 2009
VL 17
IS 3
BP 133
EP 141
AR PII 912966575
DI 10.1080/09273940903108544
PG 9
WC Ophthalmology
SC Ophthalmology
GA 467TZ
UT WOS:000267767300001
PM 19585354
ER
PT J
AU Coupland, SE
Chan, CC
Smith, J
AF Coupland, Sarah E.
Chan, Chi Chao
Smith, Justine
TI Pathophysiology of Retinal Lymphoma
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE retinal lymphoma; vitreoretinal lymphoma; vitreal lymphoma; intraocular
lymphoma; IOL; PCNSL; DLBCL
ID PRIMARY INTRAOCULAR LYMPHOMA; B-CELL-LYMPHOMA; CENTRAL-NERVOUS-SYSTEM;
INTERLEUKIN-10 GENE POLYMORPHISMS; INTRAVITREAL METHOTREXATE; MOLECULAR
DIAGNOSIS; CHEMOKINE RECEPTORS; CYTOKINE PRODUCTION; OUTCOME PREDICTION;
TISSUE MICROARRAY
AB Retinal lymphoma, the most common form of intraocular lymphoma, is a high-grade malignancy, usually of B-cell type, and is associated with a poor prognosis because of frequent central nervous system (CNS) involvement. The neoplastic B-cells of retinal lymphoma have a characteristic morphology and immunophenotype, express certain chemokines and chemokine receptors, and produce interleukins (IL), e.g. IL-10. Together with the cytological features of these tumors, the immunophenotype, presence of immunoglobulin rearrangements, and biochemical profile aid the diagnosis of retinal lymphomas. Immunophenotyping and somatic mutation analysis suggest derivation of most retinal lymphomas from an early post-germinal centre B-cell. Chromosomal translocation data would suggest, however, that a subgroup of these neoplasms may arise from germinal centre B-cells, and these could be associated with a better prognosis. Further investigations, such as gene expression profiling, are required to identify oncogenic pathways potentially involved in retinal lymphoma development, and to identify new prognostic/therapeutic markers for this tumor.
C1 [Coupland, Sarah E.] Univ Liverpool, Dept Cellular & Mol Pathol, Liverpool L69 3GA, Merseyside, England.
[Chan, Chi Chao] NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Smith, Justine] Oregon Hlth & Sci Univ, Casey Eye Inst, Portland, OR 97201 USA.
[Smith, Justine] Oregon Hlth & Sci Univ, Dept Cell & Dev Biol, Portland, OR 97201 USA.
RP Coupland, SE (reprint author), Univ Liverpool, Dept Pathol, Duncan Bldg,Daulby St, Liverpool L69 3GA, Merseyside, England.
EM s.e.coupland@liverpool.ac.uk
FU Research to Prevent Blindness; Schnitzer-Novack Foundation; ENI
Intramural Research Program; Eye Tumour Research Fund; Royal Liverpool
University Hospital, UK
FX Dr Justine Smith acknowledges support from Research to Prevent Blindness
(unrestricted grant to Casey Eye Institute) and the Schnitzer-Novack
Foundation. Dr Chi-Chao Chan acknowledges support from the ENI
Intramural Research Program. Dr Sarah Coupland would like to acknowledge
the generous support of the Eye Tumour Research Fund, Royal Liverpool
University Hospital, UK. She would also like to express her gratitude to
Professor Bertil Damato (Royal Liverpool University Hospital) for the
discussions about the manuscript. All authors would also like to thank
Dr Nathalie Cassoux and Professor Phuc LeHoang (Department of
Ophthalmology, Pitie-Salpetriere Hospital, University Paris VI, Paris,
France) for the provision of the clinical photographs.
NR 90
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U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PY 2009
VL 17
IS 4
BP 227
EP 237
AR PII 913569367
DI 10.1080/09273940903168696
PG 11
WC Ophthalmology
SC Ophthalmology
GA 480FF
UT WOS:000268717000001
PM 19657975
ER
PT J
AU Tang, J
Fillmore, G
Nussenblatt, RB
AF Tang, Johnny
Fillmore, Gary
Nussenblatt, Robert B.
TI Antiphospholipid Antibody Syndrome Mimicking Serpiginous Choroidopathy
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE antiphospholipid antibody syndrome (Hughes Syndrome); serpiginous retino
choroidopathy treatment; indocyanine green angiography; fluorescein
angiography
AB Purpose: To report a patient with antiphospholipid antibody syndrome (APS) presenting with ocular findings similar to serpiginous choroidopathy. Methods: Case report. Results: A man complained of blurred vision. Examination revealed vitritis, vasculitis, retinal ischemia, and neovascularization. Clinical and angiographic features consistent with serpiginous choroidopathy were found. An evaluation for uveitis and retinal vasculitis was remarkable for APS. Conclusion: This case expands on previously reported ocular findings associated with APS. Although the role of antiphospholipid antibodies in the pathogenesis remains undefined, the findings, including the serpiginous-like choroidopathy, can be reasonably explained by vaso-occlusion in both the retinal and choroidal vasculature.
C1 [Tang, Johnny] Case Western Reserve Univ, Univ Hosp, Inst Eye, Cleveland, OH 44106 USA.
[Tang, Johnny] Louis Stokes Cleveland DVA Med Ctr, Res Serv, Cleveland, OH USA.
[Tang, Johnny] Univ Hosp, Case Med Ctr, Cleveland, OH USA.
[Fillmore, Gary] Eye Consultants, Spokane, WA USA.
[Nussenblatt, Robert B.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Tang, J (reprint author), Case Western Reserve Univ, Univ Hosp, Inst Eye, LKSD 4107 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM bostonretina@aol.com
FU Department of Veteran's Affairs; Rehabilitation Research & Development
Career Development Award; Research to Prevent Blindness; Lions Club of
Cleveland; NIH
FX This work was supported by funding from the Department of Veteran's
Affairs, Rehabilitation Research & Development Career Development Award,
Research to Prevent Blindness, Lions Club of Cleveland, NIH Core Grant
and, in part, by the Intramural Research Program of the National
Institutes of Health.
NR 6
TC 3
Z9 3
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PY 2009
VL 17
IS 4
BP 278
EP 281
AR PII 913569175
DI 10.1080/09273940902989340
PG 4
WC Ophthalmology
SC Ophthalmology
GA 480FF
UT WOS:000268717000009
PM 19657983
ER
PT S
AU Klinman, DM
Tross, D
Klaschik, S
Shirota, H
Sato, T
AF Klinman, Dennis M.
Tross, Debbie
Klaschik, Sven
Shirota, Hidekazu
Sato, Takeshi
BE Rossi, JJ
Gait, MJ
Eckstein, F
TI Therapeutic Applications and Mechanisms Underlying the Activity of
Immunosuppressive Oligonucleotides
SO OLIGONUCLEOTIDE THERAPEUTICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 4th Annual Meeting of the Oligonucleotide-Therapeutics-Society
CY OCT 15-18, 2008
CL Harvard Med Sch, Boston, MA
HO Harvard Med Sch
DE oligonucleotide; suppressive; therapy; autoimmunity; inflammation
ID INDUCED PULMONARY INFLAMMATION; 4TH INTERNATIONAL WORKSHOP; INDUCED
IMMUNE ACTIVATION; SUPPRESSIVE OLIGODEOXYNUCLEOTIDES; INTERFERON-GAMMA;
BACTERIAL-DNA; REACTIVE ARTHRITIS; ENDOTOXIC-SHOCK; MURINE; MICE
AB Synthetic oligodeoxynucleotides (ODN) capable of "neutralizing" or "inhibiting" immune responses have been described. This review will focus on the properties of phosphorothioate ODN that mimic the immunosuppressive activity of the repetitive TTAGGG motifs present in mammalian telomeres. These TTAGGG multimers block the production of pro-inflammatory and T helper type 1 cytokines elicited when immune cells are activated by a wide variety of Toll-like receptor ligands, polyclonal activators, and antigens. Several mechanisms contribute to the suppressive activity of such ODN. Ongoing microarray studies indicate that suppressive ODN interfere with the phosphorylation of signal transducer and activator of transcription I (STATI) and STAT4, thereby blocking the inflammation mediated by STAT-associated signaling cascades. In animal models, suppressive ODN can be used to prevent or treat diseases characterized by persistent immune activation, including collagen-induced arthritis, inflammatory arthritis, systemic lupus erythematosus, silicosis, and toxic shock. These findings suggest that TTAGGG multimers may find broad use in the treatment of diseases characterized by over-exuberant/persistent immune activation.
C1 [Klinman, Dennis M.; Tross, Debbie; Klaschik, Sven; Shirota, Hidekazu; Sato, Takeshi] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.
RP Klinman, DM (reprint author), NCI, Canc & Inflammat Program, Bldg 567,Rm 205, Frederick, MD 21702 USA.
EM klinmand@mail.nih.gov
NR 50
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Z9 26
U1 0
U2 3
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND
SN 0077-8923
BN 978-1-57331-758-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2009
VL 1175
BP 80
EP 88
DI 10.1111/j.1749-6632.2009.04970.x
PG 9
WC Medicine, Research & Experimental; Multidisciplinary Sciences
SC Research & Experimental Medicine; Science & Technology - Other Topics
GA BLQ41
UT WOS:000270798600009
PM 19796080
ER
PT J
AU Raafat, A
Lawson, S
Bargo, S
Klauzinska, M
Strizzi, L
Goldhar, AS
Buono, K
Salomon, D
Vonderhaar, BK
Callahan, R
AF Raafat, A.
Lawson, S.
Bargo, S.
Klauzinska, M.
Strizzi, L.
Goldhar, A. S.
Buono, K.
Salomon, D.
Vonderhaar, B. K.
Callahan, R.
TI Rbpj conditional knockout reveals distinct functions of Notch4/Int3 in
mammary gland development and tumorigenesis
SO ONCOGENE
LA English
DT Article
DE RBP-J; Int3; tumorigenesis
ID TRUNCATED INT3 GENE; NEOPLASTIC TRANSFORMATION; CELL-DIFFERENTIATION;
NOTCH; ACTIVATION; TUMOR; EXPRESSION; EPITHELIUM; SUPPRESSOR; HAIRLESS
AB Transgenic mice expressing the Notch 4 intracellular domain (ICD) (Int3) in the mammary gland have two phenotypes: arrest of mammary alveolar/lobular development and mammary tumorigenesis. Notch4 signaling is mediated primarily through the interaction of Int3 with the transcription repressor/activator Rbpj. We have conditionally ablated the Rbpj gene in the mammary glands of mice expressing whey acidic protein (Wap)-Int3. Interestingly, Rbpj knockout mice (Wap-Cre(+)/Rbpj(-/-)/Wap-Int3) have normal mammary gland development, suggesting that the effect of endogenous Notch signaling on mammary gland development is complete by day 15 of pregnancy. RBP-J heterozygous (Wap-Cre(+)/Rbpj(-/-)/Wap-Int3) and Rbpj control (Rbpj(flox/flox)/Wap-Int3) mice are phenotypically the same as Wap-Int3 mice with respect to mammary gland development and tumorigenesis. In addition, the Wap-Cre(+)/Rbpj(-/-)/Wap-Int3- knockout mice also developed mammary tumors at a frequency similar to Rbpj heterozygous and Wap-Int3 control mice but with a slightly longer latency. Thus, the effect on mammary gland development is dependent on the interaction of the Notch ICD with the transcription repressor/activator Rbpj, and Notch-induced mammary tumor development is independent of this interaction.
C1 [Raafat, A.; Lawson, S.; Bargo, S.; Klauzinska, M.; Strizzi, L.; Goldhar, A. S.; Salomon, D.; Vonderhaar, B. K.; Callahan, R.] NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bethesda, MD 20892 USA.
[Buono, K.] NIDDKD, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
RP Callahan, R (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, NIH, 37 Convent Dr,Bldg 37,Room 1118A, Bethesda, MD 20892 USA.
EM rc54d@nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX The Rbpjflox/flox mice were kindly provided by Dr Tasuku
Honjo, Department of Medical Chemistry, Graduate School of Medicine,
Kyoto University, Kyoto, Japan, and the WAP-Cre mice were kindly
provided by Dr Lothar Hennighausen, Laboratory of Genetics and
Physiology, National Institute of Diabetes and Digestive and Kidney
Diseases, National Institutes of Health, Bethesda, MD, USA. This
research was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research.
NR 32
TC 30
Z9 30
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD JAN
PY 2009
VL 28
IS 2
BP 219
EP 230
DI 10.1038/onc.2008.379
PG 12
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 395CY
UT WOS:000262501100006
PM 18836481
ER
PT J
AU Kim, SY
Toretsky, JA
Scher, D
Helman, LJ
AF Kim, Su Young
Toretsky, Jeffrey A.
Scher, Daniel
Helman, Lee J.
TI The Role of IGF-1R in Pediatric Malignancies
SO ONCOLOGIST
LA English
DT Article
DE IGF-1R; Pediatric malignancy; Molecular targeting; Therapeutic antibody
ID GROWTH-FACTOR-I; GASTROINTESTINAL STROMAL TUMORS; EWINGS-SARCOMA;
WILMS-TUMOR; AUTOCRINE GROWTH; FACTOR RECEPTOR; METASTATIC OSTEOSARCOMA;
MONOCLONAL-ANTIBODIES; SIGNAL-TRANSDUCTION; GLIOBLASTOMA CELLS
AB The insulin-like growth factor (IGF) family consists of ligands (IGF-I, IGF-II, insulin), several receptors (including IGF-1R), and six binding proteins (IGFBP-1 through IGFBP-6). Members of this family regulate key cellular activities and they also play an important role in the development and progression of both adult and childhood cancers. Binding of a ligand to the receptor leads to its activation, followed by signal transduction along several pathways. In some childhood malignancies, IGF-1R can be activated by endocrine, autocrine, or paracrine mechanisms. Although mutations in IGF-1R have not been identified, this signaling pathway is upregulated in many childhood cancers. These findings have led to the development of a host of IGF-1R signaling modulators that are currently being tested in clinical trials. This review explores the role of IGF-1R in a range of childhood malignancies. The Oncologist 2009; 14: 83-91
C1 [Kim, Su Young; Helman, Lee J.] NCI, Ctr Canc Res, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Toretsky, Jeffrey A.; Scher, Daniel] Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Washington, DC USA.
RP Kim, SY (reprint author), NCI, Ctr Canc Res, Pediat Oncol Branch, NIH, 10 Ctr Dr,Bldg 10,CRC 1W-3750, Bethesda, MD 20892 USA.
EM kimsuyou@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]; NCI NIH HHS [R01 CA088004, R01
CA088004-08]
NR 70
TC 60
Z9 62
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD JAN
PY 2009
VL 14
IS 1
BP 83
EP 91
DI 10.1634/theoncologist.2008-0189
PG 9
WC Oncology
SC Oncology
GA 407MJ
UT WOS:000263368100011
PM 19126579
ER
PT J
AU Doroshow, JH
Croyle, RT
Niederhuber, JE
AF Doroshow, James H.
Croyle, Robert T.
Niederhuber, John E.
TI Five Strategies for Accelerating the War on Cancer in an Era of Budget
Deficits
SO ONCOLOGIST
LA English
DT Editorial Material
ID CLINICAL-TRIALS; POLICY CHANGE; DISPARITIES; ENROLLMENT; US
AB In recent years, the National Institutes of Health's largest institute, the National Cancer Institute (NCI), has adapted to difficult economic conditions by leveraging its robust infrastructure - which includes risk factor surveillance and population monitoring, research centers (focused on basic, translation, clinical, and behavioral sciences), clinical trials and health care research networks, and rigorously validated statistical models - to maximize the impact of scientific progress on the public health. To continue advancement and realize the opportunity of significant, population-level changes in cancer mortality, the NCI recommends that five national-level actions be taken: (1) significantly increase enrollment of Medicare patients into cancer clinical trials through adequate physician reimbursement, (2) increase NCI/Centers for Medicare and Medicaid Services collaboration on clinical trials research to evaluate the therapeutic efficacy of anticancer drugs, (3) establish a national outcomes research demonstration project to test strategies for measuring and improving health care quality and provide an evidence base for public policy, (4) leverage existing tobacco-control collaborations and possible new authorities at the U. S. Food and Drug Administration to realize the outstanding health gains possible from a reduction in tobacco use, and (5) increase colorectal cancer screening rates though intensified collaboration between federal agencies working to address barriers to access and use of screening. These cost-effective strategies provide the opportunity for extraordinary results in an era of budget deficits. Of the chronic diseases, cancer has the strongest national research infrastructure that can be leveraged to produce rapid results to inform budget prioritization and public policy, as well as mobilize new projects to answer critical public health questions. The Oncologist 2009; 14: 110-116
C1 [Doroshow, James H.; Croyle, Robert T.; Niederhuber, John E.] NCI, Bethesda, MD 20892 USA.
RP Doroshow, JH (reprint author), NCI, 31 Ctr Dr,Room 3A44, Bethesda, MD 20892 USA.
EM doroshoj@mail.nih.gov
NR 20
TC 3
Z9 3
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 2
BP 110
EP 116
DI 10.1634/theoncologist.2008-0270
PG 7
WC Oncology
SC Oncology
GA 417ZD
UT WOS:000264116100002
PM 19147688
ER
PT J
AU Niederhuber, JE
AF Niederhuber, John E.
TI Facilitating Patient-Centered Cancer Research and a New Era of Drug
Discovery
SO ONCOLOGIST
LA English
DT Editorial Material
C1 [Niederhuber, John E.] NCI, Bethesda, MD 20892 USA.
RP Niederhuber, JE (reprint author), Care of Lubenow A E, NCI, MPH, Off Commun, Bldg 31,Room 11A27,31 Ctr Dr,MSC 2580, Bethesda, MD 20892 USA.
EM lubenowa@occ.nci.nih.gov
NR 0
TC 2
Z9 2
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 4
BP 311
EP 312
DI 10.1634/theoncologist.2009-0051
PG 2
WC Oncology
SC Oncology
GA 439QD
UT WOS:000265641200002
PM 19365096
ER
PT J
AU Bates, SE
Benz, EJ
AF Bates, Susan E.
Benz, Edward J., Jr.
TI Troublesome Words, Linguistic Precision, and Medical Oncology
SO ONCOLOGIST
LA English
DT Editorial Material
C1 [Bates, Susan E.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Benz, Edward J., Jr.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Bates, SE (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, Bldg 10,Room 12N226,MSC 1903,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sebates@helix.nih.gov
FU Intramural NIH HHS; PHS HHS [0]
NR 14
TC 1
Z9 1
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 4
BP 445
EP 447
DI 10.1634/theoncologist.2008-0253
PG 3
WC Oncology
SC Oncology
GA 439QD
UT WOS:000265641200013
PM 19357227
ER
PT J
AU Trimble, EL
Mccaskill-Stevens, W
Denicoff, A
Minig, L
Minasian, LM
AF Trimble, Edward L.
Mccaskill-Stevens, Worta
Denicoff, Andrea
Minig, Lucas
Minasian, Lori M.
TI Learning from Experience
SO ONCOLOGIST
LA English
DT Article
C1 [Trimble, Edward L.; Mccaskill-Stevens, Worta; Denicoff, Andrea; Minig, Lucas; Minasian, Lori M.] NCI, Bethesda, MD 20892 USA.
RP Trimble, EL (reprint author), NCI, 6130 Execut Blvd,Suite 7025,MSC 7436, Bethesda, MD 20892 USA.
EM trimblet@mail.nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 5
BP 476
EP 477
DI 10.1634/theoncologist.2009-0073
PG 2
WC Oncology
SC Oncology
GA 448WV
UT WOS:000266293600004
PM 19417099
ER
PT J
AU Chuk, MK
Balis, FM
Fox, E
AF Chuk, Meredith K.
Balis, Frank M.
Fox, Elizabeth
TI Trabectedin
SO ONCOLOGIST
LA English
DT Review
DE Trabectedin; DNA repair; Drug profile
ID SOFT-TISSUE SARCOMA; CONTINUOUS INTRAVENOUS-INFUSION; MARINE ANTICANCER
DRUG; DNA-REPAIR PATHWAYS; PHASE-I; ECTEINASCIDIN-743 ET-743; HOMOLOGOUS
RECOMBINATION; NUCLEOTIDE-EXCISION; SOLID TUMORS; MOLECULAR-MECHANISMS
C1 [Chuk, Meredith K.; Balis, Frank M.; Fox, Elizabeth] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Chuk, MK (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, 10 Ctr Dr,Bldg 10 CRC,Room 1W-5750, Bethesda, MD 20892 USA.
EM chukme@mail.nih.gov
FU NIH; National Cancer Institute
FX This work was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. The views
expressed do not necessarily represent views of the National Institutes
of Health or the U. S. government.
NR 62
TC 8
Z9 8
U1 0
U2 2
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 8
BP 794
EP 799
DI 10.1634/theoncologist.2009-0104
PG 6
WC Oncology
SC Oncology
GA 489HD
UT WOS:000269409900004
PM 19684073
ER
PT J
AU Kim, A
Balis, FM
Widemann, BC
AF Kim, AeRang
Balis, Frank M.
Widemann, Brigitte C.
TI Sorafenib and Sunitinib
SO ONCOLOGIST
LA English
DT Review
DE Sorafenib; Sunitinib; Drug profile
ID REFRACTORY SOLID TUMORS; ADVANCED HEPATOCELLULAR-CARCINOMA; TYROSINE
KINASE INHIBITOR; RENAL-CELL CARCINOMA; PHASE-I; ANTITUMOR-ACTIVITY;
CANCER; PHARMACOKINETICS; BAY-43-9006; COMBINATION
C1 [Kim, AeRang; Balis, Frank M.; Widemann, Brigitte C.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Kim, A (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, 10 Ctr Dr,Bldg 10 CRC,Room 1-3872, Bethesda, MD 20892 USA.
EM kimaer@mail.nih.gov
FU NIH; National Cancer Institute
FX This was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. The views
expressed do not necessarily represent the views of the National
Institutes of Health or the U. S. government.
NR 26
TC 25
Z9 28
U1 0
U2 3
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 8
BP 800
EP 805
DI 10.1634/theoncologist.2009-0088
PG 6
WC Oncology
SC Oncology
GA 489HD
UT WOS:000269409900005
PM 19648603
ER
PT J
AU Merchant, MS
Mackall, CL
AF Merchant, Melinda S.
Mackall, Crystal L.
TI Current Approach to Pediatric Soft Tissue Sarcomas
SO ONCOLOGIST
LA English
DT Review
DE Sarcoma; Soft tissue; Pediatric malignancy; Chemotherapy; Ewing's
sarcoma; Synovial sarcoma
ID ROUND-CELL TUMOR; CHILDRENS ONCOLOGY GROUP; NERVE SHEATH TUMORS;
INTERMEDIATE RISK RHABDOMYOSARCOMA; MESENCHYMAL PROGENITOR CELLS; EARLY
LYMPHOCYTE RECOVERY; ITALIAN-COOPERATIVE-GROUP; TOTAL-BODY IRRADIATION;
HUMAN SYNOVIAL SARCOMA; END RESULTS PROGRAM
AB The development of a new soft tissue lesion in an otherwise healthy child, adolescent, or young adult can present many challenges for pediatric or medical oncology teams. Although uncommon, the diagnosis of a soft tissue malignancy should always be considered in the differential diagnosis of persistent pain, even if no mass is palpable. The definitive diagnosis and treatment of a soft tissue mass is aided by timely scans, appropriate biopsy for anatomic and molecular pathology, and a treatment approach guided by the specific diagnosis. Because pediatric soft tissue sarcomas are rare, cooperative groups play a crucial role in defining the standard of care through retrospective series and well-designed prospective clinical trials. Enrollment of newly diagnosed patients in clinical studies should be encouraged in order to continue to improve outcomes and understanding of these rare tumors. This review focuses on the current recommendations for management of sarcomas that typically occur in the soft tissues of pediatric and young adult patients. The Oncologist 2009;14:1139-1153
C1 [Merchant, Melinda S.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Merchant, MS (reprint author), NCI, Pediat Oncol Branch, NIH, 10 Ctr Dr,Bldg 10,Room 1W-3940, Bethesda, MD 20892 USA.
EM merchanm@mail.nih.gov
NR 117
TC 4
Z9 4
U1 1
U2 4
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PY 2009
VL 14
IS 11
BP 1139
EP 1153
DI 10.1634/theoncologist.2009-0160
PG 15
WC Oncology
SC Oncology
GA 524TS
UT WOS:000272166800010
PM 19897537
ER
PT J
AU Muehlbauer, P
AF Muehlbauer, Paula
TI Look Beyond Breast Cancer
SO ONCOLOGY NURSING FORUM
LA English
DT Letter
C1 NIH, Bethesda, MD 20892 USA.
RP Muehlbauer, P (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 0190-535X
J9 ONCOL NURS FORUM
JI Oncol. Nurs. Forum
PD JAN
PY 2009
VL 36
IS 1
BP 10
EP 10
PG 1
WC Oncology; Nursing
SC Oncology; Nursing
GA 396VV
UT WOS:000262620200002
ER
PT J
AU Freeman, AF
Domingo, DL
Holland, SM
AF Freeman, A. F.
Domingo, D. L.
Holland, S. M.
TI Hyper IgE (Job's) syndrome: a primary immune deficiency with oral
manifestations
SO ORAL DISEASES
LA English
DT Review
DE hyper IgE syndrome; Job's syndrome; immunodeficiency; primary teeth
retention
ID HYPERIMMUNOGLOBULIN-E SYNDROME; RECURRENT-INFECTION SYNDROME; COLD
STAPHYLOCOCCAL ABSCESSES; INTERFERON-GAMMA; PATIENT; TRANSPLANTATION;
CRYPTOCOCCOSIS; CYTOKINE; LYMPHOMA; PATHWAY
AB Autosomal dominant hyper IgE (HIES or Job's) syndrome is a rare primary immune deficiency characterized by eczema, recurrent skin and lung infections, extremely elevated serum IgE, and a variety of connective tissue and skeletal abnormalities. Individuals with HIES share a characteristic facial appearance and many oral manifestations including retained primary dentition, a high arched palate, variations of the oral mucosa and gingiva, and recurrent oral candidiasis. Mutations in STAT3 account for the majority, if not all, of the cases of autosomal dominant HIES, but the pathogenesis of the many varied features remains poorly understood. In this review, we discuss the clinical phenotype of HIES including immunologic and non-immunologic features, the genetics of HIES, and treatment.
C1 [Freeman, A. F.; Holland, S. M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Freeman, A. F.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Domingo, D. L.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RP Freeman, AF (reprint author), Bldg 10,CRC B3-4141,MSC 1684, Bethesda, MD 20892 USA.
EM smh@nih.gov
FU National Institute of Allergy and Infectious Diseases; National Cancer
Institute; National Institutes of Health [N01-CO-12400]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U. S. Government.
NR 39
TC 12
Z9 16
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1354-523X
J9 ORAL DIS
JI Oral Dis.
PD JAN
PY 2009
VL 15
IS 1
BP 2
EP 7
DI 10.1111/j.1601-0825.2008.01463.x
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 382OY
UT WOS:000261616500002
PM 19036057
ER
PT J
AU Hanna, E
Quick, J
Libutti, SK
AF Hanna, E.
Quick, J.
Libutti, S. K.
TI The tumour microenvironment: a novel target for cancer therapy
SO ORAL DISEASES
LA English
DT Review
DE tumour microenvironment; combination therapy; endothelial cells;
leucocytes; fibroblasts; extracellular matrix
ID NECROSIS-FACTOR-ALPHA; ENDOTHELIAL GROWTH-FACTOR; ACTIVATING
POLYPEPTIDE-II; ADVANCED HEPATOCELLULAR-CARCINOMA; SUBCUTANEOUS
INTERFERON-ALPHA; EXPERIMENTAL SOLID TUMORS; ADOPTIVE CELL TRANSFER;
HUMAN COLON-CANCER; CD8(+) T-CELLS; IN-VIVO
AB Cancer therapy is in the midst of a major paradigm shift. Traditionally, cancer treatments have focused on tumour cells. However, studies over the past few decades have demonstrated that cancer is a vastly complex entity with multiple components affecting a tumour's growth, invasion and metastasis. These components, collectively termed the 'tumour microenvironment', include endothelial cells, pericytes, fibroblasts, inflammatory cells, leucocytes and elements of the extracellular matrix (ECM). Biological agents that target components of the tumour microenvironment may provide an interesting alternative to traditional tumour cell-directed therapy. Because of the complexity of the tumour milieu, the most beneficial therapy will likely involve the combination of one or more agents directed at this new target. This review highlights recent preclinical and clinical studies involving agents that target tumour vasculature, leucocytes, pericytes, cancer-associated fibroblasts and ECM components. We pay particular attention to combination therapies targeting multiple components of the tumour microenvironment, and aim to demonstrate that this strategy holds promise for the future of cancer treatment.
C1 [Hanna, E.; Quick, J.; Libutti, S. K.] NCI, Tumour Angiogenesis Sect, Surg Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Quick, J.] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20892 USA.
RP Libutti, SK (reprint author), NCI, Tumour Angiogenesis Sect, Surg Branch, Ctr Canc Res,NIH, Room 4W 5940,Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM libuttis@mail.nih.gov
NR 127
TC 43
Z9 48
U1 5
U2 27
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1354-523X
J9 ORAL DIS
JI Oral Dis.
PD JAN
PY 2009
VL 15
IS 1
BP 8
EP 17
DI 10.1111/j.1601-0825.2008.01471.x
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 382OY
UT WOS:000261616500003
PM 18992016
ER
PT J
AU Sugito, T
Mineshiba, F
Zheng, C
Cotrim, AP
Goldsmith, CM
Baum, BJ
AF Sugito, T.
Mineshiba, F.
Zheng, C.
Cotrim, A. P.
Goldsmith, C. M.
Baum, B. J.
TI Transient TWEAK overexpression leads to a general salivary epithelial
cell proliferation
SO ORAL DISEASES
LA English
DT Article
DE TWEAK; gene transfer; adenoviral vector; cell division; progenitor cell
ID RAT SUBMANDIBULAR-GLAND; PROGENITOR CELLS; MULTIFUNCTIONAL CYTOKINE;
RECEPTOR; SECRETION; APOPTOSIS; PATHWAY; TARGET; MODEL; DUCT
AB Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine that has pro-apoptotic, pro-angiogenic and pro-inflammatory effects. In liver, TWEAK leads to proliferation of progenitor oval cells, but not of mature hepatocytes. This study evaluated the hypothesis that TWEAK overexpression in salivary glands would lead to the proliferation of a salivary progenitor cell.
A recombinant, serotype 5 adenoviral vector encoding human TWEAK, AdhTWEAK, was constructed, initially tested in vitro, and then administered to male Balb/c mice via cannulation of Wharton's duct. TWEAK expression in vivo was monitored as protein secreted into saliva and serum by enzyme-linked immunosorbent assays. Salivary cell proliferation was monitored by proliferating cell nuclear antigen staining and apoptosis was monitored using TUNEL staining.
AdhTWEAK administration led to a dose-dependent, transient TWEAK protein expression, detected primarily in saliva. Salivary epithelial cell proliferation was generalized, peaking on similar to days 2 and 3. TWEAK expression had no detectable effect on apoptosis of salivary epithelial cells.
Transient overexpression of TWEAK in murine salivary glands leads to a general proliferation of epithelial cells vs a selective stimulation of a salivary progenitor cell.
C1 [Sugito, T.; Mineshiba, F.; Zheng, C.; Cotrim, A. P.; Goldsmith, C. M.; Baum, B. J.] NIDCR, MPTB, NIH, Bethesda, MD 20892 USA.
RP Baum, BJ (reprint author), NIDCR, MPTB, NIH, Bldg 10,Room 1N113,MSC 1190,10 Ctr Dr, Bethesda, MD 20892 USA.
EM bbaum@dir.nidcr.nih.gov
FU National Institute of Dental and Craniofacial Research
FX This research was supported by the Intramural Research Program of the
National Institute of Dental and Craniofacial Research.
NR 35
TC 6
Z9 7
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1354-523X
J9 ORAL DIS
JI Oral Dis.
PD JAN
PY 2009
VL 15
IS 1
BP 76
EP 81
DI 10.1111/j.1601-0825.2008.01474.x
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 382OY
UT WOS:000261616500011
PM 18992019
ER
PT J
AU Simpson, DS
Lovell, KM
Lozama, A
Han, N
Day, VW
Dersch, CM
Rothman, RB
Prisinzano, TE
AF Simpson, Denise S.
Lovell, Kimberly M.
Lozama, Anthony
Han, Nina
Day, Victor W.
Dersch, Christina M.
Rothman, Richard B.
Prisinzano, Thomas E.
TI Synthetic studies of neoclerodane diterpenes from Salvia divinorum: role
of the furan in affinity for opioid receptors
SO ORGANIC & BIOMOLECULAR CHEMISTRY
LA English
DT Article
ID PLANT-DERIVED HALLUCINOGEN; AGONIST SALVINORIN-A; TEUCRIN-A;
ENANTIOSELECTIVE SYNTHESIS; RICCIOCARPIN-B; RHESUS-MONKEYS; IN-VIVO;
RATS; IDENTIFICATION; MICE
AB Further synthetic modi. cation of the furan ring of salvinorin A (1), the major active component of Salvia divinorum, has resulted in novel neoclerodane diterpenes with opioid receptor affinity and activity. A computational study has predicted 1 to be a reproductive toxicant in mammals and is suggestive that use of 1 may be associated with adverse effects. We report in this study that piperidine 21 and thiomorpholine 23 have been identified as selective partial agonists at kappa opioid receptors. This indicates that additional structural modi. cations of 1 may provide ligands with good selectivity for opioid receptors but with reduced potential for toxicity.
C1 [Simpson, Denise S.; Lovell, Kimberly M.; Lozama, Anthony; Prisinzano, Thomas E.] Univ Kansas, Dept Med Chem, Lawrence, KS 66045 USA.
[Lozama, Anthony; Han, Nina] Univ Iowa, Div Med & Nat Prod Chem, Iowa City, IA USA.
[Day, Victor W.] Univ Kansas, Dept Chem, Lawrence, KS 66045 USA.
[Dersch, Christina M.; Rothman, Richard B.] NIDA, Clin Psychopharmacol Sect, IRP, NIH,DHHS, Baltimore, MD USA.
RP Prisinzano, TE (reprint author), Univ Kansas, Dept Med Chem, Lawrence, KS 66045 USA.
EM prisinza@ku.edu
RI Prisinzano, Thomas/B-7877-2010
FU NIH [SIG S10 RR019398]; National Institute on Drug Abuse (NIDA)
[R01DA018151S1]; Intramural Research Program; National Institute on Drug
Abuse; DHHS
FX We wish to thank (Dr ToddWilliams, Mr Robert Drake, Mr Larry Sieb) of
the KU mass spectrometry laboratory for their efforts in acquiring the
ESI spectra. LCT Premier was purchased with support from NIH SIG S10
RR019398. This work was supported by Grant Numbers R01DA018151 and
R01DA018151S1 (to TEP) from the National Institute on Drug Abuse (NIDA).
Portions of this work were also supported by the Intramural Research
Program, National Institute on Drug Abuse, National Institutes of
Health, DHHS. In silico computational toxicology testing was completed
with the support of NIDA's Addiction Treatment Discovery Program through
the use of Interagency Agreement Y1DA6003. The content is the sole
responsibility of the authors and does not necessarily represent the of.
cial views of the National Institute on Drug Abuse or the National
Institutes of Health.
NR 55
TC 11
Z9 12
U1 1
U2 6
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 1477-0520
EI 1477-0539
J9 ORG BIOMOL CHEM
JI Org. Biomol. Chem.
PY 2009
VL 7
IS 18
BP 3748
EP 3756
DI 10.1039/b905148a
PG 9
WC Chemistry, Organic
SC Chemistry
GA 488CU
UT WOS:000269327500018
PM 19707679
ER
PT J
AU Ratnayake, R
Covell, D
Ransom, TT
Gustafson, KR
Beutler, JA
AF Ratnayake, Ranjala
Covell, David
Ransom, Tanya T.
Gustafson, Kirk R.
Beutler, John A.
TI Englerin A, a Selective Inhibitor of Renal Cancer Cell Growth, from
Phyllanthus engleri
SO ORGANIC LETTERS
LA English
DT Article
ID EUPHORBIACEAE; BIOASSAYS; USAGE; COMPILATION; TOXICITY; ACID
AB An extract from Phyllanthus engleri was identified in a bioinformatic analysis of NCI 60-cell natural product extract screening data that selectively Inhibited the growth of renal cancer cell lines. Bioassay-guided fractionation yielded two new gualane sesquiterpenes, englerins A (1) and B (2). Englerin A showed 1000-fold selectivity against six of eight renal cancer cell lines with GI(50) values ranging from 1-87 nM. The structures of I and 2 and their relative stereochemistry were established by spectroscopic methods,
C1 [Ratnayake, Ranjala; Ransom, Tanya T.; Gustafson, Kirk R.; Beutler, John A.] Ctr Canc Res, Mol Targets Dev Program, Frederick, MD 21702 USA.
[Covell, David] NCI, Screening Technol Branch, Dev Therapeut Program, Frederick, MD 21702 USA.
RP Beutler, JA (reprint author), Ctr Canc Res, Mol Targets Dev Program, Frederick, MD 21702 USA.
EM beutlerj@mail.nih.gov
RI Beutler, John/B-1141-2009
OI Beutler, John/0000-0002-4646-1924
FU NIH; National Cancer Institute; Center for Cancer Research;
Developmental Therapeutics Program in the Division of Cancer Treatment;
Diagnosis of the National Cancer Institute
FX We thank the Missouri Botanical Garden collectors (Roy Gereau, James
Lovett, C. O. Kyalawa, and Z. H. Mbwambo) for the plant collection,
Thomas McCloud (Natural Products Support Group, NCI-Frederick) for plant
extraction, Melinda Hollingshead (Biological Testing Branch, DTP) for
mouse toxicity studies, and Sergey Tarasov and Marzena. Dyba (Biophysics
Resource Core, Structural Biophysics Laboratory, CCR) for assistance
with high-resolution mass spectrometry. This research was supported
jointly by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research, and by the Developmental
Therapeutics Program in the Division of Cancer Treatment and Diagnosis
of the National Cancer Institute.
NR 19
TC 80
Z9 80
U1 5
U2 35
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1523-7060
J9 ORG LETT
JI Org. Lett.
PD JAN 1
PY 2009
VL 11
IS 1
BP 57
EP 60
DI 10.1021/ol802339w
PG 4
WC Chemistry, Organic
SC Chemistry
GA 388KM
UT WOS:000262018700015
PM 19061394
ER
PT J
AU Saavedra, JE
Davies, KM
Barchi, JJ
Keefer, LK
AF Saavedra, Joseph E.
Davies, Keith M.
Barchi, Joseph J., Jr.
Keefer, Larry K.
TI Unexpected Incorporation of Bromine at a Non-anomeric Position during
the Synthesis of an O-2-Glycosylated Diazeniumdiolate
SO ORGANIC PREPARATIONS AND PROCEDURES INTERNATIONAL
LA English
DT Article
ID OXIDE
C1 [Saavedra, Joseph E.] NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA.
[Davies, Keith M.] George Mason Univ, Dept Chem, Fairfax, VA 22030 USA.
[Barchi, Joseph J., Jr.] NCI, Med Chem Lab, Frederick, MD 21702 USA.
[Keefer, Larry K.] NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
RP Saavedra, JE (reprint author), NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA.
EM saavj@mail.ncifcrf.gov
RI Barchi Jr., Joseph/N-3784-2014; Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU National Cancer Institute, National Institutes of Health
[NO1-CO-2008-00001]
FX This project has been funded in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
NO1-CO-2008-00001, and in part by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. The content
of this article does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of
tradenames, commercial products, or organizations imply endorsement by
the U. S. Government.
NR 4
TC 0
Z9 0
U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0030-4948
J9 ORG PREP PROCED INT
JI Org. Prep. Proced. Int.
PY 2009
VL 41
IS 2
BP 143
EP 147
DI 10.1080/00304940902801968
PG 5
WC Chemistry, Organic
SC Chemistry
GA 587ML
UT WOS:000276996500002
ER
PT J
AU Ling, SM
Patel, DD
Garnero, P
Zhan, M
Vaduganathan, M
Muller, D
Taub, D
Bathon, JM
Hochberg, M
Abernethy, DR
Metter, EJ
Ferrucci, L
AF Ling, S. M.
Patel, D. D.
Garnero, P.
Zhan, M.
Vaduganathan, M.
Muller, D.
Taub, D.
Bathon, J. M.
Hochberg, M.
Abernethy, D. R.
Metter, E. J.
Ferrucci, L.
TI Serum protein signatures detect early radiographic osteoarthritis
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Article
DE Osteoarthritis; Proteins; Biomarkers; Inflammation; Aging
ID RHEUMATOID-ARTHRITIS; CARTILAGE; KNEE; EXPRESSION; MICROARRAYS;
AGGRECAN; HIP
AB Objective: To test the hypothesis that early knee and hand osteoarthritis (OA) development is characterized by detectable changes in serum proteins relevant to inflammation, cell growth, activation, and metabolism several years before OA becomes radiographically evident.
Methods: Using microarray platforms that simultaneously test 169 proteins relevant to inflammation, cell growth, activation and metabolism, we conducted a case-control study nested within the Baltimore Longitudinal Study of Aging (BLSA). Subjects included 22 incident cases of OA and 66 age-, sex- and body mass index (BMI)-matched controls. Serum samples tested were obtained at the time of radiographic classification as either case or control, and up to 10 years earlier at a time when all participants were free of radiographic OA. Proteins with mean signal intensities fourfold higher than background were compared between cases and controls using multivariate techniques.
Results: Sixteen proteins were different between OA cases compared to controls. Four of these proteins [matrix metalloproteinase (MMP)-7, interleukin (IL)-15, plasminogen activator inhibitor (PAI)-1 and soluble vascular adhesion protein (sVAP)-1] were already different in samples obtained 10 years before radiographic classification and remained different at the time of diagnosis. Six additional proteins were only associated with subsequent OA development and not with established OA.
Conclusions: Changes in serum proteins implicated in matrix degradation, cell activation, inflammation and bone collagen degradation products accompany early OA development and can precede radiographic detection by several years. Published by Elsevier Ltd on behalf of Ostecarthritis Research Society International.
C1 [Ling, S. M.; Zhan, M.; Vaduganathan, M.; Muller, D.; Taub, D.; Abernethy, D. R.; Metter, E. J.; Ferrucci, L.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Patel, D. D.] Univ N Carolina, Thurston Arthrit Res Ctr, Div Rheumatol Allergy & Immunol, Chapel Hill, NC USA.
[Garnero, P.] INSERM, Res Unit & Synarc 664, F-69008 Lyon, France.
[Bathon, J. M.] Johns Hopkins Med Inst, Div Rheumatol, Baltimore, MD 21205 USA.
[Hochberg, M.] Univ Maryland, Sch Med, Div Clin Immunol & Rheumatol, Baltimore, MD 21201 USA.
RP Ling, SM (reprint author), Harbor Hosp, Clin Res Branch, NM 533 3001 S Hanover St, Baltimore, MD 21225 USA.
EM lingsh@grc.nia.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Institute on Aging. Dhavalkumar Patel
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging. Dhavalkumar
Patel also has received support from Molecular Staging, Inc up until
2004. This company no longer exists. Patrick Gamero is an employee of
Synarc SAS. Synarc assays were performed in a blinded fashion, through a
material transfer agreement.
NR 24
TC 30
Z9 31
U1 2
U2 14
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 1063-4584
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD JAN
PY 2009
VL 17
IS 1
BP 43
EP 48
DI 10.1016/j.joca.2008.05.004
PG 6
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 400SS
UT WOS:000262889500007
PM 18571442
ER
PT J
AU Xie, H
Gu, XX
AF Xie, H.
Gu, X. X.
BE Park, K
Choung, YH
Park, HJ
Chun, YM
TI Regulatory mechanisms of Moraxella catarrhalis lipooligosaccharide
induced ICAM-1 expression and potential impact on otitis media with
effusion (OME)
SO OTITIS MEDIA 2009: 6TH EXTRAORDINARY INTERNATIONAL SYMPOSIUM ON RECENT
ADVANCES IN OTITIS MEDIA
LA English
DT Proceedings Paper
CT 6th Extraordinary International Symposium on Recent Advances in Otitis
Media Research
CY MAY 06-10, 2009
CL Seoul, SOUTH KOREA
SP Ajou Univ, ENT Alumni, Yonsei Univ, Chosun Univ
ID CARTILAGE PALISADE TYMPANOPLASTY; TENSA RETRACTION CHOLESTEATOMA;
FASCIA; SINUS
AB Previously we have reported that Moraxella catarrhalis lipooligosaccharide (LOS) differentially enhances intercellular adhesion molecule 1 (ICAM-1) expression on human monocytes. Further investigations have suggested that this M. catarrhalis LOS induced up-regulation of ICAM-1 required TLR4, surface CD14 and serum lipopolysaccharide binding protein (LBP), and was partially mediated through a TNF-alpha dependent autocrine mechanism. NF-kappa B p65 and JNK1 also participate in the regulation of LOS stimulated ICAM-1 expression. Moreover, the LOS activated human monocytes could stimulate adjacent naive monocytes to produce TNF-alpha, which partially depended on surface ICAM-1 and IL-8RA expression. Our results suggest that M. catarrhalis LOS could induce excessive middle ear inflammation by selectively up-regulating surface ICAM-1 expression of host cells during OME development.
C1 [Xie, H.; Gu, X. X.] Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, NIH, Rockville, MD 20850 USA.
RP Xie, H (reprint author), Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, NIH, Rockville, MD 20850 USA.
NR 6
TC 0
Z9 0
U1 2
U2 2
PU MEDIMOND S R L
PI 40128 BOLOGNA
PA VIA MASERATI 5, 40128 BOLOGNA, 00000, ITALY
BN 978-88-7587-542-8
PY 2009
BP 45
EP 52
PG 8
WC Otorhinolaryngology
SC Otorhinolaryngology
GA BQS43
UT WOS:000281730600008
ER
PT J
AU Peng, D
Gao, S
Zhang, W
Muszynski, A
Carlson, RW
Gu, XX
AF Peng, D.
Gao, S.
Zhang, W.
Muszynski, A.
Carlson, R. W.
Gu, X. X.
BE Park, K
Choung, YH
Park, HJ
Chun, YM
TI Virulence genes in Moraxella catarrhalis lipopolysaccharide biosynthesis
pathway
SO OTITIS MEDIA 2009: 6TH EXTRAORDINARY INTERNATIONAL SYMPOSIUM ON RECENT
ADVANCES IN OTITIS MEDIA
LA English
DT Proceedings Paper
CT 6th Extraordinary International Symposium on Recent Advances in Otitis
Media Research
CY MAY 06-10, 2009
CL Seoul, SOUTH KOREA
SP Ajou Univ, ENT Alumni, Yonsei Univ, Chosun Univ
ID IDENTIFICATION
AB We have previously found several potential virulence genes involved in Moraxella catarrhalis lipooligosaccharide (LOS) biosynthesis pathway. The genes include kdtA, lgt3, lpxA and lpxL/X. Using either a random transposon mutagenesis or bioinformatics approach, each corresponding knockout mutant has been generated and its truncated LOS structure confirmed by MALDI-TOF MS, glycosyl composition, linkage, and NMR analyses of de-O-acylated LOS or oligosaccharide (OS) from the mutant. Phenotypic studies revealed that the mutants showed different patterns in their growth rate, toxicity and susceptibility to hydrophobic reagents. However, most mutants with truncated LOS structure in OS and/or lipid A presented reduced resistance to the bactericidal activity of normal human serum, reduced adherence to human epithelial cells, and increased bacterial clearance in animals. Our data suggest that a complete OS moiety of the LOS is important for serum resistance and adherence to epithelial cells, and both the OS and lipid A moieties contribute to the LOS virulence.
C1 [Peng, D.; Gao, S.; Zhang, W.; Gu, X. X.] Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, NIH, Rockville, MD 20850 USA.
RP Peng, D (reprint author), Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, NIH, Rockville, MD 20850 USA.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU MEDIMOND S R L
PI 40128 BOLOGNA
PA VIA MASERATI 5, 40128 BOLOGNA, 00000, ITALY
BN 978-88-7587-542-8
PY 2009
BP 107
EP 110
PG 4
WC Otorhinolaryngology
SC Otorhinolaryngology
GA BQS43
UT WOS:000281730600018
ER
PT S
AU Farley, J
Birrer, MJ
AF Farley, John
Birrer, Michael J.
BE Stack, MS
Fishman, DA
TI Novel Therapeutic Targets
SO OVARIAN CANCER, SECOND EDITION
SE Cancer Treatment and Research
LA English
DT Article; Book Chapter
ID EPITHELIAL OVARIAN-CANCER; PHASE-II TRIAL; GYNECOLOGIC-ONCOLOGY-GROUP;
GROWTH-FACTOR RECEPTORS; MATRIX-METALLOPROTEINASE INHIBITORS;
PACLITAXEL-MEDIATED CYTOTOXICITY; METASTATIC COLORECTAL-CANCER; PRIMARY
PERITONEAL CARCINOMA; DEPENDENT KINASE INHIBITOR; MONOCLONAL-ANTIBODY
C225
C1 [Birrer, Michael J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Birrer, Michael J.] Harvard Canc Ctr, Gynecol Canc Res Program, Boston, MA 02114 USA.
[Birrer, Michael J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Farley, John] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 USA.
[Farley, John] NCI, Christina Annunziata Ctr Canc Res, Med Oncol Branch, Bethesda, MD 20892 USA.
RP Birrer, MJ (reprint author), Harvard Univ, Sch Med, 55 Fruit St, Boston, MA 02114 USA.
EM mbirrer@partners.org
NR 119
TC 2
Z9 2
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0927-3042
BN 978-0-387-98093-5
J9 CANCER TREAT RES
JI Canc. Treat. Res.
PY 2009
VL 149
BP 63
EP 84
DI 10.1007/978-0-387-98094-2_3
PG 22
WC Oncology
SC Oncology
GA BMT32
UT WOS:000273526200003
PM 19763431
ER
PT S
AU ElMasri, WM
Casagrande, G
Hoskins, E
Kimm, D
Kohn, EC
AF ElMasri, Wafic M.
Casagrande, Giovanna
Hoskins, Ebony
Kimm, Daniel
Kohn, Elise C.
BE Stack, MS
Fishman, DA
TI Cell Adhesion in Ovarian Cancer
SO OVARIAN CANCER, SECOND EDITION
SE Cancer Treatment and Research
LA English
DT Article; Book Chapter
ID ENDOTHELIAL GROWTH-FACTOR; E-CADHERIN EXPRESSION; EPITHELIAL-MESENCHYMAL
TRANSITIONS; RECEPTOR TYROSINE KINASE; MOLECULE E-CADHERIN; SOLUBLE
P-SELECTIN; SIALYL-LEWIS-X; BETA-CATENIN; TUMOR-PROGRESSION;
ALPHA-CATENIN
C1 [ElMasri, Wafic M.; Casagrande, Giovanna; Hoskins, Ebony; Kimm, Daniel; Kohn, Elise C.] Natl Canc Inst, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Kohn, EC (reprint author), Natl Canc Inst, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM kohne@mail.nih.gov
NR 164
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0927-3042
BN 978-0-387-98093-5
J9 CANCER TREAT RES
JI Canc. Treat. Res.
PY 2009
VL 149
BP 297
EP 318
DI 10.1007/978-0-387-98094-2_14
PG 22
WC Oncology
SC Oncology
GA BMT32
UT WOS:000273526200014
PM 19763442
ER
PT B
AU Okun, E
Mattson, MP
AF Okun, Eitan
Mattson, Mark P.
BE Veasey, SC
TI Neuronal Vulnerability to Oxidative Damage in Aging
SO OXIDATIVE NEURAL INJURY
SE Contemporary Clinical Neuroscience
LA English
DT Article; Book Chapter
DE ALS; Alzheimer's disease; Free radicals; Hormesis; Huntington's disease;
Hydroxynonenal; Lipid peroxidation; Parkinson's disease; Peroxynitrite
ID AMYOTROPHIC-LATERAL-SCLEROSIS; ALZHEIMERS-DISEASE; LIPID-PEROXIDATION;
NEURODEGENERATIVE DISORDERS; FREE-RADICALS; MITOCHONDRIAL DYSFUNCTION;
CALORIC RESTRICTION; PARKINSONS-DISEASE; GENE-EXPRESSION; DNA-DAMAGE
AB The aging process in the brain is as robust as it is in other body organs and manifests as decrements in cognition, sensory and motor abilities, and autonomic control of various organ systems. This is due to the fact that, with advancing age, brain cells are exposed to increasing levels of oxidative stress, disturbed energy homeostasis, and accumulation of damage to protein, lipids, and nucleic acids. While these changes occur during normal aging, they are exacerbated in neurons that are susceptible to neurodegenerative disorders. The final outcome of the balance between a person's own genetic background and the environmental changes that affect him or her determines if and when a neurodegenerative disorder will occur. Oxidative molecular alterations that occur during normal aging and that are amplified in the neurons that are affected in neurodegenerative disorders include protein nitrosylation, oxidation of amino acids and DNA bases, lipid peroxidation, and increased amounts of neurotoxic amino acid derivates such as homocysteine. Oxidative damage may render neurons vulnerable to metabolic stress, excitotoxicity, and apoptosis in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). Oxidative stress contributes to the abnormal protein aggregations specific to each disorder - amyloid beta-peptide (A beta) in AD, alpha-synuclein in PD, huntingtin in HD, and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) in ALS. These protein inclusions may arise, in part, from impaired proteasome function and autophagy. Although the utility of antioxidant ingestion as a preventative strategy for age-related neurological disorders has not yet been demonstrated, age- and disease-related oxidative damage to neurons can be decreased by dietary energy restriction and exercise and accelerated by overeating and diabetes.
C1 [Okun, Eitan; Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM omalleyk@pcg.wustl.edu; mattsonm@grc.nia.nih.gov
RI okun, eitan/K-1314-2016
OI okun, eitan/0000-0001-8474-1487
NR 72
TC 1
Z9 1
U1 1
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
BN 978-1-60327-341-1
J9 CONTEMP CLIN NEUROSC
PY 2009
BP 83
EP 95
DI 10.1007/978-1-60327-342-8_5
D2 10.1007/978-1-60327-342-8
PG 13
WC Clinical Neurology
SC Neurosciences & Neurology
GA BKK33
UT WOS:000268373600006
ER
PT S
AU Rifkind, JM
Nagababu, E
Cao, ZL
Barbiro-Michaely, E
Mayevsky, A
AF Rifkind, Joseph M.
Nagababu, Enika
Cao, Zeling
Barbiro-Michaely, Efrat
Mayevsky, Avraham
BE Liss, P
Hansell, P
Bruley, DF
Harrison, DK
TI NITRITE-INDUCED IMPROVED BLOOD CIRCULATION ASSOCIATED WITH AN INCREASE
IN A POOL OF RBC-NO WITH NO BIOACTIVITY
SO OXYGEN TRANSPORT TO TISSUE XXX
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT 35th Annual Conference of the
International-Society-on-Oxygen-Transport-to-Tissue
CY 2007
CL Uppsala, SWEDEN
SP Int Soc Oxygen Transport Tissue
ID RED-CELL; REDUCTION; OXIDATION; OXIDE; HEMOGLOBIN
AB The reduction of nitrite by RBCs producing NO can play a role in regulating vascular tone. This hypothesis was investigated in rats by measuring the effect of nitrite infusion on mean arterial blood pressure (MAP), cerebral blood flow (CBF) and cerebrovascular resistance (CVR) in conjunction with the accumulation of RBC-NO. The nitrite infusion reversed the increase in MAP and decrease in CBF produced by L-NAME inhibition of e-NOS. At the same time there was a dramatic increase in RBC-NO. Correlations of RBC-NO for individual rats support a role for the regulation or vascular tone by this pool of NO. Furthermore, data obtained prior to treatment with L-NAME or nitrite are consistent with a contribution of RBC reduced nitrite in regulating vascular tone even under normal conditions. The role of the RBC in delivering NO to the vasculature was explained by the accumulation of a pool of bioactive NO in the RBC when nitrite is reduced by deoxygenated hemoglobin chains. A comparison of R and T state hemoglobin demonstrated a potential mechanism for the release of this NO in the T-state present at reduced oxygen pressures when blood enters the microcirculation. Coupled with enhanced hemoglobin binding to the membrane under these conditions the NO can be released to the vasculature.
C1 [Rifkind, Joseph M.; Nagababu, Enika; Cao, Zeling] NIA, Mol Dynam Sect, Baltimore, MD 21224 USA.
[Barbiro-Michaely, Efrat; Mayevsky, Avraham] Bar Ilan Univ, Mina & Everard Goodman Fac Life Sci, IL-52100 Ramat Gan, Israel.
RP Rifkind, JM (reprint author), NIA, Mol Dynam Sect, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM rifkindj@mail.nih.gov
FU Intramural NIH HHS [Z01 AG000433-01]
NR 14
TC 8
Z9 9
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
SN 0065-2598
BN 978-0-387-85997-2
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2009
VL 645
BP 27
EP 34
DI 10.1007/978-0-387-85998-9_5
PG 8
WC Medicine, Research & Experimental; Physiology
SC Research & Experimental Medicine; Physiology
GA BIT62
UT WOS:000262627100005
PM 19227446
ER
PT J
AU Klebanoff, MA
AF Klebanoff, Mark A.
TI The Collaborative Perinatal Project: a 50-year retrospective
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article
ID CEREBRAL-PALSY; UNITED-STATES; BILIRUBIN; MORTALITY; AGE
C1 Eunice Kennedy Shriver NICHHD, Epidemiol Branch, NIH, Dept Hlth & Human Serv,NICHD, Bethesda, MD 20892 USA.
RP Klebanoff, MA (reprint author), Eunice Kennedy Shriver NICHHD, Epidemiol Branch, NIH, Dept Hlth & Human Serv,NICHD, 6100 Bldg,Room 7 B05, Bethesda, MD 20892 USA.
EM mk90h@nih.gov
FU NIH; National Institute of Child Health and Human Development
FX Dr Klebanoff is supported by the Intramural Research Program of the NIH,
National Institute of Child Health and Human Development.
NR 37
TC 21
Z9 21
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 2009
VL 23
IS 1
BP 2
EP 8
DI 10.1111/j.1365-3016.2008.00984.x
PG 7
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA 377TH
UT WOS:000261273000002
PM 19228308
ER
PT J
AU Davila, JA
Chiao, EY
Hasche, JC
Petersen, NJ
McGlynn, KA
Shaib, YH
AF Davila, Jessica A.
Chiao, Elizabeth Y.
Hasche, Jennifer C.
Petersen, Nancy J.
McGlynn, Katherine A.
Shaib, Yasser H.
TI Utilization and Determinants of Adjuvant Therapy Among Older Patients
Who Receive Curative Surgery for Pancreatic Cancer
SO PANCREAS
LA English
DT Article
DE pancreatic cancer; adjuvant therapy; SEER-Medicare
ID LONG-TERM SURVIVAL; DUCTAL ADENOCARCINOMA; ELDERLY-PATIENTS; RESECTION;
PANCREATICODUODENECTOMY; CHEMORADIOTHERAPY; CHEMOTHERAPY; CARCINOMA;
REGION; TRIAL
AB Objective: We conducted a population-based study to describe the utilization, determinants, and survival effects of adjuvant therapies after surgery among older patients with pancreatic cancer.
Methods: Using Surveillance, Epidemiology, and End Results-Medicare data, we identified patients older than 65 years who received surgical resection for pancreatic cancer during 1992-2002. We constructed multiple logistic regression models to examine patient, clinical, and hospital factors associated with receiving adjuvant therapy. Cox proportional hazards models were used to examine the effect of therapy on survival.
Results: Approximately 49% of patients received adjuvant therapy after surgery. Patient factors associated with increased receipt of adjuvant therapy included more recent diagnosis, younger age, stage II disease, higher income, and geographic location. Hospital factors associated with increased receipt of adjuvant therapy included cooperative group membership and larger size. Adjuvant treatments associated with a significant reduction in 2-year mortality (relative to surgery alone) were chemoradiation or radiation alone but not chemotherapy alone.
Conclusions: Our findings suggest that adjuvant chemoradiation and, to a lesser degree, radiation only are associated with a reduction in the risk of mortality among older patients who undergo surgery for pancreatic cancer. However, receipt of adjuvant therapy varied by period and geography as well as by certain patient and hospital factors.
C1 [Davila, Jessica A.; Chiao, Elizabeth Y.; Hasche, Jennifer C.; Petersen, Nancy J.; Shaib, Yasser H.] Baylor Coll Med, Sect Hlth Serv Res, Houston Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Chiao, Elizabeth Y.] Baylor Coll Med, Infect Dis Sect, Houston Vet Affairs Med Ctr, Houston, TX 77030 USA.
[McGlynn, Katherine A.] NCI DHHS, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Shaib, Yasser H.] Baylor Coll Med, Gastroenterol Sect, Houston Vet Affairs Med Ctr, Houston, TX 77030 USA.
RP Davila, JA (reprint author), Baylor Coll Med, Sect Hlth Serv Res, Houston Vet Affairs Med Ctr, 2002 Holcombe Blvd 152, Houston, TX 77030 USA.
EM jdavila@bcm.tmc.edu
FU Dan L. Duncan Cancer Center, Baylor College of Medicine
FX This study was supported by pilot funding from the Dan L. Duncan Cancer
Center, Baylor College of Medicine.
NR 18
TC 19
Z9 20
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
J9 PANCREAS
JI Pancreas
PD JAN
PY 2009
VL 38
IS 1
BP E18
EP E25
DI 10.1097/MPA.0b013e318187eb3f
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 392QP
UT WOS:000262317600025
PM 18797424
ER
PT J
AU Kreps, G
AF Kreps, Gary
BE Socha, TJ
Stamp, GH
TI Commentary Communication and Family Health and Wellness Relationships
SO PARENTS AND CHILDREN COMMUNICATING WITH SOCIETY: MANAGING RELATIONSHIPS
OUTSIDE OF THE HOME
SE Routledge Communications Series
LA English
DT Editorial Material; Book Chapter
ID CARE; BEHAVIORS
C1 [Kreps, Gary] George Mason Univ, Ctr Hlth & Risk Commun, Fairfax, VA 22030 USA.
[Kreps, Gary] George Mason Univ, Dept Commun, Fairfax, VA 22030 USA.
[Kreps, Gary] NCI, NIH, Bethesda, MD 20892 USA.
RP Kreps, G (reprint author), George Mason Univ, Ctr Hlth & Risk Commun, Fairfax, VA 22030 USA.
NR 17
TC 0
Z9 0
U1 0
U2 0
PU ROUTLEDGE
PI LONDON
PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND
BN 978-0-203-93860-7
J9 ROUTL COMMUN SER
PY 2009
BP 207
EP 212
PG 6
WC Communication; Family Studies
SC Communication; Family Studies
GA BNT23
UT WOS:000275479500013
ER
PT S
AU Kim, SY
Helman, LJ
AF Kim, Su Young
Helman, Lee J.
BE Jaffe, N
Bruland, OS
Bielack, SS
TI Strategies to Explore New Approaches in the Investigation and Treatment
of Osteosarcoma
SO PEDIATRIC AND ADOLESCENT OSTEOSARCOMA
SE Cancer Treatment and Research
LA English
DT Proceedings Paper
CT Symposium on Pediatric and Adolescent Osteosarcoma
CY MAR 06-08, 2008
CL Univ Texas, MD Anderson Canc Ctr, Houston, TX
HO Univ Texas, MD Anderson Canc Ctr
ID GROWTH-FACTOR-I; METASTATIC BEHAVIOR; OSTEOGENIC-SARCOMA; RETINOBLASTOMA
GENE; PROGNOSTIC-FACTOR; EXPRESSION; CANCER; HETEROZYGOSITY;
INVOLVEMENT; INHIBITION
AB Studies in osteosarcoma over the past 40 years have led to a steady improvement in the overall outcome of patients with osteosarcoma. In the year 2008, we can expect greater than 60% overall survival for newly diagnosed non-metastatic appendicular osteosarcoma. However, to achieve this current outcome, many patients are treated with aggressive cytotoxic chemotherapy and ultimately are not cured, and some patients who would be curable even without this aggressive approach are likely treated and cured. And finally, patients presenting with metastatic disease and those whose tumors recur after standard approaches continue to do very poorly. We believe that in order to continue to make progress in the treatment of this disease, we must achieve two main objectives. Firstly, we must find biomarkers that prospectively and accurately identify newly diagnosed non-metastatic patients who will not be cured with current modalities.
We hope that the achievement of this goal will allow for innovative clinical studies in this high-risk population while not jeopardizing those patients who currently are cured using the available treatment approaches, and ultimately accelerate progress toward caring more patients. Secondly, we must develop entirely new approaches to the treatment of metastatic and recurrent osteosarcoma. Our approach has been to develop models of highly aggressive and less aggressive osteosarcoma, and to use these models to identify genetic alterations and signaling pathways that distinguish the two phenotypic behaviors. We have identified plasma membrane-cytoskeletal linker protein, ezrin, as one pathway that identifies aggressive biological behavior in mouse and dog osteosarcoma. Using ezrin as the initial discriminator, we have high ezrin expression to activation of mTOR signaling, suggesting a possible novel target for therapy of aggressive osteosarcoma. We have also linked beta 4 integrin signaling to metastatic behavior that also appears to be linked to mTOR signaling. Most recently, we have identified a critical relationship between mTOR signaling and the IGF I signaling pathway that may help point the way to combination targeting therapy aimed at blocking both mTOR and ICF signaling in these tumors. Finally, we have proposed a novel clinical trial design to begin to test agents targeted at recurrent, metastatic disease, and this also will be discussed.
C1 [Kim, Su Young; Helman, Lee J.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Helman, LJ (reprint author), NCI, Ctr Canc Res, NIH, 31 Ctr Dr,MSC 2440, Bethesda, MD 20892 USA.
EM helmanl@mail.nih.gov
NR 34
TC 19
Z9 21
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0927-3042
BN 978-1-4419-0283-2
J9 CANCER TREAT RES
JI Canc. Treat. Res.
PY 2009
VL 152
BP 517
EP 528
DI 10.1007/978-1-4419-0284-9_31
PG 12
WC Oncology; Pediatrics
SC Oncology; Pediatrics
GA BMS92
UT WOS:000273510800031
PM 20213413
ER
PT J
AU Tran, SM
Nobrega, RQ
Kammerer, WA
Quezado, Z
AF Tran, Stephanie M.
Nobrega, Raissa Q.
Kammerer, William A.
Quezado, Zenaide
TI Familial long QT syndrome presented as ventricular tachycardia during
anesthesia
SO PEDIATRIC ANESTHESIA
LA English
DT Letter
ID RISK-FACTORS; SEVOFLURANE; CHILDREN
C1 [Tran, Stephanie M.; Nobrega, Raissa Q.; Kammerer, William A.; Quezado, Zenaide] Natl Inst Hlth, Dept Anesthesia & Surg Serv, Ctr Clin, Bethesda, MD 20892 USA.
RP Tran, SM (reprint author), Natl Inst Hlth, Dept Anesthesia & Surg Serv, Ctr Clin, Bethesda, MD 20892 USA.
EM zquezado@nih.gov
RI Quezado, Zenaide/O-4860-2016
OI Quezado, Zenaide/0000-0001-9793-4368
FU Intramural NIH HHS [ZIA CL009009-02]
NR 5
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1155-5645
J9 PEDIATR ANESTH
JI Pediatr. Anesth.
PD JAN
PY 2009
VL 19
IS 1
BP 66
EP 68
DI 10.1111/j.1460-9592.2008.02821.x
PG 4
WC Anesthesiology; Pediatrics
SC Anesthesiology; Pediatrics
GA 377RC
UT WOS:000261267300030
PM 19076523
ER
PT J
AU Kelly, KM
Thornton, JC
Hughes, D
Osunkwo, I
Weiner, M
Wang, J
Horlick, M
AF Kelly, Kara M.
Thornton, John C.
Hughes, Deborah
Osunkwo, Ifeyinwa
Weiner, Michael
Wang, Jack
Horlick, Mary
TI Total Body Bone Measurements: A Cross-Sectional Study in Children With
Acute Lymphoblastic Leukemia During and Following Completion of Therapy
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE bone mass; bone mineral density; dual-energy X-ray absorptiometry;
pediatrics
ID X-RAY ABSORPTIOMETRY; LONG-TERM SURVIVORS; MINERAL DENSITY; CRANIAL
IRRADIATION; CHILDHOOD; ADOLESCENTS; MASS; PREDNISOLONE; HOMEOSTASIS;
OSTEOPENIA
AB Background. Abnormalities in bone mineral density (BMD) occur in children treated for acute lymphoblastic leukemia (ALL). However, BMD estimates have been performed using varied instruments, reference data, and interpretations. This exploratory cross sectional study to evaluate bone mass in children with ALL, uses an algorithm that serially adjusts for variables known to affect pediatric bone measures by dual energy X-ray absorptiometry (DXA), based on models developed in 1,218 healthy children and adolescents. Procedure. Anthropometry, DXA scans, and factors with possible influence on bone mass were evaluated in 21 ALL patients receiving chemotherapy and 20 in the follow-up phase. Main Outcome was treatment group differences in Z-scores for total body bone mineral content (BMC), bone area (Area), and areal BMD (aBMD). Results. Mean Z-scores for the entire study population for BMC, Area, and aBMD were significantly less than zero. Among possible contributing factors, only calcium intake was a significant co-variate. Comparison between treatment groups showed that least-square mean Z-scores for patients on-therapy for at least 12 months were significantly lower than those off therapy for at least 12 months (P: 0.0008-0.044), except for BMC at last step of the algorithm (adjusted for sex, age, ethnicity, height, weight, and bone area). Conclusions. Evaluation of total body DXA by this algorithm is consistent with better general bone status in those off-therapy. However, in this small exploratory Study, the lack of significant difference between Z-scores for fully adjusted BMC in on- versus off-therapy groups suggests possible risk of low peak bone mass. Additional longitudinal evaluation is warranted. Pediatr Blood Cancer 2009;52:33-38. (c) 2008 Wiley-Liss, Inc.
C1 [Kelly, Kara M.; Hughes, Deborah; Osunkwo, Ifeyinwa; Weiner, Michael] Columbia Univ, Med Ctr, Div Pediat Oncol, Morgan Stanley Childrens Hosp New York Presbyteri, New York, NY 10032 USA.
[Thornton, John C.; Wang, Jack] St Lukes Roosevelt Hosp, Body Composit Unit, New York, NY USA.
[Horlick, Mary] NIDDK, Div Digest Dis & Nutr, Bethesda, MD USA.
RP Kelly, KM (reprint author), Columbia Univ, Med Ctr, Div Pediat Oncol, 161 Ft Washington Ave,Irving Pavil 7, New York, NY 10032 USA.
EM kk291@columbia.edu
FU Joseph LeRoy and Ann C. Warner Fund, Inc.
FX Grant sponsor Joseph LeRoy and Ann C. Warner Fund, Inc.
NR 30
TC 10
Z9 10
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD JAN
PY 2009
VL 52
IS 1
BP 33
EP 38
DI 10.1002/pbc.21760
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 378CZ
UT WOS:000261300000010
PM 18816694
ER
PT J
AU Newth, CJL
Venkataraman, S
Willson, DF
Meert, KL
Harrison, R
Dean, JM
Dean, M
Pollack, M
Zimmerman, J
Anand, KJS
Carcillo, JA
Nicholson, CE
AF Newth, Christopher J. L.
Venkataraman, Shekhar
Willson, Douglas F.
Meert, Kathleen L.
Harrison, Rick
Dean, J. Michael
Dean, Michael
Pollack, Murray
Zimmerman, Jerry
Anand, KanwaIjeet J. S.
Carcillo, Joseph A.
Nicholson, Carol E.
CA Eunice Shriver Kennedy Natl Inst C
TI Weaning and extubation readiness in pediatric patients
SO Pediatric Critical Care Medicine
LA English
DT Article
DE weaning; extubation; mechanical ventilation; respiratory support;
spontaneous breathing
ID RESPIRATORY-DISTRESS-SYNDROME; ACUTE LUNG INJURY; MECHANICALLY
VENTILATED INFANTS; RANDOMIZED CONTROLLED-TRIAL; PREDICTS SUCCESSFUL
EXTUBATION; PRESSURE SUPPORT VENTILATION; MAXIMAL INSPIRATORY PRESSURE;
PLACEBO-CONTROLLED TRIAL; INTENSIVE-CARE PATIENTS; ENDOTRACHEAL-TUBES
AB Objective: A systematic review of weaning and extubation for pediatric patients on mechanical ventilation. Data Selection: Pediatric and adult literature, English language.
Study Selection: Invited review.
Data Sources: Literature review using National Library of Medicine PubMed from January 1972 until April 2008, earlier cross-referenced article citations, the Cochrane Database of Systematic Reviews, and the Internet.
Conclusions: Despite the importance of minimizing time on mechanical ventilation, only limited guidance on weaning and extubation is available from the pediatric literature. A significant proportion of patients being evaluated for weaning are actually ready for extubation, suggesting that weaning is often not considered early enough in the course of ventilation. Indications for extubation are even less clear, although a trial of spontaneous breathing would seem a prerequisite. Several indices have been developed in an attempt to predict weaning and extubation success but the available literature would suggest they offer no improvement over clinical judgment. Extubation failure rates range from 2% to 20% and bear little relationship to the duration of mechanical ventilation. Upper airway obstruction is the single most common cause of extubation failure. A reliable method of assessing readiness for weaning and predicting extubation success is not evident from the pediatric literature. (Pediatr Crit Care Med 2009; 10:1-11)
C1 [Newth, Christopher J. L.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Venkataraman, Shekhar; Carcillo, Joseph A.] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Willson, Douglas F.] Univ Virginia, Dept Pediat, Childrens Hosp, Charlottesville, VA USA.
[Meert, Kathleen L.] Childrens Hosp Michigan, Detroit, MI 48201 USA.
[Harrison, Rick] Mattel Childrens Hosp, Los Angeles, CA USA.
[Dean, J. Michael] Univ Utah, Dept Pediat, Salt Lake City, UT USA.
[Pollack, Murray] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Zimmerman, Jerry] Seattle Childrens Hosp, Seattle, WA USA.
[Anand, KanwaIjeet J. S.] Arkansas Childrens Hosp, Little Rock, AR 72202 USA.
[Nicholson, Carol E.] NICHHD, Bethesda, MD 20892 USA.
RP Newth, CJL (reprint author), Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
EM cnewth@chla.usc.edu
OI Anand, Kanwaljeet/0000-0001-6498-1483
FU NICHD NIH HHS [U10 HD050012, U01 HD049934, U01HD049934, U10 HD049945,
U10 HD049981, U10 HD049983, U10 HD050012-01, U10 HD050012-02, U10
HD050012-03, U10 HD050012-04, U10 HD050012-05, U10 HD050012-06, U10
HD050096, U10HD049945, U10HD049981, U10HD049983, U10HD050012,
U10HD050096, U10HD500009, UG1 HD050096]
NR 87
TC 66
Z9 72
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1529-7535
J9 PEDIATR CRIT CARE ME
JI Pediatr. Crit. Care Med.
PD JAN
PY 2009
VL 10
IS 1
BP 1
EP 11
DI 10.1097/PCC.0b013e318193724d
PG 11
WC Critical Care Medicine; Pediatrics
SC General & Internal Medicine; Pediatrics
GA 396EK
UT WOS:000262574800001
PM 19057432
ER
PT J
AU Moss, WJ
Scott, S
Ndhlovu, Z
Monze, M
Cults, FT
Quinn, TC
Griffin, DE
AF Moss, William J.
Scott, Susana
Ndhlovu, Zaza
Monze, Mwaka
Cults, Felicity T.
Quinn, Thomas C.
Griffin, Diane E.
TI SUPPRESSION OF HUMAN IMMUNODEFICIENCY VIRUS TYPE 1 VIRAL LOAD DURING
ACUTE MEASLES
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE measles; HIV-1
ID REPLICATION; DYNAMICS; CHILDREN; THERAPY
AB Acute measle virus infection call result in a transient decrease in plasma human immunodeficiency virus type 1 (HIV-1) RNA loads. We report the kinetics of plasma HIV-1 RNA loads in 2 Zambian children with confirmed and probable measles, and show that the decline in viral load is of similar magnitude to the first-phase decay rate after initiation of antiretroviral therapy.
C1 [Moss, William J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21218 USA.
[Moss, William J.; Ndhlovu, Zaza; Griffin, Diane E.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Hlth, Baltimore, MD USA.
[Scott, Susana; Cults, Felicity T.] London Sch Hyg & Trop Med, London WC1, England.
[Monze, Mwaka] Univ Teaching Hosp, Virol Lab, Lusaka, Zambia.
[Quinn, Thomas C.] Johns Hopkins Univ, Sch Med, Div Infect Dis, Baltimore, MD 21205 USA.
[Quinn, Thomas C.] NIAID, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Moss, WJ (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St, Baltimore, MD 21218 USA.
EM wmoss@jhsph.edu
FU Wellcome Trust-Burroughs Fund Infectious Disease Initiative
[GR059114MA]; National Institutes of Health [A123047]; NIAID; National
Institutes of Health
FX Supported by grant (GR059114MA) from the Wellcome Trust-Burroughs Fund
Infectious Disease Initiative, grant A123047 from the National
Institutes of Health, and in part by the Division of Intramural
Research, NIAID, National Institutes of Health (to T.C.Q.).
NR 10
TC 8
Z9 9
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD JAN
PY 2009
VL 28
IS 1
BP 63
EP 65
DI 10.1097/INF.0b013e318184eed2
PG 3
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 391QG
UT WOS:000262247200018
PM 19057456
ER
PT J
AU Castro, M
Ramirez, MI
Gern, JE
Cutting, G
Redding, G
Hagood, JS
Whitsett, J
Abman, S
Raj, JU
Barst, R
Kato, GJ
Gozal, D
Haddad, GG
Prabhakar, NR
Gauda, E
Martinez, FD
Tepper, R
Wood, RE
Accurso, F
Teague, WG
Venegas, J
Cole, FS
Wright, RJ
AF Castro, Mario
Ramirez, Maria I.
Gern, James E.
Cutting, Garry
Redding, Greg
Hagood, James S.
Whitsett, Jeffrey
Abman, Steve
Raj, J. Usha
Barst, Robyn
Kato, Gregory J.
Gozal, David
Haddad, Gabriel G.
Prabhakar, Nanduri R.
Gauda, Estelle
Martinez, Fernando D.
Tepper, Robert
Wood, Robert E.
Accurso, Frank
Teague, W. Gerald
Venegas, Jose
Cole, F. Sessions
Wright, Rosalind J.
TI Strategic Plan for Pediatric Respiratory Diseases Research: An NHLBI
Working Group Report
SO PEDIATRIC PULMONOLOGY
LA English
DT Article
DE epigenetics; pediatric; respiratory; lung disease
ID OBSTRUCTIVE SLEEP-APNEA; SICKLE-CELL-DISEASE; GENE-EXPRESSION;
LUNG-FUNCTION; EPIGENETIC REGULATION; INTERMITTENT HYPOXIA; RHINOVIRUS
ILLNESSES; CONSTANT HYPOXIA; CHILDHOOD ASTHMA; SMOKE EXPOSURE
AB The Division of Lung Diseases of the National Heart, Lung and Blood Institute (NHLBI) recently held a workshop to identify gaps in our understanding and treatment of childhood lung diseases and to define strategies to enhance translational research in this field. Leading experts with diverse experience in both laboratory and patient-oriented research reviewed selected areas of pediatric lung diseases, including perinatal programming and epigenetic influences; mechanisms of lung injury, repair, and regeneration; pulmonary vascular disease (PVD); sleep and control of breathing; and the application of novel translational methods to enhance personalized medicine. This report summarizes the proceedings of this workshop and provides recommendations for emphasis on targeted areas for future investigation. The priority areas identified for research in pediatric pulmonary diseases included: (1) epigenetic and environmental influences on lung development that program pediatric lung diseases, (2) injury, regeneration, and repair in the developing lung, (3) PVD in children, (4) development and adaptation of ventilatory responses to postnatal life, (5) nonatopic wheezing: aberrant large airway development or injury? (6) strategies to improve assessment, diagnosis, and treatment of pediatric respiratory diseases, and (7) predictive and personalized medicine for children. PediatrPulmonol.2009;44:2-13. (c) 2008 Wiley-Liss, Inc.
C1 [Castro, Mario] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Ramirez, Maria I.] Boston Univ Med, Boston, MA USA.
[Gern, James E.] Univ Wisconsin, Madison, WI USA.
[Cutting, Garry; Gauda, Estelle] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Redding, Greg] Childrens Hosp & Reg Med Ctr, Seattle, WA USA.
[Hagood, James S.] Univ Alabama, Birmingham, AL USA.
[Whitsett, Jeffrey] Cincinnati Childrens Hosp, Med Ctr, Div Neonatol, Cincinnati, OH USA.
[Whitsett, Jeffrey] Cincinnati Childrens Hosp, Med Ctr, Div Pulm Biol, Cincinnati, OH USA.
[Abman, Steve] Univ Colorado, Sch Med, Denver, CO USA.
[Abman, Steve] Childrens Hosp, Denver, CO 80218 USA.
[Raj, J. Usha] Univ Illinois, Chicago, IL USA.
[Barst, Robyn] Columbia Univ, New York, NY USA.
[Kato, Gregory J.] NHLBI, NIH, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
[Gozal, David] Univ Louisville, Louisville, KY 40292 USA.
[Haddad, Gabriel G.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Prabhakar, Nanduri R.] Univ Chicago, Div Biol Sci, Chicago, IL 60637 USA.
[Martinez, Fernando D.] Univ Arizona, Coll Med, Tucson, AZ USA.
[Tepper, Robert] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Accurso, Frank] Univ Colorado, Pulm Med Cyst Fibrosis Ctr, Denver, CO 80202 USA.
[Teague, W. Gerald] Emory Univ, Atlanta, GA 30322 USA.
[Venegas, Jose] Dept Anesthesia & Crit, Boston, MA USA.
[Cole, F. Sessions] Washington Univ, Sch Med, St Louis, MO USA.
[Wright, Rosalind J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Castro, M (reprint author), Washington Univ, Sch Med, St Louis, MO 63130 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 77
TC 1
Z9 1
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 8755-6863
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD JAN
PY 2009
VL 44
IS 1
BP 2
EP 13
DI 10.1002/ppul.20973
PG 12
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA 393PV
UT WOS:000262386100002
ER
PT J
AU Olivier, KN
AF Olivier, Kenneth N.
TI MANAGEMENT OF NONTUBERCULOUS MYCOBATERIA
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
ID RAPIDLY GROWING MYCOBACTERIA; COMPLEX LUNG-DISEASE; MACROLIDE
RESISTANCE; CYSTIC-FIBROSIS; ABSCESSUS; INFECTION; DIAGNOSIS
C1 [Olivier, Kenneth N.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 13
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 8755-6863
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PY 2009
MA S81
BP 145
EP 146
PG 2
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA 505OL
UT WOS:000270703400029
ER
PT J
AU Glaser, TS
Prevots, DR
de Oca, RM
Holland, SM
Olivier, KN
AF Glaser, T. S.
Prevots, D. R.
de Oca, Montes R.
Holland, S. M.
Olivier, K. N.
TI TOXICITY AND EFFECTIVENESS OF INHALED AMIKACIN FOR REFRACTORY PULMONARY
NONTUBERCULOUS MYCOBACTERIAL DISEASE
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Glaser, T. S.; Prevots, D. R.; de Oca, Montes R.; Holland, S. M.; Olivier, K. N.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 8755-6863
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PY 2009
MA 363
BP 338
EP 339
PG 2
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA 505OL
UT WOS:000270703400442
ER
PT J
AU Tataranni, PA
Pannacciulli, N
Le, DSNT
Del Parigi, A
AF Tataranni, P. Antonio
Pannacciulli, Nicola
Le, Duc Son N. T.
Del Parigi, Angelo
BE Fruhbeck, G
TI Embracing Complexity: The Emergence of Functional Neuroimaging and Other
Methodologies to Study the Role of the Human Brain in the
Pathophysiology of Obesity
SO PEPTIDES IN ENERGY BALANCE AND OBESITY
SE Frontiers in Nutritional Science
LA English
DT Article; Book Chapter
ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL-BLOOD-FLOW; PRIMATE ORBITOFRONTAL
CORTEX; IN-VIVO; EATING-DISORDERS; ENERGY HOMEOSTASIS; ANOREXIA-NERVOSA;
GENE-EXPRESSION; FOOD; DOPAMINE
C1 [Tataranni, P. Antonio; Pannacciulli, Nicola; Le, Duc Son N. T.; Del Parigi, Angelo] NIDDK, NIH, US Dept HHS, Phoenix, AZ USA.
RP Tataranni, PA (reprint author), NIDDK, NIH, US Dept HHS, Phoenix, AZ USA.
NR 82
TC 0
Z9 0
U1 0
U2 1
PU CABI PUBLISHING-C A B INT
PI WALLINGFORD
PA CABI PUBLISHING, WALLINGFORD 0X10 8DE, OXON, ENGLAND
BN 978-1-84593-407-1
J9 FRONT NUTR SCI
PY 2009
IS 4
BP 309
EP 329
DI 10.1079/9781845934071.0309
PG 21
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA BWI65
UT WOS:000293952700013
ER
PT J
AU Kriegeskorte, N
AF Kriegeskorte, N.
TI Characterizing categorical and continuous visual-object codes in man,
monkey, and computational models with representational similarity
analysis
SO PERCEPTION
LA English
DT Meeting Abstract
C1 [Kriegeskorte, N.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
EM kriegeskorten@mail.nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 3
PU PION LTD
PI LONDON
PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND
SN 0301-0066
J9 PERCEPTION
JI Perception
PY 2009
VL 38
SU S
BP 62
EP 62
PG 1
WC Ophthalmology; Psychology; Psychology, Experimental
SC Ophthalmology; Psychology
GA V16YN
UT WOS:000207905000201
ER
PT J
AU Yue, X
Holt, DJ
Cassidy, BS
Devaney, KJ
Tootell, RBH
AF Yue, X.
Holt, D. J.
Cassidy, B. S.
Devaney, K. J.
Tootell, R. B. H.
TI Face selectivity is parameter-dependent in FFA
SO PERCEPTION
LA English
DT Meeting Abstract
C1 [Yue, X.; Devaney, K. J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Martinos Ctr Biomed Imaging, Boston, MA USA.
[Holt, D. J.; Cassidy, B. S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA USA.
[Tootell, R. B. H.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
EM xiaomin@nmr.mgh.harvard.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PION LTD
PI LONDON
PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND
SN 0301-0066
J9 PERCEPTION
JI Perception
PY 2009
VL 38
SU S
BP 80
EP 80
PG 1
WC Ophthalmology; Psychology; Psychology, Experimental
SC Ophthalmology; Psychology
GA V16YN
UT WOS:000207905000258
ER
PT J
AU Maier, A
Aura, C
Leopold, DA
AF Maier, A.
Aura, C.
Leopold, D. A.
TI Visual awareness correlates with layer-specific activity in primary
visual cortex
SO PERCEPTION
LA English
DT Meeting Abstract
C1 [Maier, A.] NIMH, NIH, Unit Cognit Neurophyiol & Imaging, Birmingham, AL USA.
[Leopold, D. A.] NIMH, NIH, Neurophysiol Imaging Facil, LN, Birmingham, AL USA.
[Aura, C.] Univ Alabama, Grad Program Neurosci, Birmingham, AL USA.
EM maiera@mail.nih.gov
RI Maier, Alexander/B-7489-2009
OI Maier, Alexander/0000-0002-7250-502X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PION LTD
PI LONDON
PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND
SN 0301-0066
J9 PERCEPTION
JI Perception
PY 2009
VL 38
SU S
BP 162
EP 162
PG 1
WC Ophthalmology; Psychology; Psychology, Experimental
SC Ophthalmology; Psychology
GA V16YN
UT WOS:000207905000527
ER
PT J
AU Cumming, B
AF Cumming, Bruce
TI PMF: Climbing the disparity gradient for twenty years
SO PERCEPTION
LA English
DT Editorial Material
ID BINOCULAR DISPARITY; STEREO VISION; LIMIT; TRANSPARENCY; PERCEPTION
C1 NIH, Lab Sensory Motor Res, Bethesda, MD 20892 USA.
RP Cumming, B (reprint author), NIH, Lab Sensory Motor Res, Bethesda, MD 20892 USA.
EM bgc@lsr.nei.nih.gov
NR 14
TC 0
Z9 0
U1 0
U2 1
PU PION LTD
PI LONDON
PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND
SN 0301-0066
J9 PERCEPTION
JI Perception
PY 2009
VL 38
IS 6
BP 885
EP 887
PG 3
WC Ophthalmology; Psychology; Psychology, Experimental
SC Ophthalmology; Psychology
GA 479XQ
UT WOS:000268695900029
PM 19806977
ER
PT J
AU Bornstein, MH
Gungor, D
AF Bornstein, Marc H.
Gungor, Derya
BA Bekman, S
AksuKoc, A
BF Bekman, S
AksuKoc, A
TI Organizing principles and processes from developmental science for
culture and caregiving
SO PERSPECTIVES ON HUMAN DEVELOPMENT, FAMILY, AND CULTURE
LA English
DT Article; Book Chapter
ID UNITED-STATES; INTERGENERATIONAL TRANSMISSION; CHINESE CHILDREN; JAPAN;
FRANCE; SOCIALIZATION; ARGENTINA; TODDLERS; BEHAVIOR; OUTCOMES
C1 [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res Program Dev Neurosci, Washington, DC USA.
[Bornstein, Marc H.] NICHHD, Washington, DC USA.
[Gungor, Derya] Univ Louvain, Dept Psychol, Louvain, Belgium.
[Gungor, Derya] Univ Utrecht, NL-3508 TC Utrecht, Netherlands.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res Program Dev Neurosci, Washington, DC USA.
NR 62
TC 0
Z9 0
U1 0
U2 1
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-0-521-87672-8
PY 2009
BP 69
EP 85
DI 10.1017/CBO9780511720437.008
D2 10.1017/CBO9780511720437
PG 17
WC Psychology, Developmental
SC Psychology
GA BBI90
UT WOS:000306999700007
ER
PT B
AU Russell, DG
Gordon, S
AF Russell, David G.
Gordon, Siamon
BE Russell, DG
Gordon, S
TI Phagocyte-Pathogen Interactions Macrophages and the Host Response to
Infection Preface
SO PHAGOCYTE-PATHOGEN INTERACTIONS: MACROPHAGES AND THE HOST RESPONSE TO
INFECTION
LA English
DT Editorial Material; Book Chapter
C1 [Russell, David G.] Cornell Univ, Coll Vet Med, Ithaca, NY 14853 USA.
[Gordon, Siamon] NCI, NIH, Frederick, MD 21702 USA.
[Gordon, Siamon] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
RP Russell, DG (reprint author), Cornell Univ, Coll Vet Med, Ithaca, NY 14853 USA.
NR 3
TC 10
Z9 10
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA
BN 978-1-55581-401-4
PY 2009
BP XIII
EP XIV
PG 2
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA BKL73
UT WOS:000268445000002
ER
PT B
AU Vinh, DC
Holland, SM
AF Vinh, Donald C.
Holland, Steven M.
BE Russell, DG
Gordon, S
TI Macrophage Classical Activation
SO PHAGOCYTE-PATHOGEN INTERACTIONS: MACROPHAGES AND THE HOST RESPONSE TO
INFECTION
LA English
DT Article; Book Chapter
ID CHRONIC GRANULOMATOUS-DISEASE; INTERFERON-GAMMA-RECEPTOR;
TUMOR-NECROSIS-FACTOR; WISKOTT-ALDRICH-SYNDROME; FACTOR-KAPPA-B;
ANHIDROTIC ECTODERMAL DYSPLASIA; MYCOBACTERIAL PHAGOSOME MATURATION;
CALMETTE-GUERIN INFECTION; PHAGOCYTIC CUP FORMATION; SMALL DELETION
HOTSPOT
C1 [Vinh, Donald C.; Holland, Steven M.] NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Vinh, DC (reprint author), NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 202
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA
BN 978-1-55581-401-4
PY 2009
BP 301
EP 323
PG 23
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA BKL73
UT WOS:000268445000021
ER
PT B
AU Allen, JE
Wynn, TA
AF Allen, Judith E.
Wynn, Thomas A.
BE Russell, DG
Gordon, S
TI Macrophages in Helminth Infection: Effectors, Regulators, and Wound
Healers
SO PHAGOCYTE-PATHOGEN INTERACTIONS: MACROPHAGES AND THE HOST RESPONSE TO
INFECTION
LA English
DT Article; Book Chapter
ID ALTERNATIVELY ACTIVATED MACROPHAGES; NITRIC-OXIDE SYNTHASE;
SCHISTOSOMA-MANSONI EGGS; ANTIGEN-PRESENTING CELLS; CD4(+) T-CELLS;
MIGRATION INHIBITORY FACTOR; SELECTIVE UP-REGULATION; AMINO-ACID
TRANSPORTER; GROWTH-FACTOR-BETA; BRUGIA-MALAYI
C1 [Allen, Judith E.] Univ Edinburgh, Inst Evolut Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland.
[Wynn, Thomas A.] NIAID, Immunopathogenesis Sect, NIH, Bethesda, MD 20892 USA.
RP Allen, JE (reprint author), Univ Edinburgh, Inst Evolut Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland.
NR 170
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA
BN 978-1-55581-401-4
PY 2009
BP 477
EP 490
PG 14
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA BKL73
UT WOS:000268445000033
ER
PT J
AU Betz, JM
AF Betz, Joseph M.
TI SAFETY, CAUSALITY, AND ASSOCIATION: CHALLENGES IN INVESTIGATING ADVERSE
EVENTS
SO PHARMACEUTICAL BIOLOGY
LA English
DT Meeting Abstract
C1 [Betz, Joseph M.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
EM betzj@od.nih.gov
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 1388-0209
J9 PHARM BIOL
JI Pharm. Biol.
PY 2009
VL 47
BP 14
EP 15
PG 2
WC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
SC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
GA 403OZ
UT WOS:000263093200039
ER
PT J
AU Cardellina, JH
AF Cardellina, John H., II
TI BLACK COHOSH: CONSIDERATIONS OF SAFETY AND BENEFIT
SO PHARMACEUTICAL BIOLOGY
LA English
DT Meeting Abstract
C1 [Cardellina, John H., II] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
EM jhcardellina@aol.com
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 1388-0209
J9 PHARM BIOL
JI Pharm. Biol.
PY 2009
VL 47
BP 22
EP 22
PG 1
WC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
SC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
GA 403OZ
UT WOS:000263093200060
ER
PT J
AU Betz, JM
Saldanha, LG
Fisher, KD
Coates, PM
Klein, M
Engel, J
Pho, AN
Sharpless, KE
Sander, LC
Wise, SA
Rimmer, CA
Phinney, K
AF Betz, J. M.
Saldanha, L. G.
Fisher, K. D.
Coates, P. M.
Klein, M.
Engel, J.
Pho, A. Nguyen
Sharpless, K. E.
Sander, L. C.
Wise, S. A.
Rimmer, C. A.
Phinney, K.
TI THE NIH/ODS ANALYTICAL METHODS AND REFERENCE MATERIALS PROGRAM FOR
DIETARY SUPPLEMENTS: FIVE-YEAR ACCOMPLISHMENTS AND FUTURE DIRECTIONS
SO PHARMACEUTICAL BIOLOGY
LA English
DT Meeting Abstract
C1 [Betz, J. M.; Saldanha, L. G.; Fisher, K. D.; Coates, P. M.; Klein, M.; Engel, J.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Pho, A. Nguyen] US FDA, Silver Spring, MD 20993 USA.
[Sharpless, K. E.; Sander, L. C.; Wise, S. A.; Rimmer, C. A.; Phinney, K.] Natl Inst Stand & Technol, Gaithersburg, MD 20899 USA.
EM betzj@od.nih.gov
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 1388-0209
J9 PHARM BIOL
JI Pharm. Biol.
PY 2009
VL 47
BP 29
EP 29
PG 1
WC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
SC Plant Sciences; Medical Laboratory Technology; Pharmacology & Pharmacy
GA 403OZ
UT WOS:000263093200079
ER
PT J
AU Hirunsatit, R
George, ED
Lipska, BK
Elwafi, HM
Sander, L
Yrigollen, CM
Gelernter, J
Grigorenko, EL
Lappalainen, J
Mane, S
Nairn, AC
Kleinman, JE
Simen, AA
AF Hirunsatit, Rungnapa
George, Elizabeth D.
Lipska, Barbara K.
Elwafi, Hani M.
Sander, Lisa
Yrigollen, Carolyn M.
Gelernter, Joel
Grigorenko, Elena L.
Lappalainen, Jaakko
Mane, Shrikant
Nairn, Angus C.
Kleinman, Joel E.
Simen, Arthur A.
TI Twenty-one-base-pair insertion polymorphism creates an enhancer element
and potentiates SLC6A1 GABA transporter promoter activity
SO PHARMACOGENETICS AND GENOMICS
LA English
DT Article
DE African continental ancestry group; enhancer elements;
gamma-aminobutyric acid plasma membrane transport proteins;
transcription factors; zinc fingers
ID MAGNETIC-RESONANCE-SPECTROSCOPY; TRANSCRIPTION FACTOR ZBP-89;
DEPRESSED-PATIENTS; UPTAKE INHIBITOR; GENE-EXPRESSION; VIMENTIN GENE;
OPEN-LABEL; TIAGABINE; ANXIETY; BRAIN
AB Objective Sodium-dependent and chloride-dependent gamma-aminobutyric acid (GABA) transporter 1 (SLC6A1) is the target of a number of drugs of clinical importance and is a major determinant of synaptic GABA concentrations. We resequenced the human SLC6A1 gene previously and discovered a novel 21 bp insertion in the predicted promoter region that creates a second tandem copy of the sequence. Here we sought to determine the functional relevance of this variation.
Methods We used reporter assays, mobility shift assays, quantitative PCR, and proteomics methods as well as postmortem expression analysis for this work.
Results Reporter assays showed that the insertion allele significantly increases promoter activity in multiple cell lines. The zinc finger transcription factor ZNF148 was found to significantly transactivate the promoter and increase expression when overexpressed but could not account for the differences in activity between the two alleles of the promoter. Copy number of the insertion sequence was associated with exponentially increasing activity of a downstream promoter, suggesting that the insertion sequence has enhancer activity when present in multiple copies. SLC6A1 promoter genotype was found to predict SLC6A1 RNA expression in human postmortem hippocampal samples. These results suggest that the insertion polymorphism leads to increased SLC6A1 promoter activity because, in part, of creation of an enhancer element when present as multiple copies. Genotyping individuals from Tanzania in this study suggested that the insertion allele has its origin in Africa.
Conclusion On account of the effect of the insertion on promoter activity, this relatively common polymorphism may prove useful in predicting clinical response to pharmacological modulators of SLC6A1 as well as GABAergic function in individuals of African descent. Pharmacogenetics and Genomics 19:53-65 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.
C1 [Simen, Arthur A.] Yale Univ, Sch Med, Div Mol Psychiat, Dept Psychiat, New Haven, CT 06511 USA.
[Yrigollen, Carolyn M.; Grigorenko, Elena L.] Yale Univ, Sch Med, Psychol & Child Study Ctr, New Haven, CT 06511 USA.
[Mane, Shrikant] Yale Univ, Sch Med, Yale Keck Ctr, New Haven, CT 06511 USA.
[Hirunsatit, Rungnapa; Gelernter, Joel; Lappalainen, Jaakko] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Lipska, Barbara K.; Kleinman, Joel E.] NIMH, Sect Neuropathol, Clin Brain Disorders Branch, GCAP,IRP,NIH, Bethesda, MD 20892 USA.
RP Simen, AA (reprint author), Yale Univ, Sch Med, Div Mol Psychiat, Dept Psychiat, Suite 901, New Haven, CT 06511 USA.
EM Arthur.Simen@yale.edu
OI Nairn, Angus/0000-0002-7075-0195
FU NIH [D43 TW06166, 1KL2RR024138, T32-MH14276, U24 NS051869]; VA REAP
Award; NCRR [RR19895]; NARSAD Young Investigator Award; NIDA [DA018343];
Fogarty Program [TW006764]; NICHD; Yale/NIDA Proteomics Center
FX R.H. was supported by NIH grant D43 TW06166 and a VA REAP Award. A.S.
was supported by NIH grant 1KL2RR024138, NCRR grant RR19895, a NARSAD
Young Investigator Award, and a VA REAP Award. A.S. and A.N. were
supported by NIDA grant DA018343. L.D.G. was supported by NIH grant
T32-MH14276. E.L.G. and C.Y were supported by grant TW006764 (PI:
Grigorenko) from the Fogarty Program, NIH and HD048830 (PI: Pugh) from
NICHD. J.G. was supported in part by a VA REAP Award. The authors would
like to acknowledge the support of the Yale/NIH Neuroscience Microarray
Center supported by NIH grant U24 NS051869. The authors thank Kathy
Stone and Terence Wu from the Yale/NIDA Proteomics Center as well as
Maya M. Davis. We thank Dr Thomas M. Hyde for his Involvement in
creating the brain collection and his neuroanatomical expertise, and Ms
Samhita Kumar and Mr Ross Buerlein for their technical support.
NR 33
TC 13
Z9 14
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1744-6872
J9 PHARMACOGENET GENOM
JI Pharmacogenet. Genomics
PD JAN
PY 2009
VL 19
IS 1
BP 53
EP 65
DI 10.1097/FPC.0b013e328318b21a
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
& Pharmacy
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
& Pharmacy
GA 393AE
UT WOS:000262342500006
PM 19077666
ER
PT J
AU Surh, LC
Lesko, LJ
Hobbs, S
Gutman, S
Minasian, LM
Della Pasqua, OE
Austin, MJF
Lu, K
AF Surh, Linda C.
Lesko, Lawrence J.
Hobbs, Stuart
Gutman, Steve
Minasian, Lori M.
Della Pasqua, Oscar E.
Austin, M. J. Finley
Lu, Kan
TI Fit-for-purpose pharmacogenomic biomarkers in drug development: a
project team case study with 'what-ifs'
SO PHARMACOGENOMICS
LA English
DT Article
DE biomarkers; drug development; pharmacogenetics; pharmacogenomics;
Product Label; SPC; Summary of Product Characteristics; USPI; US
Prescribing Information
AB Over the past four years, the annual US FDA-DIA pharmacogenomic workshops have brought together attendees with wide-ranging expertise spanning industry, regulatory authorities and academia. This special report summarizes a breakout session using a novel, interactive case format as a way to engage participants, raise awareness and share diverse learnings via 'real life' decisions that project teams might face in developing a new medicine. This case was situated just prior to approval by a Regulatory Authority as a project team is finalizing a new medicine label. To effectively integrate new biomarkers such as pharmacogenomics into developing new medicines, this session highlighted the importance in considering medical practice implications as relevant (or not) to information or actions by a prescriber; progressing validation beyond assay to clinical; and fitting pharmacogenomics into context with other evidence often built over decades during a drug's development. All converge onto a label that must communicate evidence-based use of a new medicine that is effective and safe.
C1 [Surh, Linda C.] GlaxoSmithKline Inc, CEDD, Global Regulatory Affairs Neurol & Pharmacogenet, Greenford UB6 0HE, Middx, England.
[Lesko, Lawrence J.] US FDA, Off Clin Pharmacol, CDER, Rockville, MD 20857 USA.
[Hobbs, Stuart; Lu, Kan] GlaxoSmithKline Inc, Strateg Prod Labelling, Res Triangle Pk, NC USA.
[Gutman, Steve] US FDA, Off In Vitro Diagonost, CDRH, Rockville, MD 20857 USA.
[Minasian, Lori M.] NCI, NIH, Bethesda, MD 20892 USA.
[Della Pasqua, Oscar E.] GlaxoSmithKline Inc, Res Triangle Pk, NC USA.
RP Surh, LC (reprint author), GlaxoSmithKline Inc, CEDD, Global Regulatory Affairs Neurol & Pharmacogenet, Greenford Rd, Greenford UB6 0HE, Middx, England.
EM lcs29779@gsk.com
NR 4
TC 4
Z9 5
U1 0
U2 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1462-2416
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD JAN
PY 2009
VL 10
IS 1
BP 137
EP 147
DI 10.2217/14622416.10.1.137
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 396BR
UT WOS:000262567700019
PM 19102723
ER
PT J
AU Greenwell, TN
Walker, BM
Cottone, P
Zorrilla, EP
Koob, GF
AF Greenwell, Thomas N.
Walker, Brendan M.
Cottone, Pietro
Zorrilla, Eric P.
Koob, George F.
TI The alpha(1) adrenergic receptor antagonist prazosin reduces heroin
self-administration in rats with extended access to heroin
administration
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Drug abuse; Escalation; Opiate; Norepinephrine; alpha-1 receptor
ID PHENYLPROPANOLAMINE-INDUCED ANOREXIA; CORTICOTROPIN-RELEASING-FACTOR;
POSTTRAUMATIC-STRESS-DISORDER; OPIATE-WITHDRAWAL; STRIA TERMINALIS;
DEPENDENT RATS; BED NUCLEUS; FEEDING PATTERNS; COCAINE SEEKING;
LOCUS-COERULEUS
AB Previous studies have reported that noradrenergic antagonists alleviate some of the symptoms of opiate withdrawal and dependence. Clinical studies also have shown that modification of the noradrenergic system may help protect patients from relapse. The present study tested the hypothesis that a dysregulated noradrenergic system has motivational significance in heroin self-administration of dependent rats. Prazosin. an alpha(1)-adrenergic antagonist (0.5, 1.0, 1.5 and 2.0 mg/kg, i.p.), was administered to adult male Wistar rats with a history of limited (1 h/day: short access) or extended (12 h/day; long access) access to intravenous heroin self-administration. Prazosin dose-dependently reduced heroin self-administration in long-access rats but not short-access rats, with 2 mg/kg of systemic prazosin significantly decreasing 1 and 2 h heroin intake. Prazosin also reversed some changes in meal pattern associated with extended heroin access. including the taking of smaller and briefer meals (at 3 h), while also increasing total food intake and slowing the eating rate within meals (both 3 h and 12 h). Thus. prazosin appears to stimulate food intake in extended access rats by restoring meals to the normal size and duration. The data Suggest that the alpha(1) adrenergic system may contribute to mechanisms that promote dependence in rats with extended access. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Greenwell, Thomas N.; Walker, Brendan M.; Cottone, Pietro; Zorrilla, Eric P.; Koob, George F.] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
RP Greenwell, TN (reprint author), NIAAA, Div Neurosci & Behav, 5635 Fishers Lane,Room 2052,MSC 9304, Bethesda, MD 20892 USA.
EM greenwellt@mail.nih.gov
RI Cottone, Pietro/F-5291-2012; Walker, Brendan /B-9219-2011; koob,
george/P-8791-2016;
OI Cottone, Pietro/0000-0003-1320-1672; Walker, Brendan
/0000-0002-7217-3950; Greenwell, Thomas/0000-0001-6069-0064
FU National Institutes of Health [DA019295]; National Institute on Drug
Abuse [DA004043]; Pearson Center for Alcoholism and Addiction Research
FX Supported by National Institutes of Health grants DA019295 (1732 to TNG)
and DA004043 (GFK) from the National Institute on Drug Abuse and the
Pearson Center for Alcoholism and Addiction Research. The authors thank
Mr. Robert Lititz for excellent technical assistance and Mr. Michael
Arends for editorial assistance.
NR 58
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U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD JAN
PY 2009
VL 91
IS 3
BP 295
EP 302
DI 10.1016/j.pbb.2008.07.012
PG 8
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 402LF
UT WOS:000263014500005
PM 18703080
ER
PT J
AU May, JA
Sharif, NA
Chen, HH
Liao, JC
Kelly, CR
Glennon, RA
Young, R
Li, JX
Rice, KC
France, CR
AF May, Jesse A.
Sharif, Najam A.
Chen, Hwang-Hsing
Liao, John C.
Kelly, Curtis R.
Glennon, Richard A.
Young, Richard
Li, Jun-Xu
Rice, Kenner C.
France, Charles R.
TI Pharmacological properties and discriminative stimulus effects of a
novel and selective 5-HT2 receptor agonist AL-38022A
[(S)-2-(8,9-dihydro-7H-pyrano[2,3-g]indazol-1-yl)-1-methylethylamine]
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Drug discrimination; 5-HT2 receptor; R-DOI; DOM; MDL 100907; Rat; Monkey
ID OCULAR HYPOTENSIVE ACTIVITY; RELATIVE EFFICACY; BINDING; ACTIVATION;
LIGANDS; CELLS; RAT; DOM; HALLUCINOGENS; ANTAGONIST
AB AL-38022A is a novel synthetic serotonergic (5-HT) ligand that exhibited high affinity for each of the 5-HT2 receptor subtypes (K-i <= 2.2 nM), but a significantly lower (> 100-fold less) affinity for other 5-HT receptors. In addition, AL-38022A displayed a very low affinity for a broad array of other receptors, neurotransmitter transport sites, ion channels, and second messenger elements, making it a relatively selective agent. AL-38022A potently stimulated functional responses via native and cloned rat (EC50 range: 1.9-22.5 nM) and human (EC5o range: 0.5-2.2 nM) 5-HT2 receptor subtypes including [Ca2+](i) mobilization and tissue contractions with apparently similar potencies and intrinsic activities and was a full agonist at all 5-HT2 receptor subtypes. The CNS activity of AL-38022A was assessed by evaluating its discriminative stimulus effects in both a rat and a monkey drug discrimination paradigm using DOM as the training drug. AL-38022A fully generalized to the DOM stimulus in each of these Studies; in monkeys MDL 100907 antagonized both DOM and AL-38022A. The pharmacological profile of AL-38022A suggests that it could be a useful tool in defining 5-HT2 receptor signaling and receptor characterization where 5-HT may function as a neurotransmitter. (c) 2008 Elsevier Inc, All rights reserved.
C1 [May, Jesse A.; Sharif, Najam A.; Chen, Hwang-Hsing; Liao, John C.; Kelly, Curtis R.] Alcon Res Ltd, Ophthalmol Discovery, Ft Worth, TX 76134 USA.
[Glennon, Richard A.; Young, Richard] Virginia Commonwealth Univ, Dept Med Chem, Sch Pharm, Richmond, VA 23298 USA.
[Li, Jun-Xu; France, Charles R.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, NIH, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, NIH, Bethesda, MD 20892 USA.
RP May, JA (reprint author), Alcon Res Ltd, Ophthalmol Discovery, Mail Stop R2-39,6201 South Freeway, Ft Worth, TX 76134 USA.
EM jesse.may@alconlabs.com
RI Li, Jun-Xu/K-9192-2013
FU Intramural research Program of the NIDA; NIAAA; NIDDKD
FX The authors thank Parvaneh Katoli, Gary Williams, and Shouxi Xu of ARL
Molecular Pharmacology Unit for their expert technical assistance. We
thank Dr. Philip Kastner of ARL In Vivo Pharmacology Unit for helpful
discussions. Organix, Inc., Woburn, MA, conducted scale-up synthesis.
This research was supported in part by the Intramural research Program
of the NIDA, the NIAAA and the NIDDKD.
NR 40
TC 6
Z9 6
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD JAN
PY 2009
VL 91
IS 3
BP 307
EP 314
DI 10.1016/j.pbb.2008.07.015
PG 8
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 402LF
UT WOS:000263014500007
PM 18718483
ER
PT J
AU Mathur, P
Graybeal, C
Feyder, M
Davis, MI
Holmes, A
AF Mathur, Poonam
Graybeal, Carolyn
Feyder, Michael
Davis, Margaret I.
Holmes, Andrew
TI Fear memory impairing effects of systemic treatment with the NMDA NR2B
subunit antagonist, Ro 25-6981, in mice: Attenuation with ageing
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Aged; Anxiety; Glutamate; Learning; Memory; NR2A; Prepulse inhibition;
Open field; Elevated plus-maze; One-trial; Western blot; C57BL/6
ID LONG-TERM-POTENTIATION; RECEPTOR EPSILON-1 SUBUNIT; AGE-RELATED-CHANGES;
SYNAPTIC PLASTICITY; LATERAL AMYGDALA; BASOLATERAL AMYGDALA; TETRAMERIC
STRUCTURE; PREPULSE INHIBITION; ALZHEIMERS-DISEASE; VISUAL-CORTEX
AB N-methyl-D-aspartate receptors (NMDARs) are mediators of synaptic plasticity and learning and are implicated in the pathophysiology Of neuropsychiatric disease and age-related cognitive dysfunction. NMDARs are heteromers, but the relative contribution of specific subunits to NMDAR-mediated learning is not fully understood. We characterized pre-conditioning systemic treatment of the NR2B subunit-selective antagonist Ro 25-6981 for effects on multi-trial, one-trial and low-shock Pavlovian fear conditioning in C57BL/6J mice. Ro 25-6981 was also profiled for effects on novel open field exploration, elevated plus-maze anxiety-like behavior, startle reactivity, prepulse inhibition of startle, and nociception. Three-month (adult) and 12-month old C57BL/6Tac mice were compared for Ro 25-6981 effects on multi-trial fear conditioning. and corticolimbic NR2B protein levels. Ro 25-6981 moderately impaired fear learning in the multi-trial and one-trial (but not low-shock) conditioning paradigms, but did not affect exploratory or anxiety-related behaviors or sensory functions. Memory impairing effects of Ro 25-6981 were absent in 12-month old mice, although NR2B protein levels were not significantly altered. Present data provide further evidence of the memory impairing effects of selective blockade of NR2B-containing NMDARs, and show loss of these effects with ageing. This work could ultimately have implications for elucidating the pathophysiology of learning dysfunction in neuropsychiatric disorders and ageing. Published by Elsevier Inc.
C1 [Mathur, Poonam; Graybeal, Carolyn; Feyder, Michael; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, Rockville, MD 20852 USA.
[Davis, Margaret I.] NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, Rockville, MD 20852 USA.
RP Holmes, A (reprint author), NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, 5625 Fishers Lane,Room 2N09, Rockville, MD 20852 USA.
EM holmesan@mail.nih.gov
RI Davis, Margaret/F-4165-2010;
OI Davis, Margaret/0000-0002-0489-8351
FU National Institute of Alcohol Abuse and Alcoholism [Z01-AA000411]
FX We would like to thank Dr. Stan Floresco for comments on an earlier
version of the manuscript. Research Supported by the Intramural Research
Program of the National Institute of Alcohol Abuse and Alcoholism
(Z01-AA000411).
NR 83
TC 20
Z9 25
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD JAN
PY 2009
VL 91
IS 3
BP 453
EP 460
DI 10.1016/j.pbb.2008.08.028
PG 8
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 402LF
UT WOS:000263014500029
PM 18809426
ER
PT J
AU Estes, KE
Penzak, SR
Calis, KA
Walsh, TJ
AF Estes, Kristina E.
Penzak, Scott R.
Calis, Karim Anton
Walsh, Thomas J.
TI Pharmacology and Antifungal Properties of Anidulafungin, a New
Echinocandin
SO PHARMACOTHERAPY
LA English
DT Review
DE anidulafungin; echinocandins; candidemia; invasive candidiasis;
esophageal candidiasis
ID PERSISTENTLY NEUTROPENIC RABBITS; EXPERIMENTAL PULMONARY ASPERGILLOSIS;
IN-VITRO; MICAFUNGIN FK463; INVASIVE ASPERGILLOSIS; CANDIDA-ALBICANS;
ESOPHAGEAL CANDIDIASIS; DOSE PHARMACOKINETICS; AMPHOTERICIN-B;
CASPOFUNGIN
AB Anidulafungin is the third echinocandin antifungal agent to receive approval from the United States Food and Drug Administration. It is indicated for the treatment of esophageal candidiasis, candidemia, and other candidal infections. Anidulafungin is fungicidal against Candida species, including Candida glabrata and isolates resistant to azoles and. polyenes. The drug's efficacy is comparable to that of fluconazole for the treatment of esophageal candidiasis, and it is effective in patients with invasive candidiasis and candidemia. Anidulafungin is distinct among the echinocandins in that it undergoes slow, nonenzymatic chemical degradation. As a consequence, impairments in renal or hepatic function do not substantially alter its pharmacokinetics. In addition, anidulafungin has not demonstrated any drug-drug interactions because it is not a substrate, inhibitor, or inducer of the cytochrome P450 enzyme system. Anidulafungin is well tolerated ill adults and pediatric patients, with few reported adverse drug events. The safety, tolerability, and potent fungicidal activity of anidulafungin against Candida species make it a reasonable alternative in the treatment of patients with serious candidal infections.
C1 [Walsh, Thomas J.] NCI, Immunocompromised Host Sect, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Estes, Kristina E.; Penzak, Scott R.; Calis, Karim Anton] NCI, Ctr Clin, Dept Pharm, NIH, Bethesda, MD 20892 USA.
RP Walsh, TJ (reprint author), NCI, Immunocompromised Host Sect, Pediat Oncol Branch, 10 Ctr Dr,1-5740, Bethesda, MD 20892 USA.
NR 66
TC 16
Z9 17
U1 1
U2 3
PU PHARMACOTHERAPY PUBLICATIONS INC
PI BOSTON
PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA
SN 0277-0008
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD JAN
PY 2009
VL 29
IS 1
BP 17
EP 30
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 392HS
UT WOS:000262294400004
PM 19113794
ER
PT J
AU Kwok, RK
Linet, MS
Chodick, G
Kleinerman, RA
Freedman, DM
Fears, T
Johnson, RE
Alexander, BH
AF Kwok, Richard K.
Linet, Martha S.
Chodick, Gabriel
Kleinerman, Ruth A.
Freedman, Daryl M.
Fears, Tom
Johnson, Ruby E.
Alexander, Bruce H.
TI Simplified Categorization of Outdoor Activities for Male and Female US
Indoor Workers-A Feasibility Study to Improve Assessment of Ultraviolet
Radiation Exposures in Epidemiologic Study Questionnaires
SO PHOTOCHEMISTRY AND PHOTOBIOLOGY
LA English
DT Article
ID SKIN-CANCER; RADIOLOGIC TECHNOLOGISTS; MULTIPLE-SCLEROSIS; UV-RADIATION;
SUN EXPOSURE; VITAMIN-D; MELANOMA; SUNLIGHT; RISK; RELIABILITY
AB Skin cancer studies depend on questionnaires to estimate exposure to ultraviolet light and subsequent risk but are limited by recall bias. We investigate the feasibility of developing a short checklist of categories comprising outdoor activities that can improve sun exposure questionnaires for use in epidemiologic studies. We recruited 124 working and retired U.S. radiologic technologists (52% women). Each subject was instructed to complete a daily activity diary, listing main indoor and outdoor activities between 9:00 A.M. and 5:00 P.M. during a 7 day period. A total of 4697 entries were associated with 1408 h (21.1%) of the total 6944 h spent outdoors. We were able to classify the activities into seven main activity categories: driving, yard work, home-maintenance, walking or performing errands, water activities, other recreational or sports activities and leisure activities or relaxing outside. These activities accounted for more than 94% of time spent outdoors both for working and retired men and women. Our data document the feasibility and guidance for developing a short checklist of outdoor activities for use in epidemiologic questionnaires for estimating sunlight exposures of working and retired indoor workers.
C1 [Kwok, Richard K.; Johnson, Ruby E.] RTI Int, Stat & Epidemiol Div, Res Triangle Pk, NC USA.
[Linet, Martha S.; Chodick, Gabriel; Kleinerman, Ruth A.; Freedman, Daryl M.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Fears, Tom] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Alexander, Bruce H.] Univ Minnesota, Div Environm Hlth Sci, Minneapolis, MN USA.
RP Kwok, RK (reprint author), RTI Int, Stat & Epidemiol Div, Res Triangle Pk, NC USA.
EM rkwok@rti.org
RI Kwok, Richard/B-6907-2017;
OI Kwok, Richard/0000-0002-6794-8360; Kleinerman, Ruth/0000-0001-7415-2478
FU National Cancer Institute [N02-CP-31013]
FX The authors gratefully acknowledge the participation of the USRT cohort
members. Thanks to Michael Phillips, Emily McFarlane, Colleen Waters
(RTI) and Diane Kampa (U Minnesota) for their assistance. This work was
supported by Contract N02-CP-31013 with the National Cancer Institute.
There are no other competing financial interests. This study has been
conducted in accord with accepted ethical and humane practices, and has
been approved by the pertinent institutional and/or governmental
oversight group(s).
NR 29
TC 6
Z9 7
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0031-8655
J9 PHOTOCHEM PHOTOBIOL
JI Photochem. Photobiol.
PD JAN-FEB
PY 2009
VL 85
IS 1
BP 45
EP 49
DI 10.1111/j.1751-1097.2008.00393.x
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 394XP
UT WOS:000262486800005
PM 18643910
ER
PT J
AU Smith, MR
Hildenbrand, H
Smith, ACM
AF Smith, Michaele R.
Hildenbrand, Hanna
Smith, Ann C. M.
TI Sensory Motor and Functional Skills of Dizygotic Twins: One with
Smith-Magenis Syndrome and a Twin Control
SO PHYSICAL & OCCUPATIONAL THERAPY IN PEDIATRICS
LA English
DT Article
DE Fine motor; genetic disorder; gross motor; sensory processing
ID SYNDROME DEL 17P11.2; MALADAPTIVE BEHAVIOR; CHILDREN; (17)(P11.2P11.2);
PHENOTYPE; PROFILES
AB Smith-Magenis syndrome (SMS), the result of an interstitial deletion within chromosome 17p11.2, is a disorder that may include minor dysmorphic features, brachydactyly, short stature, hypotonia, speech delays, cognitive deficits, signs of peripheral neuropathy, scoliosis, and neurobehavioral problems including sleep disturbances and maladaptive repetitive and self-injurious behaviors. Physical and occupational therapists provide services for children who have the syndrome, whose genetic disorder is frequently not identified or diagnosed before 1 year of age. A comprehensive physical and occupational therapy evaluation was completed in nonidentical twins with one having SMS, using the Sensory Profile; Brief Assessment of Motor Function (BAMF); Peabody Developmental Motor Scales, Second Edition (PDMS-2); and Pediatric Evaluation of Disability Inventory (PEDI). This provides a framework for conducting assessments to enhance early detection and interdisciplinary management with this specialized population.
C1 [Smith, Michaele R.; Hildenbrand, Hanna] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Smith, Ann C. M.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Smith, Ann C. M.] Georgetown Univ, Sch Med, Washington, DC 20057 USA.
RP Smith, MR (reprint author), NIH, Dept Rehabil Med, Bldg 10-CRC,Room 1-1469 NE, Bethesda, MD 20892 USA.
EM Msmith@cc.nih.gov
FU National Human Genome Research Institute, NIH; NIH Clinical Center
FX This research was supported in part by the Intramural Research Program
of the National Human Genome Research Institute, NIH, and the NIH
Clinical Center's Bench-to-Bedside Award. The authors gratefully
acknowledge the parents and children who participated in this study and
the internal reviewers from the Rehabilitation Medicine Department. The
opinions and information contained in this paper are those of the
authors and do not necessarily reflect those of the NIH or the U. S.
Public Health Service.
NR 33
TC 1
Z9 1
U1 0
U2 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0194-2638
J9 PHYS OCCUP THER PEDI
JI Phys. Occup. Ther. Pediatr.
PY 2009
VL 29
IS 3
BP 239
EP 257
DI 10.1080/01942630903028408
PG 19
WC Pediatrics; Rehabilitation
SC Pediatrics; Rehabilitation
GA V19BD
UT WOS:000208047000004
PM 19842854
ER
PT J
AU Thanos, PK
Cavigelli, SA
Michaelides, M
Olvet, DM
Patel, U
Diep, MN
Volkow, ND
AF Thanos, P. K.
Cavigelli, S. A.
Michaelides, M.
Olvet, D. M.
Patel, U.
Diep, M. N.
Volkow, N. D.
TI A Non-Invasive Method for Detecting the Metabolic Stress Response in
Rodents: Characterization and Disruption of the Circadian Corticosterone
Rhythm
SO PHYSIOLOGICAL RESEARCH
LA English
DT Article
DE Corticosterone; Stress; Fecal steroid metabolites; Circadian rhythm
ID MALE RATS; IMMUNOGLOBULIN-A; EXCRETION; PATTERNS; COCAINE; URINE; FECES;
TIME; MICE; SEX
AB Plasma corticosterone (CORT) measures are a common procedure to detect stress responses in rodents. However, the procedure is invasive and can influence CORT levels, making it less than ideal for monitoring CORT circadian rhythms. In the current paper, we examined the applicability of a non-invasive fecal CORT metabolite measure to assess the circadian rhythm. We compared fecal CORT metabolite levels to circulating CORT levels, and analyzed change in the fecal circadian rhythm following an acute stressor (i.e. blood sampling by tail veil catheter). Fecal and blood samples were collected from male adolescent rats and analyzed for CORT metabolites and circulating CORT respectively. Fecal samples were collected hourly for 24 h before and after blood draw. On average, peak fecal CORT metabolite values occurred 7-9 h after the plasma CORT peak and time-matched fecal CORT values were well correlated with plasma CORT. As a result of the rapid blood draw, fecal production and CORT levels were altered the next day. These results indicate fecal CORT metabolite measures can be used to assess conditions that disrupt the circadian CORT rhythm, and provide a method to measure long-term changes in CORT production. This can benefit research that requires long-term glucocorticoid assessment (e. g. stress mechanisms underlying health).
C1 [Thanos, P. K.; Michaelides, M.; Olvet, D. M.; Patel, U.] Brookhaven Natl Lab, Dept Med, Behav Neuropharmacol & Neuroimaging Lab, Upton, NY 11973 USA.
[Olvet, D. M.] SUNY Stony Brook, Dept Psychol, Stony Brook, NY USA.
[Thanos, P. K.; Michaelides, M.; Patel, U.; Volkow, N. D.] NIAAA, Lab Neuroimaging, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Cavigelli, S. A.; Diep, M. N.] Penn State Univ, Dept Biobehav Hlth, University Pk, PA 16802 USA.
RP Thanos, PK (reprint author), Brookhaven Natl Lab, Dept Med, Behav Neuropharmacol & Neuroimaging Lab, Bldg 490, Upton, NY 11973 USA.
EM thanos@bnl.gov
FU Intramural NIH HHS [Z01 AA000551-04]; NIAAA NIH HHS [AA11034, AA07574,
AA07611, P50 AA007611, R01 AA011034, T32 AA007574]
NR 32
TC 25
Z9 25
U1 0
U2 12
PU ACAD SCIENCES CZECH REPUBLIC, INST PHYSIOLOGY
PI PRAGUE 4
PA VIDENSKA 1083, PRAGUE 4 142 20, CZECH REPUBLIC
SN 0862-8408
J9 PHYSIOL RES
JI Physiol. Res.
PY 2009
VL 58
IS 2
BP 219
EP 228
PG 10
WC Physiology
SC Physiology
GA 442PM
UT WOS:000265853100008
PM 18380537
ER
PT J
AU Cragg, GM
Newman, DJ
AF Cragg, G. M.
Newman, D. J.
TI Nature: a vital source of leads for anticancer drug development
SO PHYTOCHEMISTRY REVIEWS
LA English
DT Article; Proceedings Paper
CT International Symposium of the Phytochemical-Society-of-Europe
CY SEP 23-26, 2008
CL Naples, ITALY
SP Phytochem Soc Europe
DE Plants; Marine organisms; Microbes; Symbionts; Multidisciplinary
collaboration
ID ADVANCED SOLID TUMORS; EVERY 3 WEEKS; BRYOSTATIN ANALOGS; POLYKETIDE
SYNTHASE; MARINE ACTINOMYCETE; PROSTATE-CANCER; PHASE-I; TUBULIN
POLYMERIZATION; BIOLOGICAL EVALUATION; THAPSIGARGIN PRODRUG
AB Over 60% of the current anticancer drugs have their origin in one way or another from natural sources. Nature continues to be the most prolific source of biologically active and diverse chemotypes, and it is becoming increasingly evident that associated microbes may often be the source of biologically active compounds originally isolated from host macro-organisms. While relatively few of the actual isolated compounds advance to become clinically effective drugs in their own right, these unique molecules may serve as models for the preparation of more efficacious analogs using chemical methodology such as total or combinatorial (parallel) synthesis, or manipulation of biosynthetic pathways. In addition, conjugation of toxic natural molecules to monoclonal antibodies or polymeric carriers specifically targeted to epitopes on tumors of interest can lead to the development of efficacious targeted therapies. The essential role played by natural products in the discovery and development of effective anticancer agents, and the importance of multidisciplinary collaboration in the generation and optimization of novel molecular leads from natural product sources is reviewed.
C1 [Cragg, G. M.; Newman, D. J.] US Natl Canc Inst, Nat Prod Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21702 USA.
RP Cragg, GM (reprint author), US Natl Canc Inst, Nat Prod Branch, Dev Therapeut Program, Div Canc Treatment & Diag, POB B, Frederick, MD 21702 USA.
EM gmcragg@verizon.net
NR 120
TC 76
Z9 82
U1 5
U2 35
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1568-7767
EI 1572-980X
J9 PHYTOCHEM REV
JI Phytochem. Rev.
PY 2009
VL 8
IS 2
SI SI
BP 313
EP 331
DI 10.1007/s11101-009-9123-y
PG 19
WC Plant Sciences
SC Plant Sciences
GA 473VK
UT WOS:000268238000002
ER
PT J
AU Park, CW
Moon, KC
Park, JS
Jun, JK
Romero, R
Yoon, BH
AF Park, Chan-Wook
Moon, Kyung Chul
Park, Joong Shin
Jun, Jong Kwan
Romero, Roberto
Yoon, Bo Hyun
TI The Involvement of Human Amnion in Histologic Chorioamnionitis is an
Indicator that a Fetal and an Intra-Amniotic Inflammatory Response is
More Likely and Severe: Clinical Implications
SO PLACENTA
LA English
DT Article
DE Amnionitis; Funisitis; Fetal inflammatory response; Intra-amnoitic
inflammatory response; Chorioamnionitis
ID C-REACTIVE PROTEIN; PRETERM PREMATURE RUPTURE; BLOOD-CELL COUNT; INTACT
MEMBRANES; FLUID INFECTION; UMBILICAL-CORD; LABOR; LESIONS; WOMEN;
INTERLEUKIN-6
AB Objective: Amnionitis (inflammation of the amnion) is the final stage of extra-placental chorioamniotic inflammation. We propose that patients with "amnionitis", rather than "chorionitis" have a more advanced form of intra-uterine inflammation/infection and, thus, would have a more intense fetal and intra-amniotic inflammatory response than those without "amnionitis".
Study design: The relationship between the presence of amnionitis, and a fetal and an intra-amniotic inflammatory response was examined in 290 singleton preterm births (<= 36 weeks) with histologic chorioamnionitis. The fetal inflammatory response was determined by plasma C-reactive protein (CRP) concentrations in umbilical cord and the presence of funisitis. The intra-amniotic inflammatory response was assessed by matrix metalloproteinase-8 (MMP-8) concentration and white blood cell (WBC) count in 156 amniotic fluid (AF) samples obtained within 5 days of birth. AF was cultured for aerobic and anaerobic bacteria and genital mycoplasmas. The CRP concentration was measured with a highly sensitive immunoassay.
Results: (1) Amnionitis was present in 43.1% of cases with histologic chorioamnionitis. (2) Patients with amnionitis had a significantly higher rate of funisitis and positive AF culture and a higher median umbilical cord plasma CRP, AF MMP-8 level and AF WBC count than those without amnionitis (p < 0.001 for each). (3) Among cases with amnionitis, the presence or absence of funisitis was not associated with significant differences in the median cord plasma CRP, AF MMP-8 level and AF WBC count. (4) However, the presence of amnionitis in cases with funisitis was associated with a higher median umbilical cord plasma CRP, AF MMP-8 level and AF WBC count than the absence of amnionitis in those with funisitis (p < 0.05 for each). (5) Multiple logistic regression analysis demonstrated that amnionitis was a better independent predictor of proven or suspected early-onset neonatal sepsis (odds ratio 3.8, 95% confidence interval (CI) 1.1-13.2, p < 0.05) than funisitis (odds ratio 1.8, 95% CI 0.5-6.1, not significant) after correction for the contribution of other potential confounding variables.
Conclusion: The involvement of the amnion in the inflammatory process of the extraplacental membranes is associated with a more intense fetal and intra-amniotic inflammatory response than chorionitis alone. This observation has clinical implications because it allows staging of the severity of the inflammatory process and assessment of the likelihood of fetal involvement. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Park, Chan-Wook; Park, Joong Shin; Jun, Jong Kwan; Yoon, Bo Hyun] Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul 110744, South Korea.
[Moon, Kyung Chul] Seoul Natl Univ, Coll Med, Dept Pathol, Seoul 151, South Korea.
[Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Detroit, MI USA.
RP Park, JS (reprint author), Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, 28 Yongon dong, Seoul 110744, South Korea.
EM jsparkmd@snu.ac.kr
RI Seoul National University, Pathology/B-6702-2012; Jun, Jong
Kwan/D-5776-2012; Yoon, Bo Hyun/H-6344-2011; Park,
Chan-Wook/J-5498-2012; Moon, Kyung Chul/J-5465-2012;
OI Jun, Jong Kwan/0000-0002-0242-1736; Park, Joong Shin/0000-0002-5246-0477
FU General Research Grants (GRG); Korea Science and Engineering Foundation,
Republic of Korea [R01-2006-000-10607-0]; Eunice Kennedy Shriver
National Institute of Child Health and Human Development, NIH, DHHS
FX This study was supported by General Research Grants (GRG), Korea Science
and Engineering Foundation, Republic of Korea (R01-2006-000-10607-0)
and, in part, by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development, NIH,
DHHS.
NR 29
TC 49
Z9 57
U1 0
U2 2
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0143-4004
J9 PLACENTA
JI Placenta
PD JAN
PY 2009
VL 30
IS 1
BP 56
EP 61
DI 10.1016/j.placenta.2008.09.017
PG 6
WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
GA 396EJ
UT WOS:000262574700009
PM 19046766
ER
PT B
AU Gottesman, MM
Hall, MD
Liang, XJ
Shen, DW
AF Gottesman, Michael M.
Hall, Matthew D.
Liang, Xing-Jie
Shen, Ding-Wu
BE Bonetti, A
Leone, R
Muggia, FM
Howell, SB
TI Resistance to Cisplatin Results from Multiple Mechanisms in Cancer Cells
SO PLATINUM AND OTHER HEAVY METAL COMPOUNDS IN CANCER CHEMOTHERAPY
SE Cancer Drug Discovery and Development
LA English
DT Proceedings Paper
CT 10th International Symposium on Platinum Coordination Compounds in
Cancer Chemotherapy
CY DEC, 2007
CL Verona, ITALY
SP Mater Salutis Hosp, Dept Oncol, Azienda Sanitaria Locale 21, Veneto Reg, Univ Verona, Dept Med & Public Hlth, Sect Pharmacol
DE Cisplatin; Resistance; Uptake; Reduced accumulation; Pleiotropic
mechanism
ID CELLULAR ACCUMULATION; MULTIDRUG-RESISTANCE; REDUCED EXPRESSION; LINES;
CHEMOTHERAPY; CARBOPLATIN
AB We have studied the development of resistance to cisplatin in cultured KB-3-1 human cervical adenocarcinoma (HeLa) cells and BEL-7404 human hepatoma cells. In a single-step selection, it is possible to develop a pleiotropic phenotype consisting of the following: (a) cross-resistance to other platinum compounds, arsenite, cadmium, methotrexate and nucleoside analogs; (b) corresponding reduced accumulation of these agents; (c) reduced receptor-mediated and fluid phase mediated endocytosis; (d) altered cytoskeleton, including disruption of actin microfilaments, filament structures, and microtubules; (e) a defect in membrane protein trafficking consisting of relocalization to intracellular vesicles of several transmembrane proteins Such as the ABBC1 transporter (MRP1, GS-X pump), glucose transporter (GluT1), and folate binding protein (FBP); and (f)altered mitochondrial morphology and function. We hypothesize that this pleiotropic phenotype reflects a basic cellular defense mechanism against cytotoxic materials that are not hydrophobic enough to enter the cell by simple diffusion, but have multiple other mechanisms of cell entry including piggybacking on existing receptors and endocytosis, and speculate that a relatively simple cellular switch can actuate this pleiotropic response.
C1 [Gottesman, Michael M.; Hall, Matthew D.; Liang, Xing-Jie; Shen, Ding-Wu] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM mgottesman@nih.gov
NR 15
TC 5
Z9 7
U1 1
U2 5
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
BN 978-1-60327-458-6
J9 CANC DRUG DISC DEV
JI Canc. Drug. Disc. Dev.
PY 2009
BP 83
EP 88
DI 10.1007/978-1-60327-459-3_11
PG 6
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA BIV36
UT WOS:000263142100011
ER
PT B
AU Tay, K
Gutierrez, M
Giaccone, G
AF Tay, Kevin
Gutierrez, Martin
Giaccone, Giuseppe
BE Bonetti, A
Leone, R
Muggia, FM
Howell, SB
TI Platinum Compounds in Lung Cancer: Current Status
SO PLATINUM AND OTHER HEAVY METAL COMPOUNDS IN CANCER CHEMOTHERAPY
SE Cancer Drug Discovery and Development
LA English
DT Proceedings Paper
CT 10th International Symposium on Platinum Coordination Compounds in
Cancer Chemotherapy
CY DEC, 2007
CL Verona, ITALY
SP Mater Salutis Hosp, Dept Oncol, Azienda Sanitaria Locale 21, Veneto Reg, Univ Verona, Dept Med & Public Hlth, Sect Pharmacol
DE Platinum compounds; Bevacizumab; Cetuximab; Excision repair
cross-complementation group 1 (ERCC1); Ribonucleotide reductace MI
(RRMI)
ID PHASE-III TRIAL; QUALITY-OF-LIFE; CISPLATIN PLUS GEMCITABINE; RANDOMIZED
CONTROLLED-TRIALS; REDUCTASE SUBUNIT M1; RIBONUCLEOTIDE REDUCTASE;
SUPPORTIVE CARE; CLINICAL-TRIALS; ADJUVANT CHEMOTHERAPY; ERCC1
EXPRESSION
AB Randomized clinical studies and meta-analyses of the literature have confirmed the improved survival of platinum-based chemotherapy doublets, that are considered standard therapy in patients with advanced non-small cell lung cancer (NSCLC) with a good performance status. The use of platinum compounds have also demonstrated a slight survival advantage over nonplatinum-based chemotherapy. Cisplatin remains the platinum agent of choice in the management of patients with NSCLC in both the advanced and adjuvant setting based on the results from recent meta-analyses. However, carboplatin may be offered to patients in advanced stages of the disease due to its more favorable toxicity profile. To date, four targeted agents (bevacizumab, cetuximab, erlotinib and gefitinib) have been studied in combination with platinum-based chemotherapy in the treatment of advanced NSCLC. Only bevacizumab has been shown to significantly prolong survival when added to carboplatin/paclitaxel as demonstrated in a large phase III study. However, issues of toxicity limit this treatment regimen to selected patients. The combination of bevacizumab with cisplatin and gemcitabine appears promising but is still awaiting the final results of the unpublished survival data. Preliminary studies indicate that molecular tumor markers may be able to identify tumors that are more likely to respond to chemotherapy. Excision repair cross-complementation group 1 (ERCC1) and Ribonucleotide Reductase MI (RRMI) are two such genes critical to DNA synthesis and DNA damage repair pathways that have been studied. The results from the first prospective phase III randomized trial suggest that customizing chemotherapy based on ERCC1 expression in patients with advanced NSCLC is a feasible approach. In the future, selection of patients based on pharmacogenetics may help identify patients who will optimally benefit from specific therapies.
C1 [Tay, Kevin; Gutierrez, Martin; Giaccone, Giuseppe] NCI, Med Oncol Branch, NIH, Bethesda, MD USA.
RP Tay, K (reprint author), NCI, Med Oncol Branch, NIH, Bethesda, MD USA.
EM giacconeg@mail.nih.gov
NR 58
TC 0
Z9 0
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
BN 978-1-60327-458-6
J9 CANC DRUG DISC DEV
JI Canc. Drug. Disc. Dev.
PY 2009
BP 231
EP 242
DI 10.1007/978-1-60327-459-3_28
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA BIV36
UT WOS:000263142100028
ER
PT J
AU Pajevic, S
Plenz, D
AF Pajevic, Sinisa
Plenz, Dietmar
TI Efficient Network Reconstruction from Dynamical Cascades Identifies
Small-World Topology of Neuronal Avalanches
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID PRIMATE CEREBRAL-CORTEX; COMPLEX BRAIN NETWORKS; FUNCTIONAL
CONNECTIVITY; GRANGER CAUSALITY; CORTICAL-NEURONS; IN-VITRO;
INFORMATION-TRANSFER; ACTIVITY PATTERNS; NEURAL SYSTEMS; ORGANIZATION
AB Cascading activity is commonly found in complex systems with directed interactions such as metabolic networks, neuronal networks, or disease spreading in social networks. Substantial insight into a system's organization can be obtained by reconstructing the underlying functional network architecture from the observed activity cascades. Here we focus on Bayesian approaches and reduce their computational demands by introducing the Iterative Bayesian (IB) and Posterior Weighted Averaging (PWA) methods. We introduce a special case of PWA, cast in nonparametric form, which we call the normalized count (NC) algorithm. NC efficiently reconstructs random and small-world functional network topologies and architectures from subcritical, critical, and supercritical cascading dynamics and yields significant improvements over commonly used correlation methods. With experimental data, NC identified a functional and structural small-world topology and its corresponding traffic in cortical networks with neuronal avalanche dynamics.
C1 [Pajevic, Sinisa] Ctr Informat Technol, Math & Stat Comp Lab, Div Computat Biosci, NIH, Bethesda, MD USA.
[Plenz, Dietmar] NIMH, Sect Crit Brain Dynam, Lab Syst Neurosci, NIH, Bethesda, MD 20892 USA.
RP Pajevic, S (reprint author), Ctr Informat Technol, Math & Stat Comp Lab, Div Computat Biosci, NIH, Bethesda, MD USA.
EM plenzd@mail.nih.gov
FU National Institute of Mental Health and the Division of Computational
Biosciences; Center for Information Technology, National Institutes of
Health
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health and the Division of Computational
Biosciences, Center for Information Technology, National Institutes of
Health.
NR 86
TC 44
Z9 46
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-734X
EI 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD JAN
PY 2009
VL 5
IS 1
AR e1000271
DI 10.1371/journal.pcbi.1000271
PG 20
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 415HG
UT WOS:000263924300005
PM 19180180
ER
PT J
AU Blankschien, MD
Potrykus, K
Grace, E
Choudhary, A
Vinella, D
Cashel, M
Herman, C
AF Blankschien, Matthew D.
Potrykus, Katarzyna
Grace, Elicia
Choudhary, Abha
Vinella, Daniel
Cashel, Michael
Herman, Christophe
TI TraR, a Homolog of a RNAP Secondary Channel Interactor, Modulates
Transcription
SO PLOS GENETICS
LA English
DT Article
ID ESCHERICHIA-COLI K-12; F-PLASMID; CRYSTAL-STRUCTURE; STATIONARY-PHASE;
OPPOSING ROLES; ALARMONE PPGPP; GENE-PRODUCTS; MICROCIN J25; IN-VIVO;
POLYMERASE
AB Recent structural and biochemical studies have identified a novel control mechanism of gene expression mediated through the secondary channel of RNA Polymerase (RNAP) during transcription initiation. Specifically, the small nucleotide ppGpp, along with DksA, a RNAP secondary channel interacting factor, modifies the kinetics of transcription initiation, resulting in, among other events, down-regulation of ribosomal RNA synthesis and up-regulation of several amino acid biosynthetic and transport genes during nutritional stress. Until now, this mode of regulation of RNAP was primarily associated with ppGpp. Here, we identify TraR, a DksA homolog that mimics ppGpp/DksA effects on RNAP. First, expression of TraR compensates for dksA transcriptional repression and activation activities in vivo. Second, mutagenesis of a conserved amino acid of TraR known to be critical for DksA function abolishes its activity, implying both structural and functional similarity to DksA. Third, unlike DksA, TraR does not require ppGpp for repression of the rrnB P1 promoter in vivo and in vitro or activation of amino acid biosynthesis/transport genes in vivo. Implications for DksA/ppGpp mechanism and roles of TraR in horizontal gene transfer and virulence are discussed.
C1 [Blankschien, Matthew D.; Grace, Elicia; Choudhary, Abha; Herman, Christophe] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Potrykus, Katarzyna; Vinella, Daniel; Cashel, Michael] NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
[Grace, Elicia; Herman, Christophe] Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA.
RP Blankschien, MD (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
EM herman@bcm.edu
RI vinella, daniel/G-5504-2012
FU NIH; HFSPO [RGY0060/2006]
FX This work is funded in part by the NICHD intramural program of the NIH
and HFSPO grant RGY0060/2006.
NR 62
TC 21
Z9 23
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD JAN
PY 2009
VL 5
IS 1
AR e1000345
DI 10.1371/journal.pgen.1000345
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 447VW
UT WOS:000266221100027
PM 19148274
ER
PT J
AU Reich, D
Nalls, MA
Kao, WHL
Akylbekova, EL
Tandon, A
Patterson, N
Mullikin, J
Hsueh, WC
Cheng, CY
Coresh, J
Boerwinkle, E
Li, M
Waliszewska, A
Neubauer, J
Li, RL
Leak, TS
Ekunwe, L
Files, JC
Hardy, CL
Zmuda, JM
Taylor, HA
Ziv, E
Harris, TB
Wilson, JG
AF Reich, David
Nalls, Michael A.
Kao, W. H. Linda
Akylbekova, Ermeg L.
Tandon, Arti
Patterson, Nick
Mullikin, James
Hsueh, Wen-Chi
Cheng, Ching-Yu
Coresh, Josef
Boerwinkle, Eric
Li, Man
Waliszewska, Alicja
Neubauer, Julie
Li, Rongling
Leak, Tennille S.
Ekunwe, Lynette
Files, Joe C.
Hardy, Cheryl L.
Zmuda, Joseph M.
Taylor, Herman A.
Ziv, Elad
Harris, Tamara B.
Wilson, James G.
TI Reduced Neutrophil Count in People of African Descent Is Due To a
Regulatory Variant in the Duffy Antigen Receptor for Chemokines Gene
SO PLOS GENETICS
LA English
DT Article
ID BENIGN FAMILIAL LEUKOPENIA; ETHNIC NEUTROPENIA; HUMAN GENOME; NEGATIVE
INDIVIDUALS; PLASMODIUM-VIVAX; HAPLOTYPE MAP; IN-VIVO; INFECTION; BLACK;
DARC
AB Persistently low white blood cell count (WBC) and neutrophil count is a well-described phenomenon in persons of African ancestry, whose etiology remains unknown. We recently used admixture mapping to identify an approximately 1-megabase region on chromosome 1, where ancestry status (African or European) almost entirely accounted for the difference in WBC between African Americans and European Americans. To identify the specific genetic change responsible for this association, we analyzed genotype and phenotype data from 6,005 African Americans from the Jackson Heart Study (JHS), the Health, Aging and Body Composition (Health ABC) Study, and the Atherosclerosis Risk in Communities (ARIC) Study. We demonstrate that the causal variant must be at least 91% different in frequency between West Africans and European Americans. An excellent candidate is the Duffy Null polymorphism (SNP rs2814778 at chromosome 1q23.2), which is the only polymorphism in the region known to be so differentiated in frequency and is already known to protect against Plasmodium vivax malaria. We confirm that rs2814778 is predictive of WBC and neutrophil count in African Americans above beyond the previously described admixture association (P = 3.8x10(-5)), establishing a novel phenotype for this genetic variant.
C1 [Reich, David; Tandon, Arti] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Reich, David; Tandon, Arti; Patterson, Nick; Waliszewska, Alicja; Neubauer, Julie] Broad Inst Harvard, Cambridge, MA USA.
[Reich, David; Tandon, Arti; Patterson, Nick; Waliszewska, Alicja; Neubauer, Julie] MIT, Cambridge, MA 02139 USA.
[Nalls, Michael A.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
[Nalls, Michael A.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
[Kao, W. H. Linda; Cheng, Ching-Yu; Coresh, Josef; Li, Man] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Akylbekova, Ermeg L.; Ekunwe, Lynette] Jackson State Univ, Jackson Heart Study Anal Grp, Jackson, MS USA.
[Mullikin, James] NHGRI, Comparat Genom Unit, Genome Technol Branch, Rockville, MD USA.
[Hsueh, Wen-Chi] Univ Calif San Francisco, Dept Epidemiol & Biostat, Inst Human Genet, Div Med Genet,Dept Med, San Francisco, CA 94143 USA.
[Cheng, Ching-Yu] NHGRI, Inherited Dis Res Branch, Baltimore, MD USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Houston, TX USA.
[Waliszewska, Alicja] Brigham & Womens Hosp, Ctr Neurol Dis, Lab Mol Immunol, Boston, MA 02115 USA.
[Li, Rongling] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Ctr Genom & Bioinformat, Memphis, TN USA.
[Leak, Tennille S.; Zmuda, Joseph M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Files, Joe C.; Hardy, Cheryl L.] Univ Mississippi, Med Ctr, Dept Med, Div Hematol, Jackson, MS 39216 USA.
[Taylor, Herman A.] Tougaloo Coll, Jackson, MS USA.
[Ziv, Elad] Univ Calif San Francisco, Dept Med, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Ziv, Elad] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Wilson, James G.] VA Med Ctr, Jackson, MS USA.
RP Reich, D (reprint author), Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
EM reich@genetics.med.harvard.edu; James.Wilson3@va.gov
RI Cheng, Ching-Yu/K-7017-2013; Ziv, Elad/L-5396-2014
OI Cheng, Ching-Yu/0000-0003-0655-885X;
FU National Heart, Lung, and Blood Institute [R01-HL-084107, N01-HC-95170,
N01-HC-95171, N01-HC-95172, N01-HC55015, N01-HC-55016, N01-HC-55018,
N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022]; National Center
on Minority Health and Health Disparities; National Institute on Aging
[N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106]; National Center for
Research Resources to the Broad Institute of Harvard and MIT [U54
RR020278]; Burroughs Wellcome Career Development; [R21DK073482];
[K01DK067207]; [U01-HG004168]
FX Research support for JHS was provided by R01-HL-084107 (JGW) from the
National Heart, Lung, and Blood Institute and contracts N01-HC-95170,
N01-HC-95171, and N01-HC-95172 from the National Heart, Lung, and Blood
Institute and the National Center on Minority Health and Health
Disparities. Research support for Health ABC was provided by the
Intramural Research Program of the National Institute on Aging, and
contracts N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106. The
Atherosclerosis Risk in Communities Study is a collaborative study
supported by National Heart, Lung, and Blood Institute contracts
N01-HC55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020,
N01-HC-55021, and N01-HC-55022. Support for the ARIC admixture mapping
studies was provided by R21DK073482 and K01DK067207 (WHLK). Genotyping
for both the JHS and Health ABC was supported by grant U54 RR020278 from
the National Center for Research Resources to the Broad Institute of
Harvard and MIT; a subsidy from this grant covered half the cost of
Health ABC genotyping. DR was supported by a Burroughs Wellcome Career
Development Award in the Biomedical Sciences, and methodological and
statistical analysis was supported by grant U01-HG004168.
NR 48
TC 127
Z9 129
U1 2
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD JAN
PY 2009
VL 5
IS 1
AR e1000360
DI 10.1371/journal.pgen.1000360
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 447VW
UT WOS:000266221100042
PM 19180233
ER
PT J
AU Tanaka, T
Shen, J
Abecasis, GR
Kisialiou, A
Ordovas, JM
Guralnik, JM
Singleton, A
Bandinelli, S
Cherubini, A
Arnett, D
Tsai, MY
Ferrucci, L
AF Tanaka, Toshiko
Shen, Jian
Abecasis, Goncalo R.
Kisialiou, Aliaksei
Ordovas, Jose M.
Guralnik, Jack M.
Singleton, Andrew
Bandinelli, Stefania
Cherubini, Antonio
Arnett, Donna
Tsai, Michael Y.
Ferrucci, Luigi
TI Genome-Wide Association Study of Plasma Polyunsaturated Fatty Acids in
the InCHIANTI Study
SO PLOS GENETICS
LA English
DT Article
ID PROLIFERATOR-ACTIVATED RECEPTOR; ALPHA-LINOLENIC ACID;
CORONARY-HEART-DISEASE; DIETARY-INTAKE; FISH CONSUMPTION;
GENETIC-VARIANTS; RISK; EXPRESSION; OMEGA-3-FATTY-ACIDS; ATHEROSCLEROSIS
AB Polyunsaturated fatty acids (PUFA) have a role in many physiological processes, including energy production, modulation of inflammation, and maintenance of cell membrane integrity. High plasma PUFA concentrations have been shown to have beneficial effects on cardiovascular disease and mortality. To identify genetic contributors of plasma PUFA concentrations, we conducted a genome-wide association study of plasma levels of six omega-3 and omega-6 fatty acids in 1,075 participants in the InCHIANTI study on aging. The strongest evidence for association was observed in a region of chromosome 11 that encodes three fatty acid desaturases (FADS1, FADS2, FADS3). The SNP with the most significant association was rs174537 near FADS1 in the analysis of arachidonic acid (AA; p = 5.95x10(-46)). Minor allele homozygotes had lower AA compared to the major allele homozygotes and rs174537 accounted for 18.6% of the additive variance in AA concentrations. This SNP was also associated with levels of eicosadienoic acid (EDA; p = 6.78x10(-9)) and eicosapentanoic acid (EPA; p = 1.07x10(-14)). Participants carrying the allele associated with higher AA, EDA, and EPA also had higher low-density lipoprotein (LDL-C) and total cholesterol levels. Outside the FADS gene cluster, the strongest region of association mapped to chromosome 6 in the region encoding an elongase of very long fatty acids 2 (ELOVL2). In this region, association was observed with EPA (rs953413; p = 1.1x10(-6)). The effects of rs174537 were confirmed in an independent sample of 1,076 subjects participating in the GOLDN study. The ELOVL2 SNP was associated with docosapentanoic and DHA but not with EPA in GOLDN. These findings show that polymorphisms of genes encoding enzymes in the metabolism of PUFA contribute to plasma concentrations of fatty acids.
C1 [Tanaka, Toshiko; Ferrucci, Luigi] Medstar Res Inst, Baltimore, MD USA.
[Tanaka, Toshiko; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Shen, Jian; Ordovas, Jose M.] Tufts Univ, Human Nutr Res Ctr Aging, JM USDA, Lab Nutr Genom, Boston, MA 02111 USA.
[Abecasis, Goncalo R.] Univ Michigan, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Kisialiou, Aliaksei; Bandinelli, Stefania; Ferrucci, Luigi] ASF, Geriatr Rehabil Unit, Florence, Italy.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Singleton, Andrew] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
[Cherubini, Antonio] Univ Perugia, Inst Gerontol & Geriatr, Dept Clin & Expt Med, I-06100 Perugia, Italy.
[Arnett, Donna] Univ Alabama, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA.
[Arnett, Donna] Univ Alabama, Clin Nutr Res Ctr, Birmingham, AL USA.
[Tsai, Michael Y.] Univ Minnesota, Lab Med & Pathol, Minneapolis, MN USA.
RP Tanaka, T (reprint author), Medstar Res Inst, Baltimore, MD USA.
EM tanakato@mail.nih.gov
RI Singleton, Andrew/C-3010-2009; Abecasis, Goncalo/B-7840-2010; Kisialiou,
Aliaksei/J-8771-2016;
OI Kisialiou, Aliaksei/0000-0001-7287-9454; Abecasis,
Goncalo/0000-0003-1509-1825; Cherubini, Antonio/0000-0003-0261-9897;
Ordovas, Jose/0000-0002-7581-5680
FU R&D contract with MedStar Research Institute; NIH; National Institute on
Aging; National Heart, Lung, and Blood Institute [U01 HL72524, HL-54776,
DK075030]; US Department of Agriculture Research Service [53-K06-5-10,
58-1950-9-001]
FX This study was supported in part by the R&D contract with MedStar
Research Institute, the Intramural Research Program of the NIH, National
Institute on Aging and by National Heart, Lung, and Blood Institute
Grant U01 HL72524, Genetic and Environmental Determinants of
Triglycerides; Grants HL-54776 and DK075030, and by contracts
53-K06-5-10 and 58-1950-9-001 from the US Department of Agriculture
Research Service.
NR 55
TC 187
Z9 191
U1 0
U2 18
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD JAN
PY 2009
VL 5
IS 1
AR e1000338
DI 10.1371/journal.pgen.1000338
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 447VW
UT WOS:000266221100020
PM 19148276
ER
PT J
AU Botosso, VF
Zanotto, PMDA
Ueda, M
Arruda, E
Gilio, AE
Vieira, SE
Stewien, KE
Peret, TCT
Jamal, LF
Pardini, MIDMC
Pinho, JRR
Massad, E
Sant'Anna, OA
Holmes, EC
Durigon, EL
AF Botosso, Viviane F.
Zanotto, Paolo M. de A.
Ueda, Mirthes
Arruda, Eurico
Gilio, Alfredo E.
Vieira, Sandra E.
Stewien, Klaus E.
Peret, Teresa C. T.
Jamal, Leda F.
Pardini, Maria I. de M. C.
Pinho, Joao R. R.
Massad, Eduardo
Sant'Anna, Osvaldo A.
Holmes, Eddie C.
Durigon, Edison L.
CA VGDN Consortium
TI Positive Selection Results in Frequent Reversible Amino Acid
Replacements in the G Protein Gene of Human Respiratory Syncytial Virus
SO PLOS PATHOGENS
LA English
DT Article
ID ATTACHMENT G-GLYCOPROTEIN; CARBOHYDRATE SIDE-CHAINS; SUBGROUP-A;
MOLECULAR EPIDEMIOLOGY; GROUP-B; CIRCULATION PATTERNS; SOUTH-AFRICA;
MONOCLONAL-ANTIBODIES; EVOLUTIONARY PATTERN; CONSECUTIVE SEASONS
AB Human respiratory syncytial virus (HRSV) is the major cause of lower respiratory tract infections in children under 5 years of age and the elderly, causing annual disease outbreaks during the fall and winter. Multiple lineages of the HRSVA and HRSVB serotypes co-circulate within a single outbreak and display a strongly temporal pattern of genetic variation, with a replacement of dominant genotypes occurring during consecutive years. In the present study we utilized phylogenetic methods to detect and map sites subject to adaptive evolution in the G protein of HRSVA and HRSVB. A total of 29 and 23 amino acid sites were found to be putatively positively selected in HRSVA and HRSVB, respectively. Several of these sites defined genotypes and lineages within genotypes in both groups, and correlated well with epitopes previously described in group A. Remarkably, 18 of these positively selected tended to revert in time to a previous codon state, producing a "flipflop'' phylogenetic pattern. Such frequent evolutionary reversals in HRSV are indicative of a combination of frequent positive selection, reflecting the changing immune status of the human population, and a limited repertoire of functionally viable amino acids at specific amino acid sites.
C1 [Botosso, Viviane F.; Sant'Anna, Osvaldo A.] Butantan Inst, Virol Branch, Sao Paulo, Brazil.
[Zanotto, Paolo M. de A.; Stewien, Klaus E.] Univ Sao Paulo, Dept Microbiol, Inst Biomed Sci, Lab Mol Evolut & Bioinformat, Sao Paulo, Brazil.
[Ueda, Mirthes] Adolfo Lutz Inst, Div Med Biol, Sao Paulo, Brazil.
[Arruda, Eurico] Univ Sao Paulo, Dept Cell Biol, Fac Med Ribeirao Preto, Sao Paulo, Brazil.
[Gilio, Alfredo E.; Vieira, Sandra E.] Univ Sao Paulo, Univ Hosp, Div Pediat, Sao Paulo, Brazil.
[Peret, Teresa C. T.] Ctr Dis Control & Prevent, Coordinating Ctr Infect Dis, Natl Ctr Immunizat & Resp Dis, Gastroenteritis & Resp Viruses Lab Branch,Div Vir, Atlanta, GA USA.
[Jamal, Leda F.] STD AIDS Reference & Training Ctr, Sao Paulo, Brazil.
[Pardini, Maria I. de M. C.] State Univ Sao Paulo, Sao Paulo, Brazil.
[Pinho, Joao R. R.] Univ Sao Paulo, Inst Trop Med, Sao Paulo, Brazil.
[Massad, Eduardo] Univ Sao Paulo, Sch Med, Dept Legal Med, Sao Paulo, Brazil.
[Holmes, Eddie C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, Mueller Lab, University Pk, PA 16802 USA.
[Holmes, Eddie C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Durigon, Edison L.] Univ Sao Paulo, Dept Microbiol, Inst Biomed Sci, Lab Clin Virol, Sao Paulo, Brazil.
RP Botosso, VF (reprint author), Butantan Inst, Virol Branch, Sao Paulo, Brazil.
EM pzanotto@usp.br
RI Botosso, Viviane/I-5591-2014; Schvartsman, Claudio/M-8706-2015; Moraes,
Claudia/K-4708-2016; Gilio, Alfredo/A-8819-2010; Massad,
Eduardo/H-6143-2011; Arruda, Eurico/E-4101-2012; vieira,
sandra/I-9456-2012; Massad, Eduardo/B-1169-2012; Toxinas,
Inct/I-1933-2013; Pinho, Joao/G-2850-2012; Proenca-Modena,
Jose/C-8231-2014; Gilio, Alfredo/J-4229-2014
OI Durigon, Edison/0000-0003-4898-6553; Grisi Candeias, Joao
Manuel/0000-0003-1515-702X; Holmes, Edward/0000-0001-9596-3552; Botosso,
Viviane/0000-0002-7876-3687; Schvartsman, Claudio/0000-0001-5695-9331;
Moraes, Claudia/0000-0001-6782-4790; vieira, sandra/0000-0001-5100-8713;
Massad, Eduardo/0000-0002-7200-2916; Pinho, Joao/0000-0003-3999-0489;
FU FAPESP [00/04205-6]; CNPq, Brazil
FX This project was made possible by the VGDN program funded by FAPESP
project #00/04205-6 and by CNPq, Brazil.
NR 55
TC 62
Z9 64
U1 1
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD JAN
PY 2009
VL 5
IS 1
AR e1000254
DI 10.1371/journal.ppat.1000254
PG 11
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 415IP
UT WOS:000263927800031
PM 19119418
ER
PT J
AU Jia, B
Ng, SK
DeGottardi, MQ
Piatak, M
Yuste, E
Carville, A
Mansfield, KG
Li, WJ
Richardson, BA
Lifson, JD
Evans, DT
AF Jia, Bin
Ng, Sharon K.
DeGottardi, M. Quinn
Piatak, Michael, Jr.
Yuste, Eloisa
Carville, Angela
Mansfield, Keith G.
Li, Wenjun
Richardson, Barbra A.
Lifson, Jeffrey D.
Evans, David T.
TI Immunization with Single-Cycle SIV Significantly Reduces Viral Loads
After an Intravenous Challenge with SIV(mac)239
SO PLOS PATHOGENS
LA English
DT Article
ID SIMIAN-IMMUNODEFICIENCY-VIRUS; MAJOR HISTOCOMPATIBILITY COMPLEX;
LIVE-ATTENUATED SIV; CD4(+) T-CELLS; VESICULAR STOMATITIS-VIRUS; RHESUS
MACAQUES; AIDS VACCINE; CLASS-I; IMMUNE-RESPONSES; NEUTRALIZING
ANTIBODIES
AB Strains of simian immunodeficiency virus (SIV) that are limited to a single cycle of infection were evaluated for the ability to elicit protective immunity against wild-type SIV(mac)239 infection of rhesus macaques by two different vaccine regimens. Six animals were inoculated at 8-week intervals with 6 identical doses consisting of a mixture of three different envelope variants of single-cycle SIV (scSIV). Six additional animals were primed with a mixture of cytoplasmic domain-truncated envelope variants of scSIV and boosted with two doses of vesicular stomatitis virus glycoprotein (VSV G) trans-complemented scSIV. While both regimens elicited detectable virus-specific T cell responses, SIV-specific T cell frequencies were more than 10-fold higher after boosting with VSV G trans-complemented scSIV (VSV G scSIV). Broad T cell recognition of multiple viral antigens and Gag-specific CD4(+) T cell responses were also observed after boosting with VSV G scSIV. With the exception of a single animal in the repeated immunization group, all of the animals became infected following an intravenous challenge with SIV(mac)239. However, significantly lower viral loads and higher memory CD4(+) T cell counts were observed in both immunized groups relative to an unvaccinated control group. Indeed, both scSIV immunization regimens resulted in containment of SIV(mac)239 replication after challenge that was as good as, if not better than, what has been achieved by other non-persisting vaccine vectors that have been evaluated in this challenge model. Nevertheless, the extent of protection afforded by scSIV was not as good as typically conferred by persistent infection with live, attenuated SIV. These observations have potentially important implications to the design of an effective AIDS vaccine, since they suggest that ongoing stimulation of virus-specific immune responses may be essential to achieving the degree of protection afforded by live, attenuated SIV.
C1 [Jia, Bin; Ng, Sharon K.; DeGottardi, M. Quinn; Yuste, Eloisa; Evans, David T.] Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick Inc, Natl Canc Inst, AIDS & Canc Virus Program, Frederick, MD USA.
[Carville, Angela; Mansfield, Keith G.] Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Pathol, Southborough, MA 01772 USA.
[Li, Wenjun] Univ Massachusetts, Sch Med, Biostat Res Grp, Div Prevent & Behav Med, Worcester, MA USA.
[Richardson, Barbra A.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Jia, B (reprint author), Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA.
EM devans@hms.harvard.edu
FU Public Health Service [AI63993, AI52751, AI71306]; National Institutes
of Health; Elizabeth Glaser Pediatric AIDS Foundation
FX This work was supported by Public Health Service grants AI63993,
AI52751, and AI71306 from the National Institutes of Health. DTE is an
Elizabeth Glaser Scientist supported by the Elizabeth Glaser Pediatric
AIDS Foundation.
NR 84
TC 28
Z9 28
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD JAN
PY 2009
VL 5
IS 1
AR e1000272
DI 10.1371/journal.ppat.1000272
PG 19
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 415IP
UT WOS:000263927800011
PM 19165322
ER
PT J
AU Ninio, S
Celli, J
Roy, CR
AF Ninio, Shira
Celli, Jean
Roy, Craig R.
TI A Legionella pneumophila Effector Protein Encoded in a Region of Genomic
Plasticity Binds to Dot/Icm-Modified Vacuoles
SO PLOS PATHOGENS
LA English
DT Article
ID NUCLEOTIDE-EXCHANGE FACTOR; IV SECRETION SYSTEM; LEGIONNAIRES-DISEASE;
ENDOPLASMIC-RETICULUM; INTRACELLULAR GROWTH; HUMAN-MONOCYTES;
TRANSLOCATED SUBSTRATE; HOST-CELLS; BACTERIUM; IDENTIFICATION
AB Legionella pneumophila is an opportunistic pathogen that can cause a severe pneumonia called Legionnaires' disease. In the environment, L. pneumophila is found in fresh water reservoirs in a large spectrum of environmental conditions, where the bacteria are able to replicate within a variety of protozoan hosts. To survive within eukaryotic cells, L. pneumophila require a type IV secretion system, designated Dot/Icm, that delivers bacterial effector proteins into the host cell cytoplasm. In recent years, a number of Dot/Icm substrate proteins have been identified; however, the function of most of these proteins remains unknown, and it is unclear why the bacterium maintains such a large repertoire of effectors to promote its survival. Here we investigate a region of the L. pneumophila chromosome that displays a high degree of plasticity among four sequenced L. pneumophila strains. Analysis of GC content suggests that several genes encoded in this region were acquired through horizontal gene transfer. Protein translocation studies establish that this region of genomic plasticity encodes for multiple Dot/Icm effectors. Ectopic expression studies in mammalian cells indicate that one of these substrates, a protein called PieA, has unique effector activities. PieA is an effector that can alter lysosome morphology and associates specifically with vacuoles that support L. pneumophila replication. It was determined that the association of PieA with vacuoles containing L. pneumophila requires modifications to the vacuole mediated by other Dot/Icm effectors. Thus, the localization properties of PieA reveal that the Dot/Icm system has the ability to spatially and temporally control the association of an effector with vacuoles containing L. pneumophila through activities mediated by other effector proteins.
C1 [Ninio, Shira; Roy, Craig R.] Yale Univ, Sch Med, Boyer Ctr Mol Med, Sect Microbial Pathogenesis, New Haven, CT 06520 USA.
[Celli, Jean] NIAID, Rocky Mt Labs, Intracellular Parasites Lab, NIH, Hamilton, MT 59840 USA.
RP Ninio, S (reprint author), Yale Univ, Sch Med, Boyer Ctr Mol Med, Sect Microbial Pathogenesis, New Haven, CT 06520 USA.
EM Craig.roy@yale.edu
OI Roy, Craig/0000-0003-4490-440X
FU NIH [2R01AI041699-12]; The Human Frontiers Science Program; Intramural
Research Program of the National Institutes of Health; National
Institute of Allergy and Infectious Diseases
FX This work was supported by NIH Grant 2R01AI041699-12 (C. R. R.), by The
Human Frontiers Science Program (S. N.), and by the Intramural Research
Program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases (J.C.).
NR 58
TC 36
Z9 36
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD JAN
PY 2009
VL 5
IS 1
AR e1000278
DI 10.1371/journal.ppat.1000278
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 415IP
UT WOS:000263927800016
PM 19165328
ER
PT J
AU Srinivasan, P
Coppens, I
Jacobs-Lorena, M
AF Srinivasan, Prakash
Coppens, Isabelle
Jacobs-Lorena, Marcelo
TI Distinct Roles of Plasmodium Rhomboid 1 in Parasite Development and
Malaria Pathogenesis
SO PLOS PATHOGENS
LA English
DT Article
ID APICAL MEMBRANE ANTIGEN-1; HOST-CELL INVASION; ERYTHROCYTE INVASION;
GLIDING MOTILITY; LIFE-CYCLE; SEXUAL DEVELOPMENT; FALCIPARUM; PROTEIN;
SURFACE; MEROZOITES
AB Invasion of host cells by the malaria parasite involves recognition and interaction with cell-surface receptors. A wide variety of parasite surface proteins participate in this process, most of which are specific to the parasite's particular invasive form. Upon entry, the parasite has to dissociate itself from the host-cell receptors. One mechanism by which it does so is by shedding its surface ligands using specific enzymes. Rhomboid belongs to a family of serine proteases that cleave cell-surface proteins within their transmembrane domains. Here we identify and partially characterize a Plasmodium berghei rhomboid protease (PbROM1) that plays distinct roles during parasite development. PbROM1 localizes to the surface of sporozoites after salivary gland invasion. In blood stage merozoites, PbROM1 localizes to the apical end where proteins involved in invasion are also present. Our genetic analysis suggests that PbROM1 functions in the invasive stages of parasite development. Whereas wild-type P. berghei is lethal to mice, animals infected with PbROM1 null mutants clear the parasites efficiently and develop long-lasting protective immunity. The results indicate that P. berghei Rhomboid 1 plays a nonessential but important role during parasite development and identify rhomboid proteases as potential targets for disease control.
C1 Johns Hopkins Sch Publ Hlth, Malaria Res Inst, Baltimore, MD USA.
Johns Hopkins Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD USA.
RP Srinivasan, P (reprint author), NIAID, Malaria Cell Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
EM srinivasanp@niaid.nih.gov
FU Johns Hopkins Malaria Research Institute; The Bloomberg Family
Foundation [R01 AI 1031478]; National Institute of Allergy and
Infectious Diseases
FX This work was supported by Johns Hopkins Malaria Research Institute, The
Bloomberg Family Foundation, and grant R01 AI 1031478 from the National
Institute of Allergy and Infectious Diseases.
NR 51
TC 22
Z9 22
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD JAN
PY 2009
VL 5
IS 1
AR e1000262
DI 10.1371/journal.ppat.1000262
PG 10
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 415IP
UT WOS:000263927800017
PM 19148267
ER
PT J
AU Sandel, ME
Wang, H
Terdiman, J
Hoffman, JM
Ciol, MA
Sidney, S
Quesenberry, C
Lu, Q
Chan, L
AF Sandel, M. Elizabeth
Wang, Hua
Terdiman, Joseph
Hoffman, Jeanne M.
Ciol, Marcia A.
Sidney, Steven
Quesenberry, Charles
Lu, Qi
Chan, Leighton
TI Disparities in Stroke Rehabilitation: Results of a Study in an
Integrated Health System in Northern California
SO PM&R
LA English
DT Article
AB Objective: To determine whether there are disparities in postacute stroke rehabilitation based on type of stroke, race/ethnicity, sex/gender, age, socioeconomic status, geographic region, or service area referral patterns in a large integrated health system with multiple levels of care.
Design: Cohort study tracking rehabilitation services for 365 days after acute hospitalization for a first stroke.
Setting: The Northern California Kaiser Permanente Health System (approximately 3.3 million membership population)
Participants: A total of 11,119 patients hospitalized for acute stroke from 1996 to 2003. The cohort includes patients discharged from acute care after a stroke. Postacute care rehabilitation services were evaluated according to the level of care ever-received within the 365 days after discharge from acute care, including inpatient rehabilitation hospital (IRH), skilled nursing facility (SNF), home health and outpatient, or no rehabilitation services.
Interventions: Not applicable.
Main Outcome Measure: Service delivery.
Results: Patients discharged to an IRH had longer lengths of stay in acute care. Patients with hemorrhagic stroke were less likely to be treated in an I RH. Patients whose highest level of rehabilitation was SNF were older and more likely to be women. After adjusting for age and other covariates, women were less likely to go to an IRH than men. Asian and black patients were more likely than white patients to be treated in an IRH or SNF. Also more likely to go to an IRH were patients from higher socioeconomic groups, from urban areas, and from geographic areas close to the regional rehabilitation hospital.
Conclusions: These results suggest variation in care delivery and extent of postacute care based on differences in patient demographics and geographic factors. Results also varied over time. Some minority populations in this cohort appeared to be more likely to receive IRH care, possibly because of disease severity, family support systems, cultural factors, or differences in referral patterns.
C1 [Sandel, M. Elizabeth] Kaiser Fdn Rehabil Ctr, Napa Solano Serv Area, Vallejo, CA 94589 USA.
[Terdiman, Joseph; Sidney, Steven; Quesenberry, Charles; Lu, Qi] Kaiser Permanente, Div Res, Oakland, CA USA.
[Hoffman, Jeanne M.; Ciol, Marcia A.] Univ Washington, Seattle, WA 98195 USA.
[Chan, Leighton] NIH, Bethesda, MD 20892 USA.
RP Sandel, ME (reprint author), Kaiser Fdn Rehabil Ctr, Napa Solano Serv Area, 975 Sereno Dr, Vallejo, CA 94589 USA.
EM elizabeth.sandel@kp.org
FU Centers for Disease Control and Prevention
FX This study was supported with funding from the Centers for Disease
Control and Prevention. Additional resources were provided by the
Intramural Research Program (Clinical Center) of the National Institutes
of Health, the Centers for Medicare and Medicaid Services, and Kaiser
Permanente.
NR 34
TC 20
Z9 20
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1934-1482
J9 PM&R
JI PM&R
PD JAN
PY 2009
VL 1
IS 1
BP 29
EP 40
DI 10.1016/j.pmrj.2008.10.012
PG 12
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA V24LD
UT WOS:000208411000006
PM 19627870
ER
PT J
AU Hardwick, JP
Osei-Hyiaman, D
Wiland, H
Abdelmegeed, MA
Song, BJ
AF Hardwick, James P.
Osei-Hyiaman, Douglas
Wiland, Homer
Abdelmegeed, Mohamed A.
Song, Byoung-Joon
TI PPAR/RXR Regulation of Fatty Acid Metabolism and Fatty Acid
omega-Hydroxylase (CYP4) Isozymes: Implications for Prevention of
Lipotoxicity in Fatty Liver Disease
SO PPAR RESEARCH
LA English
DT Review
ID ACTIVATED-RECEPTOR-ALPHA; TRIGLYCERIDE TRANSFER PROTEIN; HEPATIC
CYTOCHROME-P450 2E1; ELEMENT-BINDING PROTEIN-1C; TYPE-2
DIABETES-MELLITUS; DIET-INDUCED OBESITY; ACYL-COA OXIDASE;
VERY-LONG-CHAIN; INSULIN-RESISTANCE; NONALCOHOLIC STEATOHEPATITIS
AB Fatty liver disease is a common lipid metabolism disorder influenced by the combination of individual genetic makeup, drug exposure, and life-style choices that are frequently associated with metabolic syndrome, which encompasses obesity, dyslipidemia, hypertension, hypertriglyceridemia, and insulin resistant diabetes. Common to obesity related dyslipidemia is the excessive storage of hepatic fatty acids (steatosis), due to a decrease in mitochondria beta-oxidation with an increase in both peroxisomal beta-oxidation, and microsomal.-oxidation of fatty acids through peroxisome proliferator activated receptors (PPARs). How steatosis increases PPAR alpha activated gene expression of fatty acid transport proteins, peroxisomal and mitochondrial fatty acid beta-oxidation and omega-oxidation of fatty acids genes regardless of whether dietary fatty acids are polyunsaturated (PUFA), monounsaturated (MUFA), or saturated (SFA) may be determined by the interplay of PPARs and HNF4 alpha with the fatty acid transport proteins L-FABP and ACBP. In hepatic steatosis and steatohepatitis, the omega-oxidation cytochrome P450 CYP4A gene expression is increased even with reduced hepatic levels of PPARa. Although numerous studies have suggested the role ethanol-inducible CYP2E1 in contributing to increased oxidative stress, Cyp2e1-null mice still develop steatohepatitis with a dramatic increase in CYP4A gene expression. This strongly implies that CYP4A fatty acid.-hydroxylase P450s may play an important role in the development of steatohepatitis. In this review and tutorial, we briefly describe how fatty acids are partitioned by fatty acid transport proteins to either anabolic or catabolic pathways regulated by PPARs, and we explore how medium-chain fatty acid (MCFA) CYP4A and long-chain fatty acid (LCFA) CYP4F omega-hydroxylase genes are regulated in fatty liver. We finally propose a hypothesis that increased CYP4A expression with a decrease in CYP4F genes may promote the progression of steatosis to steatohepatitis. Copyright (C) 2009 James P. Hardwick et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
C1 [Hardwick, James P.; Wiland, Homer] NE OH Univ Coll Med & Pharm NEOUCOM NEOUCOP, Dept Integrat Med Sci, Rootstown, OH 44272 USA.
[Osei-Hyiaman, Douglas] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Osei-Hyiaman, Douglas] Nippon Boehringer Ingelheim Co Ltd, CardioMetab Dis Res Grp, Dept Mol & Cellular Biol, Kobe Pharma Res Inst,Chuo Ku, Kobe, Hyogo 6500047, Japan.
[Abdelmegeed, Mohamed A.; Song, Byoung-Joon] NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
RP Hardwick, JP (reprint author), NE OH Univ Coll Med & Pharm NEOUCOM NEOUCOP, Dept Integrat Med Sci, 4209 State Route 44, Rootstown, OH 44272 USA.
EM jph@neoucom.edu
NR 152
TC 43
Z9 43
U1 1
U2 14
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1687-4757
J9 PPAR RES
JI PPAR Res.
PY 2009
AR 952734
DI 10.1155/2009/952734
PG 20
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 670JV
UT WOS:000283418500001
ER
PT J
AU Balcazar, H
Alvarado, M
Cantu, F
Pedregon, V
Fulwood, R
AF Balcazar, Hector
Alvarado, Matilde
Cantu, Frank
Pedregon, Veronica
Fulwood, Robert
TI A Promotora de Salud Model for Addressing Cardiovascular Disease Risk
Factors in the US-Mexico Border Region
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
AB Introduction
In 2002, the National Heart, Lung, and Blood Institute partnered with the Health Resources and Services Administration's (HRSA's) Bureau of Primary Health Care and Office of Rural Health Policy to address cardiovascular health in the US-Mexico border region. From 2003 through 2005, the 2 agencies agreed to conduct an intervention program using Salud para su Corazon with promotores de salud (community health workers) in high-risk Hispanic communities served by community health centers (CHCs) in the border region to reduce risk factors and improve health behaviors.
Methods
Promotores de salud from each CHC delivered lessons from the curriculum Your Heart, Your Life. Four centers implemented a 1-group pretest-posttest study design. Educational sessions were delivered for 2 to 3 months. To test Salud para su Corazon-HRSA health objectives, the CHCs conducted the program and assessed behavioral and clinical outcomes at baseline, 3 months, 6 months, and 12 months after the intervention. A 2-sample paired t test and analyses of variance were used to evaluate differences from baseline to postintervention.
Results
Changes in heart-healthy behaviors were observed, as they have been in previous Salud para su Corazon studies, lending credibility to the effectiveness of a promotores de salud program in a clinical setting. Positive changes were also observed in low-density lipoprotein cholesterol level, triglyceride level, waist circumference, diastolic blood pressure, weight, and glycated hemoglobin (HbA1c).
Conclusion
Results suggest that integrating promotores de salud into clinical practices is a promising strategy for culturally competent and effective service delivery. Promotores de salud build coalitions and partnerships in the community. The Salud para su Corazon-HRSA initiative was successful in helping to develop an infrastructure to support a promotores de salud workforce in the US-Mexico border region.
C1 [Alvarado, Matilde; Fulwood, Robert] NHLBI, NIH, Bethesda, MD 20892 USA.
[Cantu, Frank] US Hlth Resources & Serv Adm, Rockville, MD 20857 USA.
[Pedregon, Veronica] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Balcazar, H (reprint author), Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, El Paso Reg Campus,1100 N Stanton St,Ste 100, El Paso, TX 79902 USA.
EM Hector.G.Balcazar@uth.tmc.edu
FU NHLBI; HRSA
FX We acknowledge the following community health centers and their
representatives: CSV, Melissa Aguirre; NCHS, Maria Banuelos; GCHC,
Lourdes Rangel; MCHC, Rosi Piper. We also recognize all of the
promotores from the various community health centers who participated in
the project. Lastly, we acknowledge funding for this project by NHLBI
and HRSA.
NR 13
TC 23
Z9 23
U1 1
U2 4
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD JAN
PY 2009
VL 6
IS 1
AR A02
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA V20RU
UT WOS:000208157900002
PM 19080008
ER
PT J
AU Boyington, JEA
Schoster, B
Martin, KR
Shreffler, J
Callahan, LF
AF Boyington, Josephine E. A.
Schoster, Britta
Martin, Kathryn Remmes
Shreffler, Jack
Callahan, Leigh F.
TI Perceptions of Individual and Community Environmental Influences on
Fruit and Vegetable Intake, North Carolina, 2004
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID PHYSICAL-ACTIVITY; FOOD CHOICE; CARE; CONSUMPTION; HABITS; IMPACT
AB Introduction
Increases in obesity and other chronic conditions continue to fuel efforts for lifestyle behavior changes. However, many strategies do not address the impact of environment on lifestyle behaviors, particularly healthy dietary intake. This study explored the perceptions of environment on intake of fruits and vegetables in a cohort of 2,479 people recruited from 22 family practices in North Carolina.
Methods
Participants were administered a health and social demographic survey. Formative assessment was conducted on a subsample of 32 people by using focus groups, semistructured individual interviews, community mapping, and photographs. Interviews and discussions were transcribed and content was analyzed using ATLAS.ti version 5. Survey data were evaluated for means, frequencies, and group differences.
Results
The 2,479 participants had a mean age of 52.8 years, mean body mass index (BMI) of 29.4, and were predominantly female, white, married, and high school graduates. The 32 subsample participants were older, heavier, and less educated. Some prevalent perceptions about contextual factors related to dietary intake included taste-bud fatigue (boredom with commonly eaten foods), life stresses, lack of forethought in meal planning, current health status, economic status, the ability to garden, lifetime dietary exposure, concerns about food safety, contradictory nutrition messages from the media, and variable work schedules.
Conclusion
Perceptions about intake of fruits and vegetables intake are influenced by individual (intrinsic) and community (extrinsic) environmental factors. We suggest approaches for influencing behavior and changing perceptions using available resources.
C1 [Martin, Kathryn Remmes] Univ N Carolina, Gillings Sch Publ Hlth, Thurston Arthrit Res Ctr, Inst Aging, Chapel Hill, NC USA.
[Callahan, Leigh F.] Univ N Carolina, Thurston Arthrit Res Ctr, Dept Med, Dept Orthoped,Dept Social Med, Chapel Hill, NC USA.
RP Boyington, JEA (reprint author), NINR, NIH, 1 Democracy Plaza,6701 Democracy Blvd,Suite 710, Bethesda, MD 20892 USA.
EM boyingtonje@mail.nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
[5P60-AR49465-01, 5P60-AR49465-04S1]; National Institutes of Health;
National Center on Minority Health and Health Disparities [R24
MD000167]; Department of Health and Human Services, Agency for
Healthcare Research and Quality [R24 HS013353]; National Institute on
Aging [5-T32-AG00272]; Arthritis Foundation Doctoral Dissertation Award;
ACR REF
FX This study was funded by National Institute of Arthritis and
Musculoskeletal and Skin Diseases grant no. 5P60-AR49465-01. Dr
Boyington was supported by the National Institute of Arthritis and
Musculoskeletal and Skin Diseases grant no. 5P60-AR49465-04S1, National
Institutes of Health, the National Center on Minority Health and Health
Disparities grant no. R24 MD000167, and the Department of Health and
Human Services, Agency for Healthcare Research and Quality R24 HS013353.
Ms Remmes Martin was supported by the Carolina Program on Health and
Aging Research Predoctoral Fellowship (National Institute on Aging grant
no. 5-T32-AG00272), the Arthritis Foundation Doctoral Dissertation
Award, and the ACR REF Health Professional Graduate Student Research
Preceptorship Award.
NR 34
TC 6
Z9 6
U1 0
U2 7
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD JAN
PY 2009
VL 6
IS 1
AR A04
PG 15
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA V20RU
UT WOS:000208157900004
PM 19080010
ER
PT J
AU Wolf, RL
Lepore, SJ
Vandergrift, JL
Basch, CE
Yaroch, AL
AF Wolf, Randi L.
Lepore, Stephen J.
Vandergrift, Jonathan L.
Basch, Charles E.
Yaroch, Amy L.
TI Tailored telephone education to promote awareness and adoption of fruit
and vegetable recommendations among urban and mostly immigrant black
men: A randomized controlled trial
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Diet; Randomized clinical trial; Telephone education; Fruits and
vegetables; Men; Minority; Immigrant population
ID UNITED-STATES; INCREASE CONSUMPTION; DIET INTERVENTION; AFRICAN
DIASPORA; HEALTH; ADULTS; QUESTIONNAIRE; EFFICACY; CANCER; STAGE
AB Background. Fruit and vegetable (FV) intake in black men are far below national recommendations.
Methods. Urban, primarily immigrant, black men (n=490) from the New York City metropolitan area participating in the Cancer Awareness and Prevention (CAP) Trial (2005-2007) were randomly assigned to one of two intervention groups: 1) FV Education (FVE) or 2) Prostate Education (PE). Both interventions entailed a mailed brochure plus two tailored telephone education (TTE) calls. Outcomes, measured at baseline and at eight months, included knowledge of FV recommendations, perceived benefits, stage of readiness to adopt recommendations and self-reported FV consumption.
Results. At follow-up. the WE group consumed an average of 1.2 more FV servings per day than the PE group (P<0.001; adjusted for baseline). The FVE group also demonstrated increases in knowledge about recommended FV amounts (P<0.01) and appropriate serving sizes (P<0.05), and in the percent of participants moving from a lower to a higher stage of readiness to adopt FV recommendations (P<0.05). The FVE group did not demonstrate increases in knowledge related to the importance of eating a colorful variety or in the ability to name potential health benefits.
Conclusions. TTE can be a practical and moderately effective intervention for raising awareness of FV recommendations and for Promoting FV consumption in urban and primarily immigrant black men. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Wolf, Randi L.; Basch, Charles E.] Columbia Univ, Teachers Coll, Dept Hlth & Behav Studies, New York, NY 10027 USA.
[Lepore, Stephen J.; Vandergrift, Jonathan L.] Temple Univ, Dept Publ Hlth, Philadelphia, PA 19122 USA.
[Yaroch, Amy L.] NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Wolf, RL (reprint author), Columbia Univ, Teachers Coll, Dept Hlth & Behav Studies, New York, NY 10027 USA.
EM wolf@tc.columbia.edu
FU National Cancer Institute of the National Institutes of Health [R01
CA104223]
FX This research was supported by grant R01 CA104223 from the National
Cancer Institute of the National Institutes of Health. We acknowledge
all members of the Cancer Awareness and Prevention (CAP) trial research
team, the Data Safety and Monitoring Board members, and the
participants. A special thanks to research assistants Melissa Godfrey,
Stephanie Brazis, Lindsay Wetmore-Arkader, Elizabeth McGinty and Gabriel
Pietrzak.
NR 57
TC 17
Z9 17
U1 2
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD JAN
PY 2009
VL 48
IS 1
BP 32
EP 38
DI 10.1016/j.ypmed.2008.10.015
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 401DE
UT WOS:000262918000006
PM 19010349
ER
PT S
AU Menezes, LF
Germino, GG
AF Menezes, Luis F.
Germino, Gregory G.
BE Sloboda, RD
TI Polycystic Kidney Disease, Cilia, and Planar Polarity
SO PRIMARY CILIA
SE Methods in Cell Biology
LA English
DT Review; Book Chapter
ID BARDET-BIEDL-SYNDROME; RIGHT AXIS DETERMINATION; WNT SIGNALING PATHWAYS;
BASAL BODY DYSFUNCTION; CELL POLARITY; CYST FORMATION; TRANSGENIC MICE;
GENE-PRODUCT; SUBCELLULAR-LOCALIZATION; INTRACELLULAR CALCIUM
AB Cystic kidney diseases are characterized by dilated or cystic kidney tubular segments. Changes in planar cell polarity, flow sensing, and/or proliferation have been proposed to explain these disorders. Over the last few years, several groups have suggested that ciliary dysfunction is a central component of cyst formation. We review evidence for and against each of these models, stressing some of the inconsistencies that should be resolved if an accurate understanding of cyst formation is to be achieved. We also comment on data supporting a model in which ciliary function could play different roles at different developmental stages and on the relevance of dissecting potential differences between pathways required for tubule formation and/or maintenance.
C1 [Menezes, Luis F.; Germino, Gregory G.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Germino, Gregory G.] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Menezes, LF (reprint author), Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
RI Menezes, Luis Fernando/C-7286-2015;
OI Germino, Gregory/0000-0002-3609-5588
FU Intramural NIH HHS; NIDDK NIH HHS [R37DK48006]
NR 97
TC 20
Z9 20
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-679X
BN 978-0-12-375024-2
J9 METHOD CELL BIOL
JI Methods Cell Biol.
PY 2009
VL 94
BP 273
EP +
DI 10.1016/S0091-679X(08)94014-0
PG 30
WC Cell Biology
SC Cell Biology
GA BMN63
UT WOS:000272975500015
PM 20362096
ER
PT J
AU Colbert, RA
Delay, ML
Layh-Schmitt, G
Sowders, DP
AF Colbert, Robert A.
DeLay, Monica L.
Layh-Schmitt, Gerlinde
Sowders, Dawn P.
TI HLA-B27 misfolding and spondyloarthropathies
SO PRION
LA English
DT Review
DE ankylosing spondylitis; arthritis; protein misfolding; unfolded protein
response; interleukin (IL)-17; cytokines
ID MHC CLASS-I; UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS;
HUMAN MONOCYTIC CELLS; SPONTANEOUS INFLAMMATORY DISEASE; DISULFIDE BOND
FORMATION; GENOME-WIDE ASSOCIATION; ANKYLOSING-SPONDYLITIS; TRANSGENIC
RATS; T-CELLS
AB HLA-B27 plays a central role in the pathogenesis of many spondyloarthropathies and in particular ankylosing spondylitis. The observation that the HLA-B27 heavy chain has a tendency to misfold has raised the possibility that associated diseases may belong in a rapidly expanding category of protein misfolding disorders. The synthesis of the HLA-B27 heavy chain, assembly with beta(2)m and the loading of peptide cargo, occurs in the endoplasmic reticulum ( ER) before transport to the cell surface. The evidence indicates that misfolding occurs in the ER prior to beta(2)m association and peptide optimization and is manifested in the formation of aberrant inter- and intra-chain disulfide bonds and accumulation of heavy chain bound to the chaperone BiP. Enhanced accumulation of misfolded heavy chains during the induction of class I expression by cytokines, can cause ER stress resulting in activation of the unfolded protein response (UPR).
Effects of UPR activation on cytokine production are beginning to emerge and may provide important missing links between HLA-B27 misfolding and spondyloarthritis. In this chapter we will review what has been learned about HLA-B27 misfolding in human cells and in the transgenic rat model of spondyloarthritis-like disease, considering it in the context of other protein misfolding disorders. These studies provide a framework to support much needed translational work assessing HLA-B27 misfolding and UPR activation in patient-derived material, its consequences for disease pathogenesis and ultimately how and where to focus intervention strategies.
C1 [Colbert, Robert A.; Layh-Schmitt, Gerlinde] NIAMS, NIH, Bethesda, MD 20892 USA.
[Colbert, Robert A.; DeLay, Monica L.; Layh-Schmitt, Gerlinde; Sowders, Dawn P.] Cincinnati Childrens Hosp, Med Ctr, Div Rheumatol, Cincinnati, OH USA.
RP Colbert, RA (reprint author), NIAMS, NIH, Bldg 10,CRC Rm 1-5142,10 Ctr Dr,MSC 1102, Bethesda, MD 20892 USA.
EM colbertra@mac.com
NR 129
TC 15
Z9 16
U1 1
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
SN 1933-6896
J9 PRION
JI Prion
PD JAN-MAR
PY 2009
VL 3
IS 1
BP 15
EP 26
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 436XM
UT WOS:000265449400004
PM 19363299
ER
PT B
AU Wendling, D
Johnson, T
Kaske, N
AF Wendling, Daniel
Johnson, Travis
Kaske, Neal
BE Hiller, S
Justh, K
Kyrillidou, M
Self, J
TI Student Research Behavior: Quantitative and Qualitative Research
Findings Presented with Visualizations
SO PROCEEDINGS OF THE 2008 LIBRARY ASSESSMENT CONFERENCE: BUILDING
EFFECTIVE, SUSTAINABLE, PRACTICAL ASSESSMENT
LA English
DT Proceedings Paper
CT 2008 Library Assessment Conference
CY AUG 04-07, 2008
CL Seattle, WA
SP Univ Virgina Library, Assoc Res Libraries, Univ Washington Libraries
ID INFORMATION; LIBRARY
AB The authors investigated the information-seeking patterns of 650 college students at the University of Maryland, College Park and explored ways to generate knowledge about research behaviors. Through focus groups and individual interviews, students from a wide variety of matriculation levels and subject areas described the tools they used and the order of use. Construction of the interview analysis application is described here, including interviewing techniques, inter-view form, results coding sheet, application structure, and screen shots from a Web-based prototype application that renders tables, charts, and graphs about student research behavior from the data set. This methodology helps analyze information-seeking behavior data regarding library and non-library, and Internet/non-Internet resource use. It can make comparison of this dataset with other datasets possible, and can help track emergent behaviors and tool use in the future.
The contents of this presentation reflect the views of the authors who are responsible for the opinions, facts, and the accuracy of the data presented. The contents do not necessarily reflect the official views or policies of the National Library of Medicine, National Oceanic and Atmospheric Administration, or University of Maryland Libraries.
C1 [Wendling, Daniel] Natl Lib Med, Bethesda, MD 20894 USA.
NR 34
TC 0
Z9 0
U1 1
U2 1
PU ASSOC RESEARCH LIBRARIES
PI WASHINGTON
PA 21 DUPONT CIRCLE, NW, SUITE 800, WASHINGTON, DC 20036 USA
BN 978-1-59407-814-9
PY 2009
BP 289
EP 306
PG 18
WC Information Science & Library Science
SC Information Science & Library Science
GA BJG46
UT WOS:000265657500038
ER
PT S
AU Liu, HC
Tsai, HC
Liu, SW
AF Liu, Hsiang-Chuan
Tsai, Hsien-Chang
Liu, Shin-Wu
BE Lagakos, S
Perlovsky, L
Jha, M
Covaci, B
Zaharim, A
Mastorakis, N
TI A novel predicting algorithm for Thermostable Proteins based on Hurst
exponent and Maximized L-measure
SO PROCEEDINGS OF THE AMERICAN CONFERENCE ON APPLIED MATHEMATICS: RECENT
ADVANCES IN APPLIED MATHEMATICS
SE Mathematics and Computers in Science and Engineering
LA English
DT Proceedings Paper
CT American Conference on Applied Mathematics
CY JAN 27-29, 2010
CL Harvard Univ, Cambridge, MA
SP WSEAS
HO Harvard Univ
DE Hurst exponent; Lambda-measure; P-measure; L-measure; Maximized
L-measure
ID POPS
AB Establishing a good algorithm for predicting temperature of thermostable proteins is an important issue. In this study, a new thermostable proteins prediction method by using Hurst exponent and Choquet integral regression model with respect to maximized L-measure is proposed. The main idea of this method is to integrate the physicochemical properties, long term memory property and Choquet integral regression model with respect to maximized L-measure for amino symbolic sequences of different lengths. For evaluating the performance of this new algorithm, a 5-fold Cross-Validation MSE is conducted. Experimental result shows that this new prediction algorithm is better than the Choquet integral regression model with respect to other well known fuzzy measure, Lambda-measure, P-measure, and L-measure, respectively and the traditional prediction models, ridge regression and multiple linear regression models, respectively.
C1 [Liu, Hsiang-Chuan] Asia Univ, Dept Bioinformat, 500 Lioufeng Rd, Wufeng 41354, Taichung County, Taiwan.
[Tsai, Hsien-Chang] Natl Changhua Univ Educ, Dept Biol, Changhua 50001, Taiwan.
[Liu, Shin-Wu] Natl Inst Hlth, Lab Viral Diseases, Bethesda, MD 20892 USA.
RP Liu, HC (reprint author), Asia Univ, Dept Bioinformat, 500 Lioufeng Rd, Wufeng 41354, Taichung County, Taiwan.
EM lhc@asia.edu.tw; bihft@cc.ncue.edu.tw; liushin@mail.nih.gov
FU National Science Council grant of Taiwan Government [NSC
98-2410-H-468-014]
FX This paper is partially supported by the National Science Council grant
of Taiwan Government (NSC 98-2410-H-468-014)
NR 14
TC 0
Z9 0
U1 0
U2 0
PU WORLD SCIENTIFIC AND ENGINEERING ACAD AND SOC
PI ATHENS
PA AG LOANNOU THEOLOGOU 17-23, 15773 ZOGRAPHOU, ATHENS, GREECE
SN 1792-4308
BN 978-960-474-150-2
J9 MATH COMPUT SCI ENG
PY 2009
BP 304
EP +
PG 2
WC Mathematics, Applied
SC Mathematics
GA BPM82
UT WOS:000279344900044
ER
PT B
AU Lin, DC
Shreiber, DI
Dimitriadis, EK
Horkay, F
AF Lin, David C.
Shreiber, David I.
Dimitriadis, Emilios K.
Horkay, Ferenc
GP ASME
TI A HYPERELASTIC CONTACT MODEL FOR THE INDENTATION OF CHONDROCYTES AND
CARTILAGE EXTRACELLULAR MATRIX
SO PROCEEDINGS OF THE ASME SUMMER BIOENGINEERING CONFERENCE 2008, PTS A AND
B
LA English
DT Proceedings Paper
CT ASME Summer Bioengineering Conference
CY JUN 25-29, 2008
CL Marco Isl, FL
SP Amer Soc Mech Engineers, Bioengn Div
ID ATOMIC-FORCE MICROSCOPY; ARTICULAR-CARTILAGE; ZONE
C1 [Lin, David C.; Horkay, Ferenc] NICHHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA.
RP Lin, DC (reprint author), NICHHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA.
OI Shreiber, David/0000-0001-8248-419X
NR 5
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MECHANICAL ENGINEERS
PI NEW YORK
PA THREE PARK AVENUE, NEW YORK, NY 10016-5990 USA
BN 978-0-7918-4321-5
PY 2009
BP 1069
EP 1070
PG 2
WC Engineering, Biomedical
SC Engineering
GA BIW31
UT WOS:000263364700535
ER
PT B
AU Korecki, CL
Walter, BA
Godburn, KE
Iatridis, JC
AF Korecki, Casey L.
Walter, Benjamin A.
Godburn, Karolyn E.
Iatridis, James C.
GP ASME
TI ASYMMETRIC LOADING PROMOTES EARLY SIGNS OF INTERVERTEBRAL DISC
DEGENERATION IN LARGE ANIMAL ORGAN CULTURE
SO PROCEEDINGS OF THE ASME SUMMER BIOENGINEERING CONFERENCE - 2009, PT A
AND B
LA English
DT Proceedings Paper
CT ASME Summer Bioengineering Conference
CY JUN 17-21, 2009
CL Lake Tahoe, CA
SP ASME Bioengn Div
C1 [Korecki, Casey L.] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Korecki, CL (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MECHANICAL ENGINEERS
PI NEW YORK
PA THREE PARK AVENUE, NEW YORK, NY 10016-5990 USA
BN 978-0-7918-4891-3
PY 2009
BP 151
EP 152
PG 2
WC Cell & Tissue Engineering; Engineering, Biomedical
SC Cell Biology; Engineering
GA BPV38
UT WOS:000280089000076
ER
PT B
AU Lin, DC
Horkay, F
AF Lin, David C.
Horkay, Ferenc
GP ASME
TI MAPPING THE ELASTIC AND OSMOTIC PROPERTIES OF CARTILAGE EXTRACELLULAR
MATRIX
SO PROCEEDINGS OF THE ASME SUMMER BIOENGINEERING CONFERENCE - 2009, PT A
AND B
LA English
DT Proceedings Paper
CT ASME Summer Bioengineering Conference
CY JUN 17-21, 2009
CL Lake Tahoe, CA
SP ASME Bioengn Div
ID GELS
C1 [Lin, David C.; Horkay, Ferenc] NIH, Sect Tissue Biophys & Biomimet, Bethesda, MD 20892 USA.
RP Lin, DC (reprint author), NIH, Sect Tissue Biophys & Biomimet, Bldg 10, Bethesda, MD 20892 USA.
NR 6
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MECHANICAL ENGINEERS
PI NEW YORK
PA THREE PARK AVENUE, NEW YORK, NY 10016-5990 USA
BN 978-0-7918-4891-3
PY 2009
BP 677
EP 678
PG 2
WC Cell & Tissue Engineering; Engineering, Biomedical
SC Cell Biology; Engineering
GA BPV38
UT WOS:000280089000339
ER
PT J
AU Ding, XY
Patel, M
Chan, CC
AF Ding, Xiaoyan
Patel, Mrinali
Chan, Chi-Chao
TI Molecular pathology of age-related macular degeneration
SO PROGRESS IN RETINAL AND EYE RESEARCH
LA English
DT Review
DE Age-related macular degeneration; Inflammation; Single nucleotide
polymorphism; Genetics Retinal pigment epithelium; Retinal
photoreceptors; Drusen; Vascular endothelial growth factor; Bruch's
membrane; Molecular pathology
ID COMPLEMENT FACTOR-H; RETINAL-PIGMENT EPITHELIUM; C-REACTIVE PROTEIN;
EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION; APOLIPOPROTEIN-E GENE; BLUE
MOUNTAINS EYE; HTRA1 PROMOTER POLYMORPHISM; MITOCHONDRIAL-DNA DAMAGE;
CASE-CONTROL SAMPLES; GROWTH-FACTOR-BETA
AB Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the world. Although the etiology and pathogenesis of AMD remain largely unclear, a complex interaction of genetic and environmental factors is thought to exist. AMD pathology is characterized by degeneration involving the retinal photoreceptors, retinal pigment epithelium, and Bruch's membrane, as well as, in some cases, alterations in choroidal capillaries. Recent research on the genetic and molecular underpinnings of AMD brings to light several basic molecular pathways and pathophysiological processes that might mediate AMD risk, progression, and/or response to therapy. This review summarizes, in detail, the molecular pathological findings in both humans and animal models, including genetic variations in CFH, CX3CR1, and ARMS2/HtrA1, as well as the role of numerous molecules implicated in inflammation, apoptosis, cholesterol trafficking, angiogenesis, and oxidative stress. Published by Elsevier Ltd.
C1 [Ding, Xiaoyan; Patel, Mrinali; Chan, Chi-Chao] NEI, Immunopathol Sect, Immunol Lab, Bethesda, MD 20892 USA.
[Ding, Xiaoyan] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, Guangzhou 510060, Guangdong, Peoples R China.
[Patel, Mrinali] Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Chan, CC (reprint author), NEI, Immunopathol Sect, Immunol Lab, 10 Ctr Dr,10-10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
FU NEI Intramural Research Program
FX We would like to thank Dr. Robert B. Nussenblatt for his critical
review. The support for this study was provided by the NEI Intramural
Research Program.
NR 209
TC 258
Z9 268
U1 12
U2 73
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1350-9462
J9 PROG RETIN EYE RES
JI Prog. Retin. Eye Res.
PD JAN
PY 2009
VL 28
IS 1
BP 1
EP 18
DI 10.1016/j.preteyeres.2008.10.001
PG 18
WC Ophthalmology
SC Ophthalmology
GA 420RF
UT WOS:000264306200001
PM 19026761
ER
PT J
AU Sublette, ME
Milak, MS
Hibbeln, JR
Freed, PJ
Oquendo, MA
Malone, KM
Parsey, RV
Mann, JJ
AF Sublette, M. Elizabeth
Milak, Matthew S.
Hibbeln, Joseph R.
Freed, Peter J.
Oquendo, Maria A.
Malone, Kevin M.
Parsey, Ramin V.
Mann, J. John
TI Plasma polyunsaturated fatty acids and regional cerebral glucose
metabolism in major depression
SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
LA English
DT Article
DE Major Depressive Disorder; Bipolar Disorder; PET; Docosahexaenoic acid;
Arachidonic acid; Eicosapentaenoic acid; PUFA
ID POSITRON-EMISSION-TOMOGRAPHY; POSTMORTEM ORBITOFRONTAL CORTEX;
BLOOD-CELL MEMBRANES; RHESUS-MONKEY; DOCOSAHEXAENOIC ACID;
ARACHIDONIC-ACID; BIPOLAR DISORDER; SEROTONERGIC CHALLENGE;
FRONTAL-CORTEX; PREFRONTAL CONNECTIONS
AB Deficiencies in polyunsaturated essential fatty acids (PUFA) are implicated in mood disorders, although mechanisms of action and regional specificity in the brain are unknown. We hypothesized that plasma phospholipid PUFA levels are correlated with regionally specific relative cerebral metabolic rates of glucose (rCMRglu). Medication-free depressed subjects (N=29) were studied using [(18)F]-fluoro-2-deoxyglucose positron emission tomography. Docosahexaenoic acid (22:6n-3), arachidonic acid (20:4n-6), and eicosapentaenoic acid (20:5n-3) were assessed as a percentage of total phospholipid PUFA (DHA%, AA%, and EPA%, respectively). DHA% and AA% correlated positively with rCMRglu in temporoparietal cortex. In addition, DHA% correlated negatively with rCMRglu in prefrontal cortex and anterior cingulate. No correlations were seen with EPA%. Thus, under conditions of low plasma DHA, rCMRglu was higher in temporoparietal cortex and lower in anterior cingulate/prefrontal cortex. Opposing effects of DHA on these regions is a hypothesis that could be addressed in future prospective studies with n-3 supplementation. This pilot study is the first to demonstrate fatty acid and regionally specific correlations in the brain between plasma PUFA and rCMRglu in humans. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Sublette, M. Elizabeth; Milak, Matthew S.; Freed, Peter J.; Oquendo, Maria A.; Parsey, Ramin V.; Mann, J. John] Columbia Univ, New York State Psychiat Inst, Dept Mol Imaging & Neuropathol, New York, NY 10032 USA.
[Sublette, M. Elizabeth; Milak, Matthew S.; Freed, Peter J.; Oquendo, Maria A.; Parsey, Ramin V.; Mann, J. John] Columbia Univ, Dept Psychiat, New York, NY 10032 USA.
[Mann, J. John] Columbia Univ, Dept Radiol, New York, NY 10032 USA.
[Hibbeln, Joseph R.] NIAAA, NIH, Bethesda, MD USA.
[Malone, Kevin M.] Univ Coll Dublin, Sch Med & Med Sci, Dublin, Ireland.
RP Sublette, ME (reprint author), Columbia Univ, New York State Psychiat Inst, Dept Mol Imaging & Neuropathol, 1051 Riverside Dr,Unit 42, New York, NY 10032 USA.
EM es2316@columbia.edu
RI Sublette, M/A-8391-2009; Milak, Matthew/Q-7170-2016;
OI Sublette, M/0000-0001-7378-4262; Malone, Kevin M/0000-0001-5665-4706
FU NCRR NIH HHS [M01 RR000645, M01 RR000645-280727, RR00645]; NIMH NIH HHS
[MH40695, MH62185, P50 MH062185, P50 MH062185-09, R01 MH040695, R01
MH040695-17, R01 MH048514]
NR 97
TC 40
Z9 41
U1 4
U2 9
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0952-3278
J9 PROSTAG LEUKOTR ESS
JI Prostaglandins Leukot. Essent. Fatty Acids
PD JAN
PY 2009
VL 80
IS 1
BP 57
EP 64
DI 10.1016/j.plefa.2008.11.004
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
GA 422NH
UT WOS:000264434500008
PM 19128951
ER
PT J
AU Ramsden, CE
Hibbeln, JR
Lands, WE
AF Ramsden, Christopher E.
Hibbeln, Joseph R.
Lands, William E.
TI Letter to the Editor re: Linoleic acid and coronary heart disease.
SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
LA English
DT Letter
C1 [Ramsden, Christopher E.] Univ N Carolina, Sch Med, Chapel Hill, NC 27599 USA.
[Hibbeln, Joseph R.] NIH, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
[Hibbeln, Joseph R.] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Ramsden, CE (reprint author), Univ N Carolina, Sch Med, CB 7200, Chapel Hill, NC 27599 USA.
EM cramsden@med.unc.edu
NR 10
TC 3
Z9 3
U1 1
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0952-3278
J9 PROSTAG LEUKOTR ESS
JI Prostaglandins Leukot. Essent. Fatty Acids
PD JAN
PY 2009
VL 80
IS 1
BP 77
EP 77
DI 10.1016/j.plefa.2008.12.002
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
GA 422NH
UT WOS:000264434500011
PM 19147338
ER
PT J
AU Kelly, MP
Lee, ST
Lee, FT
Smyth, FE
Davis, ID
Brechbiel, MW
Scott, AM
AF Kelly, Marcus P.
Lee, Sze Ting
Lee, F. -T.
Smyth, Fiona E.
Davis, Ian D.
Brechbiel, Martin W.
Scott, Andrew M.
TI Therapeutic Efficacy of Lu-177-CHX-A ''-DTPA-hu3S193 Radioimmunotherapy
in Prostate Cancer Is Enhanced by EGFR Inhibition or Docetaxel
Chemotherapy
SO PROSTATE
LA English
DT Article
DE hu3S193; prostate cancer; radioimmunotherapy; combined modality
ID EPIDERMAL-GROWTH-FACTOR; HUMANIZED MONOCLONAL-ANTIBODY; PHASE-I TRIAL;
COMBINED-MODALITY RADIOIMMUNOTHERAPY; LEWIS-Y ANTIGEN; SOLID TUMORS;
COLORECTAL-CARCINOMA; MEMBRANE ANTIGEN; BREAST-CANCER; LUNG-CANCER
AB BACKGROUND. This study investigated the biodistribution and therapeutic efficacy of Lutetium-177 (Lu-177) radiolabeled anti-Lewis Y monoclonal antibody hu3S193 radioimmnunotherapy (RIT) in mice bearing prostate cancer xenografts. The. ability of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor AG1478 and docetaxel chemotherapy to enhance the efficacy of RIT was also assessed in vivo.
METHODS. The in vitro cytotoxicity of Lu-177 labeled hu3S193 on Le(y) positive DUI 45 prostate cancer cells was assessed using proliferation assays, with induction of apoptosis measured by ELISA. The in vivo biodistribution and tumor localization of Lu-177-hu3S193 was assessed ill mice bearing established DU145 tumor xenografts. The efficacy and maximum tolerated dose of Lu-177-hu3S193 RIT in vivo was determined by a dose escalation study. EGFR inhibitor AG1478 or docetaxel chemotherapy was administered at sub-therapeutic doses in conjunction with RIT in vivo.
RESULTS. Lu-177-hu3S193 mediated significant induction of cytotoxicity and apoptosis in vitro. In vivo analysis of Lu-177-hu3S193 biodistribution demonstrated specific targeting of DU145 prostate cancer xenografts, with maximal tumor uptake of 33.2 +/- 3.9%ID/g observed at 120 hr post-injection. In RIT studies, Lu-177-hu3S193 caused specific and dose-dependent inhibition of prostate cancer tumor growth. A maximum tolerated dose of 350 mu Ci was determined for Lu-177-hu3S193. Combination of Lu-177-hu3S193 RIT with EGFR inhibitor AG1478 or docetaxel chemotherapy both significantly improved efficacy.
CONCLUSIONS. Lu-177-hu3S193 RIT is effective as a single agent in the treatment of Le(y) positive prostate cancer models. The enhancement of RIT by AG1478 or docetaxel indicates the promise of combined modality strategies. Prostate 69: 92-104, 2009. (C) 2008 Wiley-Liss. Inc.
C1 [Kelly, Marcus P.; Lee, Sze Ting; Lee, F. -T.; Smyth, Fiona E.; Scott, Andrew M.] Austin Hosp, Melbourne Ctr Clin Sci, Ludwig Inst Canc Res, Tumour Targeting Lab, Heidelberg, Vic 3084, Australia.
[Davis, Ian D.] Austin Hosp, Ludwig Inst Canc Res, Urooncol Lab, Heidelberg, Vic 3084, Australia.
[Brechbiel, Martin W.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Kelly, MP (reprint author), Austin Hosp, Melbourne Ctr Clin Sci, Ludwig Inst Canc Res, Tumour Targeting Lab, 145-163 Studley Rd, Heidelberg, Vic 3084, Australia.
EM mpkelly2@hotmail.com
RI Davis, Ian/A-1430-2012
OI Davis, Ian/0000-0002-9066-8244
FU NHMRC Program [280912]; NIH; National Cancer Institute; Center for
Cancer Research; Melbourne Research Scholarship, University of
Melbourne, Melbourne, Australia; Victorian Cancer Agency Clinician
Researcher Fellowship
FX We thank the staff from the Department of Nuclear Medicine, Austin
Hospital, for their assistance in the CT scanning and gamma camera
imaging of animals and staff of the Tumour Targeting Program for
assistance in biodistribution studies. This work was supported in part
by an NH&MRC Program Grant No. 280912 and the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research. MPK was supported by a Melbourne Research Scholarship,
University of Melbourne, Melbourne, Australia. IDD is supported in part
by a Victorian Cancer Agency Clinician Researcher Fellowship. MWB is
supported by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 50
TC 23
Z9 23
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-4137
J9 PROSTATE
JI Prostate
PD JAN 1
PY 2009
VL 69
IS 1
BP 92
EP 104
DI 10.1002/pros.20856
PG 13
WC Endocrinology & Metabolism; Urology & Nephrology
SC Endocrinology & Metabolism; Urology & Nephrology
GA 390EZ
UT WOS:000262148400010
PM 18942092
ER
PT S
AU Chung, JY
Hewitt, SM
AF Chung, Joon-Yong
Hewitt, Stephen M.
BE Kurien, BT
Scofield, RH
TI Transfer and Multiplex Immunoblotting of a Paraffin Embedded Tissue
SO PROTEIN BLOTTING AND DETECTION: METHODS AND PROTOCOLS
SE Methods in Molecular Biology
LA English
DT Article; Book Chapter
DE Immunoassay; Histology; Proteomics; Expressional profiling
ID LASER CAPTURE MICRODISSECTION; ELECTROPHORESIS; MICROARRAYS; EXPRESSION;
PROTEINS; CANCER
AB In the functional proteome era, the proteomic profiling of clinicopathologic annotated tissues is an essential step for mining and evaluations of candidate biomarkers for disease. Previously, application of routine proteomic methodologies to clinical tissue specimens has provided unsatisfactory results. Multiplex tissue immunoblotting is a method of transferring proteins from a formalin-fixed, paraffin-embedded tissue section to a stack of membranes which can be applied to a conventional immunoblotting method. A single tissue section can be transferred to up to ten membranes, each of which is probed with antibodies and detected with fluorescent tags. By this approach, total protein and target signals can be simultaneously determined on each membrane; hence each antibody is internally normalized. Phosphorylation-specific antibodies as well as antibodies that do not readily work well with paraffin-embedded tissue are applicable to the membranes, expanding the menu of antibodies that can be utilized with formalin-fixed tissue. This novel platform can provide quantitative detection retaining histomorphologic detail in clinical samples and has great potential to facilitate discovery and development of new diagnostic assays and therapeutic agents.
C1 [Chung, Joon-Yong; Hewitt, Stephen M.] NCI, Bethesda, MD 20892 USA.
RP Chung, JY (reprint author), NCI, Bethesda, MD 20892 USA.
OI Hewitt, Stephen/0000-0001-8283-1788; Chung,
Joon-Yong/0000-0001-5041-5982
NR 15
TC 3
Z9 3
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1064-3745
BN 978-1-934115-73-2
J9 METHODS MOL BIOL
JI Methods Mol. Biol.
PY 2009
VL 536
BP 139
EP +
DI 10.1007/978-1-59745-542-8_16
D2 10.1007/978-1-59745-542-8
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA BKJ86
UT WOS:000268334600016
PM 19378053
ER
PT S
AU Root, DD
Wang, K
AF Root, Douglas D.
Wang, Kuan
BE Walker, JM
TI Kinetic Silver Staining of Proteins
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID MICROTITER PLATES
C1 [Root, Douglas D.] Univ N Texas, Dept Biol Sci, Denton, TX 76203 USA.
[Wang, Kuan] NIAMS, Muscle Biol Lab, NIH, LPB, Bethesda, MD USA.
RP Root, DD (reprint author), Univ N Texas, Dept Biol Sci, Denton, TX 76203 USA.
NR 4
TC 0
Z9 0
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 51
EP 54
DI 10.1007/978-1-59745-198-7_8
D2 10.1007/978-1-59745-198-7
PG 4
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300008
ER
PT S
AU Lemkin, PF
Thornwall, GC
Evans, JA
AF Lemkin, Peter F.
Thornwall, Gregory C.
Evans, Jai A.
BE Walker, JM
TI Comparing 2D Electrophoretic Gels Across Internet Databases: An Open
Source Application
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID HUMAN PLASMA PROTEOME; SWISS-2DPAGE DATABASE; BIOMARKER DISCOVERY;
META-DATABASE; IMAGES; PROTEINS; IDENTIFICATION; MICROARRAYS; PROSPECTS;
SOFTWARE
C1 [Evans, Jai A.] Lockheed Martin Corp, Washington, DC USA.
[Thornwall, Gregory C.] LECB NCI FCRDC, Frederick, MD USA.
NR 34
TC 0
Z9 0
U1 2
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 409
EP 441
DI 10.1007/978-1-59745-198-7_40
D2 10.1007/978-1-59745-198-7
PG 33
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300040
ER
PT S
AU Miles, AP
Saul, A
AF Miles, Aaron P.
Saul, Allan
BE Walker, JM
TI Using SDS-PAGE and Scanning Laser Densitometry to Measure Yield and
Degradation of Proteins
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID POLYACRYLAMIDE-GEL ELECTROPHORESIS; ASSAY
C1 [Miles, Aaron P.] George Washington Univ, Dept Microbiol Immunol & Trop Med, Human Hookworm Vaccine Initiat, Washington, DC 20052 USA.
[Saul, Allan] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Miles, AP (reprint author), George Washington Univ, Dept Microbiol Immunol & Trop Med, Human Hookworm Vaccine Initiat, Washington, DC 20052 USA.
NR 12
TC 1
Z9 1
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 487
EP 496
DI 10.1007/978-1-59745-198-7_44
D2 10.1007/978-1-59745-198-7
PG 10
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300044
ER
PT S
AU Root, DD
Wang, K
AF Root, Douglas D.
Wang, Kuan
BE Walker, JM
TI Copper Iodide Staining of Proteins and Its Silver Enhancement
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID MEMBRANES
C1 [Root, Douglas D.] Univ N Texas, Dept Biol Sci, Denton, TX 76203 USA.
[Wang, Kuan] NIAMS, Muscle Biol Lab, NIH, LPB, Bethesda, MD USA.
RP Root, DD (reprint author), Univ N Texas, Dept Biol Sci, Denton, TX 76203 USA.
NR 9
TC 1
Z9 1
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 723
EP 728
DI 10.1007/978-1-59745-198-7_72
D2 10.1007/978-1-59745-198-7
PG 6
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300072
ER
PT S
AU Makrides, SC
Gasbarro, C
Bello, JM
AF Makrides, Sawas C.
Gasbarro, Christina
Bello, Job M.
BE Walker, JM
TI The Use of Quantum Dot Luminescent Probes for Western Blot Analysis
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID STAPHYLOCOCCAL PROTEIN-A; RECOMBINANT PROTEINS; BIOLOGICAL DETECTION;
ESCHERICHIA-COLI; IMMOBILIZATION; BIOTINYLATION; NANOCRYSTALS;
PURIFICATION; SPECIFICITY; SUBSTRATE
C1 [Makrides, Sawas C.] NCI, Special Review & Logist Branch, Div Extramural Activ, NIH, Bethesda, MD 20892 USA.
[Makrides, Sawas C.] Covance Inc, Chantilly, VA USA.
[Gasbarro, Christina; Bello, Job M.] EIC Labs Inc, Norwood, MA 02062 USA.
RP Makrides, SC (reprint author), NCI, Special Review & Logist Branch, Div Extramural Activ, NIH, Bethesda, MD 20892 USA.
NR 25
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 807
EP 818
DI 10.1007/978-1-59745-198-7_79
D2 10.1007/978-1-59745-198-7
PG 12
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300079
ER
PT S
AU Amero, SA
James, TC
Elgin, SCR
AF Amero, Sally Ann
James, Tharappel C.
Elgin, Sarah C. R.
BE Walker, JM
TI Production of Antibodies Using Proteins in Gel Bands
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID MONOCLONAL-ANTIBODIES; CHROMOSOMAL PROTEIN; DROSOPHILA; GENE
C1 [Amero, Sally Ann] NIH, Ctr Sci Review, Bethesda, MD 20892 USA.
[Elgin, Sarah C. R.] Washington Univ, Dept Biol, St Louis, MO 63130 USA.
RP Amero, SA (reprint author), NIH, Ctr Sci Review, Bldg 10, Bethesda, MD 20892 USA.
NR 17
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 1687
EP 1691
DI 10.1007/978-1-59745-198-7_170
D2 10.1007/978-1-59745-198-7
PG 5
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300170
ER
PT S
AU Hager-Braun, C
Tomer, KB
AF Hager-Braun, Christine
Tomer, Kenneth B.
BE Walker, JM
TI Determination of Epitopes by Mass Spectrometry
SO PROTEIN PROTOCOLS HANDBOOK, THIRD EDITION
SE Springer Protocols Handbooks
LA English
DT Article; Book Chapter
ID IMMUNODEFICIENCY-VIRUS TYPE-1; DIFFERENTIAL CHEMICAL-MODIFICATION;
MONOCLONAL-ANTIBODY; DISCONTINUOUS EPITOPE; LIMITED PROTEOLYSIS;
PROTEIN; PEPTIDE; IDENTIFICATION; COMPLEX; GLYCOPROTEIN
C1 [Hager-Braun, Christine] NIEHS, Res Triangle Pk, NC 27709 USA.
[Tomer, Kenneth B.] Struct Biol Lab, Mass Spectrometry Grp, Res Triangle Pk, NC USA.
RP Hager-Braun, C (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 34
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1949-2448
BN 978-1-60327-474-6
J9 SPRINGER PROTOC HAND
PY 2009
BP 1859
EP 1872
DI 10.1007/978-1-59745-198-7_197
D2 10.1007/978-1-59745-198-7
PG 14
WC Microbiology
SC Microbiology
GA BLR02
UT WOS:000270829300197
ER
PT J
AU Rajapaksha, M
Eichler, JF
Hajduch, J
Anderson, DE
Kirk, KL
Bann, JG
AF Rajapaksha, Maheshinie
Eichler, Jack F.
Hajduch, Jan
Anderson, David E.
Kirk, Kenneth L.
Bann, James G.
TI Monitoring anthrax toxin receptor dissociation from the protective
antigen by NMR
SO PROTEIN SCIENCE
LA English
DT Article
DE anthrax; protective antigen; histidine; pH; membrane; pore; fluorine
ID LETHAL FACTOR; PROTEIN TRANSLOCATION; PORE FORMATION; CHANNEL; BINDING;
IDENTIFICATION; COMPLEX; DOMAIN; CELLS
AB The binding of the Bacillus anthracis protective antigen (PA) to the host cell receptor is the first step toward the formation of the anthrax toxin, a tripartite set of proteins that include the enzymatic moieties edema factor (EF), and lethal factor (LF). PA is cleaved by a furin-like protease on the cell surface followed by the formation of a donut-shaped heptameric prepore. The prepore undergoes a major structural transition at acidic pH that results in the formation of a membrane spanning pore, an event which is dictated by interactions with the receptor and necessary for entry of EF and LF into the cell. We provide direct evidence using 1-dimensional (13)C-edited (1)H NMR that low pH induces dissociation of the Von-Willebrand factor A domain of the receptor capillary morphogenesis protein 2 (CMG2) from the prepore, but not the monomeric full length PA. Receptor dissociation is also observed using a carbon-13 labeled, 2-fluorohistidine labeled CMG2, consistent with studies showing that protonation of His-121 in CMG2 is not a mechanism for receptor release. Dissociation is likely caused by the structural transition upon formation of a pore from the prepore state rather than protonation of residues at the receptor PA or prepore interface.
C1 [Rajapaksha, Maheshinie; Eichler, Jack F.; Bann, James G.] Wichita State Univ, Dept Chem, Wichita, KS 67260 USA.
[Eichler, Jack F.] Emory Univ, Oxford Coll, Div Nat Sci & Math, Oxford, GA 30054 USA.
[Hajduch, Jan; Kirk, Kenneth L.] Natl Inst Diabet & Kidney Dis, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Anderson, David E.] Natl Inst Diabet & Kidney Dis, Prote & Mass Spectrometry Facil, NIH, Bethesda, MD 20892 USA.
RP Bann, JG (reprint author), Wichita State Univ, Dept Chem, 1845 Fairmount, Wichita, KS 67260 USA.
EM jim.bann@wichita.edu
FU Research Sites for Educators postdoctoral fellowship; NIDDK; National
Institutes of Health [US4 AJ1057160]; IDeA-COBRE-PSF award (through the
University of Kansas)
FX The authors thank Dr. Carl Frieden (Washington University in St. Louis)
for use of the fluorine cryoprobe and comments on the manuscript, and
Dr. Gregory DeKoster for his assistance with the SMRC experiments. They
also thank Dr. Jose Rizo Rey (UT-Southwestern) and Dr. Jacob Schaefer
(Washington University) for helpful comments on the manuscript. J.F.E.
was supported by a Research Sites for Educators postdoctoral fellowship.
K.L.K., J.H., and D.E.A were funded by the intramural research program
of NIDDK.; National Institutes of Health; Grant number: US4 AJ1057160;
Grant sponsor: IDeA-COBRE-PSF award (through the University of Kansas).
NR 31
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Z9 11
U1 0
U2 4
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD JAN
PY 2009
VL 18
IS 1
BP 17
EP 23
DI 10.1002/pro.26
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 396TI
UT WOS:000262613700004
PM 19177347
ER
PT J
AU Lountos, GT
Tropea, JE
Zhang, D
Jobson, AG
Pommier, Y
Shoemaker, RH
Waugh, DS
AF Lountos, George T.
Tropea, Joseph E.
Zhang, Di
Jobson, Andrew G.
Pommier, Yves
Shoemaker, Robert H.
Waugh, David S.
TI Crystal structure of checkpoint kinase 2 in complex with NSC 109555, a
potent and selective inhibitor
SO PROTEIN SCIENCE
LA English
DT Article
DE checkpoint kinase inhibitor; structure-assisted drug design; cocrystal
structure
ID DNA-DAMAGE CHECKPOINT; PROTEIN-KINASE; CHK2 KINASE; CANCER-THERAPY;
TUMOR-CELLS; DRUG DESIGN; ACTIVATION; AUTOPHOSPHORYLATION; RADIATION;
DOMAIN
AB Checkpoint kinase 2 (Chk2), a ser/thr kinase involved in the ATM-Chk2 checkpoint pathway, is activated by genomic instability and DNA damage and results in either arrest of the cell cycle to allow DNA repair to occur or apoptosis if the DNA damage is severe. Drugs that specifically target Chk2 could be beneficial when administered in combination with current DNA-damaging agents used in cancer therapy. Recently, a novel inhibitor of Chk2, NSC 109555, was identified that exhibited high potency (IC(50) = 240 nM) and selectivity. This compound represents a new chemotype and lead for the development of novel Chk2 inhibitors that could be used as therapeutic agents for the treatment of cancer. To facilitate the discovery of new analogs of NSC 109555 with even greater potency and selectivity, we have solved the crystal structure of this inhibitor in complex with the catalytic domain of Chk2. The structure confirms that the compound is an ATP-competitive inhibitor, as the electron density clearly reveals that it occupies the ATP-binding pocket. However, the mode of inhibition differs from that of the previously studied structure of Chk2 in complex with debromohymenialdisine, a compound that inhibits both Chk1 and Chk2. A unique hydrophobic pocket in Chk2, located very close to the bound inhibitor, presents an opportunity for the rational design of compounds with higher binding affinity and greater selectivity.
C1 [Lountos, George T.; Tropea, Joseph E.; Zhang, Di; Waugh, David S.] NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA.
[Jobson, Andrew G.; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Shoemaker, Robert H.] NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21702 USA.
RP Waugh, DS (reprint author), NCI, Macromol Crystallog Lab, POB B, Frederick, MD 21702 USA.
EM waughd@ncifcrf.gov
RI Lountos, George/B-3983-2015
FU NIH; National Cancer Institute; Center for Cancer Research; U.S.
Department of Energy, Office of Science, Office of Basic Energy Sciences
[W-31-109-Eng-38]
FX NIH, National Cancer Institute, Center for Cancer Research.;
Electrospray mass spectrometry experiments were conducted on the LC/ESMS
instrument maintained by the Biophysics Resource in the Structural
Biophysics Laboratory, Center for Cancer Research, National Cancer
Institute at Frederick. X-ray diffraction data were collected at the
Southeast Regional Collaborative Access Team (SER-CAT) beamline 22-ID at
the Advanced Photon Source, Argonne National Laboratory. Supporting
institutions may be found at http://www.ser-cat.org/members. html. Use
of the Advanced Photon Source was supported by the U.S. Department of
Energy, Office of Science, Office of Basic Energy Sciences, under
contract no. W-31-109-Eng-38.
NR 53
TC 18
Z9 19
U1 0
U2 4
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD JAN
PY 2009
VL 18
IS 1
BP 92
EP 100
DI 10.1002/pro.16
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 396TI
UT WOS:000262613700011
PM 19177354
ER
PT J
AU Degenhardt, L
Chiu, WT
Conway, K
Dierker, L
Glantz, M
Kalaydjian, A
Merikangas, K
Sampson, N
Swendsen, J
Kessler, RC
AF Degenhardt, L.
Chiu, W. T.
Conway, K.
Dierker, L.
Glantz, M.
Kalaydjian, A.
Merikangas, K.
Sampson, N.
Swendsen, J.
Kessler, R. C.
TI Does the 'gateway' matter? Associations between the order of drug use
initiation and the development of drug dependence in the National
Comorbidity Study Replication
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Alcohol; cannabis; dependence; gateway; illicit drugs; National
Comorbidity Survey Replication; tobacco
ID WORLD-HEALTH-ORGANIZATION; MENTAL-HEALTH; CANNABIS USE;
GENERAL-POPULATION; YOUNG ADULTHOOD; NCS-R; PROGRESSION; MARIJUANA;
ALCOHOL; COHORT
AB Background. The 'gateway' pattern of drug initiation describes a normative sequence, beginning with alcohol and tobacco use, followed by cannabis, then other illicit drugs. Previous work has suggested that 'violations' of this sequence may be predictors of later problems but other determinants were not considered. We have examined the role of pre-existing mental disorders and sociodemographics in explaining the predictive effects of violations using data from the US National Comorbidity Survey Replication (NCS-R).
Method. The NCS-R is a nationally representative face-to-face household survey of 9282 English-speaking respondents aged 18 years and older that used the World Health Organization (WHO) Composite International Diagnostic Interview (CIDI) to assess DSM-IV mental and substance disorders. Drug initiation was estimated using retrospective age-of-onset reports and 'violations' defined as inconsistent with the normative initiation order. Predictors of violations were examined using multivariable logistic regressions. Discrete-time survival analysis was used to see whether violations predicted progression to dependence.
Results. Gateway violations were largely unrelated to later dependence risk, with the exception of small increases in risk of alcohol and other illicit drug dependence for those who initiated use of other illicit drugs before cannabis. Early-onset internalizing disorders were predictors of gateway violations, and both internalizing and externalizing disorders increased the risks of dependence among users of all drugs.
Conclusions. Drug use initiation follows a strong normative pattern, deviations from which are not strongly predictive of later problems. By contrast, adolescents who have already developed mental health problems are at risk for deviations from the normative sequence of drug initiation and for the development of dependence.
C1 [Degenhardt, L.] Univ New S Wales, Natl Drug & Alcohol Res Ctr, Sydney, NSW 2052, Australia.
[Chiu, W. T.; Sampson, N.; Kessler, R. C.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Conway, K.] Natl Inst Drug Abuse, Div Epidemiol Serv & Prevent Res, US Natl Inst Hlth, Bethesda, MD USA.
[Dierker, L.] Wesleyan Univ, Dept Psychol, Middletown, CT USA.
[Kalaydjian, A.; Merikangas, K.] NIMH, Bethesda, MD 20892 USA.
[Swendsen, J.] Univ Bordeaux, Psychopathol Res Lab, Bordeaux, France.
RP Degenhardt, L (reprint author), Univ New S Wales, Natl Drug & Alcohol Res Ctr, Sydney, NSW 2052, Australia.
EM l.degenhardt@unsw.edu.au
RI Degenhardt, Louisa/D-4515-2012;
OI Degenhardt, Louisa/0000-0002-8513-2218; Conway,
Kevin/0000-0002-7638-339X
FU National Institute of Mental Health [U01-MH60220]; National Institute of
Drug Abuse (NIDA); Substance Abuse and Mental Health Services
Administration (SAMHSA); Robert Wood Johnson Foundation [044708]; John
W. Alden Trust; National Institutes of Health [K01 DA15454, R01
DA012058]; NIDA (Dierker); Patrick and Catherine Weldon Donaghue Medical
Research Foundation; Australian Government Department of Health and
Ageing (Degenhardt); Australian National Health and Medical Research
Council (NHMRC); US NIMH [R01MH070884]; John D. and Catherine T.
MacArthur Foundation; Pfizer Foundation; US Public Health Service
[R13-MH066849, R01-MH069864, R01 DA016558]; Fogarty International Center
[FIRCA R01-TW006481]; Pan American Health Organization; Eli Lilly and
Company; Ortho-McNeil Pharmaceutical, Inc.; GlaxoSmithKline;
Bristol-Myers Squibb
FX The US National Comorbidity Survey Replication (NCS-R) is supported by
the National Institute of Mental Health (NIMH; U01-MH60220) with
supplemental support from the National Institute of Drug Abuse (NIDA),
the Substance Abuse and Mental Health Services Administration (SAMHSA),
the Robert Wood Johnson Foundation (RWJF; Grant 044708), and the John W.
Alden Trust. Data analyses and manuscript preparation were undertaken
with support from an Intramural Research Program of the National
Institutes of Health, NIMH (Kalaydjian, Merikangas), grants K01 DA15454
and R01 DA012058 from the NIDA (Dierker), and an Investigator Award from
the Patrick and Catherine Weldon Donaghue Medical Research Foundation
(Dierker). The National Drug and Alcohol Research Centre is funded by
the Australian Government Department of Health and Ageing (Degenhardt),
and Degenhardt is the recipient of an Australian National Health and
Medical Research Council (NH&MRC) Senior Research Fellowship. The NCS-R
is carried out in conjunction with the World Health Organization World
Mental Health (WMH) Survey Initiative. We thank the WMH staff for
assistance with instrumentation, fieldwork and data analysis. These
activities were supported by the US NIMH (R01MH070884), the John D. and
Catherine T. MacArthur Foundation, the Pfizer Foundation, the US Public
Health Service (R13-MH066849, R01-MH069864, and R01 DA016558), the
Fogarty International Center (FIRCA R01-TW006481), the Pan American
Health Organization, Eli Lilly and Company, Ortho-McNeil Pharmaceutical,
Inc., GlaxoSmithKline, and Bristol-Myers Squibb. A complete list of WMH
publications can be found at www.hcp.med.harvard.edu/wmh/.
NR 38
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U1 2
U2 10
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD JAN
PY 2009
VL 39
IS 1
BP 157
EP 167
DI 10.1017/S0033291708003425
PG 11
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 396DJ
UT WOS:000262572100016
PM 18466664
ER
PT J
AU Mallinger, AG
Frank, E
Thase, ME
Barwell, MM
DiazGranados, N
Luckenbaugh, DA
Kupfer, DJ
AF Mallinger, Alan G.
Frank, Ellen
Thase, Michael E.
Barwell, Michelle M.
DiazGranados, Nancy
Luckenbaugh, David A.
Kupfer, David J.
TI Revisiting the Effectiveness of Standard Antidepressants in Bipolar
Disorder: Are Monoamine Oxidase Inhibitors Superior?
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article
DE antidepressive agents; bipolar disorder; depressive disorder; clinical
trial; monoamine oxidase inhibitors; treatment outcome
ID RATING-SCALE; DEPRESSION; IMIPRAMINE; TRANYLCYPROMINE; MOCLOBEMIDE
AB Objective: The role of antidepressants in treating bipolar disorder is controversial, and the comparative effectiveness of specific drugs is insufficiently studied. We report here a comparison of monoamine oxidase inhibitors (MAOIs) with the serotonin reuptake inhibitor paroxetine (PAROX). Experimental Design: We conducted a retrospective analysis of data from a larger study, using the first antidepressant trial administered either after entry (n = 46) or after a recurrent episode during study participation (n = 6). Twenty two patients were treated with PAROX and 30 with an MAOI. Durable recovery was determined from Hamilton depression and Young mania scores, based on published criteria. Principal Observations: PAROX treatment led to durable recovery in 27% of patients, a result very similar to the 24% recovery rate found in a recent STEP-BD trial. In contrast, patients treated with an MAOI had a 53% durable recovery rate. Survival analysis showed a significantly faster onset of durable recovery with MAOIs (chi(2) = 4.77, p = 0.029). Among subjects who were able to complete an adequate treatment trial of at least four weeks duration, durable recovery was attained in a significantly greater proportion of those treated with an MAOI (16 of 23, 70%) as compared to PAROX (6 of 18, 33%)(Fisher's Exact Test, p = 0.023). Conclusions: In these patients with bipolar depression, the antidepressant effectiveness of PAROX was unacceptably low, but rates of recovery with MAOIs were significantly higher. Psychopharmacology Bulletin. 2009;42(2):64-74.
C1 [Mallinger, Alan G.; Frank, Ellen; Thase, Michael E.; Barwell, Michelle M.; Kupfer, David J.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
[Mallinger, Alan G.; DiazGranados, Nancy] NIMH, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Thase, Michael E.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Mallinger, AG (reprint author), NIMH, Mood & Anxiety Disorders Program, DIRP, NIH, Bldg 10,Room 3N210,MSC 1290, Bethesda, MD 20892 USA.
EM mallingera@mail.nih.gov
FU National Institute of Mental Health [MH29618, MH49115, MH30915]; NIH,
National Institute of Mental Health
FX This research was supported in part by Grants MH29618, MH49115 and
MH30915 from the National Institute of Mental Health, and in part by the
Intramural Program of the NIH, National Institute of Mental Health. This
work was initially performed at the University of Pittsburgh, prior to
Dr. Mallinger's official duties as a Government employee. The views
expressed in this paper do not necessarily represent the views of the
United States Government or any of its agencies. This study is
registered with ClinicalTrials.gov (Identifier: NCT00227968).
NR 14
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Z9 13
U1 0
U2 2
PU MEDWORKS MEDIA GLOBAL, LLC
PI HERMOS BEACH
PA 670 FIFTH STREET, STE A, HERMOS BEACH, CA 90254 USA
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 2009
VL 42
IS 2
BP 64
EP 74
PG 11
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 641OH
UT WOS:000281137100004
PM 19629023
ER
PT J
AU Meltzer, JA
Fonzo, GA
Constable, RT
AF Meltzer, Jed A.
Fonzo, Greg A.
Constable, R. Todd
TI Transverse patterning dissociates human EEG theta power and hippocampal
BOLD activation
SO PSYCHOPHYSIOLOGY
LA English
DT Article
DE fMRI; Alpha; Default mode; Negative BOLD; LORETA
ID FRONTAL MIDLINE THETA; WORKING-MEMORY TASK; ANTERIOR CINGULATE CORTEX;
ALPHA-RHYTHM; GAMMA-OSCILLATIONS; PREFRONTAL CORTEX; VISUAL-CORTEX;
PHASE-LOCKING; ELECTROMAGNETIC TOMOGRAPHY; RECOGNITION MEMORY
AB Theta oscillations (4-8 Hz) are often modulated in human electroencephalogram (EEG) studies of memory, whereas overlapping frequencies dominate rodent hippocampal EEG. An emerging parallelism between theta reactivity and hippocampal functional magnetic resonance imaging activation has suggested a homology between theta activity in humans and rodents, representing a process of cortico-hippocampal interaction involved in memory. In the present study, we investigated EEG reactivity during performance of a relational memory task that induces a negative hippocampal blood oxygenation level dependent (BOLD) signal change, compared to a nonrelational control condition. Relational trials induced theta increases and alpha decreases. Low Resolution Electromagnetic Brain Tomography estimates localized theta and alpha modulation to frontal midline and parietal midline cortices, respectively, both of which exhibit negative BOLD responses in this task. Thus, theta and alpha dynamics are dissociable from positive BOLD activation, and may, in fact, colocalize with negative BOLD responses.
C1 [Meltzer, Jed A.; Constable, R. Todd] Yale Univ, Interdepartmental Neurosci Program, New Haven, CT USA.
[Fonzo, Greg A.; Constable, R. Todd] Yale Univ, Dept Diagnost Radiol, New Haven, CT 06510 USA.
[Constable, R. Todd] Yale Univ, Dept Biomed Engn, New Haven, CT 06510 USA.
[Constable, R. Todd] Yale Univ, Dept Neurosurg, New Haven, CT 06510 USA.
RP Meltzer, JA (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, Bldg 10,Rm 5C410,10 Ctr Dr, Bethesda, MD 20892 USA.
EM jed.meltzer@aya.yale.edu
OI Meltzer, Jed/0000-0002-4301-1901
FU NIH [R01-NS38467]; American Epilepsy Society
FX This research was supported by NIH R01-NS38467 and by a predoctoral
fellowship from the American Epilepsy Society (J. A. M.). We thank
Ulrich Schridde for helpful comments on the manuscript and Robert Astur
for development of the transverse patterning task.
NR 90
TC 13
Z9 16
U1 1
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0048-5772
J9 PSYCHOPHYSIOLOGY
JI Psychophysiology
PD JAN
PY 2009
VL 46
IS 1
BP 153
EP 162
DI 10.1111/j.1469-8986.2008.00719.x
PG 10
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 387WW
UT WOS:000261983300017
PM 18823411
ER
PT J
AU Peyk, P
Schupp, HT
Keil, A
Elbert, T
Junghofer, M
AF Peyk, Peter
Schupp, Harald T.
Keil, Andreas
Elbert, Thomas
Junghoefer, Markus
TI Parallel processing of affective visual stimuli
SO PSYCHOPHYSIOLOGY
LA English
DT Article
DE ERP; Emotion; Attention; Rapid serial visual presentation
ID NEURAL MECHANISMS; BRAIN MECHANISMS; ERP ANALYSIS; EMOTION; ATTENTION;
PERCEPTION; ACTIVATION; CORTEX; POTENTIALS; AWARENESS
AB Event-related potential (ERP) studies of affective picture processing have demonstrated an early posterior negativity (EPN) for emotionally arousing pictures that are embedded in a rapid visual stream. The present study examined the selective processing of emotional pictures while systematically varying picture presentation rates between 1 and 16 Hz. Previous results with presentation rates up to 5 Hz were replicated in that emotional compared to neutral pictures were associated with a greater EPN. Discrimination among emotional and neutral contents was maintained up to 12 Hz. To explore the notion of parallel processing, convolution analysis was used: EPNs generated by linear superposition of slow rate ERPs explained 70%-93% of the variance of measured EPNs, giving evidence for an impressive capacity of parallel affective discrimination in rapid serial picture presentation.
C1 [Peyk, Peter] Univ Basel, Dept Psychol, Basel, Switzerland.
[Schupp, Harald T.; Elbert, Thomas] Univ Konstanz, Dept Psychol, Constance, Germany.
[Keil, Andreas] Univ Florida, NIMH, Ctr Study Emot & Attent, Gainesville, FL USA.
[Junghoefer, Markus] Univ Munster, Inst Biomagnetism & Biosignalanalysis, Munster, Germany.
RP Peyk, P (reprint author), Univ Basel, Dept Clin Psychol & Psychotherapy, Missionsstr 60-62, CH-4055 Basel, Switzerland.
EM peter.peyk@unibas.ch
RI Elbert, Thomas/C-8556-2009; Frank, David/E-8213-2012; Keil,
Andreas/F-9427-2011
OI Keil, Andreas/0000-0002-4064-1924
FU NIMH NIH HHS [P50 MH072850, P50 MH072850-04]
NR 30
TC 22
Z9 23
U1 1
U2 10
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0048-5772
J9 PSYCHOPHYSIOLOGY
JI Psychophysiology
PD JAN
PY 2009
VL 46
IS 1
BP 200
EP 208
DI 10.1111/j.1469-8986.2008.00755.x
PG 9
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 387WW
UT WOS:000261983300022
PM 19055507
ER
PT J
AU Kuh, D
Cooper, R
Hardy, R
Guralnik, J
Richards, M
AF Kuh, Diana
Cooper, Rachel
Hardy, Rebecca
Guralnik, Jack
Richards, Marcus
CA Musculoskeletal Study Team
TI Lifetime Cognitive Performance is Associated With Midlife Physical
Performance in a Prospective National Birth Cohort Study
SO PSYCHOSOMATIC MEDICINE
LA English
DT Article
DE lifetime cognition; physical performance; birth cohort; developmental
differences
ID LATE ADULTHOOD; GRIP STRENGTH; OLDER-ADULTS; HEALTH; AGE; AMERICANS;
VARIABLES; DECLINE; BALANCE; BRAIN
AB Objectives: To examine whether measures of cognitive performance across life are related to physical performance at age 53 years, allowing for potential confounders. Methods: In a large representative British birth cohort of men and women (N = 2135) the associations between cognitive performance across life (i.e., standardized cognition scores at ages 15, 43, and 53 years and changes in verbal memory and search speed scores between 43 and 53 years) and measures of physical performance at age 53 years (i.e., standing balance, chair rising, and grip strength) were examined. Adjustments were made for body size, physical activity levels, health status, and socioeconomic conditions at age 53 years. Results: Higher cognitive scores on all childhood and adult tests, and a slower decline in verbal memory and search speed, were associated with better standing balance. Higher verbal fluency scores and a slower decline in verbal memory and search speed were more strongly related than scores on tests of general cognitive ability to chair rising. The relationships between cognitive performance and grip strength were inconsistent and weak. Conclusions: The differential patterns of association found are consistent with the degree to which each is dependent on central nervous system function. Our findings suggest that initial developmental differences as well as shared ageing processes may underlie associations found between cognitive and physical performance.
C1 [Kuh, Diana; Cooper, Rachel; Hardy, Rebecca; Richards, Marcus] Royal Free & Univ Coll Med Sch, MRC NSHD, MRC Unit Lifelong Hlth & Ageing, Dept Epidemiol & Publ Hlth, London WC1B 5JU, England.
[Guralnik, Jack] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
RP Kuh, D (reprint author), Royal Free & Univ Coll Med Sch, MRC NSHD, MRC Unit Lifelong Hlth & Ageing, Dept Epidemiol & Publ Hlth, 33 Bedford Pl, London WC1B 5JU, England.
EM d.kuh@nshd.mrc.ac.uk
OI Cooper, Rachel/0000-0003-3370-5720
FU Medical Research Council, United Kingdom; Intramural Research Program;
National Institute on Aging; NIH
FX Supported by the Medical Research Council, United Kingdom and in part by
the Intramural Research Program, National Institute on Aging, NIH; MRC
(to DK, RC, RH, and MR) and NIA (to J.G.).
NR 40
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U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD JAN
PY 2009
VL 71
IS 1
BP 38
EP 48
DI 10.1097/PSY.0b013e31818a1620
PG 11
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA 395ZR
UT WOS:000262562500008
PM 19124616
ER
PT J
AU Rice, SC
Zonderman, AB
Metter, EJ
Najjar, SS
Waldstein, SR
AF Rice, S. Carrington
Zonderman, Alan B.
Metter, E. Jeffrey
Najjar, Samer S.
Waldstein, Shari R.
TI Absence of Relation Between Depressive Symptoms and Carotid Intimal
Medial Thickness in the Baltimore Longitudinal Study of Aging
SO PSYCHOSOMATIC MEDICINE
LA English
DT Article
DE atherosclerosis; carotid intimal medial thickness; depression
ID CORONARY HEART-DISEASE; RISK-FACTOR; CARDIOVASCULAR-DISEASE;
MYOCARDIAL-INFARCTION; NEGATIVE EMOTIONS; ARTERIAL-WALL;
ATHEROSCLEROSIS; ASSOCIATION; PROGRESSION; REFLECTION
AB Objective: To examine the relation between longitudinal trajectories of depressive symptoms as well as history of significant symptoms and subsequent carotid intimal media] thickness (IMT) among participants enrolled in the Baltimore Longitudinal Study of Aging and to assess longitudinal covariation of depressive symptoms and carotid IMT over two time points. Prior literature has identified inconsistent cross-sectional associations between depressive symptoms and carotid IMT in healthy persons, and existing longitudinal work has relied on depression assessment at a single time point. Methods: A total of 556 participants (303 women and 253 men), aged 20 to 93 years (mean +/- standard deviation = 55.8 +/- 15.9 years), completed the Center for Epidemiological Studies-Depression (CES-D) scale from one to eight times over I to 15 years. Participants later underwent high-resolution B-mode ultrasonography to assess IMT of the far wall of the common carotid artery. A subset of these participants (n = 68) underwent reassessment of IMT an average of 3.9 years later. Linear and mixed-effects regression models were adjusted for sex, race, education, systolic blood pressure, low-density lipoprotein cholesterol, body mass index, diabetes, smoking, and anti hypertensive, lipid-lowering, and antidepressant medications. Results: There was no relation between trajectory of depressive symptoms or history of significant depressive symptoms and future carotid IMT. There was also no evidence for longitudinal covariation of depressive symptoms and IMT over time. Additional analyses similarly revealed a lack of significant associations. Conclusion: There is no association between depressive symptoms and carotid IMT in the present sample of healthy community-dwelling volunteers.
C1 [Rice, S. Carrington; Waldstein, Shari R.] Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21250 USA.
[Rice, S. Carrington; Zonderman, Alan B.; Metter, E. Jeffrey; Najjar, Samer S.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
[Waldstein, Shari R.] NIH, Bethesda, MD 20892 USA.
[Waldstein, Shari R.] Univ Maryland, Sch Med, Dept Med, Div Gerontol, Baltimore, MD 21201 USA.
[Waldstein, Shari R.] Ctr Geriatr Res Educ & Clin, Baltimore, MD USA.
RP Rice, SC (reprint author), Univ Maryland Baltimore Cty, Dept Psychol, 1000 Hilltop Circle, Baltimore, MD 21250 USA.
EM rice3@umbc.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU National Institutes of Health
FX Supported by The National Institute on Aging Intramural Research Program
of the National Institutes of Health (S.C.R., A.B.Z., E.J.M., S.S.N.).
NR 32
TC 15
Z9 15
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD JAN
PY 2009
VL 71
IS 1
BP 70
EP 76
DI 10.1097/PSY.0b013e3181865f73
PG 7
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA 395ZR
UT WOS:000262562500012
PM 18842746
ER
PT J
AU Wideroff, L
Phillips, KA
Randhawa, G
Ambs, A
Armstrong, K
Bennett, CL
Brown, ML
Donaldson, MS
Follen, M
Goldie, SJ
Hiatt, RA
Khoury, MJ
Lewis, G
McLeod, HL
Piper, M
Powell, I
Schrag, D
Schulman, KA
Scott, J
AF Wideroff, Louise
Phillips, Kathryn A.
Randhawa, Gurvaneet
Ambs, Anita
Armstrong, Katrina
Bennett, Charles L.
Brown, Martin L.
Donaldson, Molla S.
Follen, Michele
Goldie, Sue J.
Hiatt, Robert A.
Khoury, Muin J.
Lewis, Graham
McLeod, Howard L.
Piper, Margaret
Powell, Isaac
Schrag, Deborah
Schulman, Kevin A.
Scott, Joan
TI A Health Services Research Agenda for Cellular, Molecular and Genomic
Technologies in Cancer Care
SO PUBLIC HEALTH GENOMICS
LA English
DT Review
DE Genomics; Health services research; Emerging technologies; Translational
research
ID COST-EFFECTIVENESS ANALYSIS; METASTATIC BREAST-CANCER; REPORTS RADAR
PROJECT; ADVERSE DRUG EVENTS; CLINICAL-PRACTICE; RACIAL-DIFFERENCES;
CERVICAL-CANCER; PUBLIC-HEALTH; PROPHYLACTIC VACCINES; PROSTATE-CANCER
AB Background: In recent decades, extensive resources have been invested to develop cellular, molecular and genomic technologies with clinical applications that span the continuum of cancer care. Methods: In December 2006, the National Cancer Institute sponsored the first workshop to uniquely examine the state of health services research on cancer-related cellular, molecular and genomic technologies and identify challenges and priorities for expanding the evidence base on their effectiveness in routine care. Results: This article summarizes the workshop outcomes, which included development of a comprehensive research agenda that incorporates health and safety endpoints, utilization patterns, patient and provider preferences, quality of care and access, disparities, economics and decision modeling, trends in cancer outcomes, and health-related quality of life among target populations. Conclusions: Ultimately, the successful adoption of useful technologies will depend on understanding and influencing the patient, provider, health care system and societal factors that contribute to their uptake and effectiveness in 'real-world' settings. Copyright (C) 2009 S. Karger AG, Basel
C1 [Wideroff, Louise; Ambs, Anita; Brown, Martin L.] NCI, Bethesda, MD 20892 USA.
[Phillips, Kathryn A.; Hiatt, Robert A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Randhawa, Gurvaneet] Agcy Healthcare Res & Qual, Rockville, MD USA.
[Armstrong, Katrina] Univ Penn, Philadelphia, PA 19104 USA.
[Bennett, Charles L.] Northwestern Univ, Evanston, IL USA.
[Donaldson, Molla S.] George Washington Univ, Washington, DC USA.
[Follen, Michele] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Goldie, Sue J.] Harvard Univ, Boston, MA 02115 USA.
[Schrag, Deborah] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[McLeod, Howard L.] Univ N Carolina, Chapel Hill, NC USA.
[Piper, Margaret] Blue Cross Blue Shield Assoc Technol Evaluat Ctr, Chicago, IL USA.
[Powell, Isaac] Wayne State Univ, Detroit, MI USA.
[Schulman, Kevin A.] Duke Univ, Durham, NC USA.
[Scott, Joan] Johns Hopkins Univ, Baltimore, MD USA.
[Lewis, Graham] Univ York, Heslington, England.
RP Wideroff, L (reprint author), Natl Inst Drug Abuse, Epidemiol Res Branch, Div Epidemiol Serv & Prevent Res, 6001 Executive Blvd,Suite 5153 MSC 9589, Bethesda, MD 20892 USA.
EM Wideroff@nih.gov
RI Hernandez, Jessica/G-6527-2011;
OI Piper, Margaret/0000-0002-6231-9653
FU NCI [263-MQ-610769, 263-MQ-612315, 263-MQ-612317, 263MQ-700870,
263-MQ-701381, 263-MQ612321, 263-MQ-611969, 263-MQ-612316,
263-MQ-612323, 263-MQ-611964, 263MQ-612324, 263-MQ-611967];
[HHSN261200700005C]
FX The study was funded by the NCI (263-MQ-610769 to K. A. P.;
263-MQ-612315 to K. A.; 263-MQ-612317 to C. L. B.; 263MQ-700870 to M. S.
D.; 263-MQ-701381 to M. F.; 263-MQ612321 to S. J. G.; 263-MQ-611969 to
R. A. H.; 263-MQ-612316 to H. L. M.; 263-MQ-612323 to I. P.;
263-MQ-611964 to D. S.; 263MQ-612324 to K. A. S.; 263-MQ-611967 to the
University of York; HHSN261200700005C to Scientific Consulting Group for
organizational and editorial assistance).
NR 83
TC 12
Z9 12
U1 2
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-4246
J9 PUBLIC HEALTH GENOMI
JI Pub. Health Genomics
PY 2009
VL 12
IS 4
BP 233
EP 244
DI 10.1159/000203779
PG 12
WC Genetics & Heredity; Public, Environmental & Occupational Health
SC Genetics & Heredity; Public, Environmental & Occupational Health
GA 432LX
UT WOS:000265136600004
PM 19367091
ER
PT J
AU Newport, MJ
Rotimi, CN
AF Newport, Melanie J.
Rotimi, Charles N.
TI Reducing the Global Genomic Inequity Gap: Development of an African
Genome Project
SO PUBLIC HEALTH GENOMICS
LA English
DT Article
C1 [Newport, Melanie J.] Brighton & Sussex Med Sch, Dept Med, Brighton BN1 9PS, E Sussex, England.
[Rotimi, Charles N.] NHGRI, Ctr Res Genom & Global Hlth, NIH, Bethesda, MD 20892 USA.
RP Newport, MJ (reprint author), Brighton & Sussex Med Sch, Dept Med, Brighton BN1 9PS, E Sussex, England.
EM M.J.Newport@bsms.ac.uk
NR 1
TC 6
Z9 6
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-4246
J9 PUBLIC HEALTH GENOMI
JI Pub. Health Genomics
PY 2009
VL 12
IS 4
BP 251
EP 252
DI 10.1159/000197973
PG 2
WC Genetics & Heredity; Public, Environmental & Occupational Health
SC Genetics & Heredity; Public, Environmental & Occupational Health
GA 432LX
UT WOS:000265136600006
PM 19182477
ER
PT J
AU Morens, DM
Taubenberger, JK
Folkers, GK
Fauci, AS
AF Morens, David M.
Taubenberger, Jeffery K.
Folkers, Gregory K.
Fauci, Anthony S.
TI An Historical Antecedent of Modern Guidelines for Community Pandemic
influenza Mitigation
SO PUBLIC HEALTH REPORTS
LA English
DT Editorial Material
ID US CITIES; INTERVENTIONS
C1 [Morens, David M.; Taubenberger, Jeffery K.; Folkers, Gregory K.; Fauci, Anthony S.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Morens, DM (reprint author), NIAID, NIH, Bldg 31,Room 7A-10,31 Ctr Dr,MSC 2520, Bethesda, MD 20892 USA.
EM dmorens@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 17
TC 3
Z9 3
U1 0
U2 0
PU ASSOC SCHOOLS PUBLIC HEALTH
PI WASHINGTON
PA 1101 15TH ST NW, STE 910, WASHINGTON, DC 20005 USA
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD JAN-FEB
PY 2009
VL 124
IS 1
BP 22
EP 25
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 385NI
UT WOS:000261820500006
PM 19413024
ER
PT J
AU Sigurdson, AJ
Land, CE
Bhatti, P
Pineda, M
Brenner, A
Carr, Z
Gusev, BI
Zhumadilov, Z
Simon, SL
Bouville, A
Rutter, JL
Ron, E
Struewing, JP
AF Sigurdson, Alice J.
Land, Charles E.
Bhatti, Parveen
Pineda, Marbin
Brenner, Alina
Carr, Zhanat
Gusev, Boris I.
Zhumadilov, Zhaxibay
Simon, Steven L.
Bouville, Andre
Rutter, Joni L.
Ron, Elaine
Struewing, Jeffery P.
TI Thyroid Nodules, Polymorphic Variants in DNA Repair and RET-Related
Genes, and Interaction with Ionizing Radiation Exposure from Nuclear
Tests in Kazakhstan
SO RADIATION RESEARCH
LA English
DT Article
ID DEGREE RELATIVES; POOLED ANALYSIS; CANCER; RISK; HAPLOTYPES; CARCINOMA;
DISEASES; ASSOCIATION; MECHANISMS; MUTATIONS
AB Risk factors for thyroid cancer remain largely unknown except for ionizing radiation exposure during childhood and a history of benign thyroid nodules. Because thyroid nodules are more common than thyroid cancers and are associated with thyroid cancer risk, we evaluated several polymorphisms potentially relevant to thyroid tumors and assessed interaction with ionizing radiation exposure to the thyroid gland. Thyroid nodules were detected in 1998 by ultrasound screening of 2997 persons who lived near the Semipalatinsk nuclear test site in Kazakhstan when they were children (1949-1962). Cases with thyroid nodules (n = 907) were frequency matched (1:1) to those without nodules by ethnicity (Kazakh or Russian), gender and age at screening. Thyroid gland radiation doses were estimated from fallout deposition patterns, residence history and diet. We analyzed 23 polymorphisms in 13 genes and assessed interaction with ionizing radiation exposure using likelihood ratio tests (LRT). Elevated thyroid nodule risks were associated with the minor alleles of RET S836S (rs1800862, P = 0.03) and GFRA1 -193C>G (rs not assigned, P = 0.05) and decreased risk with XRCC1 R194W (rs1799782, P trend = 0.03) and TGFB1 T263I (rs1800472, P = 0.009). Similar patterns of association were observed for a small number of papillary thyroid cancers (n = 25). Ionizing radiation exposure to the thyroid gland was associated with significantly increased risk of thyroid nodules (age and gender adjusted excess odds ratio/Gy = 0.30, 95% CI 0.05-0.56), with evidence for interaction by genotype found for XRCC1 R194W (LRT P value = 0.02). Polymorphisms in RET signaling, DNA repair and proliferation genes may be related to risk of thyroid nodules, consistent with some previous reports on thyroid cancer. Borderline support for gene-radiation interaction was found for a variant in XRCC1, a key base excision repair protein. Other pathways such as genes in double-strand break repair, apoptosis and genes related to proliferation should also be pursued. (C) 2009 by Radiation Research Society
C1 [Sigurdson, Alice J.; Land, Charles E.; Bhatti, Parveen; Brenner, Alina; Carr, Zhanat; Simon, Steven L.; Bouville, Andre; Ron, Elaine] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Pineda, Marbin; Rutter, Joni L.; Struewing, Jeffery P.] NCI, Lab Populat Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Gusev, Boris I.] Kazakhstan State Res Inst Radiat Med & Ecol, Semipalatinsk, Kazakhstan.
[Zhumadilov, Zhaxibay] Semipalatinsk State Med Acad, Semipalatinsk, Kazakhstan.
RP Sigurdson, AJ (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,EPS 7060,MSC 7238, Bethesda, MD 20892 USA.
EM sigurdsa@mail.nih.gov
RI Struewing, Jeffery/I-7502-2013;
OI Struewing, Jeffery/0000-0002-4848-3334; Rutter, Joni/0000-0002-6502-2361
FU Division of Cancer Epidemiology and Genetics of the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services; Harkin Award
FX We are very grateful to the residents of the Kazakhstan villages who
participated in this study. This study was supported in part by the
Intramural Research Program of the Division of Cancer Epidemiology and
Genetics of the National Cancer Institute, National Institutes of
Health, Department of Health and Human Services and by the Harkin Award
for research on thyroid cancer.
NR 35
TC 23
Z9 25
U1 1
U2 6
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD JAN
PY 2009
VL 171
IS 1
BP 77
EP 88
DI 10.1667/RR1327.1
PG 12
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 390TX
UT WOS:000262187700008
PM 19138047
ER
PT J
AU Weinberger, D
Berger, G
AF Weinberger, Daniel
Berger, Gregor
BE Jackson, HJ
McGorry, PD
TI Genetic vulnerability
SO RECOGNITION AND MANAGEMENT OF EARLY PSYCHOSIS: A PREVENTIVE APPROACH,
2ND EDITION
LA English
DT Article; Book Chapter
ID CATECHOL-O-METHYLTRANSFERASE; NEUROTROPHIC FACTOR GENE; CHILDHOOD-ONSET
SCHIZOPHRENIA; VAL(108/158) MET GENOTYPE; FACTOR BDNF GENE; BIPOLAR
DISORDER; SUSCEPTIBILITY GENE; ALZHEIMERS-DISEASE; PREFRONTAL CORTEX;
MONOZYGOTIC TWINS
C1 [Weinberger, Daniel] NIMH, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
[Berger, Gregor] Univ Basel Hosp, Dept Psychiat, CH-4031 Basel, Switzerland.
[Berger, Gregor] Schlossli Clin, Zurich, Switzerland.
[Berger, Gregor] Univ Melbourne, Parkville, Vic 3052, Australia.
RP Weinberger, D (reprint author), NIMH, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
NR 140
TC 0
Z9 0
U1 1
U2 1
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-0-521-61731-4
PY 2009
BP 31
EP 46
DI 10.1017/CBO9780511576287.004
D2 10.1017/CBO9780511576287
PG 16
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA BDR82
UT WOS:000314590300004
ER
PT S
AU Ogawa, M
Kosaka, N
Urano, Y
Choyke, PL
Kobayashi, H
AF Ogawa, Mikako
Kosaka, Nobuyuki
Urano, Yasuteru
Choyke, Peter L.
Kobayashi, Hisataka
BE Achilefu, S
Raghavachari, R
TI Activatable optical imaging probes with various fluorophore-quencher
combinations
SO REPORTERS, MARKERS, DYES, NANOPARTICLES, AND MOLECULAR PROBES FOR
BIOMEDICAL APPLICATIONS
SE Proceedings of SPIE-The International Society for Optical Engineering
LA English
DT Proceedings Paper
CT Conference on Reporters, Markers, Dyes, Nanoparticles, and Molecular
Probes for Biomedical Applications
CY JAN 26-29, 2009
CL San Jose, CA
SP SPIE
DE molecular imaging; cancer; activatable probe; fluorophore-quencher pair
ID FLUORESCENCE PROBE; CANCER; CONJUGATE; DIMERS; FRET
AB Molecular imaging probes rely on high target-to-background ratios (TBR) to achieve maximum sensitivity and specificity. We utilized "quenchers" to turn off the background signal from the unbound probe and investigated the ability of specific fluorophore-quencher pairs to activate at target tissues. Both fluorophore and quencher were conjugated to a single cancer targeting molecule, either avidin or antibody. Fluorescence signal from these targeting molecules was "turned off" by the quencher in the unbound state, but was "turned on" only when the molecules bound to the cell surface target and was internalized.
We tested the following fluorophore-quencher combinations based on fluorescence resonance energy transfer (FRET) pairs; OregonG-BHQ1, RhodG-BHQ1/ATTO540Q, TAMRA-QSY7/QSY21, TexRed-QSY21, Alexa647-QSY21, Cy5.5-QSY21/BHQ3 and Alexa680-QSY21/BHQ3. Among these, only RhodG-ATTO540Q and TAMRA-QSY7/21 pair showed activation upon cell binding/internalization. Among these combinations, TAMRA-QSY7 pair showed the highest activation (40-fold and 13-fold for avidin and antibody conjugate, respectively) as measured with an in vitro dissociation assay. The activation was dependent on the method used to conjugate fluorophores and quenchers to the targeting molecule. In vitro microscopic studies with TAMRA-QSY7 pair conjugated to avidin or antibody showed high fluorescent signal inside the target cancer cells, indicating activation after internalization. In vivo imaging studies in tumor bearing mice demonstrated that tumors could be clearly detected with low background.
Although the precise quenching mechanism remains to be determined, this activation system can achieve high TBR in vivo molecular imaging.
C1 [Ogawa, Mikako; Kosaka, Nobuyuki; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ogawa, M (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 13
TC 0
Z9 0
U1 0
U2 3
PU SPIE-INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA
SN 0277-786X
BN 978-0-8194-7436-0
J9 P SOC PHOTO-OPT INS
PY 2009
VL 7190
AR 71900Z
DI 10.1117/12.808326
PG 8
WC Biophysics; Engineering, Biomedical; Nanoscience & Nanotechnology;
Optics
SC Biophysics; Engineering; Science & Technology - Other Topics; Optics
GA BSS51
UT WOS:000285710200018
ER
PT J
AU O'Brien, SJ
AF O'Brien, Stephen J.
TI Comparative genomics in vertebrates: a role for the platypus
SO REPRODUCTION FERTILITY AND DEVELOPMENT
LA English
DT Editorial Material
ID SEX-CHROMOSOMES; EVOLUTION
C1 NCI, Lab Genom Divers, Frederick, MD 21702 USA.
RP O'Brien, SJ (reprint author), NCI, Lab Genom Divers, Frederick, MD 21702 USA.
EM stephen.obrien@nih.gov
NR 16
TC 0
Z9 0
U1 0
U2 1
PU CSIRO PUBLISHING
PI COLLINGWOOD
PA 150 OXFORD ST, PO BOX 1139, COLLINGWOOD, VICTORIA 3066, AUSTRALIA
SN 1031-3613
J9 REPROD FERT DEVELOP
JI Reprod. Fertil. Dev.
PY 2009
VL 21
IS 8
BP VII
EP IX
DI 10.1071/RDv21n8_IN
PG 3
WC Developmental Biology; Reproductive Biology; Zoology
SC Developmental Biology; Reproductive Biology; Zoology
GA 512KH
UT WOS:000271247100002
PM 20092045
ER
PT B
AU Martensen, R
AF Martensen, Robert
BE Campbell, L
Wiesen, A
TI Landscape Designers, Doctors, and the Making of Healthy Urban Spaces in
19th Century America
SO RESTORATIVE COMMONS: CREATING HEALTH AND WELL-BEING THROUGH URBAN
LANDSCAPES
SE USDA Forest Service Northern Research Station General Technical Report
GTR-NRS
LA English
DT Proceedings Paper
CT Meristem 2007 Forum
CY 2007
CL New York Acad Med, New York, NY
SP Harvard-Loeb Fellowship Forum, PC Landscape Architecture, Inst Landscape Studies, Terrapin Bright Green, David Kamp FASLA, LF Dirtworks
HO New York Acad Med
C1 [Martensen, Robert] NIH, Off NIH Hist & Museum, Bethesda, MD USA.
NR 8
TC 0
Z9 0
U1 0
U2 1
PU USDA FOREST SERVICE
PI NEWTOWN SQUARE
PA 11 CAMPUS BLVD, STE 200, NEWTOWN SQUARE, PA 19073-3294 USA
J9 USDA FOR SERV NRS GT
PY 2009
IS P-39
BP 27
EP 37
PG 11
WC Horticulture; Public, Environmental & Occupational Health; Urban Studies
SC Agriculture; Public, Environmental & Occupational Health; Urban Studies
GA BJI17
UT WOS:000266060700001
ER
PT J
AU Chen, J
Tsai, SY
Vazin, T
Coggiano, M
Freed, WJ
AF Chen, Jia
Tsai, Shang-Yi
Vazin, Tandis
Coggiano, Mark
Freed, William J.
TI Human embryonic stem cells which express hrGFP in the undifferentiated
state and during dopaminergic differentiation
SO RESTORATIVE NEUROLOGY AND NEUROSCIENCE
LA English
DT Article
DE Human embryonic stem cells; EF1-hrGFP reporter gene; nucleofection;
BGO1V2-EFG; histone deacetylase; neural differentiation; dopaminergic
ID TYROSINE-HYDROXYLASE; HISTONE DEACETYLASE; NEURAL PRECURSORS;
GENE-EXPRESSION; PROMOTER; NEURONS; LINE; BUTYRATE; INHIBITORS; CULTURE
AB Purpose: human embryonic stem cells (hESCs) which express a reporter gene consistently during all phases of differentiation would be valuable for basic research on cell transplantation. In this study, we describe karyotypically-abnormal variant hESCs, BGO1V2-EFG, which express hrGFP driven by the EF1 promoter.
Methods: BGO1V2-EFG cells were analyzed by using immunocytochemistry, single cell-based confocal image, and in vitro differentiation, including dopaminergic differentiation.
Results: Undifferentiated BGO1V2-EFG cells expressed pluripotent ESC markers and retained the ability to differentiate into cell types of all three germ layers. BGO1V2-EFG cells maintained stable and robust hrGFP expression in vitro in the undifferentiated state and during differentiation. The EF1 promoter retained activity during dopaminergic differentiation, as 76% of tyrosine hydroxlase (TH)-positive cells co-expressed hrGFP by confocal analysis. Treated with sodium butyrate (0.02 mM to 2.0 mM), an inhibitor of histone deacetylase (HDAC), during differentiation did not affect hrGFP expression, although TH expression was reduced by higher concentrations of sodium butyrate.
Conclusion: BGO1V2-EFG cells maintain stable and robust hrGFP expression in the undifferentiated state and during neural differentiation. Especially, the EF1 promoter was effective in driving hrGFP expression during dopaminergic differentiation. BGO1V2-EFG cells may be useful for transplantation studies in Parkinson disease animal models.
C1 [Chen, Jia; Tsai, Shang-Yi; Vazin, Tandis; Coggiano, Mark; Freed, William J.] NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Chen, J (reprint author), NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, 333 Cassell Dr,Triad Bldg,Room 3505, Baltimore, MD 21224 USA.
EM jichen@mail.nih.gov
FU NIDA; NIH; DHHS
FX Research was supported by the IRP of NIDA, NIH, DHHS.
NR 30
TC 6
Z9 9
U1 0
U2 5
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0922-6028
J9 RESTOR NEUROL NEUROS
JI Restor. Neurol. Neurosci.
PY 2009
VL 27
IS 4
BP 359
EP 370
DI 10.3233/RNN-2009-0521
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 492BS
UT WOS:000269629700010
PM 19738328
ER
PT J
AU Aboud, S
Mhalu, F
Bakari, M
Lifson, J
Lyamuya, E
Marovich, M
Cox, J
Sandstrom, E
Biberfeld, G
Nilsson, C
AF Aboud, S.
Mhalu, F.
Bakari, M.
Lifson, J.
Lyamuya, E.
Marovich, M.
Cox, J.
Sandstrom, E.
Biberfeld, G.
Nilsson, C.
TI HIV-specific T-lymphocyte proliferative responses induced by a multigene
multiclade HIV-1 DNA/MVA heterologous vaccine in Tanzanian volunteers
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Aboud, S.; Mhalu, F.; Bakari, M.; Lyamuya, E.] Muhimbili Univ Hlth & Allied Sci, Dept Microbiol & Immunol, Dar Es Salaam, Tanzania.
[Lifson, J.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Marovich, M.; Cox, J.] US Mil HIV Res Program, Rockville, MD USA.
[Sandstrom, E.] Karolinska Univ Hosp, Stockholm, Sweden.
[Biberfeld, G.] Swedish Inst Infect Dis Control, Stockholm, Sweden.
[Biberfeld, G.] Karolinska Inst, Stockholm, Sweden.
[Nilsson, C.] Swedish Inst Infect Dis Control SMI, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P191
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300242
ER
PT J
AU Allen, MA
Gray, G
Churchyard, G
Bekker, L
Nchabeleng, M
Mlisana, K
Metch, B
Moodie, Z
Roux, S
Mathebula, M
Bennie, T
Kublin, J
AF Allen, M. A.
Gray, G.
Churchyard, G.
Bekker, L.
Nchabeleng, M.
Mlisana, K.
Metch, B.
Moodie, Z.
Roux, S.
Mathebula, M.
Bennie, T.
Kublin, J.
TI Social impact events in Phambili, the first phase 2B HIV vaccine trial
in South Africa
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Allen, M. A.] NIAID, DAIDS VRP, NIH, Bethesda, MD 20892 USA.
[Gray, G.] Perinatal HIV Res Unit, Soweto, South Africa.
[Gray, G.] Univ Witwatersrand, Soweto, South Africa.
[Churchyard, G.] Univ Cape Town, Klerksdorp, South Africa.
[Bekker, L.; Roux, S.] Desmond Tutu HIV Ctr, Cape Town, South Africa.
[Allen, M. A.; Nchabeleng, M.; Mathebula, M.] MeCRU, Medunsa, South Africa.
[Mlisana, K.; Bennie, T.] Ctr AIDS Programme Res S Africa CAPRISA, Durban, South Africa.
[Metch, B.; Moodie, Z.] Stat Ctr HIV AIDS Res & Prevent, FHCRC, Seattle, WA USA.
[Kublin, J.] Fred Hutchinson Canc Res Ctr, HIV Vaccine Trials Network, Seattle, WA 98104 USA.
[Churchyard, G.] Aurum Inst Hlth Res, Klerksdorp, South Africa.
OI Allen, Mary/0000-0001-8163-0714
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P190
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300241
ER
PT J
AU Bachu, M
Murali, RV
Babu, AMHKH
Yedavalli, VSRK
Jeang, KT
Ranga, U
AF Bachu, Mahesh
Murali, Rajesh V.
Babu, Anil M. H. K. H.
Yedavalli, Venkat S. R. K.
Jeang, Kuan-Teh
Ranga, Udaykumar
TI Fourth NF-kappa B site in HIV-1 subtype-C LTR confers functional
advantage to viral gene expression
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Bachu, Mahesh; Murali, Rajesh V.; Babu, Anil M. H. K. H.; Ranga, Udaykumar] Jawaharlal Nehru Ctr Adv Sci Res, Mol Virol Lab, Mol Biol & Genet Unit, Bangalore, Karnataka, India.
[Yedavalli, Venkat S. R. K.; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RI Jeang, Kuan-Teh/A-2424-2008
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P3
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200055
ER
PT J
AU Bakari, M
Aboud, S
Nilsson, C
Francis, J
Buma, D
Moshiro, C
Aris, EA
Lyamuya, E
Janabi, M
Mbwana, J
Mwanyika, L
Stout, R
Hejdeman, B
Brave, A
Robb, M
Marovich, M
Michael, N
Earl, P
Moss, B
Wahren, B
Biberfeld, G
Pallangyo, K
Mhalu, F
Sandstrom, E
AF Bakari, M.
Aboud, S.
Nilsson, C.
Francis, J.
Buma, D.
Moshiro, C.
Aris, E. A.
Lyamuya, E.
Janabi, M.
Mbwana, J.
Mwanyika, L.
Stout, R.
Hejdeman, B.
Brave, A.
Robb, M.
Marovich, M.
Michael, N.
Earl, P.
Moss, B.
Wahren, B.
Biberfeld, G.
Pallangyo, K.
Mhalu, F.
Sandstrom, E.
TI A low dose of multigene, multiclade HIV DNA given intradermally induces
strong and broad immune responses after boosting with heterologous HIV
MVA
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Bakari, M.; Aboud, S.; Francis, J.; Moshiro, C.; Lyamuya, E.; Mbwana, J.; Pallangyo, K.; Mhalu, F.] MUHAS, Dar Es Salaam, 20892, Tanzania.
[Nilsson, C.; Brave, A.; Wahren, B.; Biberfeld, G.] Swedish Inst Infect Dis Control, Stockholm, Sweden.
[Nilsson, C.; Brave, A.; Wahren, B.; Biberfeld, G.] Karolinska Inst, Stockholm, Sweden.
[Buma, D.; Aris, E. A.; Janabi, M.] Muhimbili Natl Hosp, Dar Es Salaam, Tanzania.
[Mwanyika, L.] Tanzania Police Force, Dar Es Salaam, Tanzania.
[Hejdeman, B.; Sandstrom, E.] Soder Sjukhuset, KI, Stockholm, Sweden.
[Robb, M.; Marovich, M.; Michael, N.] Walter Reed Army Inst Res, Rockville, MD USA.
[Earl, P.; Moss, B.] NIAID, NIH, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P403
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300454
ER
PT J
AU Bar, KJ
Keele, BF
Decker, J
McLellan, J
Salazar-Gonzales, J
Salazar, M
Li, H
Wang, S
Yang, Y
Hahn, BH
Kwong, PD
Shaw, GM
AF Bar, K. J.
Keele, B. F.
Decker, J.
McLellan, J.
Salazar-Gonzales, J.
Salazar, M.
Li, H.
Wang, S.
Yang, Y.
Hahn, B. H.
Kwong, P. D.
Shaw, G. M.
TI Neutralizing antibody responses against conformational envelope epitopes
in early HIV-1 infection
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Bar, K. J.; Decker, J.; Salazar-Gonzales, J.; Salazar, M.; Li, H.; Wang, S.; Hahn, B. H.; Shaw, G. M.] Univ Alabama, Birmingham, AL USA.
[Keele, B. F.] NCI, Frederick, MD 21701 USA.
[McLellan, J.; Yang, Y.; Kwong, P. D.] NIH, Bethesda, MD 20892 USA.
RI McLellan, Jason/A-6874-2010
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P71
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300123
ER
PT J
AU Bar, KJ
Li, H
Keele, B
Grayson, T
Sun, R
Chamberland, A
Tremblay, C
Markowitz, M
Schumacher, J
Hahn, B
Shaw, G
AF Bar, K. J.
Li, H.
Keele, B.
Grayson, T.
Sun, R.
Chamberland, A.
Tremblay, C.
Markowitz, M.
Schumacher, J.
Hahn, B.
Shaw, G.
TI Multiplicity of infection by HIV-1 in injection drug users, men who have
sex with men and heterosexuals
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Bar, K. J.; Li, H.; Grayson, T.; Sun, R.; Schumacher, J.; Hahn, B.; Shaw, G.] Univ Alabama, Birmingham, AL USA.
[Keele, B.] NCI, Frederick, MD 21701 USA.
[Chamberland, A.; Tremblay, C.] Univ Montreal, Montreal, PQ, Canada.
[Markowitz, M.] Aaron Diamond AIDS Res Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O37
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300038
ER
PT J
AU Casazza, JP
Bowman, K
Adzaku, S
Ambrozak, DA
Roederer, M
Bailer, RT
Enama, M
Nason, M
Ledgerwood, JE
Graham, BS
Koup, RA
AF Casazza, J. P.
Bowman, K.
Adzaku, S.
Ambrozak, D. A.
Roederer, M.
Bailer, R. T.
Enama, M.
Nason, M.
Ledgerwood, J. E.
Graham, B. S.
Koup, R. A.
TI Increased HIV-specific immunity in HIV-infected individuals vaccinated
with a DNA prime, rAd5 boost regimen
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Casazza, J. P.; Bowman, K.; Adzaku, S.; Ambrozak, D. A.; Roederer, M.; Bailer, R. T.; Enama, M.; Nason, M.; Ledgerwood, J. E.; Graham, B. S.; Koup, R. A.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P315
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300366
ER
PT J
AU Chang, J
Kulkarni, S
Meier, A
Lindsay, RJ
Bazner, S
Lifson, JD
Bosch, RJ
Carrington, M
Altfeld, M
AF Chang, J.
Kulkarni, S.
Meier, A.
Lindsay, R. J.
Bazner, S.
Lifson, J. D.
Bosch, R. J.
Carrington, M.
Altfeld, M.
TI TLR-mediated pDC responses to HIV-1 ligands
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Chang, J.; Meier, A.; Lindsay, R. J.; Bazner, S.; Altfeld, M.] MIT & Harvard, Ragon Inst MGH, Boston, MA USA.
[Kulkarni, S.; Carrington, M.] NCI, SAIC Frederick, Lab Genom Divers, Frederick, MD 21701 USA.
[Lifson, J. D.] NCI, SAIC Frederick, AIDS & Canc Virus Program, Frederick, MD 21701 USA.
[Bosch, R. J.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O11
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300012
ER
PT J
AU Chattopadhyay, PK
Brodie, T
Ganesan, A
Mascola, JR
Michael, NL
Roederer, M
AF Chattopadhyay, P. K.
Brodie, T.
Ganesan, A.
Mascola, J. R.
Michael, N. L.
Roederer, M.
TI The first year: early correlates of long-term HIV progression
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Chattopadhyay, P. K.; Mascola, J. R.; Roederer, M.] NIH, ImmunoTechnol Sect, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Brodie, T.] Inst Biomed Res, Bellinzona, Switzerland.
[Ganesan, A.] Natl Naval Med Ctr, Bethesda, MD USA.
[Michael, N. L.] US Mil HIV Res Program, Rockville, MD USA.
RI Chattopadhyay, Pratip/B-9227-2008;
OI Chattopadhyay, Pratip/0000-0002-5457-9666
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P257
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300308
ER
PT J
AU Chen, W
Xiao, X
Streaker, E
Wang, Y
Markowitz, M
Haynes, B
AF Chen, W.
Xiao, X.
Streaker, E.
Wang, Y.
Markowitz, M.
Haynes, B.
TI Monoclonal antibodies from patient with acute HIV-1 infection
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Chen, W.; Xiao, X.; Streaker, E.; Wang, Y.] NCI, CCRNP, NIH, Frederick, MD 21701 USA.
[Markowitz, M.] Rockefeller Univ, Aaron Diamond AIDS Res Center, New York, NY 10021 USA.
[Haynes, B.] Human Vaccine Inst, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P36
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300089
ER
PT J
AU Cherkasova, E
Lerman, MI
Childs, R
AF Cherkasova, Elena
Lerman, Michael I.
Childs, Richard
TI Transcriptional regulation of HERV-E expression in clear cell renal
carcinoma
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Cherkasova, Elena; Lerman, Michael I.; Childs, Richard] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P23
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200075
ER
PT J
AU Cicala, C
Martinelli, E
Mcnally, JP
Pascucio, M
Patel, N
Jelicic, K
Wei, D
Van Ryk, D
Fauci, AS
Arthos, J
AF Cicala, C.
Martinelli, E.
Mcnally, J. P.
Pascucio, M.
Patel, N.
Jelicic, K.
Wei, D.
Van Ryk, D.
Fauci, A. S.
Arthos, J.
TI The gut mucosal homing receptor integrin alpha 4 beta 7 forms a complex
with CD4 and defines a T cell subset that is highly susceptible to
infection by HIV-1
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Cicala, C.; Martinelli, E.; Mcnally, J. P.; Pascucio, M.; Patel, N.; Jelicic, K.; Wei, D.; Van Ryk, D.; Fauci, A. S.; Arthos, J.] Natl Inst Allergy & Infect Dis USA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P99
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300151
ER
PT J
AU Currier, JR
De Souza, M
Ratto-Kim, S
Paris, R
Nguay, V
Cox, J
Earl, P
Moss, B
Sriplienchan, S
Thongcharoen, P
Kim, J
Robb, M
Michael, N
Marovich, M
AF Currier, J. R.
De Souza, M.
Ratto-Kim, S.
Paris, R.
Nguay, V.
Cox, J.
Earl, P.
Moss, B.
Sriplienchan, S.
Thongcharoen, P.
Kim, J.
Robb, M.
Michael, N.
Marovich, M.
TI Characterization of cell-mediated immune responses generated by
recombinant modified vaccinia Ankara (rMVA)-HIV-1 in a phase I vaccine
trial
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Currier, J. R.; Ratto-Kim, S.; Nguay, V.; Kim, J.; Robb, M.; Michael, N.; Marovich, M.] Mil HIV Res Program, Dept Vaccine Res & Dev, Rockville, MD USA.
[De Souza, M.; Paris, R.; Sriplienchan, S.; Thongcharoen, P.] AFRIMS, Bangkok, Thailand.
[Cox, J.] IAVI, Rockville, MD USA.
[Earl, P.; Moss, B.] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O27
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300028
ER
PT J
AU Didierlaurent, L
Houzet, L
Paillart, JC
Morichaud, Z
Smagulova, F
Maurel, S
Marquet, R
Mougel, M
AF Didierlaurent, Ludovic
Houzet, Laurent
Paillart, Jean-Christophe
Morichaud, Zakia
Smagulova, Fatima
Maurel, Stephan
Marquet, Roland
Mougel, Marylene
TI HIV-1 specifically encapsidates other nucleic acids than its genomic RNA
SO RETROVIROLOGY
LA English
DT Meeting Abstract
ID VIRIONS
C1 [Didierlaurent, Ludovic; Houzet, Laurent; Morichaud, Zakia; Smagulova, Fatima; Maurel, Stephan; Mougel, Marylene] Equipe Assemblage & Replicat Retrovirus, UMII CPBS, UMI, CNRS,UMR 5236, Montpellier, France.
[Houzet, Laurent] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Paillart, Jean-Christophe; Marquet, Roland] ULP, CNRS, UPR9002, Architecture & React ARN, Strasbourg, France.
RI Paillart, Jean-Christophe/A-4171-2010; Mougel, Marylene/K-7958-2013
OI Mougel, Marylene/0000-0002-0345-1427
NR 4
TC 0
Z9 0
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P31
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200083
ER
PT J
AU Dosenovic, P
Guenaga, J
Ofek, G
Baker, D
Schief, W
Kwong, PD
Hedestam, GBK
Wyatt, RT
AF Dosenovic, P.
Guenaga, J.
Ofek, G.
Baker, D.
Schief, W.
Kwong, P. D.
Hedestam, G. B. Karlsson
Wyatt, R. T.
TI Analysis of antibody and B cell responses following inoculation with
computationally designed HIV-1 2F5 epitope scaffold proteins
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Dosenovic, P.; Hedestam, G. B. Karlsson] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.
[Guenaga, J.; Ofek, G.; Kwong, P. D.; Wyatt, R. T.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Baker, D.; Schief, W.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
RI Baker, David/K-8941-2012
OI Baker, David/0000-0001-7896-6217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P178
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300229
ER
PT J
AU Douagi, I
Forsell, MM
Sundling, C
O'dell, S
Seder, R
Mascola, JR
Lore, K
Wyatt, RT
AF Douagi, I.
Forsell, M. M.
Sundling, C.
O'dell, S.
Seder, R.
Mascola, J. R.
Lore, K.
Wyatt, R. T.
TI Impact of in vivo CD4 binding during HIV-1 Env trimer immunizations of
rhesus macaques
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Douagi, I.; Forsell, M. M.; Sundling, C.] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.
[O'dell, S.; Seder, R.; Mascola, J. R.; Wyatt, R. T.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Lore, K.] Karolinska Inst, Ctr Infect Med, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O35
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300036
ER
PT J
AU Eller, L
Ouma, B
Oballah, P
Eller, MA
de Souza, MS
Wabwire-Mangen, F
Laeyendecker, O
Quinn, T
Kiwanuka, N
Serwadda, D
Sewankambo, N
Wawer, M
Gray, R
Michael, NL
Robb, ML
Montefiori, D
Brown, BK
Polonis, VR
AF Eller, L.
Ouma, B.
Oballah, P.
Eller, M. A.
de Souza, M. S.
Wabwire-Mangen, F.
Laeyendecker, O.
Quinn, T.
Kiwanuka, N.
Serwadda, D.
Sewankambo, N.
Wawer, M.
Gray, R.
Michael, N. L.
Robb, M. L.
Montefiori, D.
Brown, B. K.
Polonis, V. R.
TI Breadth and magnitude of neutralizing antibody responses in subjects
infected with HIV-1 subtype D or recombinants in Rakai district, Uganda
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Eller, L.; Eller, M. A.; Michael, N. L.; Robb, M. L.; Brown, B. K.; Polonis, V. R.] Makerere Univ, Walter Reed Project, US Mil HIV Res Program, Kampala, Uganda.
[de Souza, M. S.] Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand.
[Wabwire-Mangen, F.; Kiwanuka, N.; Serwadda, D.] Makerere Univ, Walter Reed Makerere Univ, Sch Publ Hlth, Kampala, Uganda.
[Laeyendecker, O.; Quinn, T.; Wawer, M.; Gray, R.] NIAID, Johns Hopkins Sch Med, NIH, Baltimore, MD USA.
[Sewankambo, N.] Makerere Univ, Coll Hlth Sci, Kampala, Uganda.
[Montefiori, D.] Duke Univ, Durham, NC USA.
RI Laeyendecker, Oliver/B-9331-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P56
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300109
ER
PT J
AU Enama, ME
Novik, L
Holman, L
Gordon, I
Nason, M
Ledgerwood, J
Graham, BS
AF Enama, M. E.
Novik, L.
Holman, L.
Gordon, I.
Nason, M.
Ledgerwood, J.
Graham, B. S.
TI Safety and tolerability of VRC DNA and rAd5 HIV-1 vaccine delivery by
intramuscular, subcutaneous and intradermal administration in healthy
adults
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Enama, M. E.; Novik, L.; Holman, L.; Gordon, I.; Ledgerwood, J.; Graham, B. S.] NIAID, VRC, NIH, Bethesda, MD 20892 USA.
[Nason, M.] NIAID, BRB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P200
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300251
ER
PT J
AU Felber, BK
Valentin, A
von Gegerfelt, A
Jalah, R
Patel, V
Kulkarni, V
Alicea, C
Rosati, M
Khan, A
Draghia-Akli, R
Pavlakis, GN
AF Felber, B. K.
Valentin, A.
von Gegerfelt, A.
Jalah, R.
Patel, V.
Kulkarni, V.
Alicea, C.
Rosati, M.
Khan, A.
Draghia-Akli, R.
Pavlakis, G. N.
TI Persistent virological benefit in SIV-infected macaques upon therapeutic
vaccination upon vaccination with DNA vectors
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Felber, B. K.; Jalah, R.; Kulkarni, V.; Alicea, C.; Rosati, M.] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
[Valentin, A.; von Gegerfelt, A.; Patel, V.; Pavlakis, G. N.] NCI, HRS, VB, Frederick, MD 21701 USA.
[Khan, A.; Draghia-Akli, R.] VGX Pharmaceut Inc, The Woodlands, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P318
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300369
ER
PT J
AU Felber, BK
Kim, E
Pal, R
Desrosiers, RC
Wolinsky, SM
Pavlakis, GN
AF Felber, B. K.
Kim, E.
Pal, R.
Desrosiers, R. C.
Wolinsky, S. M.
Pavlakis, G. N.
TI Monospecific expansion of SIVmac251 during acute infection masks
multiple transmitted virus variants revealed during the chronic phase
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Felber, B. K.] NCI, Canc Res Ctr, HRPS, VB, Frederick, MD 21701 USA.
[Kim, E.; Wolinsky, S. M.] Northwestern Univ, Chicago, IL 60611 USA.
[Desrosiers, R. C.] Harvard Univ, Sch Med, New England Reg Primate Res Ctr, Southborough, MA 01772 USA.
[Pavlakis, G. N.] NCI, HRS, VB, Frederick, MD 21701 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O38
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300039
ER
PT J
AU Fischer, W
Apetrei, C
Hahn, BH
Letvin, NL
Nabel, GJ
Korber, BT
AF Fischer, W.
Apetrei, C.
Hahn, B. H.
Letvin, N. L.
Nabel, G. J.
Korber, B. T.
TI Gene-to-gene differences in evolutionary rate between HIV-1 and natural
SIV from sooty mangabeys: implications for vaccine tests in non-human
primates
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Fischer, W.; Korber, B. T.] Los Alamos Natl Lab, Los Alamos, NM USA.
[Apetrei, C.] Tulane Univ, Dept Trop Med, New Orleans, LA 70118 USA.
[Hahn, B. H.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Letvin, N. L.] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
[Letvin, N. L.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Nabel, G. J.] NAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
MA P425
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300476
ER
PT J
AU Flatz, LR
Kong, W
Ko, S
Roychoudhuri, R
Wang, L
Xu, L
Yang, Z
Honda, M
Pinschewer, DD
Nabel, GJ
AF Flatz, L. R.
Kong, W.
Ko, S.
Roychoudhuri, R.
Wang, L.
Xu, L.
Yang, Z.
Honda, M.
Pinschewer, D. D.
Nabel, G. J.
TI Replication-defective lymphocytic choriomeningitis virus vectors boost
cellular and humoral immunity after DNA or adenovirus vector priming
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Flatz, L. R.; Kong, W.; Ko, S.; Roychoudhuri, R.; Wang, L.; Xu, L.; Yang, Z.; Honda, M.; Nabel, G. J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Pinschewer, D. D.] Univ Geneva, Dept Pathol & Immunol, CMU, Geneva, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P357
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300408
ER
PT J
AU Franchini, G
AF Franchini, G.
TI Improvement of the efficacy of ALVAC-HIV vaccine candidates for humans
in non human primates
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Franchini, G.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P415
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300466
ER
PT J
AU Freel, SA
Chattopadhyay, PK
Lamoreaux, L
Zarkowsky, D
Overman, RG
Ochsenbauer-Jambor, C
Kappes, JC
Cunningham, CK
Denny, TN
Weinhold, KJ
Ferrari, G
Koup, RA
Graham, BS
Haynes, BF
Roederer, M
Tomaras, GD
AF Freel, S. A.
Chattopadhyay, P. K.
Lamoreaux, L.
Zarkowsky, D.
Overman, R. G.
Ochsenbauer-Jambor, C.
Kappes, J. C.
Cunningham, C. K.
Denny, T. N.
Weinhold, K. J.
Ferrari, G.
Koup, R. A.
Graham, B. S.
Haynes, B. F.
Roederer, M.
Tomaras, G. D.
TI Phenotypic analyses of CD8+T cells that mediate virus inhibition from
HIV-1 vaccinees and HIV-1+virus controllers
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Freel, S. A.] Duke Univ, Sch Med, DHVI & Surg, Durham, NC USA.
[Chattopadhyay, P. K.; Roederer, M.] NIAID, Immunotechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Lamoreaux, L.; Zarkowsky, D.; Koup, R. A.] NIAID, Immunol Core Sect, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Overman, R. G.; Denny, T. N.; Weinhold, K. J.; Haynes, B. F.; Tomaras, G. D.] Duke Univ, Med Ctr, DHVI & Surg, Durham, NC USA.
[Ochsenbauer-Jambor, C.; Kappes, J. C.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Cunningham, C. K.] Duke Univ, Med Ctr, Dept Pediat, Durham, NC USA.
[Ferrari, G.] Duke Univ, Med Ctr, Dept Surg, Durham, NC USA.
[Graham, B. S.] NIAID, Viral Pathogenesis Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RI Chattopadhyay, Pratip/B-9227-2008; Tomaras, Georgia/J-5041-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O1
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300002
ER
PT J
AU Gray, GE
Bekker, L
Churchyard, G
Nchabeleng, M
Mlisana, K
de Bruyn, G
Roux, S
Mathebula, M
Latka, M
Bennie, T
Metch, B
Moodie, Z
Allen, M
Eaton, N
Kublin, J
AF Gray, G. E.
Bekker, L.
Churchyard, G.
Nchabeleng, M.
Mlisana, K.
de Bruyn, G.
Roux, S.
Mathebula, M.
Latka, M.
Bennie, T.
Metch, B.
Moodie, Z.
Allen, M.
Eaton, N.
Kublin, J.
TI Did unblinding affect HIV risk behaviour and risk perception in the
HVTN503/Phambili study?
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Gray, G. E.; de Bruyn, G.] Perinatal HIV Res Unit, Soweto, South Africa.
[Bekker, L.; Roux, S.] Desmond Tutu HIV Fdn, Cape Town, South Africa.
[Churchyard, G.; Latka, M.] Aurum Inst Hlth Res, Cape Town, South Africa.
[Nchabeleng, M.; Mathebula, M.; Bennie, T.] Medunsa HIV Clin Res Unit MeCRU, Tswane, South Africa.
[Mlisana, K.] CAPRISA, Durban, South Africa.
[Metch, B.; Moodie, Z.] FHCRC, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA USA.
[Allen, M.] NIAID, NIH, Bethesda, MD 20892 USA.
[Eaton, N.; Kublin, J.] Fred Hutchinson Canc Res Ctr, HIV Vaccine Trials Network, Seattle, WA 98104 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P209
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300260
ER
PT J
AU Harris, LD
Estes, JD
Klatt, NR
Taft, B
Barclay, R
Douek, DC
Silvestri, G
Liffson, J
Brenchley, J
AF Harris, L. D.
Estes, J. D.
Klatt, N. R.
Taft, B.
Barclay, R.
Douek, D. C.
Silvestri, G.
Liffson, J.
Brenchley, J.
TI Extensive intestinal damage underlies microbial translocation in the GI
tract of chronically SIV-infected Rhesus macaques
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Harris, L. D.; Klatt, N. R.; Brenchley, J.] NIAID, Immunopathogenesis Unit, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Estes, J. D.; Taft, B.; Liffson, J.] NCI, AIDS & Canc Virus Program, SAIC, NIH, Frederick, MD 21701 USA.
[Barclay, R.] Univ Edinburgh, Ctr Regenerat Med, Edinburgh, Midlothian, Scotland.
[Douek, D. C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Silvestri, G.] Univ Penn, Dept Pathol, Philadelphia, PA 19104 USA.
[Silvestri, G.] Univ Penn, Lab Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P146
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300198
ER
PT J
AU Hirao, LA
Wu, L
Khan, AS
Dai, A
Karl, J
Lank, S
Wiseman, R
O'Connor, D
Watkins, D
Miller, N
Betts, MR
Sardesai, NY
Boyer, JD
Weiner, DB
AF Hirao, L. A.
Wu, L.
Khan, A. S.
Dai, A.
Karl, J.
Lank, S.
Wiseman, R.
O'Connor, D.
Watkins, D.
Miller, N.
Betts, M. R.
Sardesai, N. Y.
Boyer, J. D.
Weiner, D. B.
TI DNA vaccination with IL-12 lowers viral replication following SIVmac251
challenge
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Hirao, L. A.; Wu, L.; Dai, A.; Betts, M. R.; Boyer, J. D.; Weiner, D. B.] Univ Penn, Philadelphia, PA 19104 USA.
[Khan, A. S.; Sardesai, N. Y.] VGX Pharmaceut, The Woodlands, TX USA.
[Karl, J.; Lank, S.; Wiseman, R.; O'Connor, D.; Watkins, D.] Univ Wisconsin, Madison, WI USA.
[Miller, N.] NIAID, Bethesda, MD 20892 USA.
RI Weiner, David/H-8579-2014
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P28
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300081
ER
PT J
AU Jeang, KT
AF Jeang, Kuan-Teh
TI Novel cellular processes that regulate post-transcriptional expression
of HIV-1 transcripts
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Jeang, Kuan-Teh] NIH, Bethesda, MD 20892 USA.
RI Jeang, Kuan-Teh/A-2424-2008
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR I15
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200016
ER
PT J
AU Johnson, D
Merino, Y
Berkowitz, N
Vasilenko, O
Larkin, B
Young, S
Graham, B
Ledgerwood, JM
AF Johnson, D.
Merino, Y.
Berkowitz, N.
Vasilenko, O.
Larkin, B.
Young, S.
Graham, B.
Ledgerwood, J. M.
TI An evaluation of prescreen recruitment data: enrolling racial/ethnic
minorities in Phase I HIV vaccine clinical trials
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Johnson, D.; Merino, Y.; Berkowitz, N.; Vasilenko, O.; Larkin, B.; Young, S.; Graham, B.; Ledgerwood, J. M.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P406
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300457
ER
PT J
AU Kannanganat, S
Nigam, P
Velu, V
Earl, P
Lai, L
Lawson, B
Chennareddi, L
Wilson, R
Kozlowski, P
Moss, B
Robinson, H
Amara, R
AF Kannanganat, S.
Nigam, P.
Velu, V.
Earl, P.
Lai, L.
Lawson, B.
Chennareddi, L.
Wilson, R.
Kozlowski, P.
Moss, B.
Robinson, H.
Amara, R.
TI Influence of preexisting vaccinia immunity on a DNA/MVA SIV vaccine,
decreased cellular immunity but enhanced control of a pathogenic SIV
challenge
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Earl, P.; Moss, B.] NIH, Viral Dis Lab, Bethesda, MD 20892 USA.
[Wilson, R.; Kozlowski, P.] Louisiana State Univ, Hlth Sci Ctr, New Orleans, LA USA.
[Robinson, H.] Geovax Inc, Atlanta, GA USA.
[Kannanganat, S.; Nigam, P.; Velu, V.; Lai, L.; Lawson, B.; Chennareddi, L.; Amara, R.] Emory Univ, Yerkes Natl Primate Ctr, Atlanta, GA 30322 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O51
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300052
ER
PT J
AU Ko, S
Wang, L
Cheng, C
Kong, W
Gall, J
King, R
Nabel, GJ
AF Ko, S.
Wang, L.
Cheng, C.
Kong, W.
Gall, J.
King, R.
Nabel, G. J.
TI Development of recombinant adenovirus 28 vectors for HIV vaccines
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Ko, S.; Wang, L.; Cheng, C.; Kong, W.; Nabel, G. J.] NIAID, Virol Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Gall, J.; King, R.] Genvec Inc, Gaithersburg, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P309
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300360
ER
PT J
AU Latka, M
Grey, G
Fielding, K
Bekker, L
Mlisana, K
Nchabeleng, M
DeBruin, G
Allen, M
Kublin, J
Churchyard, G
AF Latka, M.
Grey, G.
Fielding, K.
Bekker, L.
Mlisana, K.
Nchabeleng, M.
DeBruin, G.
Allen, M.
Kublin, J.
Churchyard, G.
TI Factors associated with pregnancy during the HVTN 503/Phambili trial, a
phase IIB HIV trial of the Merck Ad-5 multi-clade HIV vaccine
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Latka, M.; Churchyard, G.] Aurum Inst, Houghton, South Africa.
[Grey, G.; DeBruin, G.] Univ Witwatersrand, Perinatal Hlth Res Unit, Johannesburg, South Africa.
[Fielding, K.] London Sch Hyg & Trop Med, London WC1, England.
[Bekker, L.] Desmond Tutu HIV Ctr, Cape Town, South Africa.
[Mlisana, K.] CAPRISA, Durban, South Africa.
[Nchabeleng, M.] MEDUNSA, Pretoria, South Africa.
[Allen, M.] NIH, Washington, DC USA.
[Kublin, J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P187
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300238
ER
PT J
AU Lau, C
Swann, EM
Gaist, P
Allen, MA
AF Lau, C.
Swann, E. M.
Gaist, P.
Allen, M. A.
TI Behavioral and social science in HIV vaccine clinical research: workshop
recommendations
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Lau, C.; Swann, E. M.; Gaist, P.; Allen, M. A.] NIH, Behav & Social Sci Grp, DAIDS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P219
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300270
ER
PT J
AU Ledgerwood, JE
Novik, L
Enama, ME
Gordon, IJ
Holman, LA
Nason, MC
Bailer, RT
Roederer, M
Koup, RA
Mascola, JR
Nabel, GJ
Graham, BS
AF Ledgerwood, J. E.
Novik, L.
Enama, M. E.
Gordon, I. J.
Holman, L. A.
Nason, M. C.
Bailer, R. T.
Roederer, M.
Koup, R. A.
Mascola, J. R.
Nabel, G. J.
Graham, B. S.
TI Comparable immunogenicity of VRC DNA and rAd5 HIV-1 vaccines delivered
by intramuscular, subcutaneous and intradermal routes in healthy adults
(VRC 011)
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Ledgerwood, J. E.; Novik, L.; Enama, M. E.; Gordon, I. J.; Holman, L. A.; Nason, M. C.; Bailer, R. T.; Roederer, M.; Koup, R. A.; Mascola, J. R.; Nabel, G. J.; Graham, B. S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P198
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300249
ER
PT J
AU Letvin, N
Mascola, J
Rao, S
Buzby, A
Roederer, M
Hudgens, M
Gilbert, P
Seder, R
Douek, D
Koup, R
Graham, B
Nabel, G
AF Letvin, N.
Mascola, J.
Rao, S.
Buzby, A.
Roederer, M.
Hudgens, M.
Gilbert, P.
Seder, R.
Douek, D.
Koup, R.
Graham, B.
Nabel, G.
TI Gene-based vaccination protects against mucosal infection by a
heterologous highly pathogenic SIV isolate in rhesus monkeys
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Letvin, N.; Buzby, A.] Harvard Univ, Sch Med, Beth Israel Deaconess Hosp, Boston, MA USA.
[Mascola, J.; Rao, S.; Roederer, M.; Seder, R.; Douek, D.; Koup, R.; Graham, B.; Nabel, G.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Hudgens, M.] Univ N Carolina, Chapel Hill, NC USA.
[Gilbert, P.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P421
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300472
ER
PT J
AU Maenetje, PW
Casazza, J
Riou, C
Ambrozak, D
Gray, G
de Bruyn, G
Koup, R
Gray, C
AF Maenetje, P. W.
Casazza, J.
Riou, C.
Ambrozak, D.
Gray, G.
de Bruyn, G.
Koup, R.
Gray, C.
TI A less differentiated memory phenotype of Gag-specific CD4+T-cells
during primary HIV infection associates with viral control at 12 months
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Maenetje, P. W.; Riou, C.; Ambrozak, D.; Koup, R.; Gray, C.] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Casazza, J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Gray, G.; de Bruyn, G.] Perinatal HIV Res Unit Soweto, Johannesburg, South Africa.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O44
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300045
ER
PT J
AU Malherbe, DC
Doria-Rose, N
Misher, L
Beckett, T
Blay-Puryear, W
Barnett, S
Srivastava, I
Richardson, B
Stamatatos, L
Haigwood, NL
AF Malherbe, D. C.
Doria-Rose, N.
Misher, L.
Beckett, T.
Blay-Puryear, W.
Barnett, S.
Srivastava, I.
Richardson, B.
Stamatatos, L.
Haigwood, N. L.
TI Sequential immunization with a subtype B HIV-1 envelope quasispecies
elicits broader neutralization than vaccination with a single envelope
clone
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Malherbe, D. C.; Haigwood, N. L.] Oregon Hlth & Sci Univ, Beaverton, OR USA.
[Doria-Rose, N.] NIH, Bethesda, MD 20892 USA.
[Misher, L.; Beckett, T.] Trub Pharmaceut, Seattle, WA USA.
[Blay-Puryear, W.] Boston Univ, Boston, MA 02215 USA.
[Barnett, S.; Srivastava, I.] Novartis Vaccines & Diagnost, Cambridge, MA USA.
[Richardson, B.] Univ Washington, Seattle, WA 98195 USA.
[Stamatatos, L.] Seattle Biomed Res Inst, Seattle, WA 98109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P86
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300138
ER
PT J
AU Manches, O
Munn, D
Fallahi, A
Lifson, J
Chaperot, L
Plumas, J
Bhardwaj, N
AF Manches, O.
Munn, D.
Fallahi, A.
Lifson, J.
Chaperot, L.
Plumas, J.
Bhardwaj, N.
TI HIV-activated human plasmacytoid DCs induce Tregs through an indoleamine
2,3-dioxygenase-dependent mechanism
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Manches, O.; Fallahi, A.; Bhardwaj, N.] NYU, Langone Med Ctr, Inst Canc, New York, NY USA.
[Munn, D.] Med Coll Georgia, Augusta, GA 30912 USA.
[Lifson, J.] NCI, Frederick, MD 21701 USA.
[Chaperot, L.; Plumas, J.] EFS Rhone Alpes, INSERM, U823, La Tronche, France.
RI Plumas, Joel/N-2516-2013; chaperot, laurence/N-2927-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P281
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300332
ER
PT J
AU Mariani, SA
Crotti, A
Vicenzi, E
Huang, DW
Lempicky, R
Cicala, C
Arthos, J
Poli, G
AF Mariani, Samanta A.
Crotti, Andrea
Vicenzi, Elisa
Huang Dawei
Lempicky, Richard
Cicala, Claudia
Arthos, James
Poli, Guido
TI Post-entry events of efficient R5 vs. inefficient X4 HIV-1 replication
in primary CD4(+) T lymphocytes, a transcriptome analysis
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Mariani, Samanta A.; Crotti, Andrea; Vicenzi, Elisa; Poli, Guido] Ist Sci San Raffaele, Dept Immunol Transplantat & Infect Dis, I-20132 Milan, Italy.
[Huang Dawei; Lempicky, Richard] Sci Applicat Int Corp, Frederick, MD 21702 USA.
[Cicala, Claudia; Arthos, James] NIAID, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
SU 2
AR I19
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200020
ER
PT J
AU Mark, D
Middelkoop, K
Roux, S
Gray, G
Mlisana, K
Nchabaleng, M
Churchyard, G
De Bruyn, G
Latka, M
Magagula, D
Kublin, J
Allen, M
Bekker, L
AF Mark, D.
Middelkoop, K.
Roux, S.
Gray, G.
Mlisana, K.
Nchabaleng, M.
Churchyard, G.
De Bruyn, G.
Latka, M.
Magagula, D.
Kublin, J.
Allen, M.
Bekker, L.
CA T NIAID HIV Vaccine Trials Network
TI HVTN 503(Phambili) trial discontinuation of enrolment/vaccination: the
impact on trial participant attitudes to vaccine trials and scientific
research
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Mark, D.; Middelkoop, K.; Roux, S.; Bekker, L.; T NIAID HIV Vaccine Trials Network] Univ Cape Town, Desmond Tutu HIV Ctr, ZA-7925 Cape Town, South Africa.
[Gray, G.; De Bruyn, G.] Univ Witwatersrand, Perinatal HIV Res Unit, Johannesburg, South Africa.
[Mlisana, K.; Magagula, D.] Univ KwaZulu Natal, CAPRISA, Durban, South Africa.
[Nchabaleng, M.] Univ Limpopo, Medunsa Clin Res Unit, Pretoria, South Africa.
[Churchyard, G.; Latka, M.] Aurum Inst Hlth Res, Johannesburg, South Africa.
[Kublin, J.] HIV Vaccine Trials Network, Seattle, WA USA.
[Allen, M.] NIAID, DAIDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P214
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300265
ER
PT J
AU Mir, KD
Milush, JM
Brenchley, JM
Reeves, JD
Gordon, SN
Else, JG
O'Neill, E
Silvestri, G
Sodora, DL
AF Mir, K. D.
Milush, J. M.
Brenchley, J. M.
Reeves, J. D.
Gordon, S. N.
Else, J. G.
O'Neill, E.
Silvestri, G.
Sodora, D. L.
TI Preserved adaptive immune responses and limited immune activation in
CD4-low SIV-positive sooty mangabeys
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Mir, K. D.; Sodora, D. L.] Seattle Biomed Res Inst, Viral Vaccines Program, Seattle, WA 98109 USA.
[Milush, J. M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Brenchley, J. M.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Reeves, J. D.] Monogram Biosci, San Francisco, CA USA.
[Gordon, S. N.; Silvestri, G.] Univ Penn, Philadelphia, PA 19104 USA.
[Else, J. G.] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[O'Neill, E.] Ctr Dis Control Influenza Div, Atlanta, GA USA.
RI Reeves, Jacqueline/I-5379-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P26
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300079
ER
PT J
AU Morner, A
Scholler, J
Bunnik, E
Jansson, M
Wehlin, L
Bergqvist, L
Pihlainen, EH
Shaw, O
Seidl, T
Wang, Y
Bergmeier, LA
Singh, M
Vaughan, R
Yang, G
Shao, Y
Wyatt, RT
Schuitemaker, H
Biberfeld, G
Thorstensson, R
Lehner, T
AF Morner, A.
Scholler, J.
Bunnik, E.
Jansson, M.
Wehlin, L.
Bergqvist, L.
Pihlainen, E. Hansson
Shaw, O.
Seidl, T.
Wang, Y.
Bergmeier, L. A.
Singh, M.
Vaughan, R.
Yang, G.
Shao, Y.
Wyatt, R. T.
Schuitemaker, H.
Biberfeld, G.
Thorstensson, R.
Lehner, T.
TI Immunisation with recombinant HLA class I and II, HIV-1gp140 and SIVp27
antigens elicits protection against SHIV-SF162P4 infection in rhesus
macaques
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Morner, A.; Jansson, M.; Wehlin, L.; Bergqvist, L.; Pihlainen, E. Hansson; Biberfeld, G.; Thorstensson, R.] Swedish Inst Infect Dis Control, Dept Immunol & Vaccinol, Solna, Sweden.
[Scholler, J.] Immudex, Copenhagen, Denmark.
[Bunnik, E.; Schuitemaker, H.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
[Shaw, O.; Vaughan, R.] Guys Kings & St Thomas Hosp, London, England.
[Seidl, T.; Wang, Y.; Lehner, T.] Kings Coll London, Guys Hosp, London WC2R 2LS, England.
[Bergmeier, L. A.] Barts & London Queen Marys Sch Med & Dent, London, England.
[Singh, M.] LIONEX Diagnost & Therapeut, Braunschweig, Germany.
[Yang, G.; Shao, Y.] Chinese Ctr Dis Control, Beijing, Peoples R China.
[Wyatt, R. T.] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P328
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300379
ER
PT J
AU Pahwa, S
Pallikkuth, S
Rogers, KA
Doster, M
Villinger, F
Franchini, G
AF Pahwa, S.
Pallikkuth, S.
Rogers, K. A.
Doster, M.
Villinger, F.
Franchini, G.
TI Interleukin (IL)-21 induces cytolytic molecule perforin in CD4 and CD8 T
cells without CD4 activation in chronically SIV infected rhesus macaques
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Pahwa, S.; Pallikkuth, S.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Rogers, K. A.; Villinger, F.] Emory Univ, Atlanta, GA 30322 USA.
[Doster, M.; Franchini, G.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P276
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300327
ER
PT J
AU Pancera, M
Majeed, S
Ban, Y
Chen, L
Huang, C
Kong, L
Kwon, Y
Stuckey, J
Zhou, T
Robinson, J
Schief, W
Sodroski, J
Wyatt, R
Kwong, P
AF Pancera, M.
Majeed, S.
Ban, Y.
Chen, L.
Huang, C.
Kong, L.
Kwon, Y.
Stuckey, J.
Zhou, T.
Robinson, J.
Schief, W.
Sodroski, J.
Wyatt, R.
Kwong, P.
TI Structure of HIV-1 gp41 interactive region: layered architecture and
basis of conformational mobility
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Pancera, M.; Majeed, S.; Chen, L.; Huang, C.; Kong, L.; Kwon, Y.; Stuckey, J.; Zhou, T.; Wyatt, R.; Kwong, P.] NIAID, NIH, VRC, Bethesda, MD 20892 USA.
[Ban, Y.; Schief, W.] Univ Washington, Seattle, WA 98195 USA.
[Robinson, J.] Tulane Univ, Med Ctr, Dept Pediat, New Orleans, LA 70118 USA.
[Sodroski, J.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
RI Zhou, Tongqing/A-6880-2010
OI Zhou, Tongqing/0000-0002-3935-4637
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P126
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300178
ER
PT J
AU Patterson, J
Li, Q
Kuate, S
McKinnon, K
DiPasquale, J
Haase, AT
Robert-Guroff, M
AF Patterson, J.
Li, Q.
Kuate, S.
McKinnon, K.
DiPasquale, J.
Haase, A. T.
Robert-Guroff, M.
TI Replicating adenovirus type 5 host range recombinant vaccine
biodistribution in rhesus macaques following multiple mucosal routes of
immunization
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Patterson, J.; Kuate, S.; McKinnon, K.; DiPasquale, J.; Robert-Guroff, M.] NCI, Bethesda, MD 20892 USA.
[Li, Q.; Haase, A. T.] Univ Minnesota, Sch Med, Dept Microbiol, Minneapolis, MN 55455 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P355
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300406
ER
PT J
AU Pavlakis, GN
Rosati, M
Patel, V
Valentin, A
Bergamaschi, C
Kulkarni, V
Jalah, R
von Gegerfelt, A
Ohlen, C
Khan, A
Draghia-Akli, R
Van Rompay, K
Felber, BK
AF Pavlakis, G. N.
Rosati, M.
Patel, V.
Valentin, A.
Bergamaschi, C.
Kulkarni, V.
Jalah, R.
von Gegerfelt, A.
Ohlen, C.
Khan, A.
Draghia-Akli, R.
Van Rompay, K.
Felber, B. K.
TI Intramuscular DNA delivery by electroporation leads to greatly enhanced
systemic and mucosal immune responses and control of SIVmac251 challenge
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Pavlakis, G. N.; Rosati, M.; Patel, V.; Valentin, A.; Bergamaschi, C.; von Gegerfelt, A.] NCI, Ctr Canc Res, HRS, VB, Frederick, MD 21701 USA.
[Ohlen, C.] NCI, SAIC Frederick Inc, ACVP, Frederick, MD 21701 USA.
[Khan, A.; Draghia-Akli, R.] VGX Pharmaceut Inc, The Woodlands, TX USA.
[Van Rompay, K.] Calif Natl Reg Primate Res Ctr, Davis, CA USA.
[Kulkarni, V.; Jalah, R.; Felber, B. K.] NCI, HRPS, VB, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P196
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300247
ER
PT J
AU Pegu, A
Migone, T
Freimuth, W
Donaldson, M
Foulds, K
Roederer, M
Nabel, GJ
AF Pegu, A.
Migone, T.
Freimuth, W.
Donaldson, M.
Foulds, K.
Roederer, M.
Nabel, G. J.
TI A human blocking antibody to CCR5 partially protects against lentiviral
infection in non-human primates
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Pegu, A.; Donaldson, M.; Foulds, K.; Roederer, M.; Nabel, G. J.] NIH, Bethesda, MD 20892 USA.
[Migone, T.; Freimuth, W.] Human Genome Sci, Rockville, MD USA.
OI Pegu, Amarendra/0000-0003-3564-6453
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P402
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300453
ER
PT J
AU Pegu, A
Boyington, JC
Kong, W
Shi, W
Kwong, PD
Nabel, GJ
AF Pegu, A.
Boyington, J. C.
Kong, W.
Shi, W.
Kwong, P. D.
Nabel, G. J.
TI Crystal structure and function of a monoclonal antibody against primate
CD4 that blocks HIV/SIV infection
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Pegu, A.; Boyington, J. C.; Kong, W.; Shi, W.; Kwong, P. D.; Nabel, G. J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
OI Pegu, Amarendra/0000-0003-3564-6453
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P183
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300234
ER
PT J
AU Robinson, HL
Amara, RR
Lai, L
Xu, Y
De Rosa, S
Defawe, O
Sato, A
Tomaras, GD
Qin, L
Moss, B
Wyatt, LS
Hay, C
Goepfert, P
AF Robinson, H. L.
Amara, R. R.
Lai, L.
Xu, Y.
De Rosa, S.
Defawe, O.
Sato, A.
Tomaras, G. D.
Qin, L.
Moss, B.
Wyatt, L. S.
Hay, C.
Goepfert, P.
TI Comparison of the immunogenicity in humans and rhesus macaques of
vaccines consisting of DNA priming and MVA boosting and MVA priming and
boosting
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Robinson, H. L.; Xu, Y.] GeoVax Inc, Atlanta, GA USA.
[Amara, R. R.; Lai, L.] Yerkes Natl Primate Res Ctr, Atlanta, GA USA.
[Amara, R. R.; Lai, L.] Emory Vaccine Ctr, Atlanta, GA USA.
[De Rosa, S.; Defawe, O.; Sato, A.] Fred Hutchinson Canc Res Ctr, HVTN Lab Program, Seattle, WA 98104 USA.
[Tomaras, G. D.] Duke Univ, Med Ctr, Durham, NC USA.
[Qin, L.] Fred Hutchinson Canc Res Ctr, HVTN SCHARP, Seattle, WA 98104 USA.
[Wyatt, L. S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Hay, C.] Univ Rochester, Rochester, NY USA.
[Goepfert, P.] Univ Alabama, Alabama Vaccine Res Clin, Birmingham, AL USA.
RI Tomaras, Georgia/J-5041-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P422
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300473
ER
PT J
AU Rood, JE
Migueles, SA
Berkley, AM
Compton, AA
Joshi, RP
Duerr, A
McElrath, J
Connors, M
AF Rood, J. E.
Migueles, S. A.
Berkley, A. M.
Compton, A. A.
Joshi, R. P.
Duerr, A.
McElrath, J.
Connors, M.
TI HIV-specific CD8+T-cells of vaccinees exhibit proliferative and
cytotoxic capacities comparable to those of progressors
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Rood, J. E.; Migueles, S. A.; Berkley, A. M.; Compton, A. A.; Joshi, R. P.; Connors, M.] NIH, Bethesda, MD 20892 USA.
[Duerr, A.; McElrath, J.] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Unit, Seattle, WA 98104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O49
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300050
ER
PT J
AU Sanville, B
Buckler-White, A
Yan, YH
Dolan, M
Wollenberg, K
Kozak, CA
AF Sanville, Bradley
Buckler-White, Alicia
Yan, Yuhe
Dolan, Michael
Wollenberg, Kurt
Kozak, Christine A.
TI Adaptive evolution of the virus resistance gene Apobec in the genus Mus
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Sanville, Bradley; Buckler-White, Alicia; Yan, Yuhe; Kozak, Christine A.] NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
[Dolan, Michael; Wollenberg, Kurt] NIAID, Bioinformat & Computat Biosci Branch, Off Cyber Infrastruct & Computat Biol, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O7
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200032
ER
PT J
AU Sarzotti-Kelsoe, M
Cox, J
Cleland, N
Denny, T
Hural, J
Needham, L
Ozaki, D
Rodriguez-Chavez, IR
Stevens, G
Stiles, T
Tarragona-Fiol, T
Simkins, A
AF Sarzotti-Kelsoe, M.
Cox, J.
Cleland, N.
Denny, T.
Hural, J.
Needham, L.
Ozaki, D.
Rodriguez-Chavez, I. R.
Stevens, G.
Stiles, T.
Tarragona-Fiol, T.
Simkins, A.
TI Evaluation and recommendations on good clinical laboratory practice
(GCLP) guidelines for phase I-III HIV vaccine clinical trials
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Sarzotti-Kelsoe, M.] Duke Univ, Med Ctr, Durham, NC USA.
[Sarzotti-Kelsoe, M.] Int AIDS Vaccine Initiat, Rockville, MD USA.
[Cleland, N.] NIAID, DAIDS, NIH, Bethesda, MD 20892 USA.
[Denny, T.; Needham, L.] CHAVI, Duke Human Vaccine Inst, Durham, NC USA.
[Hural, J.] HIV Vaccine Trials Network, Seattle, WA USA.
[Ozaki, D.] CAVD CA VIMC Cent QAU, Durham, NC USA.
[Rodriguez-Chavez, I. R.] NIDCR, AIDS & Immunosuppress Program, IBIDB, DER,NIH, Bethesda, MD USA.
[Stiles, T.] Qual Ltd, Kettering, England.
[Cox, J.; Stevens, G.; Tarragona-Fiol, T.] Univ London Imperial Coll Sci Technol & Med, Int AIDS Vaccine Initiat Core Lab, London, England.
[Simkins, A.] AlphaVax Human Vaccines Inc, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P206
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300257
ER
PT J
AU Sirivichayakul, S
Felber, B
Kulkarni, V
Pavlakis, G
Buranapraditkun, S
Thantiworasit, P
Pitakpolrat, P
Allen, T
Leitner, T
Korber, B
Ruxrungtham, K
AF Sirivichayakul, S.
Felber, B.
Kulkarni, V.
Pavlakis, G.
Buranapraditkun, S.
Thantiworasit, P.
Pitakpolrat, P.
Allen, T.
Leitner, T.
Korber, B.
Ruxrungtham, K.
TI Pre-clinical immunogenicity of mosaic Asian AE/B HIV-1 DNA vaccine in
mice
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Sirivichayakul, S.; Buranapraditkun, S.; Thantiworasit, P.; Pitakpolrat, P.; Ruxrungtham, K.] Chulalongkorn Univ, Fac Med, Dept Med, Bangkok 10330, Thailand.
[Felber, B.; Kulkarni, V.; Pavlakis, G.] NCI, Frederick, MD 21701 USA.
[Allen, T.] Harvard Univ, Sch Med, Boston, MA USA.
[Leitner, T.; Korber, B.] Los Alamos Natl Lab, Los Alamos, NM USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P321
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300372
ER
PT J
AU Sitar, S
Hartman, BI
Graham, BS
Ledgerwood, JE
AF Sitar, S.
Hartman, B. I.
Graham, B. S.
Ledgerwood, J. E.
TI Social media as a tool for engaging and educating audiences around HIV
vaccine research and clinical trial participation
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Sitar, S.; Hartman, B. I.; Graham, B. S.; Ledgerwood, J. E.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 1
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P218
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300269
ER
PT J
AU Strbo, N
Vaccari, M
Pahwa, S
Kolber, MA
Fisher, E
Gonzalez, L
Felber, BK
Pavlakis, GN
Franchini, G
Podack, ER
AF Strbo, N.
Vaccari, M.
Pahwa, S.
Kolber, M. A.
Fisher, E.
Gonzalez, L.
Felber, B. K.
Pavlakis, G. N.
Franchini, G.
Podack, E. R.
TI Gp96-Ig-SIV vaccines induce predominant immune responses at mucosal
sites
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Strbo, N.; Pahwa, S.; Kolber, M. A.; Fisher, E.; Gonzalez, L.; Podack, E. R.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Vaccari, M.; Felber, B. K.; Pavlakis, G. N.; Franchini, G.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR O34
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300035
ER
PT J
AU Strebel, K
AF Strebel, Klaus
TI Antagonizing the effects of Bst-2/tetherin: multiple ways to accomplish
a common goal
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Strebel, Klaus] NIAID, Viral Biochem Sect, LMM, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR I10
PG 1
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200011
ER
PT J
AU Sui, Y
Zhu, Q
Gagnon, S
Dzutsev, A
Terabe, M
Vaccari, M
Venzon, D
Klinman, D
Strober, W
Kelsall, B
Franchini, G
Belyakov, IM
Berzofsky, JA
AF Sui, Y.
Zhu, Q.
Gagnon, S.
Dzutsev, A.
Terabe, M.
Vaccari, M.
Venzon, D.
Klinman, D.
Strober, W.
Kelsall, B.
Franchini, G.
Belyakov, I. M.
Berzofsky, J. A.
TI Role of vaccine-induced innate and adaptive immunity in controlling
mucosal transmission of SIV in macaques
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Venzon, D.] NCI, Biostat Branch, NIH, Bethesda, MD 20892 USA.
[Klinman, D.] NCI, Expt Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Strober, W.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Kelsall, B.] NIAID, Lab Molec Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P414
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300465
ER
PT J
AU Sundling, C
Soldemo, M
Chakrabarti, B
Forsell, MN
Lore, K
Wyatt, RT
Douagi, I
AF Sundling, C.
Soldemo, M.
Chakrabarti, B.
Forsell, M. N.
Lore, K.
Wyatt, R. T.
Douagi, I.
TI Evaluation of peripheral and bone marrow B cell responses in rhesus
macaques after immunization with soluble HIV-1 gp140 trimers
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Sundling, C.; Soldemo, M.; Douagi, I.] Karolinska Inst, Stockholm, Sweden.
[Chakrabarti, B.; Forsell, M. N.; Wyatt, R. T.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Lore, K.] Karolinska Inst, Ctr Infect Med, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P83
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300135
ER
PT J
AU Valentin, A
von Gegerfelt, A
Alicea, C
Patel, V
Marthas, ML
Van Rompay, K
Pavlakis, GN
Felber, BK
AF Valentin, A.
von Gegerfelt, A.
Alicea, C.
Patel, V.
Marthas, M. L.
Van Rompay, K.
Pavlakis, G. N.
Felber, B. K.
TI Altered mucosal distribution of SIV-specific T cells in Rhesus macaques
infected with the live-attenuated Rev-independent SIV
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Valentin, A.; von Gegerfelt, A.; Patel, V.; Pavlakis, G. N.] NCI, Ctr Canc Res, HRS, VB, Frederick, MD 21701 USA.
[Alicea, C.; Felber, B. K.] NCI, HRPS, VB, Frederick, MD 21701 USA.
[Marthas, M. L.; Van Rompay, K.] Calif Natl Reg Primate Res Ctr, Davis, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P164
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300215
ER
PT J
AU Verkoczy, L
Diaz, M
Holl, TM
Ouyang, Y
Bouton-Verville, H
Alam, SM
Liao, H
Kelsoe, G
Haynes, BF
AF Verkoczy, L.
Diaz, M.
Holl, T. M.
Ouyang, Y.
Bouton-Verville, H.
Alam, S. M.
Liao, H.
Kelsoe, G.
Haynes, B. F.
TI Immunological tolerance prevents the expression of a broadly reactive
neutralizing HIV-1 antibody
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Verkoczy, L.; Bouton-Verville, H.; Alam, S. M.; Liao, H.; Haynes, B. F.] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC USA.
[Diaz, M.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Holl, T. M.; Kelsoe, G.] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA.
[Ouyang, Y.] Xenogen Biosci, Cranbury, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P54
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300107
ER
PT J
AU Wang, Y
Whittall, T
Scholler, J
Wyatt, R
Singh, M
Bergmeier, LA
Bunnik, E
Schuitemaker, H
Shaw, O
Vaughan, R
Pido-Lopez, J
Seidl, T
Babaahmady, K
Yang, G
Thorstensson, R
Biberfeld, G
Lehner, T
AF Wang, Y.
Whittall, T.
Scholler, J.
Wyatt, R.
Singh, M.
Bergmeier, L. A.
Bunnik, E.
Schuitemaker, H.
Shaw, O.
Vaughan, R.
Pido-Lopez, J.
Seidl, T.
Babaahmady, K.
Yang, G.
Thorstensson, R.
Biberfeld, G.
Lehner, T.
TI Allogeneic stimulation of the anti-viral APOBEC3G in human CD4+T cells
and prevention of SHIV infectivity in macaques immunized with HLA
antigens
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Wang, Y.; Whittall, T.; Bergmeier, L. A.; Shaw, O.; Vaughan, R.; Pido-Lopez, J.; Seidl, T.; Babaahmady, K.; Lehner, T.] Kings Coll London, Mucosal Immunol Unit, London WC2R 2LS, England.
[Scholler, J.] Immunodex, Copenhagen, Denmark.
[Wyatt, R.] NIH, Bethesda, MD 20892 USA.
[Singh, M.] Lionex Diagnost & Therapeut, Braunschweig, Germany.
[Bunnik, E.; Schuitemaker, H.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
[Yang, G.] Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China.
[Thorstensson, R.; Biberfeld, G.] Swedish Inst Infect Dis Control, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P340
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300391
ER
PT J
AU Wu, X
Zhou, T
O'Dell, S
Wyatt, RT
Kwong, PD
Mascola, JR
AF Wu, X.
Zhou, T.
O'Dell, S.
Wyatt, R. T.
Kwong, P. D.
Mascola, J. R.
TI Mechanism of HIV-1 resistance to a monoclonal antibody that effectively
targets the site of CD4 attachment
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Wu, X.; Zhou, T.; O'Dell, S.; Wyatt, R. T.; Kwong, P. D.; Mascola, J. R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RI Zhou, Tongqing/A-6880-2010
OI Zhou, Tongqing/0000-0002-3935-4637
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P118
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300170
ER
PT J
AU Wyatt, L
Earl, P
Moss, B
AF Wyatt, L.
Earl, P.
Moss, B.
TI Assessing and restructuring foreign gene insertion sites for enhanced
stability of modified Vaccinia virus ankara recombinants expressing HIV
genes
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Wyatt, L.; Earl, P.; Moss, B.] NIAID, LVD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P416
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300467
ER
PT J
AU Xiao, X
Feng, Y
Chen, W
Longo, N
Dimitrov, DS
AF Xiao, X.
Feng, Y.
Chen, W.
Longo, N.
Dimitrov, D. S.
TI Guiding the immune system through complex maturation pathways: a novel
multi-immunogen approach for elicitation of broadly neutralizing
antibodies
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Xiao, X.; Feng, Y.; Chen, W.; Dimitrov, D. S.] NCI, CCRNP, NIH, Frederick, MD 21701 USA.
[Longo, N.] NIAMSD, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P35
PG 2
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300088
ER
PT J
AU Yu, B
Houzet, L
Didierlaurent, L
Chamontin, C
Morichaud, Z
Darlix, JL
Mougel, M
AF Yu, Bing
Houzet, Laurent
Didierlaurent, Ludovic
Chamontin, Celia
Morichaud, Zakia
Darlix, Jean Luc
Mougel, Marylene
TI A new role of the HIV-1 nucleocapsid in the spatiotemporal control of
the reverse transcription throughout the virus replication cycle
SO RETROVIROLOGY
LA English
DT Meeting Abstract
ID MUTATIONS; TYPE-1
C1 [Yu, Bing; Houzet, Laurent; Didierlaurent, Ludovic; Chamontin, Celia; Morichaud, Zakia; Mougel, Marylene] Inst Biol, CPBS Equipe Assemblage & Replicat Retrovirus, UMI UMII, CNRS UMR 5236, Montpellier, France.
[Yu, Bing] Huazhong Univ Sci & Technol, Dept Pathogen Biol, Tongji Med Coll, Wuhan 430074, Peoples R China.
[Houzet, Laurent] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Darlix, Jean Luc] ENS, IFR 128, INSERM, Unite Virol Humaine,LaboRetro,U758, Lyon, France.
RI Mougel, Marylene/K-7958-2013
OI Mougel, Marylene/0000-0002-0345-1427
NR 5
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P14
PG 2
WC Virology
SC Virology
GA 498MX
UT WOS:000270146200066
ER
PT J
AU Zhou, T
Yang, Z
Xu, L
Hessell, AJ
Burton, DR
Nabel, GJ
Kwong, PD
AF Zhou, T.
Yang, Z.
Xu, L.
Hessell, A. J.
Burton, D. R.
Nabel, G. J.
Kwong, P. D.
TI Crystal structure of gp120 in complex with the CD4-binding-site antibody
b13 suggests precise targeting is needed for neutralization
SO RETROVIROLOGY
LA English
DT Meeting Abstract
C1 [Zhou, T.; Yang, Z.; Xu, L.; Nabel, G. J.; Kwong, P. D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Hessell, A. J.; Burton, D. R.] Scripps Res Inst, La Jolla, CA 92037 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PY 2009
VL 6
AR P66
PG 1
WC Virology
SC Virology
GA 509KL
UT WOS:000271015300118
ER
PT J
AU Cammarata, M
Eybert, L
Ewald, F
Reichenbach, W
Wulff, M
Anfinrud, P
Schotte, F
Plech, A
Kong, QY
Lorenc, M
Lindenau, B
Rabiger, J
Polachowski, S
AF Cammarata, Marco
Eybert, Laurent
Ewald, Friederike
Reichenbach, Wolfgang
Wulff, Michael
Anfinrud, Philip
Schotte, Friedrich
Plech, Anton
Kong, Qingyu
Lorenc, Maciej
Lindenau, Bernd
Raebiger, Juergen
Polachowski, Stephan
TI Chopper system for time resolved experiments with synchrotron radiation
SO REVIEW OF SCIENTIFIC INSTRUMENTS
LA English
DT Article
DE beam choppers; high-speed techniques; synchrotron radiation; X-ray
apparatus
ID X-RAY-DIFFRACTION; STRUCTURAL DYNAMICS; MECHANICAL SHUTTER; BEAM
CHOPPER; CRYSTALLOGRAPHY; REALIZATION; PROTEIN; COMPLEX; ESRF
AB A chopper system for time resolved pump-probe experiments with x-ray beams from a synchrotron is described. The system has three parts: a water-cooled heatload chopper, a high-speed chopper, and a millisecond shutter. The chopper system, which is installed in beamline ID09B at the European Synchrotron Radiation Facility, provides short x-ray pulses for pump-probe experiments with ultrafast lasers. The chopper system can produce x-ray pulses as short as 200 ns in a continuous beam and repeat at frequencies from 0 to 3 kHz. For bunch filling patterns of the synchrotron with pulse separations greater than 100 ns, the high-speed chopper can isolate single 100 ps x-ray pulses that are used for the highest time resolution. A new rotor in the high-speed chopper is presented with a single pulse (100 ps) and long pulse (10 mu s) option. In white beam experiments, the heatload of the (noncooled) high-speed chopper is lowered by a heatload chopper, which absorbs 95% of the incoming power without affecting the pulses selected by the high speed chopper.
C1 [Cammarata, Marco; Eybert, Laurent; Ewald, Friederike; Reichenbach, Wolfgang; Wulff, Michael] European Synchrotron Radiat Facil, F-38043 Grenoble, France.
[Anfinrud, Philip; Schotte, Friedrich] NIH, Chem Phys Lab, Bethesda, MD 20892 USA.
[Plech, Anton] Forschungszentrum Karlsruhe, Inst Synchrotron Radiat ISS, D-76021 Karlsruhe, Germany.
[Kong, Qingyu] Synchrotron SOLEIL, F-91192 Gif Sur Yvette, France.
[Lorenc, Maciej] Univ Rennes 1, CNRS, UMR6626, Grp Mat Condensee & Mat, F-35042 Rennes, France.
[Lindenau, Bernd; Raebiger, Juergen; Polachowski, Stephan] Forschungszentrum Julich, Cent Technol Div ZAT, D-52425 Julich, Germany.
RP Wulff, M (reprint author), European Synchrotron Radiat Facil, BP 220, F-38043 Grenoble, France.
EM wulff@esrf.fr
RI Cammarata, Marco/C-2322-2008; Plech, Anton/E-4895-2010; Lorenc,
Maciej/N-7594-2014;
OI Cammarata, Marco/0000-0003-3013-1186; Plech, Anton/0000-0002-6290-9303
NR 22
TC 48
Z9 48
U1 3
U2 22
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0034-6748
J9 REV SCI INSTRUM
JI Rev. Sci. Instrum.
PD JAN
PY 2009
VL 80
IS 1
AR 015101
DI 10.1063/1.3036983
PG 10
WC Instruments & Instrumentation; Physics, Applied
SC Instruments & Instrumentation; Physics
GA 401TT
UT WOS:000262966000035
PM 19191457
ER
PT S
AU Chao, CC
Garland, DL
Dasch, GA
Ching, WM
AF Chao, Chien-Chung
Garland, Donita L.
Dasch, Gregory A.
Ching, Wei-Mei
BE Hechemy, KE
Brouqui, P
Samuel, JE
Raoult, DA
TI Comparative Proteomic Analysis of Antibiotic-Sensitive and Insensitive
Isolates of Orientia tsutsugamushi
SO RICKETTSIOLOGY AND RICKETTSIAL DISEASES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 5th International Conference on Rickettsiae and Rickettsial Diseases
CY MAY 18-20, 2008
CL Marseilles, FRANCE
DE Orientia tsutsugamushi; Proteomic; antibiotic sensitive
ID SCRUB TYPHUS; RESISTANCE
AB Scrub typhus, caused by infection with Orientia tsutsugamushi, is probably the most common severe rickettsial disease. Early diagnosis followed by treatment with antibiotics such as doxycycline or chloramphenicol usually quickly decreases fever in patients, and they often recover well from other symptoms of the disease. However, poorly responsive cases have been reported from northern Thailand and southern India. In order to identify protein factors that may be partially responsible for differential drug sensitivity of isolates of Orientia, we compared the protein profiles of doxycycline sensitive (Karp) versus (vs.) insensitive (AFSC4 and AFSC7) isolates. Tryptic peptides from both total water-soluble proteins and from protein spots separated by 2D-PAGE were analyzed using LC-MS/MS. The identity of each protein was established using the published genomic sequence of Boryong strain O. tsutsugamushi. The profiles of protein released into water from these isolates were quite different. There were 10 proteins detected only in AFSC4, 3 only in Karp, and I only in AFSC7. Additionally, there were 2 proteins not detected only in AFSC4,4 not found only in Karp, and 3 not found only in AFSC-7. A comparison of 2D-PAGE protein profiles of drug sensitive strain versus (vs.) insensitive isolates has led to the identification of 14 differentially expressed or localized proteins, including elongation factor Ts and Tu, DNA-directed RNA polymerase alpha-subunit, ATP synthase beta-subunit, and several hypothetical proteins. These data confirm the tremendous proteomic diversity of isolates of Orientia and suggest that drug insensitivity in this species may arise from multiple mechanisms.
C1 [Chao, Chien-Chung; Ching, Wei-Mei] USN, VRDD, IDD, Med Res Ctr, Silver Spring, MD 20910 USA.
[Garland, Donita L.] NEI, NIH, Bethesda, MD 20892 USA.
[Dasch, Gregory A.] Ctr Dis Control & Prevent, Rickettsial Zoonoses Branch, Atlanta, GA 30333 USA.
[Ching, Wei-Mei] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
RP Chao, CC (reprint author), USN, VRDD, IDD, Med Res Ctr, 503 Robert Grant Ave,RM3N71, Silver Spring, MD 20910 USA.
EM chien-chung.chao@med.navy.mil
RI Chao, Chien-Chung/A-8017-2011;
OI Dasch, Gregory/0000-0001-6090-1810
FU Work Unit Number (WUN [6000.RAD1.J.A0310]
FX The authors wish to thank Ms. Kynita Winn for her help in 2D-PAGE
analysis and Dr. Paul Graf for his review of the manuscript. This work
was Supported by Work Unit Number (WUN) 6000.RAD1.J.A0310. The opinions
and assertions contained herein are the private ones of the authors and
are not to be construed as official or as reflecting the views of the
Department of the Navy, the naval service at large, the Department of
Defense, the Centers for Disease Control and Prevention, the Department
of Health and Human Services, or the U. S. Government. Authors C. C.
Chao, G. A. Dasch, and W M. Ching are employees of the U. S. Government.
This work was prepared as part of official duties.
NR 18
TC 4
Z9 4
U1 1
U2 3
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND
SN 0077-8923
BN 978-1-57331-750-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2009
VL 1166
BP 27
EP 37
DI 10.1111/j.1749-6632.2009.04525.x
PG 11
WC Infectious Diseases; Multidisciplinary Sciences; Parasitology
SC Infectious Diseases; Science & Technology - Other Topics; Parasitology
GA BJV56
UT WOS:000267264400003
PM 19538261
ER
PT S
AU Graubard, BI
Korn, EL
AF Graubard, Barry I.
Korn, Edward L.
BE Pfeffermann, D
Rao, CR
TI Scatterplots with Survey Data
SO SAMPLE SURVEYS: INFERENCE AND ANALYSIS, VOL 29B
SE Handbook of Statistics
LA English
DT Article; Book Chapter
C1 [Graubard, Barry I.] NCI, Biostat Branch, Bethesda, MD 20892 USA.
[Korn, Edward L.] NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Graubard, BI (reprint author), NCI, Biostat Branch, Execut Plaza,South Bldg,6120 Execut Blvd,Room 802, Bethesda, MD 20892 USA.
EM graubarb@mail.nih.gov; korne@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0169-7161
BN 978-0-08-096354-9
J9 HANDB STAT
PY 2009
VL 29B
BP 397
EP 419
DI 10.1016/S0169-7161(09)00237-5
PG 23
WC Statistics & Probability
SC Mathematics
GA BCR02
UT WOS:000311051300018
ER
PT J
AU Scherer, ML
Aspelund, T
Sigurdsson, S
Detrano, R
Garcia, M
Mitchell, GF
Launer, LJ
Thorgeirsson, G
Gudnason, V
Harris, TB
AF Scherer, Matthew L.
Aspelund, Thor
Sigurdsson, Sigurdur
Detrano, Robert
Garcia, Melissa
Mitchell, Gary F.
Launer, Lenore J.
Thorgeirsson, Gudmundur
Gudnason, Vilmundur
Harris, Tamara B.
TI Abnormal T-wave axis is associated with coronary artery calcification in
older adults
SO SCANDINAVIAN CARDIOVASCULAR JOURNAL
LA English
DT Article; Proceedings Paper
CT 47th Annual Conference on Cardiovascular Disease Epidemiology and
Prevention
CY FEB 28-MAR 03, 2007
CL Orlando, FL
SP Amer Heart Assoc, Council Epidemiol & Prevent, Council Nutr, Phys Activ & Metab, Natl Heart, Lung & Blood Inst
DE Epidemiology; electrocardiography; aging; computed tomography;
atherosclerosis
ID BEAM COMPUTED-TOMOGRAPHY; PREDICTS CARDIAC DEATH;
CARDIOVASCULAR-DISEASE; GENERAL-POPULATION; HEART-DISEASE; CHEST-PAIN;
RISK; MEN; ATHEROSCLEROSIS; ANGLE
AB Objective. To determine whether T-wave axis on the resting electrocardiogram (ECG) is associated with coronary artery calcification (CAC) score, a measurement of coronary atherosclerosis, in older adults. Methods. The sample consisted of 2004 adults aged 66 and over participating in the prospective, population-based Age-Gene/Environment Susceptibility-Reykjavik Study. The cohort was divided into gender-stratified quartiles based upon Agatston CAC score derived from computerized tomography. Frontal T-axis deviation from 45 degrees was assessed using surface ECG. Statistical analysis was performed with Tobit regression models adjusted for demographic and cardiovascular risk factors. Results. In the entire study population, T-axis deviation from 45 degrees was significantly associated with increasing CAC score in men (p0.001) and women (p=0.03). In men without clinically recognized coronary heart disease (CHD), the association with CAC score remained statistically significant (p=0.02). This association was significant among women without CHD once male CAC cut points were used (p=0.05). Conclusion. An abnormal T-wave axis is associated with an increasing CAC score in this population of Icelandic older adults. This association remains in the subgroup of subjects without clinical CHD.
C1 [Scherer, Matthew L.; Garcia, Melissa; Launer, Lenore J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Scherer, Matthew L.] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20817 USA.
[Aspelund, Thor; Sigurdsson, Sigurdur; Thorgeirsson, Gudmundur; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Detrano, Robert] Univ Calif Los Angeles, Los Angeles, CA USA.
[Mitchell, Gary F.] Cardiovasc Engn Inc, Waltham, MA USA.
RP Harris, TB (reprint author), 7201 Wisconsin Ave,Suite 3C-309, Bethesda, MD 20892 USA.
EM harris99@mail.nih.gov
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
FU Intramural NIH HHS [Z01 AG007380-03]; NIA NIH HHS [N01AG12100]
NR 27
TC 2
Z9 2
U1 0
U2 1
PU TAYLOR & FRANCIS AS
PI OSLO
PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY
SN 1401-7431
J9 SCAND CARDIOVASC J
JI Scand. Cardiovasc. J.
PY 2009
VL 43
IS 4
BP 240
EP 248
AR PII 904520580
DI 10.1080/14017430802471483
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 474JS
UT WOS:000268280200005
PM 18937149
ER
PT J
AU Barch, DM
Carter, CS
Arnsten, A
Buchanan, RW
Cohen, JD
Geyer, M
Green, MF
Krystal, JH
Nuechterlein, K
Robbins, T
Silverstein, S
Smith, EE
Strauss, M
Wykes, T
Heinssen, R
AF Barch, Deanna M.
Carter, Cameron S.
Arnsten, Amy
Buchanan, Robert W.
Cohen, Jonathan D.
Geyer, Mark
Green, Michael F.
Krystal, John H.
Nuechterlein, Keith
Robbins, Trevor
Silverstein, Steven
Smith, Edward E.
Strauss, Milton
Wykes, Til
Heinssen, Robert
TI Selecting Paradigms From Cognitive Neuroscience for Translation into Use
in Clinical Trials: Proceedings of the Third CNTRICS Meeting
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
ID IMPROVE COGNITION; SCHIZOPHRENIA; TARGETS; ENHANCEMENT; RECEPTORS;
DEFICITS; AGONISTS; TASKS; SIZE
AB This overview describes the goals and objectives of the third conference conducted as part of the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS) initiative. This third conference was focused on selecting specific paradigms from cognitive neuroscience that measured the constructs identified in the first CNTRICS meeting, with the goal of facilitating the translation of these paradigms into use in clinical trials contexts. To identify such paradigms, we had an open nomination process in which the field was asked to nominate potentially relevant paradigms and to provide information on several domains relevant to selecting the most promising tasks for each construct (eg, construct validity, neural bases, psychometrics, availability of animal models). Our goal was to identify 1-2 promising tasks for each of the 11 constructs identified at the first CNTRICS meeting. In this overview article, we describe the on-line survey used to generate nominations for promising tasks, the criteria that were used to select the tasks, the rationale behind the criteria, and the ways in which breakout groups worked together to identify the most promising tasks from among those nominated. This article serves as an introduction to the set of 6 articles included in this special issue that provide information about the specific tasks discussed and selected for the constructs from each of 6 broad domains (working memory, executive control, attention, long-term memory, perception, and social cognition).
C1 [Barch, Deanna M.] Washington Univ, St Louis, MO 63130 USA.
[Carter, Cameron S.] Univ Calif Davis, Davis, CA 95616 USA.
[Arnsten, Amy; Krystal, John H.] Yale Univ, New Haven, CT USA.
[Buchanan, Robert W.] Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA.
[Cohen, Jonathan D.] Princeton Univ, Princeton, NJ 08544 USA.
[Geyer, Mark] Univ Calif San Diego, San Diego, CA 92103 USA.
[Green, Michael F.] Univ Calif Los Angeles, Semel Inst, Los Angeles, CA USA.
[Green, Michael F.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Nuechterlein, Keith] Univ Calif Los Angeles, Los Angeles, CA USA.
[Robbins, Trevor] Univ Cambridge, Cambridge, England.
[Silverstein, Steven] Univ Med & Dent New Jersey, Rutgers, NJ USA.
[Smith, Edward E.] Columbia Univ, New York, NY USA.
[Strauss, Milton] Univ New Mexico, Albuquerque, NM USA.
[Wykes, Til] Kings Coll London, Inst Psychiat, London, England.
[Heinssen, Robert] NIMH, Bethesda, MD 20892 USA.
RP Barch, DM (reprint author), Washington Univ, St Louis, MO 63130 USA.
EM dbarch@artsci.wustl.edu
RI Wykes, Til/B-7894-2008; Wykes, Til/B-3812-2011; Barch,
Deanna/G-8638-2013
OI Wykes, Til/0000-0002-5881-8003;
FU National Institute of Mental Health (NIMH); Robert Wood Johnson
Foundation; National Alliance for Research on Schizophrenia and
Depression (NARSAD); McDonnell Foundation; National Institute of Drugs
and Alcohol; US Veteran's Administration VISN 22 Mental Illness
Research, Education, and Clinical Center; Janssen; Pfizer; GSK Inc
FX We would also like to thank Jody Conrad, Carol Cox, and Deb Tussing,
whose efforts have been invaluable in the CNTRICS process. Financial
Disclosures: Carter receives funding from the National Institute of
Mental Health (NIMH), the Robert Wood Johnson Foundation, and National
Alliance for Research on Schizophrenia and Depression (NARSAD). Dr
Carter has served as a consultant for Pfizer, Eli Lilly, and Roche.
Barch receives funding from the NIMH, the McDonnell Foundation, and
NARSAD. Dr Buchanan is currently a Data Safety and Management Board
(DSMB) member for Pfizer and in the past has served as a DSMB member for
Wyeth. He has served as a consultant for: Pfizer, Roche, Memory,
GlaxoSmithKline, Astra-Zeneca, Solvay, Sanofi-Aventis, and Organon and
has received study medications from Janssen and Ortho-McNeil
Neurologics. Dr Geyer has received consulting compensation from Abbott,
Acadia, Addex, Amgen, AstraZeneca, Bristol-Myers Squibb, Jazz, Organon,
Nura, San Diego Instruments, Serono, and Wyeth-Ayerst. Dr Geyer also has
research grant support from National Institute of Drugs and Alcohol,
NIMH, and the US Veteran's Administration VISN 22 Mental Illness
Research, Education, and Clinical Center. Dr Green received funding form
the NIMH and serves as a consultant to Amgen, Acadia, Astellas,
Bristol-Myers Squibb, Dainippon Sumitomo Pharma, Eli Lilly, Lundbeck,
Memory Pharmaceuticals, Otsuka Pharmaceutical, Sanofi-Aventis
Pharmaceuticals, and Solvay. Dr Krystal receives research funding from
the NIMH and has served as an advisor or consultant for AstraZeneca
Pharmaceuticals; LP Bristol-Myers Squibb; Cypress Bioscience, Inc; Eli
Lilly and Co; Forest Laboratories; GlaxoSmithKline; HoustonPharma;
Lohocla Research Corporation; Merz Pharmaceuticals; Organon
Pharmaceuticals; Pfizer Pharmaceuticals; Tetragenex Pharmaceuticals; and
Transcept Pharmaceuticals, Inc. Dr Nuechterlein has received research
funding from the NIMH and from Janssen, L. P., and has served as a
consultant for Janssen, L. P. Dr Robbins is a stockholder in CeNeS and
has share options in Cambridge Cognition. He has served as a consultant
to Eli Lilly, GSK, Wyeth, and Allon and has received research funding
from Pfizer, GSK Inc and received speaking honoraria from Merck, Sharp
and Dohme, Lundbeck, Cephalon, and Cortex. Dr Silverstein Medical
Research Institute, Janssen, and AstraZeneca. Dr Strauss, Dr Heinssen,
Dr Smith, and Dr Wykes reported no biomedical financial interests or
conflicts of interest. Dr Cohen receives research funding from the NIMH.
NR 17
TC 73
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U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PD JAN
PY 2009
VL 35
IS 1
BP 109
EP 114
DI 10.1093/schbul/sbn163
PG 6
WC Psychiatry
SC Psychiatry
GA 383OK
UT WOS:000261682700014
PM 19023126
ER
PT J
AU Stroup, TS
Lieberman, JA
McEvoy, JR
Davis, SM
Swartz, MS
Keefe, RSE
Miller, AL
Rosenheck, RA
Hsiao, JK
AF Stroup, T. Scott
Lieberman, Jeffrey A.
McEvoy, Joseph R.
Davis, Sonia M.
Swartz, Marvin S.
Keefe, Richard S. E.
Miller, Alexander L.
Rosenheck, Robert A.
Hsiao, John K.
CA Catie Investigators
TI Results of phase 3 of the CATIE schizophrenia trial
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Schizophrenia; Clinical trial; Antipsychotic; Effectiveness
ID INTERVENTION EFFECTIVENESS CATIE; CLINICAL ANTIPSYCHOTIC TRIALS;
RANDOMIZED CONTROLLED-TRIAL; RESISTANT SCHIZOPHRENIA; DRUGS;
2ND-GENERATION; RISPERIDONE; OLANZAPINE; QUETIAPINE; CLOZAPINE
AB Objective: The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study examined the comparative effectiveness of antipsychotic treatments for individuals with chronic schizophrenia. Patients who had discontinued antipsychotic treatment in phases I and 2 were eligible for phase 3, in which they selected one of nine antipsychotic regimens with the help of their study doctor. We describe the characteristics of the patients who selected each treatment option and their outcomes.
Method: Two hundred and seventy patients entered phase 3. The open-label treatment options were monotherapy with oral aripiprazole, dozapine, clanzapine, perphenazine, quetiapine, risperidone, ziprasidone, long-acting injectable fluphenazine decanoate, or a combination of any two of these treatments.
Results: Few patients selected fluphenazine decanoate (n=9) or perphenazine (n=4). Similar numbers selected each of the other options (range 33-41). Of the seven common choices, those who selected clozapine and combination antipsychotic treatment were the most symptomatic, and those who selected aripiprazole and ziprasidone had the highest body mass index. Symptoms improved for all groups, although the improvements were modest for the groups starting with relatively mild levels of symptoms. Side effect profiles of the medications varied considerably but medication discontinuations due to intolerability were rare (7% overall).
Conclusions: Patients and their doctors made treatment selections based on clinical factors, including severity of symptoms, response to prior treatments, and physical health status. Fluphenazine decanoate was rarely used among those with evidence of treatment non-adherence and clozapine was underutilized for those with poor previous response. Combination antipsychotic treatment warrants further study. (c) 2008 Elsevier BY. All rights reserved.
C1 [Stroup, T. Scott; Davis, Sonia M.] Univ N Carolina, Dept Psychiat, Sch Med, Chapel Hill, NC 27599 USA.
[Lieberman, Jeffrey A.] Columbia Univ, New York State Psychiat Inst, Coll Phys & Surg, Dept Psychiat, New York, NY USA.
[McEvoy, Joseph R.] Duke Univ, Med Ctr, John Umstead Hosp, Dept Biol Psychiat, Durham, NC 27706 USA.
[McEvoy, Joseph R.; Swartz, Marvin S.; Keefe, Richard S. E.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27706 USA.
[Davis, Sonia M.] Quintiles Inc, Res Triangle Pk, NC USA.
[Miller, Alexander L.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
[Rosenheck, Robert A.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06520 USA.
[Hsiao, John K.] NIMH, Div Serv & Intervent Res, NIH, Bethesda, MD 20892 USA.
RP Stroup, TS (reprint author), Univ N Carolina, Dept Psychiat, Sch Med, CB 7160, Chapel Hill, NC 27599 USA.
EM sstroup@med.unc.edu
RI Stroup, Thomas/F-9188-2014
OI Stroup, Thomas/0000-0002-3123-0672
FU National Institute of Mental Health [NO1 MH90001]
FX Acknowledgement This article was based on results from the Clinical
Antipsychotic Trials of Intervention Effectiveness project, supported by
the National Institute of Mental Health (NO1 MH90001). The aim of this
project is to examine the comparative effectiveness of antipsychotic
drugs in conditions for which their use is clinically indicated,
including schizophrenia and Alzheimer's disease. The project was carried
out by principal investigators from the University of North Carolina,
Duke University, the University of Southern California, the University
of Rochester, and Yale University in association with Quintiles, Inc.;
the program staff of the Division of interventions and Services Research
of the NIMH; and investigators from 56 sites in the United States (CATIE
Study Investigators Group). AstraZeneca Pharmaceuticals LP,
Bristol-Myers Squibb Company, Forest Pharmaceuticals. Inc., Janssen
Pharmaceutica Products, L.P., Eli Lilly and Company. Otsuka
Pharmaceutical Co., Ltd., Pfizer Inc., and Zenith Goldline
Pharmaceuticals, Inc., provided medications for the studies.
NR 14
TC 65
Z9 67
U1 2
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD JAN
PY 2009
VL 107
IS 1
BP 1
EP 12
DI 10.1016/j.schres.2008.10.011
PG 12
WC Psychiatry
SC Psychiatry
GA 404KW
UT WOS:000263151500001
PM 19027269
ER
PT B
AU Carbone, KM
AF Carbone, Kathryn M.
BE Fratamico, PM
Smith, JL
Brogden, KA
TI Infectious Causes of Chronic Disease: from Hypothesis to Proof
SO SEQUELAE AND LONG-TERM CONSEQUENCES OF INFECTIOUS DISEASES
LA English
DT Article; Book Chapter
ID PNEUMOCYSTIS-CARINII PNEUMONIA; COST-EFFECTIVENESS ANALYSIS;
BLOOD-STREAM INFECTIONS; LYME-DISEASE; ACQUIRED IMMUNODEFICIENCY;
PREVENTIVE STRATEGIES; ECONOMIC BURDEN; HOMOSEXUAL MEN; HIV-INFECTION;
SYNDROME AIDS
C1 NIH, Bethesda, MD 20892 USA.
RP Carbone, KM (reprint author), NIH, MSC 4326,8800 Rockville Pike, Bethesda, MD 20892 USA.
NR 76
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA
BN 978-1-55581-430-4
PY 2009
BP 1
EP 8
PG 8
WC Infectious Diseases
SC Infectious Diseases
GA BKK70
UT WOS:000268393800001
ER
PT J
AU Singh, AP
Harada, S
Mishina, Y
AF Singh, A. P.
Harada, S.
Mishina, Y.
TI Downstream Genes of Sox8 That Would Affect Adult Male Fertility
SO SEXUAL DEVELOPMENT
LA English
DT Article
DE Blood-testis barrier; Male fertility; Sertoli cell; SRY-box;
Spermatogenesis
ID TRANSCRIPTION FACTOR SOX8; SERTOLI-CELL FUNCTION; JUNCTION DYNAMICS; SEX
DETERMINATION; TESTIS; MOUSE; DIFFERENTIATION; EXPRESSION; MICE;
SPERMATOGENESIS
AB Sertoli cells provide nutritional and physical support to germ cells during spermatogenesis. Sox8 encodes a high mobility group transcription factor closely related to Sox9 and Sox10. Sertoli cells produce SOX8 protein, and its elimination results in an age-dependent deregulation of spermatogenesis resulting in male infertility. This suggests that Sox8 is a critical regulator of Sertoli cell function for the maintenance of male fertility beyond the first wave of spermatogenesis. To better understand the roles of Sox8 in testicular development and maintenance of male fertility, we have performed a detailed analysis to explore its downstream genes. We have used mRNA expression profiling to identify affected genes in Sertoli cells in the mutant testes of 2-month-old mice. Expression profiling of the heterozygous and homozygous Sox8 mutant testes indicates alterations in several important spermatogenesis and blood-testis barrier genes, providing insight into the molecular basis of the defects in Sox8(-/-) testes beyond the first wave of spermatogenesis. Copyright (C) 2009 S. Karger AG, Basel
C1 [Mishina, Y.] Univ Michigan, Sch Dent, Dept Biol Mat Sci, Ann Arbor, MI 48109 USA.
[Harada, S.] Merck Res Labs, Dept Bone Biol & Osteoporosis Res, West Point, PA USA.
[Singh, A. P.; Mishina, Y.] Natl Inst Environm Hlth Sci, Mol Dev Biol Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC USA.
RP Mishina, Y (reprint author), Univ Michigan, Sch Dent, Dept Biol Mat Sci, Ann Arbor, MI 48109 USA.
EM mishina@umich.edu
RI Singh, Ajeet/G-3935-2013
FU NIH, National Institute of Environmental Health Sciences [ES071003-11];
Indo-US Collaboration on Environment and Occupational Health Grant;
RIKEN Brain Science Institute [833-3944]
FX The authors would like to dedicate this manuscript to Dr. Shun Harada, a
great colleague and a wonderful friend, who made significant
contributions to the field of SOX biology. We gratefully thank the NIEHS
Microarrays Core Facility led by Dr. Rich Paules. We thank Dr. Leping Li
for sequence analyses, Drs. Mitch Eddy, Manas Ray, and Greg Scott for
helpful discussion and critical reading of the manuscript. We also thank
Mss. Ijeoma Nwosu, Gloria MacDonald, and Kelly McCann for their
technical support, Ms. Tonya Miller for her excellent service of
maintenance of the mouse colonies. This work was supported in part by
the Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences (ES071003-11), by the Indo-US
Collaboration on Environment and Occupational Health Grant, and by a
gift from RIKEN Brain Science Institute (833-3944) to Y.M.
NR 30
TC 8
Z9 8
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1661-5425
J9 SEX DEV
JI Sex. Dev.
PY 2009
VL 3
IS 1
BP 16
EP 25
DI 10.1159/000200078
PG 10
WC Developmental Biology
SC Developmental Biology
GA 428SV
UT WOS:000264871100002
PM 19339814
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Shellfish Mariculture in Drakes Estero, Point Reyes National Seashore,
California Summary
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Editorial Material; Book Chapter
ID OYSTERS CRASSOSTREA-GIGAS; EELGRASS ZOSTERA-MARINA; SUBMERGED AQUATIC
VEGETATION; SUSPENSION-FEEDING BIVALVES; HAPLOSPORIDIUM-NELSONI MSX;
PACIFIC-NORTHWEST ESTUARY; PHOCA-VITULINA-RICHARDSI; CLIMATE-CHANGE
IMPACTS; SAN-FRANCISCO BAY; HARBOR SEALS
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 246
TC 0
Z9 0
U1 3
U2 4
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 1
EP +
PG 22
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300001
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Shellfish Mariculture in Drakes Estero, Point Reyes National Seashore,
California Introduction to Drakes Estero
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Editorial Material; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 9
EP 24
PG 16
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300002
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Benthic/Pelagic Coupling-Nutrients and Particulates
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 25
EP 29
PG 5
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300003
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Eelgrass
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 30
EP 34
PG 5
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300004
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Fish
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 35
EP 37
PG 3
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300005
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Benthic Invertebrates in Soft Sediments
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 38
EP 40
PG 3
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300006
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Harbor Seals
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 41
EP 49
PG 9
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300007
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Nonnative Species
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 50
EP 56
PG 7
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300008
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Birds
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 57
EP 60
PG 4
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300009
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Human-Use Values-Economics, Recreation, and Aesthetics
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 61
EP 66
PG 6
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300010
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Scientific Conclusions That Can Be Drawn
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 67
EP 70
PG 4
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300011
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI Accuracy of the Scientific Conclusions Released by NPS to the Public
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 71
EP 79
PG 9
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300012
ER
PT J
AU Peterson, CH
Costa-Pierce, BA
Dumbauld, BR
Friedman, C
Hofmann, EE
Kite-Powell, H
Manahan, DT
O'Beirn, F
Paine, RT
Thompson, P
Whitlatch, R
Roberts, S
Bostrom, J
Chiarello, H
Mcnutt, MK
Boesch, DF
Corredor, JE
Criddle, KR
Feeley, MH
Hernandez, D
Holman, RA
Kim, K
Knuth, BA
Lawson, RA
Matsumoto, GI
Pearlman, JS
Rosenberg, AA
Rudnick, DL
Serafin, RJ
Trehu, AM
Tyack, PL
Wright, DJ
Yoder, JA
Roberts, S
Mengelt, C
Park, S
Bostrom, J
Glickson, D
Banskota, S
Lewis, P
Chiarello, H
Justice, J
AF Peterson, Charles (Pete) H.
Costa-Pierce, Barry A.
Dumbauld, Brett R.
Friedman, Carolyn
Hofmann, Eileen E.
Kite-Powell, Hauke
Manahan, Donal T.
O'Beirn, Francis
Paine, Robert T.
Thompson, Paul
Whitlatch, Robert
Roberts, Susan
Bostrom, Jodi
Chiarello, Heather
Mcnutt, Marcia K.
Boesch, Donald F.
Corredor, Jorge E.
Criddle, Keith R.
Feeley, Mary (Missy) H.
Hernandez, Debra
Holman, Robert A.
Kim, Kiho
Knuth, Barbara A.
Lawson, Robert A.
Matsumoto, George I.
Pearlman, Jay S.
Rosenberg, Andrew A.
Rudnick, Daniel L.
Serafin, Robert J.
Trehu, Anne M.
Tyack, Peter L.
Wright, Dawn J.
Yoder, James A.
Roberts, Susan
Mengelt, Claudia
Park, Susan
Bostrom, Jodi
Glickson, Deborah
Banskota, Shubha
Lewis, Pamela
Chiarello, Heather
Justice, Jeremy
CA Pt Reyes Natl Seashore
Ocean Studies Board
GP Natl Res Council
TI How Scientific Conclusions Affected NPS Decision Making
SO SHELLFISH MARICULTURE IN DRAKES ESTERO, POINT REYES NATIONAL SEASHORE,
CALIFORNIA
LA English
DT Article; Book Chapter
C1 [Peterson, Charles (Pete) H.] Univ N Carolina, Morehead City, NC 28557 USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Rhode Isl Sea Grant Coll Program, Narragansett, RI USA.
[Costa-Pierce, Barry A.] Univ Rhode Isl, Fisheries Aquaculture & Oceanog, Narragansett, RI USA.
[Dumbauld, Brett R.] ARS, USDA, Newport, OR USA.
[Friedman, Carolyn] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA.
[Hofmann, Eileen E.] Old Dominion Univ, Ctr Coastal Phys Oceanog, Oceanog, Norfolk, VA USA.
[Kite-Powell, Hauke] Woods Hole Oceanog Inst, Marine Policy Ctr, Woods Hole, MA USA.
[Manahan, Donal T.] Univ So Calif, Biol Sci, Los Angeles, CA USA.
[O'Beirn, Francis] Inst Marine, Galway, Ireland.
[Paine, Robert T.] Univ Washington, Dept Biol, Seattle, WA 98195 USA.
[Thompson, Paul] Univ Aberdeen, Sch Biol Sci, Zool, Aberdeen AB9 1FX, Scotland.
[Whitlatch, Robert] Univ Connecticut, Marine Sci, Groton, CT USA.
[Roberts, Susan; Bostrom, Jodi; Chiarello, Heather] Ocean Studies Board, Washington, DC USA.
[Roberts, Susan] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Roberts, Susan] NIH, Bethesda, MD USA.
[Chiarello, Heather] Natl Acad, New York, NY USA.
[Mcnutt, Marcia K.; Matsumoto, George I.] Monterey Bay Aquarium Res Inst, Moss Landing, CA USA.
[Boesch, Donald F.] Univ Maryland, Ctr Environm Sci, Cambridge, MD USA.
[Corredor, Jorge E.] Univ Puerto Rico, Mayaguez, PR USA.
[Criddle, Keith R.] Univ Alaska Fairbanks, Juneau, AK USA.
[Feeley, Mary (Missy) H.] ExxonMobil Explorat Co, Houston, TX USA.
[Hernandez, Debra] Hernandez & Co, Isle Of Palms, SC USA.
[Holman, Robert A.; Trehu, Anne M.; Wright, Dawn J.] Oregon State Univ, Corvallis, OR 97331 USA.
[Kim, Kiho] Amer Univ, Washington, DC 20016 USA.
[Knuth, Barbara A.] Cornell Univ, Ithaca, NY USA.
[Lawson, Robert A.] Sci Applicat Int Corp, San Diego, CA 92121 USA.
[Pearlman, Jay S.] Boeing Co, Port Angeles, WA USA.
[Rosenberg, Andrew A.] Univ New Hampshire, Durham, NH 03824 USA.
[Rudnick, Daniel L.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA.
[Serafin, Robert J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA.
[Tyack, Peter L.; Yoder, James A.] Woods Hole Oceanog Inst, Woods Hole, MA USA.
RP Peterson, CH (reprint author), Univ N Carolina, Morehead City, NC 28557 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-13898-7
PY 2009
BP 80
EP 87
PG 8
WC Ecology; Fisheries
SC Environmental Sciences & Ecology; Fisheries
GA BC3XK
UT WOS:000352027300013
ER
PT J
AU Goel, P
Sherman, A
AF Goel, Pranay
Sherman, Arthur
TI The Geometry of Bursting in the Dual Oscillator Model of Pancreatic
beta-cells
SO SIAM JOURNAL ON APPLIED DYNAMICAL SYSTEMS
LA English
DT Article
DE bursting; oscillations; calcium; insulin; pancreatic beta-cells; sliding
bars; dual oscillator model; composite bifurcation diagram; fast-slow
systems; coupled oscillators
ID ELECTRICAL-ACTIVITY; INSULIN-SECRETION; CALCIUM; ISLETS; MEMBRANE;
RETICULUM
AB We describe an extended fast-slow analysis for the dual oscillator model (DOM) for bursting oscillations in pancreatic beta-cells, which occur on a wide range of time scales, from seconds to minutes. This wide dynamic range has been suggested to result from the interactions of a very slow metabolic, possibly glycolytic, oscillator and a faster electrical oscillator, itself containing several negative feedback mechanisms with a range of time scales. Although the high dimensionality of the slow subsystem would defeat a straightforward fast-slow analysis, we show that an approximate geometrical analysis that exploits particular features of the DOM and is based on superimposing the bifurcation diagrams of the component oscillators leads to new insights into the functioning of the system.
C1 [Goel, Pranay; Sherman, Arthur] Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Goel, P (reprint author), Natl Inst Hlth, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM pgoel@iiserpune.ac.in; asherman@nih.gov
RI Goel, Pranay/D-1081-2013;
OI Goel, Pranay/0000-0002-2249-0288
FU NIH [R01-DK-46409B]
FX We thank Bard Ermentrout and Brad Peercy for useful discussions, and
Richard Bertram and Les Satin for comments on the manuscript. This
theoretical work was made possible by experiments performed in the
laboratory of Dr. Leslie Satin, supported by NIH grant R01-DK-46409B.
NR 31
TC 12
Z9 12
U1 1
U2 2
PU SIAM PUBLICATIONS
PI PHILADELPHIA
PA 3600 UNIV CITY SCIENCE CENTER, PHILADELPHIA, PA 19104-2688 USA
SN 1536-0040
J9 SIAM J APPL DYN SYST
JI SIAM J. Appl. Dyn. Syst.
PY 2009
VL 8
IS 4
BP 1664
EP 1693
DI 10.1137/08074427X
PG 30
WC Mathematics, Applied; Physics, Mathematical
SC Mathematics; Physics
GA 518VN
UT WOS:000271723300008
ER
PT J
AU Norian, JM
Levens, ED
DeCherney, AH
Adamson, GD
AF Norian, John M.
Levens, Eric D.
DeCherney, Alan H.
Adamson, G. David
BE Gerris, J
Adamson, GD
DeSutter, P
Racowsky, C
TI An American perspective on single embryo transfer
SO SINGLE EMBRYO TRANSFER
LA English
DT Article; Book Chapter
ID IN-VITRO FERTILIZATION; ASSISTED REPRODUCTIVE TECHNOLOGIES; RANDOMIZED
CONTROLLED-TRIAL; PREIMPLANTATION GENETIC DIAGNOSIS; INTRACYTOPLASMIC
SPERM INJECTION; MULTIPLE-GESTATION PREGNANCIES; LOW-BIRTH-WEIGHT;
BLASTOCYST TRANSFER; CONGENITAL-MALFORMATIONS; UNITED-STATES
C1 [Norian, John M.; Levens, Eric D.; DeCherney, Alan H.] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA.
[Adamson, G. David] Fertil Phys No Calif, Palo Alto, CA USA.
RP Norian, JM (reprint author), NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA.
NR 87
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-0-521-88834-9
PY 2009
BP 269
EP 281
PG 13
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA BDN18
UT WOS:000313966300028
ER
PT S
AU Hunt, R
Sauna, ZE
Ambudkar, SV
Gottesman, MM
Kimchi-Sarfaty, C
AF Hunt, Ryan
Sauna, Zuben E.
Ambudkar, Suresh V.
Gottesman, Michael M.
Kimchi-Sarfaty, Chava
BE Komar, AA
TI Silent (Synonymous) SNPs: Should We Care About Them?
SO SINGLE NUCLEOTIDE POLYMORPHISMS: METHODS AND PROTOCOLS, SECOND EDITION
SE Methods in Molecular Biology
LA English
DT Article; Book Chapter
DE Single nucleotide polymorphism; messenger RNA splicing; messenger RNA
stability; messenger RNA structure; protein folding; synonymous
mutations; nonsynonymous mutations; codon frequency; codon usage
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; MESSENGER-RNA STABILITY; SEQUENCE
EVOLUTION; CODON USAGE; PROTEIN; GENE; MUTATIONS; SCHIZOPHRENIA;
POPULATION; EXPRESSION
AB One of the surprising findings of the Human Genome Project was that single nucleotide polymorphisms (SNPs), which, by definition, have a minor allele frequency greater than 1%, occur at higher rates than previously suspected. When occurring in the gene coding regions, SNPs can be synonymous (i.e., not causing a change in the amino acid) or nonsynonymous (when the amino acid is altered). It has long been assumed that synonymous SNPs arc inconsequential, as the primary sequence of the protein is retained. A number of studies have questioned this assumption over the last decade, shoving that synonymous mutations arc also under evolutionary pressure and they can be implicated in disease. More importantly, several of the mechanisms by which synonymous mutations alter the structure, function, and expression level of proteins are now being elucidated. Studies have demonstrated that synonymous polymorphisms can affect messenger RNA splicing, stability, and structure as well as protein folding. These changes can have a significant effect on the function of proteins, change cellular response to therapeutic targets, and often explain the different responses of individual patients to a certain medication.
C1 [Hunt, Ryan; Sauna, Zuben E.; Kimchi-Sarfaty, Chava] US FDA, Lab Hemostasis, Div Hematol, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Ambudkar, Suresh V.; Gottesman, Michael M.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Hunt, R (reprint author), US FDA, Lab Hemostasis, Div Hematol, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
FU Intramural NIH HHS
NR 56
TC 88
Z9 96
U1 0
U2 6
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1064-3745
BN 978-1-60327-410-4
J9 METHODS MOL BIOL
JI Methods Mol. Biol.
PY 2009
VL 578
BP 23
EP 39
DI 10.1007/978-1-60327-411-1_2
D2 10.1007/978-1-60327-411-1
PG 17
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BNM36
UT WOS:000274946200002
PM 19768585
ER
PT J
AU Buckley, A
Jennison, K
Buckley, J
Spence, S
Thurm, A
Fasano, R
Sato, S
Susan, S
AF Buckley, A.
Jennison, K.
Buckley, J.
Spence, S.
Thurm, A.
Fasano, R.
Sato, S.
Susan, S.
TI POLYSOMNOGRAPHIC ABNORMALITIES AND PARENT REPORT IN YOUNG CHILDREN WITH
AUTISM
SO SLEEP
LA English
DT Meeting Abstract
CT 23rd Annual Meeting of the Associated-Professional-Sleep-Societies
CY JUN 06-11, 2009
CL Seattle, WA
SP Associated Profess Sleep Soc
C1 [Buckley, A.; Jennison, K.; Spence, S.; Thurm, A.; Susan, S.] NIMH, Pediat & Dev Neuropsychiat Branch, Bethesda, MD 20892 USA.
[Buckley, J.] NYU, Steihardt Sch Culture Educ & Human Dev, Dept Humanities & Social Sci, New York, NY USA.
[Fasano, R.; Sato, S.] Natl Inst Neurol Dis, EEG Sect, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 2009
VL 32
MA 1079
BP A352
EP A352
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 438FT
UT WOS:000265542001426
ER
PT J
AU Chen, T
Wilk, JB
O'Connor, GT
Gottlieb, DJ
AF Chen, T.
Wilk, J. B.
O'Connor, G. T.
Gottlieb, D. J.
TI GENETICS OF SLEEP PHENOTYPES IN THE NHLBI'S FRAMINGHAM HEART STUDY
OFFSPRING COHORT
SO SLEEP
LA English
DT Meeting Abstract
CT 23rd Annual Meeting of the Associated-Professional-Sleep-Societies
CY JUN 06-11, 2009
CL Seattle, WA
SP Associated Profess Sleep Soc
C1 [Gottlieb, D. J.] Vet Affairs Boston Healthcare Syst, Boston, MA USA.
[O'Connor, G. T.; Gottlieb, D. J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Chen, T.; O'Connor, G. T.; Gottlieb, D. J.] Boston Univ, Dept Med, Sect Pulm Allergy & Crit Care, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 2009
VL 32
MA 1226
BP A401
EP A401
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 438FT
UT WOS:000265542001572
ER
PT J
AU Coddington, N
Carr, W
Picchioni, D
Horovitz, SG
Fukunaga, M
Duyn, JH
Braun, AR
Balkin, TJ
AF Coddington, N.
Carr, W.
Picchioni, D.
Horovitz, S. G.
Fukunaga, M.
Duyn, J. H.
Braun, A. R.
Balkin, T. J.
TI ACTIVATION DIFFERENCES DURING ASCENDING AND DESCENDING TRENDS IN A-WAVE
POWER WHILE SLEEPING
SO SLEEP
LA English
DT Meeting Abstract
CT 23rd Annual Meeting of the Associated-Professional-Sleep-Societies
CY JUN 06-11, 2009
CL Seattle, WA
SP Associated Profess Sleep Soc
C1 [Coddington, N.] Thomas Jefferson High Sch Sci & Technol, Alexandria, VA USA.
[Coddington, N.; Carr, W.] USN, Med Res Ctr, Silver Spring, MI USA.
[Carr, W.; Picchioni, D.; Braun, A. R.] Natl Inst Deafness & Other Commun Disorders, Bethesda, MD USA.
[Picchioni, D.; Balkin, T. J.] Walter Reed Army Inst Res, Silver Spring, MD USA.
[Horovitz, S. G.; Fukunaga, M.; Duyn, J. H.] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
RI Duyn, Jozef/F-2483-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 2009
VL 32
MA 0061
BP A20
EP A20
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 438FT
UT WOS:000265542000063
ER
PT J
AU Picchioni, D
Horovitz, SG
Fukunaga, M
Carr, WS
Balkin, TJ
Duyn, JH
Braun, AR
AF Picchioni, D.
Horovitz, S. G.
Fukunaga, M.
Carr, W. S.
Balkin, T. J.
Duyn, J. H.
Braun, A. R.
TI HOW SLOW CAN YOU GO? UNIQUE FMRI CORRELATIONS WITH EEG ACTIVITY BELOW
0.1 HZ DURING SLEEP
SO SLEEP
LA English
DT Meeting Abstract
CT 23rd Annual Meeting of the Associated-Professional-Sleep-Societies
CY JUN 06-11, 2009
CL Seattle, WA
SP Associated Profess Sleep Soc
C1 [Picchioni, D.; Balkin, T. J.] Walter Reed Army Inst Res, Silver Spring, MD USA.
[Horovitz, S. G.; Fukunaga, M.; Duyn, J. H.; Braun, A. R.] NIH, Bethesda, MD 20892 USA.
[Carr, W. S.] USN, Med Res Ctr, Silver Spring, MD USA.
RI Duyn, Jozef/F-2483-2010; Fukunaga, Masaki/F-6441-2013
OI Fukunaga, Masaki/0000-0003-1010-2644
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 2009
VL 32
MA 0033
BP A11
EP A11
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 438FT
UT WOS:000265542000035
ER
PT J
AU Rogers, VE
Lewin, DS
Geiger-Brown, J
Winnie, G
AF Rogers, V. E.
Lewin, D. S.
Geiger-Brown, J.
Winnie, G.
TI OBSTRUCTIVE SLEEP APNEA AND SICKLE CELL DISEASE SEVERITY IN CHILDREN
SO SLEEP
LA English
DT Meeting Abstract
CT 23rd Annual Meeting of the Associated-Professional-Sleep-Societies
CY JUN 06-11, 2009
CL Seattle, WA
SP Associated Profess Sleep Soc
C1 [Rogers, V. E.; Geiger-Brown, J.] Univ Maryland, Baltimore, MD 21201 USA.
[Lewin, D. S.] NHLBI, Div Lung Dis, Bethesda, MD 20892 USA.
[Winnie, G.] Childrens Natl Med Ctr, Dept Allergy Pulm & Sleep Med, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 2009
VL 32
MA 0272
BP A91
EP A91
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 438FT
UT WOS:000265542000274
ER
PT J
AU McCall, C
Blascovich, J
Young, A
Persky, S
AF McCall, Cade
Blascovich, Jim
Young, Ariana
Persky, Susan
TI Proxemic behaviors as predictors of aggression towards Black (but not
White) males in an immersive virtual environment
SO SOCIAL INFLUENCE
LA English
DT Article
DE Aggression; Implicit attitudes; Proxemics; Prejudice; Nonverbal behavior
ID SOCIAL COGNITION; PREJUDICE; QUESTIONNAIRE; TECHNOLOGY; ATTITUDES;
DISTANCE; POSTURE; SELF
AB This study investigated the relationship between participant proxemic behavior and overt aggression during interactions with Black and White agents in an immersive virtual environment. In a series of two tasks, participants first interacted with two male agents (each of the same race) and then engaged in a violent shooting game with those agents. Participants' proxemic behaviors (interpersonal distance and head movements) during the first task predicted aggressive and hostile participant shots against Black but not White agents in the subsequent task. Results supported the value of proxemic variables in predicting aggression and the utility of IVET for experimental social psychology.
C1 [McCall, Cade] Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA.
[Persky, Susan] NHGRI, Bethesda, MD 20892 USA.
RP McCall, C (reprint author), Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA.
EM mccall@psych.ucsb.edu
NR 30
TC 18
Z9 19
U1 3
U2 7
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 1553-4510
J9 SOC INFLUENCE
JI Soc. Influ.
PY 2009
VL 4
IS 2
BP 138
EP 154
DI 10.1080/15534510802517418
PG 17
WC Psychology, Social
SC Psychology
GA 687GQ
UT WOS:000284767400004
ER
PT J
AU Beaton, EA
Schmidt, LA
Schulkin, J
Antony, MM
Swinson, RP
Hall, GB
AF Beaton, Elliott A.
Schmidt, Louis A.
Schulkin, Jay
Antony, Martin M.
Swinson, Richard P.
Hall, Geoffrey B.
TI Different fusiform activity to stranger and personally familiar faces in
shy and social adults
SO SOCIAL NEUROSCIENCE
LA English
DT Article
ID HUMAN EXTRASTRIATE CORTEX; FACIAL EXPRESSIONS; SELECTIVE ATTENTION;
FUNCTIONAL MRI; SHYNESS; PERCEPTION; AUTISM; PHOBIA; AREA; CHILDREN
AB Although shyness is associated with deficits in different aspects of face processing including face recognition and facial emotions, we know relatively little about the neural correlates of face processing among individuals who are shy. Here we show reduced activation to stranger faces among shy adults in a key brain area involved in face processing. Event-related functional magnetic resonance imaging scans were acquired on 12 shy and 12 social young adults during the rapid presentation of stranger and personally familiar neutral faces. Shy adults exhibited significantly less bilateral activation in the fusiform face area (FFA) in response to stranger faces and significantly greater bilateral activation in the same region to personally familiar faces than their social counterparts. Shy adults also exhibited significantly greater right amygdala activation in response to stranger faces than social adults. Among social adults, stranger faces elicited greater FFA activation than personally familiar faces. Findings suggest that there are distinct patterns of neural activation in the FFA in response to viewing stranger and personally familiar faces among shy and social adults.
C1 [Schmidt, Louis A.] McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada.
[Schulkin, Jay] NIH, Bethesda, MD 20892 USA.
[Schulkin, Jay] Georgetown Univ, Washington, DC USA.
[Antony, Martin M.] Ryerson Univ, Toronto, ON, Canada.
[Antony, Martin M.; Hall, Geoffrey B.] St Josephs Healthcare, Hamilton, ON, Canada.
RP Schmidt, LA (reprint author), McMaster Univ, Dept Psychol Neurosci & Behav, 1280 Main St W, Hamilton, ON L8S 4K1, Canada.
EM schmidtl@mcmaster.ca; hallg@mcmaster.ca
RI Antony, Martin/K-1991-2012;
OI Antony, Martin/0000-0002-3508-377X; Beaton, Elliott/0000-0001-7631-4637
FU Natural Sciences and Engineering Council of Canada (NSERC); Louis
Schmidt and a Father Sean O'Sullivan Research Centre (FSORC)
Post-doctoral Fellowship
FX The first author is now at the M. I. N. D. Institute at the University
of California, Davis. This research was funded by a grant from the
Natural Sciences and Engineering Council of Canada (NSERC) awarded to
Louis Schmidt and a Father Sean O'Sullivan Research Centre (FSORC)
Post-doctoral Fellowship awarded to Elliott Beaton. We wish to thank Sue
McKee for her assistance with data collection and Jami Sawyer and
Jessica Shelley for their help with data entry.
NR 39
TC 15
Z9 17
U1 4
U2 11
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 1747-0919
J9 SOC NEUROSCI
JI Soc. Neurosci.
PY 2009
VL 4
IS 4
BP 308
EP 316
AR PII 909874996
DI 10.1080/17470910902801021
PG 9
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 462QY
UT WOS:000267371900003
PM 19322727
ER
PT J
AU Zamboni, G
Gozzi, M
Krueger, F
Duhamel, JR
Sirigu, A
Grafman, J
AF Zamboni, Giovanna
Gozzi, Marta
Krueger, Frank
Duhamel, Jean-Rene
Sirigu, Angela
Grafman, Jordan
TI Individualism, conservatism, and radicalism as criteria for processing
political beliefs: A parametric fMRI study
SO SOCIAL NEUROSCIENCE
LA English
DT Article
DE Politics; Multidimensional scaling; Parametric fMRI; Social cognition;
Medial prefrontal cortex; Temporoparietal junction; Ventral striatum
ID DORSOLATERAL PREFRONTAL CORTEX; COGNITIVE NEUROSCIENCE; WORKING-MEMORY;
FRONTAL-CORTEX; NEURAL BASIS; AUTOBIOGRAPHICAL MEMORY; DECISION-MAKING;
SOCIAL-BEHAVIOR; HUMAN BRAIN; INSIGHTS
AB Politics is a manifestation of the uniquely human ability to debate, decide, and reach consensus on decisions affecting large groups over long durations of time. Recent neuroimaging studies on politics have focused on the association between brain regions and specific political behaviors by adopting party or ideological affiliation as a criterion to classify either experimental stimuli or subjects. However, it is unlikely that complex political beliefs (i.e., othe government should protect freedom of speecho) are evaluated only on a liberal-to-conservative criterion. Here we used multidimensional scaling and parametric functional magnetic resonance imaging to identify which criteria/dimensions people use to structure complex political beliefs and which brain regions are concurrently activated. We found that three independent dimensions explained the variability of a set of statements expressing political beliefs and that each dimension was reflected in a distinctive pattern of neural activation: individualism (medial prefrontal cortex and temporoparietal junction), conservatism (dorsolateral prefrontal cortex), and radicalism (ventral striatum and posterior cingulate). The structures we identified are also known to be important in self-other processing, social decision-making in ambivalent situations, and reward prediction. Our results extend current knowledge on the neural correlates of the structure of political beliefs, a fundamental aspect of the human ability to coalesce into social entities.
C1 [Grafman, Jordan] Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
[Zamboni, Giovanna; Gozzi, Marta] Univ Modena, I-41100 Modena, Italy.
[Duhamel, Jean-Rene; Sirigu, Angela] CNRS, Bron, France.
RP Grafman, J (reprint author), Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bldg 10,Room 7D43,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
RI Zamboni, Giovanna/F-3583-2017;
OI Zamboni, Giovanna/0000-0002-6133-3373; Grafman, Jordan
H./0000-0001-8645-4457
FU National Institute of Neurological Disorders and Stroke Intramural
Research Program; Italian Ministry of University and Research
FX We thank Davide Prandi for computer programming, Dimitrios Kapogiannis
for performing neurological exams, Aron Barbey and Maren Strenziok for
valuable suggestions, and Roland Zahn and Kris Knutson for astute
imaging analysis advice. This study was supported by the National
Institute of Neurological Disorders and Stroke Intramural Research
Program (to GZ, MG, FK, and JG) and the Italian Ministry of University
and Research (MIUR) (to GZ and MG). GZ is currently at the Nuffield
Department of Clinical Medicine, University of Oxford, UK.
NR 62
TC 24
Z9 25
U1 7
U2 38
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 1747-0919
J9 SOC NEUROSCI
JI Soc. Neurosci.
PY 2009
VL 4
IS 5
BP 367
EP 383
AR PII 912764185
DI 10.1080/17470910902860308
PG 17
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 492OP
UT WOS:000269668500001
PM 19562629
ER
PT J
AU Blair, RJR
Blair, KS
AF Blair, R. J. R.
Blair, Karina S.
BE Decety, J
Ickes, W
TI Empathy, Morality, and Social Convention: Evidence from the Study of
Psychopathy and Other Psychiatric Disorders
SO SOCIAL NEUROSCIENCE OF EMPATHY
LA English
DT Article; Book Chapter
ID PRESCHOOL CHILDRENS CONCEPTIONS; PEDIATRIC BIPOLAR DISORDER;
EVENT-RELATED FMRI; RESPONSE-REVERSAL; NEURAL BASIS; AUTISM; FACES;
EXPRESSIONS; MECHANISMS; ATTENTION
C1 [Blair, R. J. R.; Blair, Karina S.] NIMH, Bethesda, MD 20892 USA.
RP Blair, RJR (reprint author), NIMH, Bethesda, MD 20892 USA.
NR 66
TC 14
Z9 14
U1 1
U2 6
PU M I T PRESS
PI CAMBRIDGE
PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA
BN 978-0-262-01297-3
PY 2009
BP 139
EP 152
PG 14
WC Psychology, Clinical; Psychology, Psychoanalysis
SC Psychology
GA BPL39
UT WOS:000279132400012
ER
PT B
AU Shamir, L
AF Shamir, Lior
BE Giordano, AJ
Costa, GE
TI SOFT COMPUTING IN ASTRONOMY
SO SOFT COMPUTING: NEW RESEARCH
LA English
DT Article; Book Chapter
ID COSMIC-RAY REJECTION; DIGITAL SKY SURVEY; SURVEY TELESCOPE; SINGLE
IMAGES; IDENTIFICATION; ALGORITHM; PERSEUS; CAMERAS; SYSTEM; PATROL
AB In the past few years, the primary tools that serve observational astronomy have been changing significantly. Thus, manually controlled telescopes are gradually being replaced by autonomous robotic systems, which produce vast pipelines of astronomical data. These include multi-million dollar ventures that are considered the primary projects in modem observational astronomy, such as SDSS (Sloan Digital Sky Survey), PAN-STARRS, LSST (Large Synoptic Survey Telescope), and also semi-autonomous space telescopes such as JWST (James Webb Space Telescope). Many smaller-scale ground and space based robotic telescopes also operate, and substantially contribute to the efforts of searching supernovae, planetary eclipses, comets, and asteroids that might pose a future threat to Earth.
However, while very many astronomical data are constantly being generated, human identifications are many times impracticably slow. Therefore, one can reasonably assume that many discoveries of significant scientific value are hidden inside the databases generated by robotic telescopes, but cannot be found due to the complex task of mining these data for discoveries. In order to optimize the scientific return of robotic sky surveys, the data should be analyzed in an automated fashion that can detect single events of scientific interest in data sets of millions of recorded astronomical objects.
Automated search for scientific discoveries in astronomical images is a formidable task that requires complex decision making. This complexity is caused by the vague definition of events that can be considered "interesting", as there is no "typical" astronomical discovery. Other contributors to this complexity are inaccuracies of the optics and instruments, ever-changing sky opacity and weather conditions, and the presence of artificial satellites and space junks that reflects sunlight in a fashion that is often unpredicted, yet offer no scientific interest.
Since astronomical pipeline can generate very many images per day, where each image consists of thousands of astronomical objects, even a small percentage of false positives can make a proposed solution impractical.
The complex environment introduced by the increasing importance of autonomous sky surveys initiated a continuous effort of development and implementation of soft computing-based solutions to astronomical pipeline processing. In this chapter we describe the: challenging problems of automating the analysis of astronomical images, present existing soft computing-based solutions, and discuss future directions of soft computing in observational astronomy.
C1 [Shamir, Lior] Michigan Technol Univ, Dept Phys, Houghton, MI 49931 USA.
[Shamir, Lior] NIA, NIH, Bethesda, MD 20892 USA.
RP Shamir, L (reprint author), Michigan Technol Univ, Dept Phys, Houghton, MI 49931 USA.
NR 77
TC 0
Z9 0
U1 1
U2 1
PU NOVA SCIENCE PUBLISHERS, INC
PI HAUPPAUGE
PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA
BN 978-1-60456-883-7
PY 2009
BP 229
EP 262
PG 34
WC Computer Science, Artificial Intelligence; Computer Science, Theory &
Methods
SC Computer Science
GA BMR68
UT WOS:000273414600010
ER
PT B
AU Soekadar, SR
Caria, A
Murguialday, AR
Birbaumer, N
AF Soekadar, Surjo R.
Caria, Andrea
Murguialday, Ander Ramos
Birbaumer, Niels
BE Johnsen, N
Agerskov, R
TI Rehabilitation After Stroke Using Brain-Computer-Interfaces and
Neurostimulation
SO SOMATOSENSORY CORTEX: ROLES, INTERVENTIONS AND TRAUMAS
SE Neurology Laboratory and Clinical Research Series
LA English
DT Article; Book Chapter
DE neurotechnology; brain-computer-interface; neurostimulation;
neuro-rehabilitation; stroke
ID TRANSCRANIAL MAGNETIC STIMULATION; SLOW CORTICAL POTENTIALS; PRIMARY
MOTOR CORTEX; ELECTRICAL-STIMULATION; CONTROLLED-TRIAL; CEREBRAL-CORTEX;
SELF-REGULATION; MOVEMENT; COMMUNICATION; SIGNALS
AB This chapter deals with the current state and perspective of neurotechnology, particular the use of brain computer interfaces (BCI) and neurostimulation in the rehabilitation of stroke. While 20 years ago brain-computer-interfaces that utilize neurophysiologic or metabolic signals originating in the brain to activate or deactivate external devices or computers have been used by a handful of research groups only, there are now - after the decade of the brain - several hundred groups world-wide working in this field. Additionally, the modulation of brain activity by non-invasive cortical stimulation undergoes a renaissance. New and innovative techniques to modulate or even enhance brain functions have emerged. After a short introduction of the BCI-systems that have been developed and successfully used in patients with intractable epilepsy, attention deficit disorder, ALS and chronic pain since 1979 by the University of Tuebingen group, recent developments in the use of BCI technology and neurostimulation for stroke survivors will be sketched and exemplified by our latest results. Limits and current challenges in the use of BCI technology and brain stimulation will be highlighted and discussed. The chapter closes with an outlook on future developments and prospects introducing promising developments such as the combination of BCI systems with non-invasive forms of neurostimulation and e.g. functional electric stimulation (FES).
C1 [Soekadar, Surjo R.] Univ Tubingen, Dept Psychiat & Psychotherapy, Neurostimulat Unit, D-72074 Tubingen, Germany.
[Soekadar, Surjo R.] NINDS, NIH, Human Cort Physiol & Stroke Neurorehabil Sect, Bethesda, MD 20892 USA.
[Caria, Andrea; Murguialday, Ander Ramos; Birbaumer, Niels] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, D-72074 Tubingen, Germany.
RP Soekadar, SR (reprint author), Univ Tubingen, Dept Psychiat & Psychotherapy, Neurostimulat Unit, D-72074 Tubingen, Germany.
NR 101
TC 0
Z9 0
U1 0
U2 2
PU NOVA SCIENCE PUBLISHERS, INC
PI HAUPPAUGE
PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA
BN 978-1-60741-876-4
J9 NEUROL LAB CLIN RES
PY 2009
BP 101
EP 119
PG 19
WC Clinical Neurology
SC Neurosciences & Neurology
GA BPD20
UT WOS:000278553000005
ER
PT J
AU Li, SY
Lu, Q
Fu, WJ
Romero, R
Cui, YH
AF Li, Shaoyu
Lu, Qing
Fu, Wenjiang
Romero, Roberto
Cui, Yuehua
TI A Regularized Regression Approach for Dissecting Genetic Conflicts that
Increase Disease Risk in Pregnancy
SO STATISTICAL APPLICATIONS IN GENETICS AND MOLECULAR BIOLOGY
LA English
DT Article
DE complex disease; genetic conflicts; genomic imprinting; maternal-fetal
genotype incompatibility; penalized mixture logistic regression
ID FOR-GESTATIONAL-AGE; INTRAUTERINE GROWTH RESTRICTION; PENALIZED
LOGISTIC-REGRESSION; FETAL-GROWTH; IMPRINTED GENES; MFG TEST;
ASSOCIATION; DEFINITION; EXPRESSION; MORBIDITY
AB Human diseases developed during pregnancy could be caused by the direct effects of both maternal and fetal genes, and/or by the indirect effects caused by genetic conflicts. Genetic conflicts exist when the effects of fetal genes are opposed by the effects of maternal genes, or when there is a conflict between the maternal and paternal genes within the fetal genome. The two types of genetic conflicts involve the functions of different genes in different genomes and are genetically distinct. Differentiating and further dissecting the two sets of genetic conflict effects that increase disease risk during pregnancy present statistical challenges, and have been traditionally pursued as two separate endeavors. In this article, we develop a unified framework to model and test the two sets of genetic conflicts via a regularized regression approach. Our model is developed considering real situations in which the paternal information is often completely missing; an assumption that fails most of the current family-based studies. A mixture model-based penalized logistic regression is proposed for data sampled from a natural population. We develop a variable selection procedure to select significant genetic features. Simulation studies show that the model has high power and good false positive control under reasonable sample sizes and disease allele frequency. A case study of small for gestational age (SGA) is provided to show the utility of the proposed approach. Our model provides a powerful tool for dissecting genetic conflicts that increase disease risk during pregnancy, and offers a testable framework for the genetic conflict hypothesis previously proposed.
C1 [Li, Shaoyu; Lu, Qing; Fu, Wenjiang; Cui, Yuehua] Michigan State Univ, E Lansing, MI 48824 USA.
[Romero, Roberto] NIH, NICHD, Bethesda, MD USA.
RP Li, SY (reprint author), Michigan State Univ, E Lansing, MI 48824 USA.
EM lishaoyu@stt.msu.edu; qlu@epi.msu.edu; fuw@epi.msu.edu;
prbchiefstaff@med.wayne.edu; cui@stt.msu.edu
FU NSF [DMS-0707031]; Eunice Kennedy Shriver National Institute of Child
Health and Human Developmen; NIH; DHHS
FX The authors thank the editor and two anonymous referees for their
constructive comments and useful suggestions that greatly improved the
manuscript. This work was supported in part by NSF grant DMS-0707031 and
by the Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, NIH, DHHS.
Address for correspondence: Dr. Yuehua Cui, Department of Statistics &
Probability, Michigan State University, East Lansing, MI 48824.
NR 49
TC 14
Z9 14
U1 0
U2 2
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 2194-6302
EI 1544-6115
J9 STAT APPL GENET MOL
JI Stat. Appl. Genet. Mol. Biol.
PY 2009
VL 8
IS 1
AR 45
DI 10.2202/1544-6115.1474
PG 30
WC Biochemistry & Molecular Biology; Mathematical & Computational Biology;
Statistics & Probability
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology;
Mathematics
GA 513IP
UT WOS:000271316200002
ER
PT J
AU Yuan, M
Tian, X
Zheng, G
Yang, YN
AF Yuan, Min
Tian, Xin
Zheng, Gang
Yang, Yaning
TI Adaptive Transmission Disequilibrium Test for Family Trio Design
SO STATISTICAL APPLICATIONS IN GENETICS AND MOLECULAR BIOLOGY
LA English
DT Article
DE adaptive TDT; conditional power; efficiency robustness; genetic model
selection; Hardy-Weinberg disequilibrium; MAX-type tests; TDT-type
tests; FBAT; constrained likelihood ratio test
ID CANDIDATE-GENE ASSOCIATION; HARDY-WEINBERG DISEQUILIBRIUM; GENOTYPE
RELATIVE-RISKS; ROBUST LINKAGE TESTS; UNIFIED APPROACH; AFFECTED SIBS;
PARENTS; POWER; LOCI; IDDM
AB The transmission disequilibrium test (TDT) is a standard method to detect association using family trio design. It is optimal for an additive genetic model. Other TDT-type tests optimal for recessive and dominant models have also been developed. Association tests using family data, including the TDT-type statistics, have been unified to a class of more comprehensive and flexable family-based association tests (FBAT). TDT-type tests have high efficiency when the genetic model is known or correctly specified, but may lose power if the model is mis-specified. Hence tests that are robust to genetic model mis-specification yet efficient are preferred. Constrained likelihood ratio test (CLRT) and MAX-type test have been shown to be efficiency robust. In this paper we propose a new efficiency robust procedure, referred to as adaptive TDT (aTDT). It uses the Hardy-Weinberg disequilibrium coefficient to identify the potential genetic model underlying the data and then applies the TDT-type test (or FBAT for general applications) corresponding to the selected model. Simulation demonstrates that aTDT is efficiency robust to model mis-specifications and generally outperforms the MAX test and CLRT in terms of power. We also show that aTDT has power close to, but much more robust, than the optimal TDT-type test based on a single genetic model. Applications to real and simulated data from Genetic Analysis Workshop (GAW) illustrate the use of our adaptive TDT.
C1 [Yuan, Min; Yang, Yaning] Univ Sci & Technol China, Hefei, Peoples R China.
[Tian, Xin; Zheng, Gang] NHLBI, Bethesda, MD 20892 USA.
RP Yuan, M (reprint author), Univ Sci & Technol China, Hefei, Peoples R China.
EM myuan@mail.ustc.edu.cn; tianx@nhlbi.nih.gov; zhengg@nhlbi.nih.gov;
ynyang@gmail.com
FU China NSF
FX Yang was partially supported by China NSF grant.
NR 40
TC 4
Z9 4
U1 0
U2 1
PU BERKELEY ELECTRONIC PRESS
PI BERKELEY
PA 2809 TELEGRAPH AVENUE, STE 202, BERKELEY, CA 94705 USA
SN 1544-6115
J9 STAT APPL GENET MOL
JI Stat. Appl. Genet. Mol. Biol.
PY 2009
VL 8
IS 1
AR 30
DI 10.2202/1544-6115.1451
PG 22
WC Biochemistry & Molecular Biology; Mathematical & Computational Biology;
Statistics & Probability
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology;
Mathematics
GA 465QI
UT WOS:000267601500004
ER
PT J
AU Vexler, A
Wu, CQ
Liu, AY
Whitcomb, BW
Schisterman, EF
AF Vexler, Albert
Wu, Chengqing
Liu, Aiyi
Whitcomb, Brian W.
Schisterman, Enrique F.
TI An extension of a change-point problem
SO STATISTICS
LA English
DT Article
DE Doob decomposition; change-point; classification; CUSUM statistics;
likelihood ratio; limit of detection; martingale; martingale transforms;
Shiryayev-Roberts statistics
ID SEQUENTIAL-ANALYSIS; LINEAR-REGRESSION; DETECTION LIMITS; FALSE ALARM;
RUN-LENGTH; SURVEILLANCE; EXPOSURE; ALTERNATIVES; TESTS; MODEL
AB We consider a specific classification problem in the context of change-point detection. We present generalized classical maximum likelihood tests for homogeneity of the observed sample in a simple form which avoids the complex direct estimation of unknown parameters. This paper proposes a martingale approach to transformation of test statistics. For sequential and retrospective testing problems, we propose the adapted Shiryayev-Roberts statistics in order to obtain simple tests with asymptotic power one. An important application of the developed methods is in the analysis of exposure's measurements subject to limits of detection in occupational medicine.
C1 [Vexler, Albert] SUNY Buffalo, Dept Biostat, Buffalo, NY 14260 USA.
[Wu, Chengqing; Liu, Aiyi; Whitcomb, Brian W.; Schisterman, Enrique F.] NICHD, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD USA.
RP Vexler, A (reprint author), SUNY Buffalo, Dept Biostat, Buffalo, NY 14260 USA.
EM avexler@buffalo.edu
OI Liu, Aiyi/0000-0002-6618-5082; Schisterman, Enrique/0000-0003-3757-641X
NR 33
TC 2
Z9 2
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 0233-1888
J9 STATISTICS
JI Statistics
PY 2009
VL 43
IS 3
BP 213
EP 225
AR PII 907042540
DI 10.1080/02331880802395930
PG 13
WC Statistics & Probability
SC Mathematics
GA 448ED
UT WOS:000266245000001
ER
PT J
AU Zheng, G
Balakrishnan, N
Park, S
AF Zheng, Gang
Balakrishnan, N.
Park, Sangun
TI Fisher information in ordered data: A review
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Asymptotics; censored data; characterizations; hazard functions; life
testing; order statistics; ranked set sampling
ID II CENSORED-DATA; QUANTITATIVE-TRAIT LOCI; RANKED SET SAMPLES;
EXPONENTIATED EXPONENTIAL FAMILY; EXACT LIKELIHOOD INFERENCE; TUKEYS
LINEAR SENSITIVITY; DISCORDANT SIB PAIRS; RECORD VALUES;
WEIBULL-DISTRIBUTION; CORRELATION-COEFFICIENT
AB Fisher information is a fundamental concept of statistical inference and plays an important role in many areas of statistical analysis. Research in Fisher information in order statistics started around 1965 by John Tukey. Recently, the research in this area has been extended from classical order statistics and Type-I and Type-II censored data to other situations, including hybrid censoring, random censoring, progressive censoring, record values, and concomitants, with new applications in genetic linkage analysis. In this article, we provide a comprehensive review of various developments concerning the theory and applications of Fisher information in ordered data, show how Fisher information provides insight into properties of many statistical procedures involving order statistics.
C1 [Zheng, Gang] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Balakrishnan, N.] McMaster Univ, Dept Math & Stat, Hamilton, ON L8S 4K1, Canada.
[Park, Sangun] Yonsei Univ, Dept Appl Stat, Seoul 120749, South Korea.
RP Zheng, G (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM zhengg@nhlbi.nih.gov; bala@univmail.cis.mcmaster.ca; sangun@yonsei.ac.kr
FU Yonsei University
FX Partially supported by Yonsei University Research Fund of 2007.
NR 106
TC 6
Z9 6
U1 2
U2 5
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 1
BP 101
EP 113
PG 13
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660MY
UT WOS:000282648900010
ER
PT J
AU Gail, MH
AF Gail, Mitchell H.
TI Applying the Lorenz curve to disease risk to optimize health benefits
under cost constraints
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Absolute risk; cost constraints; constrained optimization; cumulative
incidence; disease prevention; Lorenz curve; risk prediction model
ID OF-FIT TEST; BREAST-CANCER; GINI-INDEX; MODELS
AB This paper shows how the Lorenz curve can be used, together with models of disease risk, to allocate scarce resources so as to optimize a health benefit. Consider the example of breast cancer mortality. If there were sufficient resources to provide all women with mammograms, a certain maximal number of lives could be saved. Suppose, however, that only a fraction of that amount of money is available for prevention activities. Suppose that a questionnaire could be given to assess a woman's risk of dying of breast cancer. Depending on the amount of money available, on the ratio of the cost of a questionnaire to the cost of a mammogram, and on the Lorenz curve of the distribution of risks of breast cancer mortality, I calculate the proportion of women who should be given questionnaires, the proportion of women given the questionnaires who should be given mammograms because they have high risks, and the proportion of women not given questionnaires who should be assigned to receive mammograms at random so as to maximize the number of lives saved.
C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Gail, MH (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM gailm@exchange.nih.gov
FU National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Cancer Institute.
NR 9
TC 8
Z9 8
U1 0
U2 3
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 2
BP 117
EP 121
PG 5
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660NG
UT WOS:000282649700002
PM 19779595
ER
PT J
AU Chatterjee, N
Graubard, BI
Gastwirth, JL
AF Chatterjee, Nilanjan
Graubard, Barry I.
Gastwirth, Joseph L.
TI The use of the risk percentile curve in the analysis of epidemiologic
data
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Relative risk; Absolute risk; Population attributable risk; Logistic
regression; Cox proportional hazard regression; Case-control study;
Cohort study; Attributable risk reduction curve; Expectancy curve;
Survey data
ID ADJUSTMENT; CANCER
AB Economists and social scientists have used percentile-based curves, e.g., the Lorenz curve, to summarize data from positive random variables, especially skewed data such as income. Measures of interest, e.g., the Gini index of relative inequality, correspond to areas defined by the curves. In this paper we explore the usefulness of risk-percentile and related curves in epidemiology, especially when the exposure data is skewed. These curves are defined and risk measures, e.g. the population attributable risk are related to areas under them for data from either a cohort or a case-control study. Regression spline methods of estimating these curves are used as they do not require a pre-specified risk model. The concepts are illustrated by analyzing data from a cohort study of dietary red meat consumption and all-cause mortality and a case-control study of serum homocysteine level and colorectal cancer. These examples show that the risk percentile curves often are more useful than presenting the risk as a function of the raw exposure data as the later graph is often dominated by the tails when the data is skewed. Furthermore, the risk percentile curve is more informative than the commonly used method of presenting the average risk in categories defined by several fixed percentiles such as quartiles or quintiles. Indeed, the risk averages for these categories can be obtained from the risk-percentile curve.
C1 [Chatterjee, Nilanjan; Graubard, Barry I.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Gastwirth, Joseph L.] George Washington Univ, Dept Stat, Washington, DC 20052 USA.
RP Chatterjee, N (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM graubarb@mail.nih.gov
NR 20
TC 0
Z9 0
U1 0
U2 2
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 2
BP 123
EP 131
PG 9
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660NG
UT WOS:000282649700003
ER
PT J
AU Buckman, DW
Li, ZH
AF Buckman, Dennis W.
Li, Zhaohai
TI Missing data methods for linkage analysis of IBS and incomplete IBD from
affected sib-pairs
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Incomplete data; Missing at random; Identity-by-descent;
Identity-by-state; Complex traits; Required sample size; Power; Type I
error
ID QUANTITATIVE-TRAIT LOCI; GENETICALLY COMPLEX TRAITS; AFFECTED RELATIVE
PAIRS; EXTREME DISCORDANT; STRATEGIES; IDENTITY; HUMANS; INFERENCE;
MODELS; POWER
AB We derive linkage statistics for situations where the number of marker alleles shared identical-by-descent (IBD) is incomplete, and the number of marker alleles shared identical-by-state (IBS) is known. The linkage statistics are based on the assumption that the parental genotypes are missing at random (MAR). We first assume the marker IBD is unambiguous for a sib-pair if the parental genotypes are available. Then we relax this assumption to assess the impact of marker ambiguity. The derivation of each statistic involves a Taylor series expansion of a log likelihood that is a function of the recombination fraction and nuisance parameters and incorporates the missing data situation. The first derivative of the log likelihood is zero under the null hypothesis of no recombination, so the Taylor series expansion of the log likelihood reveals a linkage statistic that is proportional to the second derivative of the log likelihood evaluated at the null hypothesis value of the recombination fraction. We prove that the standardized linkage statistics have asymptotic normal distributions, and we provide required sample sizes and simulation results and consider the impact of parent availability and marker ambiguity.
C1 [Buckman, Dennis W.] Informat Management Serv Inc, Silver Spring, MD 20904 USA.
[Buckman, Dennis W.; Li, Zhaohai] George Washington Univ, Dept Stat, Washington, DC 20052 USA.
[Li, Zhaohai] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Buckman, DW (reprint author), Informat Management Serv Inc, 2501 Prosper Dr,Suite 200, Silver Spring, MD 20904 USA.
EM buckmand@imsweb.com; zli@gwu.edu
FU NIH [EY014478]
FX The work of the second author was supported in part by NIH grant
EY014478.
NR 32
TC 0
Z9 0
U1 0
U2 1
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 2
BP 133
EP 144
PG 12
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660NG
UT WOS:000282649700004
ER
PT J
AU Zheng, G
Joo, J
Tian, X
Wu, CO
Lin, JP
Stylianou, M
Waclawiw, MA
Geller, NL
AF Zheng, Gang
Joo, Jungnam
Tian, Xin
Wu, Colin O.
Lin, Jing-Ping
Stylianou, Mario
Waclawiw, Myron A.
Geller, Nancy L.
TI Robust genome-wide scans with genetic model selection using case-control
design
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Case-control design; Efficiency robustness; Genetic model selection;
Genome-wide studies; MAX
ID CASE-CONTROL ASSOCIATION; TREND TESTS; SAMPLE-SIZE; DISEQUILIBRIUM;
EFFICIENT; SURVIVAL; DISEASES; POWER; LOCI
AB In a genome-wide association study with more than 100, 000 (100K) to 1 million single nucleotide polymorphisms (SNPs), the first step is usually a genome-wide scan to identify candidate chromosome regions for further analyses. The goal of the genome-wide scan is to rank all the SNPs based on their association tests or p-values and select the top SNPs. A good ranking procedure ranks the SNPs with true associations as near to the top as possible. This enhances the probability of selecting at least one SNP with a true association. However, if the disease-associated SNPs have moderate genetic effects, the probability that a large number of null SNPs will have extremely small p-values (or large test statistics) is high when screening more than 300K SNPs. Therefore, when selecting a small fraction of top SNPs (usually less than 5%), the probability of selecting at least one SNP with a true association is usually less than 80% unless the sample size is large. Robust statistics have been proposed to rank all the SNPs (e.g., MAX3 and MIN2). In this article we consider genome-wide scans with a genetic model selection and compare this proposed method to the existing approaches. Results from simulation studies are presented.
C1 [Zheng, Gang; Joo, Jungnam; Tian, Xin; Wu, Colin O.; Lin, Jing-Ping; Stylianou, Mario; Waclawiw, Myron A.; Geller, Nancy L.] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
RP Zheng, G (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM zhengg@nhlbi.nih.gov; jooj@nhlbi.nih.gov; tianx@nhlbi.nih.gov;
wuc@nhlbi.nih.gov; linj@nhlbi.nih.gov; stylianm@nhlbi.nih.gov;
waclawim@nhlbi.nih.gov; gellern@nhlbi.nih.gov
NR 30
TC 5
Z9 5
U1 0
U2 3
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 2
BP 145
EP 151
PG 7
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660NG
UT WOS:000282649700005
ER
PT J
AU Li, QZ
Liu, AY
Yu, K
Yu, KF
AF Li, Qizhai
Liu, Aiyi
Yu, Kai
Yu, Kai F.
TI A weighted rank-sum procedure for comparing samples with multiple
endpoints
SO STATISTICS AND ITS INTERFACE
LA English
DT Article
DE Asymptotic normality; Behrens-Fisher problem; Case-Control; Clinical
trials; Multiple endpoints; Rank-sum statistics; Weights
ID BEHRENS-FISHER PROBLEM; TRIALS; TESTS
AB For comparing the distribution of two samples with multiple endpoints, O'Brien (1984) proposed rank-sum-type test statistics. Huang et al. (2005) extended these statistics to the general nonparametric Behrens-Fisher hypothesis problem and obtained improved test statistics by replacing the ad hoc variance with the asymptotic variance of the rank-sum statistics. In this paper we generalize the work of O'Brien (1984) and Huang et al. (2005) and propose a weighted rank-sum statistic. We show that the weighted rank-sum statistic is asymptotically normally distributed, permitting the computation of power, p-values and confidence intervals. We further demonstrate via simulation that the weighted rank-sum statistic is efficient in controlling the type I error rate and under certain alternatives, is more powerful than the statistics of O'Brien (1984) and Huang et al. (2005).
C1 [Li, Qizhai; Yu, Kai] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Li, Qizhai] Chinese Acad Sci, Acad Math & Syst Sci, Beijing 100864, Peoples R China.
EM liqz@amss.ac.cn; liua@mail.nih.gov; yuka@mail.nih.gov; yukf@mail.nih.gov
FU National Institutes of Health; Chinese Academy of Sciences
FX This research has been supported by the Intramural Research Program of
the National Institutes of Health and the Knowledge Innovation Program
of the Chinese Academy of Sciences.
NR 9
TC 1
Z9 1
U1 0
U2 4
PU INT PRESS BOSTON, INC
PI SOMERVILLE
PA PO BOX 43502, SOMERVILLE, MA 02143 USA
SN 1938-7989
J9 STAT INTERFACE
JI Stat. Interface
PY 2009
VL 2
IS 2
BP 197
EP 201
PG 5
WC Mathematical & Computational Biology; Mathematics, Interdisciplinary
Applications
SC Mathematical & Computational Biology; Mathematics
GA 660NG
UT WOS:000282649700010
PM 19823699
ER
PT J
AU Kovacic, JC
Boehm, M
AF Kovacic, Jason C.
Boehm, Manfred
TI Resident vascular progenitor cells: An emerging role for non-terminally
differentiated vessel-resident cells in vascular biology
SO STEM CELL RESEARCH
LA English
DT Review
ID HEMATOPOIETIC STEM-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; MUSCLE-LIKE
CELLS; EMBRYONIC ENDOTHELIAL-CELLS; APOE-DEFICIENT MICE; IN-VITRO;
SMOOTH-MUSCLE; YOLK-SAC; MOUSE EMBRYO; DORSAL AORTA
AB Throughout development and adult life the vasculature exhibits a remarkably dynamic capacity for growth and repair. The vasculature also plays a pivotal role in the execution of other diverse biologic processes, such as the provisioning of early hematopoietic stem cells during embryonic development or the regulation of vascular tone and blood pressure. Adding to this importance, from an anatomical perspective, the vasculature is clearly an omnipresent organ, with few areas of the body that it does not penetrate. Given these impressive characteristics, it is perhaps to be expected that the vasculature should require, or at least be associated with, a ready supply of stem and progenitor cells. However, somewhat surprisingly, it is only now just beginning to be broadly appreciated that the vasculature plays host to a range of vessel-resident stem and progenitor cells. The possibility that these vessel-resident cells are implicated in processes as diverse as tumor vascularization and adaptive vascular remodeling appears likely, and several exciting avenues for clinical translation are already under investigation. This review explores the various stem and progenitor cell populations that are resident in the microvasculature, endothelium, and vessel watts and vessel-resident cells capable of phenotypic transformation. Published by Elsevier B.V.
C1 [Kovacic, Jason C.; Boehm, Manfred] NHLBI, Translat Med Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
RP Boehm, M (reprint author), NHLBI, Translat Med Branch, Div Intramural Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM boehmm2@mail.nih.gov
FU NHLBI; NIH
FX We acknowledge the professional skills and advice of Dr. Christian A.
Combs and Dr. Daniela Matide (Light Microscopy Core Facility, National
Heart, Lung, and Blood Institute, National Institutes of Health) for
their assistance with Fig. 1. J.K. and M.B. are funded by the intramural
research program of the NHLBI, NIH.
NR 118
TC 39
Z9 39
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1873-5061
J9 STEM CELL RES
JI Stem Cell Res.
PD JAN
PY 2009
VL 2
IS 1
BP 2
EP 15
DI 10.1016/j.scr.2008.05.005
PG 14
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 495QL
UT WOS:000269909000002
PM 19383404
ER
PT J
AU Kuznetsov, SA
Mankani, MH
Bianco, P
Robey, PG
AF Kuznetsov, Sergei A.
Mankani, Mahesh H.
Bianco, Paolo
Robey, Pamela G.
TI Enumeration of the colony-forming units-fibroblast from mouse and human
bone marrow in normal and pathological conditions
SO STEM CELL RESEARCH
LA English
DT Review
ID MESENCHYMAL STEM-CELLS; FETAL CALF SERUM; FORMATION IN-VITRO; STROMAL
CELLS; CFU-F; PROGENITOR CELLS; PRECURSOR-CELLS; MYELOPROLIFERATIVE
DISORDERS; PROLIFERATIVE CAPACITY; OSTEOPROGENITOR CELLS
AB Bone marrow stromal cell populations, containing a subset of multipotential skeletal stem cells, are increasingly contemplated for use in tissue engineering and stem cell therapy, whereas their involvement in the pathogenetic mechanisms of skeletal disorders is far less recognized. We compared the concentrations of stromal clonogenic cells, colony forming units-fibroblast (CFU-Fs), in norm and pathology. Initially, culture conditions were optimized by demonstrating that fetal bovine serum heat inactivation could significantly repress colony formation. Using non-heat-inactivated fetal bovine serum, the concentration of CFU-Fs; (colony-forming efficiency, CFE) ranged from 3.5 +/- 1.0 to 11.5 +/- 4.0 per 1 X 10(5) nucleated cells in five inbred mouse strains. In four transgenic lines with profound bone involvement, CFE was either significantly reduced or increased compared to wild-type littermates. In normal human donors, CFE decreased slightly with age and averaged 52.2 +/- 4.1 for children and 32.3 +/- 3.0 for adults. CFE was significantly altered in patients with several skeletal, metabolic, and hematological disorders: reduced in congenital generalized lipodystrophy, achondroplasia (SADDAN), pseudoachondroplasia, and Paget disease of bone and elevated in alcaptonuria and sickle cell anemia. Our findings indicate that under appropriate culture conditions, CFE values may provide useful insights into bone/bone marrow pathophysiology. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Kuznetsov, Sergei A.; Mankani, Mahesh H.; Robey, Pamela G.] Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Bianco, Paolo] Univ Roma La Sapienza, Dipartimento Med Sperimentale & Patol, I-00161 Rome, Italy.
RP Kuznetsov, SA (reprint author), Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, NIH, US Dept HHS, 30 Convent Dr MSC 4370, Bethesda, MD 20892 USA.
EM skuznets@mail.nih.gov
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
FU National Institute of Dental and Craniofacial Research; IRP; NIH; DHHS
FX The authors are grateful to Drs. Michael Collins (NIDCR, NIH); Jose Luis
Franco and Steven M. Holland (NIAID, NIH); Glen Nuckolls (NIAMS, NIH);
Clair A. Francomano (NIA, NIH); Elif Arioglu Oral and Philip Gorden
(NIDDK, NIH); William Gahl (NHGRI, NIH); Arabella Leet, Paul Sponsetter,
Neat Fedarko, and lain McIntosh (Johns Hopkins University, Baltimore,
MD); John W.T. Walker and Stephen L.-K. Yen (Children's Hospital, Los
Angeles, CA); Fred Singer (John Wayne Cancer Institute, Santa Monica,
CA); Alan Aaron and Brian Evans (Georgetown University, Washington, DC);
Paul A. Manner (George Washington University, Washington, DC); and
Michael Keating (Children's National Medicine Center, Washington, DC)
for providing human bone and bone marrow. We are indebted to Drs. Kenn
Holmbeck (NIDCR, NIH); Tomoko Iwata and Clair A. Francomano (NIA, NIH);
Cui-Ling Li and Chu-Xia Deng (NIDDK, NIH); Lorraine A. Fitzpatrick
(GtaxoSmithKline, Collegeville, PA); and Laura Calvi, Henry M.
Kronenberg, and Ernestina Schipani (Massachusetts General Hospital and
Harvard Medical School, Boston, MA) for providing transgenic mice with
skeletal phenotypes. This research was supported by the Division of
Intramural Research of the National Institute of Dental and Craniofacial
Research, IRP, NIH, DHHS.
NR 107
TC 36
Z9 38
U1 2
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1873-5061
J9 STEM CELL RES
JI Stem Cell Res.
PD JAN
PY 2009
VL 2
IS 1
BP 83
EP 94
DI 10.1016/j.scr.2008.07.007
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 495QL
UT WOS:000269909000010
PM 19383412
ER
PT J
AU Pistollato, F
Chen, HL
Rood, BR
Zhang, HZ
D'Avella, D
Denaro, L
Gardiman, M
Kronnie, GT
Schwartz, PH
Favaro, E
Indraccolo, S
Basso, G
Panchision, DM
AF Pistollato, Francesca
Chen, Hui-Ling
Rood, Brian R.
Zhang, Hui-Zhen
D'Avella, Domenico
Denaro, Luca
Gardiman, Marina
Kronnie, Geertruy Te
Schwartz, Philip H.
Favaro, Elena
Indraccolo, Stefano
Basso, Giuseppe
Panchision, David M.
TI Hypoxia and HIF1 alpha Repress the Differentiative Effects of BMPs in
High-Grade Glioma
SO STEM CELLS
LA English
DT Article
DE Brain tumor; High-grade glioma; Oxygen; Bone morphogenetic proteins;
Smad; Hypoxia inducible factor 1 alpha
ID BONE MORPHOGENETIC PROTEINS; TUMOR-INITIATING CELLS; GROWTH-FACTOR
RECEPTOR; NEURAL STEM-CELLS; INDUCIBLE FACTOR-1-ALPHA; OXYGEN-TENSION;
PROGENITOR CELLS; GENE-EXPRESSION; RADIAL GLIA; MOUSE-BRAIN
AB Hypoxia commonly occurs in solid tumors of the central nervous system (CNS) and often interferes with therapies designed to stop their growth. We found that pediatric high-grade glioma (HGG)-derived precursors showed greater expansion under lower oxygen tension, typical of solid tumors, than normal CNS precursors. Hypoxia inhibited p53 activation and subsequent astroglial differentiation of HGG precursors. Surprisingly, although HGG precursors generated endogenous bone morphogenetic protein (BMP) signaling that promoted mitotic arrest under high oxygen tension, this signaling was actively repressed by hypoxia. An acute increase in oxygen tension led to Smad activation within 30 minutes, even in the absence of exogenous BMP treatment. Treatment with BMPs further promoted astroglial differentiation or death of HGG precursors under high oxygen tension, but this effect was inhibited under hypoxic conditions. Silencing of hypoxia-inducible factor 1 alpha (HIF1 alpha) led to Smad activation even under hypoxic conditions, indicating that HIF1 alpha is required for BMP repression. Conversely, BMP activation at high oxygen tension led to reciprocal degradation of HIF1 alpha; this BMP-induced degradation was inhibited in low oxygen. These results show a novel, mutually antagonistic interaction of hypoxia-response and neural differentiation signals in HGG proliferation, and suggest differences between normal and HGG precursors that may be exploited for pediatric brain cancer therapy. STEM CELLS 2009; 27: 7-17
C1 [Pistollato, Francesca; Kronnie, Geertruy Te; Basso, Giuseppe] Univ Padua, Dept Pediat, Hematooncol Lab, Padua, Italy.
[D'Avella, Domenico; Denaro, Luca] Univ Padua, Dept Neurosurg, Padua, Italy.
[Gardiman, Marina] Univ Padua, Dept Pathol, I-35100 Padua, Italy.
[Favaro, Elena] Univ Padua, Dept Oncol & Surg Sci, I-35100 Padua, Italy.
[Pistollato, Francesca; Chen, Hui-Ling; Rood, Brian R.; Zhang, Hui-Zhen; Panchision, David M.] Childrens Natl Med Ctr, Childrens Res Inst, Neurosci Res Ctr, Washington, DC 20010 USA.
[Schwartz, Philip H.] Childrens Hosp Orange Cty, Res Inst, Orange, CA 92668 USA.
[Schwartz, Philip H.] Univ Calif Irvine, Irvine, CA USA.
[Indraccolo, Stefano] IRCCS, Ist Oncol Veneto, Padua, Italy.
RP Panchision, DM (reprint author), NIMH, Dev Neurobiol Program, NIH, 6001 Execut Blvd,MSC 9641, Bethesda, MD 20892 USA.
EM panchisiond@mail.nih.gov
RI Indraccolo, Stefano/E-9541-2012; Waha, Andreas/J-2950-2014; Favaro,
Elena/Q-4566-2016;
OI Indraccolo, Stefano/0000-0002-4810-7136; Favaro,
Elena/0000-0001-5376-5515; BASSO, GIUSEPPE/0000-0002-2634-9302
FU Frank and Nancy Parsons Fund; Zickler Fund; Georgia Derrico and Rod
Porter Fund; Italian Association AIRC regional grant; FIRB grant;
Italian Association for the Fight against Neuroblastoma (Pensiero
Project); Italian Ministry of Health Oncology Program 2006; CNMC
Research Advisory Council; CHOC Foundation; CNMC Board of Visitors
FX This study was supported by funds from the Frank and Nancy Parsons Fund,
the Zickler Fund, the Georgia Derrico and Rod Porter Fund for the
CNMC/University of Padova Sister Program, the Italian Association AIRC
regional grant, the FIRB grant, the Italian Association for the Fight
against Neuroblastoma (Pensiero Project), the Italian Ministry of Health
Oncology Program 2006, the CNMC Research Advisory Council, the CHOC
Foundation for Children, and grants from the CNMC Board of Visitors. We
thank Dr Elisabeth Rushing, Armed Forces Institute of Pathology,
Washington, DC, and Prof. Felice Giangaspero, Neurosurgery Department,
Umberto I Hospital, Rome, Italy, for providing the external secondary
neuropathological review.
NR 60
TC 36
Z9 36
U1 0
U2 5
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 1
BP 7
EP 17
DI 10.1634/stemcells.2008-0402
PG 11
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 402SC
UT WOS:000263032400003
PM 18832593
ER
PT J
AU Rao, RC
Boyd, J
Padmanabhan, R
Chenoweth, JG
McKay, RD
AF Rao, Rajesh C.
Boyd, Justin
Padmanabhan, Raji
Chenoweth, Josh G.
McKay, Ronald D.
TI Efficient Serum-Free Derivation of Oligodendrocyte Precursors from
Neural Stem Cell-Enriched Cultures
SO STEM CELLS
LA English
DT Article
DE Oligodendrocytes; Multipotent stem cells; Platelet-derived growth
factor; Glycolysis; Extracellular signal-regulated mitogen-activated
protein kinases Phosphatidylinositol 3-kinase
ID CENTRAL-NERVOUS-SYSTEM; GLIAL PROGENITOR-CELL; RAT-BRAIN
OLIGODENDROCYTES; GROWTH-FACTOR RECEPTOR; SIMIAN SARCOMA-VIRUS; IN-VIVO;
GENE-EXPRESSION; ALPHA-RECEPTOR; WHITE-MATTER; PDGF
AB Oligodendrocytes derived in the laboratory from stem cells have been proposed as a treatment for acute and chronic injury to the central nervous system. Platelet-derived growth factor (PDGF) receptor alpha (PDGFR alpha) signaling is known to regulate oligodendrocyte precursor cell numbers both during development and adulthood. Here, we analyze the effects of PDGFR alpha signaling on central nervous system (CNS) stem cell-enriched cultures. We find that AC133 selection for CNS progenitors acutely isolated from the fetal cortex enriches for PDGF-AA-responsive cells. PDGF-AA treatment of fibroblast growth factor 2-expanded CNS stem cell-enriched cultures increases nestin(+) cell number, viability, proliferation, and glycolytic rate. We show that a brief exposure to PDGF-AA rapidly and efficiently permits the derivation of O4(+) oligodendrocyte-lineage cells from CNS stem cell-enriched cultures. The derivation of oligodendrocyte-lineage cells demonstrated here may support the effective use of stem cells in understanding fate choice mechanisms and the development of new therapies targeting this cell type. STEM CELLS 2009; 27: 116-125
C1 [Rao, Rajesh C.; Boyd, Justin; Padmanabhan, Raji; Chenoweth, Josh G.; McKay, Ronald D.] Natl Inst Neurol Disorders & Stroke, Mol Biol Lab, NIH, Bethesda, MD USA.
[Rao, Rajesh C.] Howard Hughes Med Inst, NIH, Res Scholars Program, Bethesda, MD 20817 USA.
[Rao, Rajesh C.] Yale Univ, Sch Med, New Haven, CT 06510 USA.
RP McKay, RD (reprint author), 35 Convent Dr,MSC 4092, Bethesda, MD 20892 USA.
EM mckay@codon.nih.gov
OI Rao, Rajesh/0000-0002-5776-8366
FU NIH-National Institute of Neurological Disorders and Stroke; Howard
Hughes Medical Institute-NIH Research Scholars Program; NIH Research
Award [T35 HL07649]
FX The authors thank Jeanette Beers and Ramesh Potla for assistance with
fluorescence-activated cell sorter analysis and glycolytic rate assays.
We acknowledge Sachiko Murase for critical discussion of the manuscript.
We also thank Andreas Theotokis-Androutsellis, Andrei Kuzmichev, Dan
Hoeppner, Rea Ravin, and Steven Poser for their advice and suggestions
to optimize cell culture and other assays. We are grateful to Hirohide
Takebayashi (National Institute for Physiological Sciences, Okazaki,
Japan) for his gift of Olig2 antibody. This work was supported by the
Intramural Program of the NIH-National Institute of Neurological
Disorders and Stroke. R. C. R. was supported by the Howard Hughes
Medical Institute-NIH Research Scholars Program and by a T35 HL07649 NIH
Research Award through Yale University School of Medicine. R. C. R is
currently affiliated with the Department of Ophthalmology, Massachusetts
Eye & Ear Infirmary, Harvard Medical School, Boston, MA.
NR 81
TC 11
Z9 11
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 1
BP 116
EP 125
DI 10.1634/stemcells.2007-0205
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 402SC
UT WOS:000263032400014
PM 18403757
ER
PT J
AU Hayakawa, J
Hsieh, MM
Uchida, N
Phang, O
Tisdale, JF
AF Hayakawa, Jun
Hsieh, Matthew M.
Uchida, Naoya
Phang, Oswald
Tisdale, John F.
TI Busulfan Produces Efficient Human Cell Engraftment in NOD/LtSz-Scid IL2R
gamma(Null) Mice
SO STEM CELLS
LA English
DT Article
DE Cord blood; Peripheral blood stem cell transplantation; Severe combined
immunodeficient mice; Transferrin; Xenograft transplant; Busulfan;
Erythropoiesis; Hematopoietic stem cells
ID HEMATOPOIETIC STEM-CELLS; BLOOD CD34(+) CELLS; BONE-MARROW-CELLS;
NOD/SCID MICE; NULL MICE; INTRAFEMORAL TRANSPLANTATION; REPOPULATING
ABILITY; CD122(+) CELLS; MODEL; RECEPTOR
AB Xenografting immunodeficient mice after low-dose irradiation has been used as a surrogate human hematopoietic stem cell (HSC) assay; however, irradiation requires strict and meticulous animal support and can produce significant mortality rates, limiting the usefulness of this model. In this work, we examined the use of parenteral busulfan as an alternative conditioning agent. Busulfan led to dose-dependent human HSC engraftment in NOD/LtSz-scid/IL2R gamma(null) mice, with marked improvement in survival rates. Terminally differentiated B and T lymphocytes made up most of the human CD45+ cells observed during the initial 5 weeks post-transplant when unselected cord blood (CB) products were infused, suggesting derivation from existing mature elements rather than HSCs. Beyond 5 weeks, CD34+ enriched products produced and sustained superior engraftment rates compared with unselected grafts (CB CD34+, 65.8% +/- 5.35%, vs. whole CB, 4.27% +/- 0.67%, at 24 weeks). CB CD34+ group achieved significantly higher levels of engraftment than mobilized CD34+ enriched peripheral blood (PB CD34+). At 8 weeks, all leukocyte subsets were detected, yet human red blood cells (RBCs) were not observed. Transfused human red cells persisted in the chimeric mice for up to 3 days; an accompanying rise in total bilirubin suggested hemolysis as a contributing factor to their clearance. Recipient mouse-derived human HSCs had the capacity to form erythroid colonies in vitro at various time points post-transplant in the presence of human transferrin (Tf). When human Tf was administered singly or in combination with anti-CD122 antibody and human cytokines, up to 0.1% human RBCs were detectable in the peripheral blood. This long evasive model should prove valuable for the study of human erythroid cells. STEM CELLS 2009; 27: 175-182
C1 [Hayakawa, Jun; Hsieh, Matthew M.; Uchida, Naoya; Phang, Oswald; Tisdale, John F.] Natl Inst Diabet & Digest & Kidney Disorders, Mol & Clin Hematol Branch, Bethesda, MD 20892 USA.
[Hayakawa, Jun; Hsieh, Matthew M.; Uchida, Naoya; Phang, Oswald; Tisdale, John F.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Tisdale, JF (reprint author), Natl Inst Diabet & Digest & Kidney Disorders, Mol & Clin Hematol Branch, 9000 Rockville Pike,Bldg 10,Room 9N 116, Bethesda, MD 20892 USA.
EM johntis@mail.nih.gov
FU Intramural Research Program; NIH; National Institute of Diabetes and
Digestive and Kidney Diseases; National Heart, Lung, and Blood Institute
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases and the
National Heart, Lung, and Blood Institute at the NIH. We thank Elizabeth
Joyal for collection of the cord blood samples, Martha Kirby for cell
sorting, and D. Eric Anderson for mass spectroscopy. This work was
supported by the Intramural Research Program of the NIH, National
Institute of Diabetes and Digestive and Kidney Diseases.
NR 31
TC 24
Z9 24
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 1
BP 175
EP 182
DI 10.1634/stemcells.2008-0583
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 402SC
UT WOS:000263032400020
PM 18927475
ER
PT J
AU Nemeth, MJ
Mak, KK
Yang, YZ
Bodine, DM
AF Nemeth, Michael J.
Mak, Kingston K.
Yang, Yingzi
Bodine, David M.
TI beta-Catenin Expression in the Bone Marrow Microenvironment Is Required
for Long-Term Maintenance of Primitive Hematopoietic Cells
SO STEM CELLS
LA English
DT Article
DE Wnt; Myeloid Progenitor Cells; Hematopoietic Stem Cells; Transgenic Mice
ID WNT SIGNALING PATHWAY; STEM-CELLS; PROGENITOR CELLS; STROMAL CELLS;
PARATHYROID-HORMONE; GENE-EXPRESSION; N-CADHERIN; IN-VITRO; MICE;
DIFFERENTIATION
AB Hematopoiesis is dependent upon the bone marrow microenvironment, which is comprised of multiple mesenchymal cell types, including fibroblasts,endothelial cells, osteoblasts, and stroma progenitors. The canonical Wnt signaling pathway, which relies on the beta-catenin protein to mediate its signal, is necessary for the normal development of mesenchymal tissue. We hypothesized that canonical Wnt signaling regulates the cellular composition and function of the bone marrow microenvironment. We observed that a beta-catenin-deficient bone marrow microenvironment maintained hematopoietic stem cells but exhibited a decreased capacity to support primitive hematopoietic cells. These results correlated with decreased numbers of osteoblasts and with decreased production of basic fibroblast growth factor, stem cell factor, and vascular cell adhesion molecule-1. From these data, we propose a model in which beta-catenin in the microenvironment is required noncell autonomously for long-term maintenance of hematopoietic progenitors. STEM CELLS 2009;27:1109-1119
C1 [Nemeth, Michael J.; Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
[Nemeth, Michael J.] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
[Nemeth, Michael J.] Roswell Pk Canc Inst, Dept Immunol, Buffalo, NY 14263 USA.
[Mak, Kingston K.; Yang, Yingzi] NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA.
RP Bodine, DM (reprint author), NHGRI, Genet & Mol Biol Branch, 49 Convent Dr,Rm 4A04, Bethesda, MD 20892 USA.
EM tedyaz@nhgri.nih.gov
FU Roswell Park Cancer Institute
FX We thank Dr. Mark M. Taketo for his generous gift of the
Catnblox(ex3)/+ transgenic mouse line. M.J.N. was supported
in part by institutional funds provided by Roswell Park Cancer
Institute.
NR 54
TC 39
Z9 40
U1 1
U2 7
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 5
BP 1109
EP 1119
DI 10.1002/stem.32
PG 11
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 447GL
UT WOS:000266179500014
PM 19415781
ER
PT J
AU Fliedner, TM
Chao, NJ
Bader, JL
Boettger, A
Case, C
Chute, J
Confer, DL
Ganser, A
Gorin, NC
Gourmelon, P
Graessle, DH
Krawisz, R
Meineke, V
Niederwieser, D
Port, M
Powles, R
Sirohi, B
Weinstock, DM
Wiley, A
Coleman, CN
AF Fliedner, Theodor M.
Chao, Nelson J.
Bader, Judith L.
Boettger, Axel
Case, Cullen, Jr.
Chute, John
Confer, Dennis L.
Ganser, Arnold
Gorin, Norbert-Claude
Gourmelon, Patrick
Graessle, Dieter H.
Krawisz, Robert
Meineke, Viktor
Niederwieser, Dietger
Port, Matthias
Powles, Ray
Sirohi, Bhawna
Weinstock, David M.
Wiley, Albert
Coleman, C. Norman
TI Stem Cells, Multiorgan Failure in Radiation Emergency Medical
Preparedness: A US/European Consultation Workshop
SO STEM CELLS
LA English
DT Article
DE Hemopoietic growth factor; Irradiation; Stem cell transplantation; Stem
cell-microenvironment interactions
ID HEMATOPOIETIC STEM; NUCLEAR EVENTS; HUMAN EMBRYO; NICHE; BLOOD;
MANAGEMENT; EXPOSURE; CONSEQUENCES; RESPONSES; SEVERITY
AB The concern of the public regarding terrorist actions involving nuclear emergencies resulted in the reopening of the discussion regarding the best ways to cope with the inevitable health impairments. Medical experts from the US and from Europe considered it of importance to harmonize at an international level the diagnostic and therapeutic approaches regarding the radiation-induced health impairments. The present contribution is the result of the first U.S./European Consultation Workshop addressing approaches to radiation emergency preparedness and assistance, which was held recently at Ulm University, Ulm, Germany. Discussions dealt with the assessment of the extent of damage after total body exposure and, in particular, the quantity and quality of the damage to the hematopoietic stem cell pool. Secondly, the pathogenesis of the multiorgan failure was considered because of the organ-to-organ interactions. Thirdly, approaches were considered to harmonize the "triage-methods'' used on an international level using the "Response Category'' approach as developed for the European Communities. These discussions lead to the conclusion that there is a strong need for continuing education of physicians, nurses, and support personnel to address the issues posed by the management of patients suffering from radiation syndromes. Finally, the discussions expressed the need for more international cooperation in research and development of more refined methods to treat patients with any type of radiation syndromes. STEM CELLS 2009;27:1205-1211
C1 [Chao, Nelson J.; Chute, John] Duke Univ, Div Cellular Therapy, Dept Med, RadCCORE Radiat Countermeasures Ctr Res Excellenc, Durham, NC 27710 USA.
[Fliedner, Theodor M.; Graessle, Dieter H.] Univ Ulm, Radiat Med Res Grp, D-89069 Ulm, Germany.
[Bader, Judith L.; Coleman, C. Norman] NCI, NIH, Bethesda, MD 20892 USA.
[Bader, Judith L.; Coleman, C. Norman] Off Assistant Secretary Preparedness & Response, Dept Hlth & Human Serv, Washington, DC USA.
[Boettger, Axel] Fed Minist Environm Nat Protect & Nucl Safety, Dept Radiat Protect, Bonn, Germany.
[Case, Cullen, Jr.; Confer, Dennis L.] NMDP, Minneapolis, MN USA.
[Ganser, Arnold; Port, Matthias] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, D-3000 Hannover, Germany.
[Gorin, Norbert-Claude] Hosp St Antoine, Dept Hematol & Cell Therapy, Paris, France.
[Gourmelon, Patrick] IRSN, Fontenay Aux Roses, France.
[Krawisz, Robert] Amer Soc Blood & Marrow Transplantat, Arlington Hts, IL USA.
[Meineke, Viktor] Bundeswehr Inst Radiobiol, Munich, Germany.
[Niederwieser, Dietger] Univ Leipzig, Dept Hematol & Oncol, Leipzig, Germany.
[Powles, Ray] Parkside Oncol Clin, London, England.
[Sirohi, Bhawna] Addenbrookes Hosp, Dept Med Oncol, Cambridge, England.
[Weinstock, David M.] DFCI, Div Hematol Neoplasia, Boston, MA USA.
[Wiley, Albert] Radiat Emergency Assistance Ctr Training Site, Oak Ridge, TN USA.
RP Chao, NJ (reprint author), Duke Univ, Div Cellular Therapy, Dept Med, RadCCORE Radiat Countermeasures Ctr Res Excellenc, 2400 Pratt St,Suite 9100, Durham, NC 27710 USA.
EM Chao0002@mc.duke.edu
RI Port, Matthias/D-5230-2011
FU NIAID NIH HHS [U19 AI067798, U19 AI067798-07]
NR 38
TC 23
Z9 23
U1 0
U2 3
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 5
BP 1205
EP 1211
DI 10.1002/stem.16
PG 7
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 447GL
UT WOS:000266179500023
PM 19418462
ER
PT J
AU Smith, GH
Salomon, DS
Vonderhar, BK
AF Smith, Gilbert H.
Salomon, David S.
Vonderhar, Barbara K.
TI "Evidence that an Early Pregnancy Causes a Persistent Decrease in the
Number of Functional Mammary Epithelial Stem Cells-Implications for
Pregnancy-Induced Protection Against Breast Cancer'' by Siwko et al.
SO STEM CELLS
LA English
DT Letter
ID TUMORIGENESIS; ENVIRONMENT; GLAND; RATS
C1 [Smith, Gilbert H.; Salomon, David S.; Vonderhar, Barbara K.] NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Smith, GH (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bldg37,Rm 1106,MSC4254, Bethesda, MD 20892 USA.
EM gs4d@nih.gov
NR 6
TC 1
Z9 1
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 5
BP 1223
EP 1223
DI 10.1002/stem.19
PG 1
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 447GL
UT WOS:000266179500025
PM 19418459
ER
PT J
AU Blaisdell, CJ
Gail, DB
Nabel, EG
AF Blaisdell, Carol J.
Gail, Dorothy B.
Nabel, Elizabeth G.
TI National Heart, Lung, and Blood Institute Perspective: Lung Progenitor
and Stem Cells-Gaps in Knowledge and Future Opportunities
SO STEM CELLS
LA English
DT Article
DE Lung cell biology; Lung regeneration; Reprogramming
ID SIDE POPULATION CELLS; NEUROEPITHELIAL BODY MICROENVIRONMENT;
ENHANCER-BINDING PROTEIN; BONE-MARROW; BRONCHOPULMONARY DYSPLASIA;
EPITHELIAL-CELLS; GROWTH-FACTORS; SMOOTH-MUSCLE; BASAL-CELLS; AIRWAY
AB Because the lung stem cell field is so new, there remain many unanswered questions that are being addressed regarding the identification, location, and role of exogenous and endogenous stem and progenitor cell populations in growth, regeneration, and repair of the lung. Advancing lung stem cell biology will require multidisciplinary teams and a long term effort to unravel the biologic processes of stem cells in the lung. While no clinical research in lung stem cell therapies are currently funded by NHLBI, the knowledge gained by understanding the basic biology of the lung stem cell populations will be needed to translate to diagnostic and therapeutic strategies in the future. STEM CELLS 2009; 27: 2263-2270
C1 [Blaisdell, Carol J.] NHLBI, NIH, Div Lung Dis, Bethesda, MD 20892 USA.
RP Blaisdell, CJ (reprint author), NHLBI, NIH, Div Lung Dis, 6701 Rockledge Dr,10042, Bethesda, MD 20892 USA.
EM blaisdellcj@nhlbi.nih.gov
NR 54
TC 10
Z9 10
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 2009
VL 27
IS 9
BP 2263
EP 2270
DI 10.1002/stem.148
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 497IX
UT WOS:000270053700023
PM 19522010
ER
PT B
AU Smith, GH
AF Smith, Gilbert H.
BE Bagley, RG
Teicher, BA
TI Mouse Mammary Tumor Virus: Stem Cells and Mammary Cancer
SO STEM CELLS AND CANCER
SE Cancer Drug Discovery and Development
LA English
DT Article; Book Chapter
DE Stem cell; MMTV; Mammary; Cancer; Transplantation; Mice
ID TEMPLATE DNA STRANDS; EPITHELIAL-CELLS; BREAST-CANCER; CHEMICAL
CARCINOGENESIS; TGF-BETA-1 EXPRESSION; GLAND; TUMORIGENESIS; MICE;
SENESCENCE; PATHWAYS
AB The paradigm of mammary cancer induction by the mouse mammary tumor virus (MMTV) is used to illustrate the body of evidence that supports the hypothesis that mammary epithelial stem/progenitor cells represent targets for oncogenic transformation. It is argued that this is not a special case applicable only to MMTV-induced mammary cancer, because MMTV acts as an environmental mutagen producing random interruptions in the somatic DNA of infected cells by insertion of proviral DNA copies. In addition to disrupting the host genome, the proviral DNA also influences gene expression through its associated enhancer sequences over significant intergenomic distances. Genes commonly affected by MMTV insertion in multiple individual tumors include, the Writ genes, the FGF gene family, and the Notch gene family. All of these gene families are known to play essential roles in stem cell maintenance and behavior in a variety of organs. The MMTV-induced mutations accumulate in cells that are long lived and possess the properties of stem cells, namely, self-renewal and the capacity to produce divergent epithelial progeny through asymmetric division. The evidence shows that epithelial cells with these properties are present in normal mammary glands, may be infected with MMTV, and become transformed to produce epithelial hyperplasia through MMTV-induced mutagenesis and progress to frank mammary malignancy. Retroviral marking via MMTV proviral insertion demonstrates that this process progresses from a single mammary epithelial cell that possesses all of the features ascribed to tissue-specific stem cells.
C1 NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Smith, GH (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 43
TC 0
Z9 0
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
BN 978-1-60327-932-1
J9 CANCER DRUG DISCOV D
JI Canc. Drug. Disc. Dev.
PY 2009
BP 127
EP 140
DI 10.1007/978-1-60327-933-8_10
D2 10.1007/978-1-60327-933-8
PG 14
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA BKK41
UT WOS:000268379100010
ER
PT S
AU Marotta, F
Yadav, H
Pathak, S
Minelli, E
Signorelli, P
Lorenzetti, A
Marandola, P
AF Marotta, F.
Yadav, H.
Pathak, S.
Minelli, E.
Signorelli, P.
Lorenzetti, A.
Marandola, P.
BE Bradlow, HL
Carruba, G
TI Inhibition of Human Breast Cancer Cell Growth and Enzymatic Activity by
a Fermented Nutraceutical
SO STEROID ENZYMES AND CANCER
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 9th Advanced Course on Steroid Enzymes and Cancer
CY MAY 03-08, 2008
CL Erice, ITALY
DE breast cancer cell lines; in vivo breast cancer model; Manda-Koso
ID BCL-2; ANTIOXIDANT; CARCINOMA; APOPTOSIS
AB Human breast cancer cell lines MCF-7 (ER-positive) and Hs578T (ER-negative) were cultured and one lot incubated for 48 It with 5-50 mu g/ml of a fermented phytocompound (MK: Manda-Koso, Innoshima, Japan). lit vitro, it appeared a dose-dependent decrease of cell viability (5-57%) in MK group in both cell lines (P < 0.001, plateau: 30 mu g/ml), decreased beta-galactosidase activity, enhanced apoptosis, and inversely increased Bax/Bcl2 ratio (P < 0.01) with an upregulation of p53 (P < 0.05). In the ill vivo model, Balb-c mice were inoculated with tumor cells and the treatment group was fed with 20 mg of MK. Tumor weight in MK-fed group was time-course reduced by 22%, to 51% at 2 and 4 weeks, respectively (P < 0.05) with increased survival (P < 0.05). Tumour tissue of MK-fed mice showed a downregulated Bcl-2 with increased Bax/Bcl-2 ratio, reduced PCNA, and activated caspase 3. Although more studies are ongoing to foster the clinical applicability of MK integrated within a rational chemopreventive and therapeutic strategy, a p53-triediated mechanism is likely to play a relevant role, besides its reported antioxidant capacity, NK cell activity enhancement, cancer-cytostatic activity properties.
C1 [Marotta, F.; Signorelli, P.; Lorenzetti, A.; Marandola, P.] GAIA Age Management Fdn, Nutraceut Nutrigenom Unit, Pavia, Italy.
[Yadav, H.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Pathak, S.] Univ Kalyani, Cytogenet & Mol Biol Lab, Kalyani 741235, W Bengal, India.
[Marotta, F.; Minelli, E.] Univ Milan, WHO Ctr Biotech & Nat Med, Milan, Italy.
RP Marotta, F (reprint author), Piazza Firenze 12, I-20151 Milan, Italy.
EM fmarchimede@libero.it
NR 15
TC 1
Z9 1
U1 0
U2 2
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND
SN 0077-8923
BN 978-1-57331-745-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2009
VL 1155
BP 273
EP 277
DI 10.1111/j.1749-6632.2008.03684.x
PG 5
WC Oncology; Multidisciplinary Sciences
SC Oncology; Science & Technology - Other Topics
GA BJC65
UT WOS:000264751500031
PM 19250216
ER
PT B
AU Wang, PY
Wenthold, RJ
AF Wang, Philip Y.
Wenthold, Robert J.
BE Hortsch, M
Umemori, H
TI Synaptic Adhesion-Like Molecules (SALMs)
SO STICKY SYNAPSE: CELL ADHESION MOLECULES AND THEIR ROLE IN SYNAPSE
FORMATION AND MAINTENANCE
LA English
DT Article; Book Chapter
DE Synapse; Dendrite; Axon; PDZ proteins; LRR; Growth cone; Heteromeric;
Homomeric; Neurite outgrowth
ID LONG-TERM POTENTIATION; LEUCINE-RICH REPEATS; CELL-ADHESION; NEURITE
OUTGROWTH; EXCITATORY SYNAPSES; GROWTH CONE; N-CADHERIN; TRANSMEMBRANE
PROTEINS; DENDRITE ARBORIZATION; RECEPTOR TRAFFICKING
AB The synaptic adhesion-like molecules (SALMs) are a newly discovered family of cell adhesion molecules that have a variety of functions in neuronal development, including aspects of neurite Outgrowth and synapse formation (Ko et al. Neuron 50:233-245, 2006, Morimura et al. Gene 380:72-83, 2006, Wang et al. J Neurosci 26:2174-2183, 2006, Seabold et al. J Biol Chem 283:8395-8405, 2008, Wang et al. Mol Cell Neurosci, 39:83-94, 2008). Also known as Lrfn (leucine-rich and fibronectin III domain-containing), five family members have been identified thus far: SALM1/Lrfn2, SALM2/Lrfn1, SALM3/Lrfn4, SALM4/Lrfn3, and SALM5/Lrfn5. The SALMs have been shown to interact with NMDA receptors and the PSD-95 family of MAGUK proteins. Recent studies also indicate that the individual SALMs, while similar in structure, play distinct roles in heteromeric and homomeric protein interactions and neurite outgrowth (Seabold et al. J Blot Chem 283:8395-8405, 2008, Wang et al. Mol Cell Neurosci, 39:83-94, 2008). Neurite outgrowth and synapse formation are fundamental mechanisms in the development of the nervous System. While a considerable amount of information is known about both phenomena, the mechanism connecting the two is still enigmatic. SALMs join a growing mosaic of synaptic proteins that contribute to both neurite outgrowth and synapse formation during the course of development. Investigating SALMs and related proteins is essential for addressing fundamental questions of neuronal development.
C1 [Wang, Philip Y.; Wenthold, Robert J.] Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Philip Y.] Univ Maryland, Coll Chem & Life Sci, Dept Biol, College Pk, MD 20742 USA.
[Wang, Philip Y.] Univ Maryland, Neurosci & Cognit Sci Program, College Pk, MD 20742 USA.
RP Wenthold, RJ (reprint author), Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
EM wenthold@nidcd.nih.gov
NR 67
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-0-387-92707-7
PY 2009
BP 367
EP 383
DI 10.1007/978-0-387-92708-4_18
D2 10.1007/978-0-387-92708-4
PG 17
WC Cell Biology; Neurosciences
SC Cell Biology; Neurosciences & Neurology
GA BKY34
UT WOS:000269610400018
ER
PT B
AU Chitakornkijsil, P
AF Chitakornkijsil, Pranee
BE Xiaowen, J
Erming, X
Schneider, I
TI SMEs Entrepreneurship and Development Strategies
SO STRATEGIC MANAGEMENT ENGINEERING: ENTERPRISE, ENVIRONMENT AND CRISIS
LA English
DT Proceedings Paper
CT International Conference on Strategic Management
CY JUN 25-30, 2009
CL Chengdu, PEOPLES R CHINA
DE SMEs; International Entrepreneurship; Export; Import; International
Market Place
AB In this study, the method for SMEs to go international is considered. The study shows the new international development to expand for international market. Besides, it introduces how entrepreneurs are able to take advantage of exporting opportunities. Moreover it illustrates the entrepreneurial benefits of importing. In addition, it explains the benefits of foreign direct investment by entrepreneur. More than that, it demonstrates the disadvantages and advantages of entrepreneurial joint ventures. Furthermore, it exhibits advantages and disadvantages of licensing arrangements. Eventually, it establishes key steps for enhancing the international market place.
C1 [Chitakornkijsil, Pranee] NIDA, Grad Sch Business Adm, Bangkok 10240, Thailand.
NR 36
TC 0
Z9 0
U1 0
U2 1
PU SICHUAN UNIV PRESS
PI CHENGDU
PA 29 WANGJIANGLU, JIUYANQIAO, CHENGDU, PEOPLES R CHINA
BN 978-7-5614-4376-7
PY 2009
BP 214
EP 218
PG 5
WC Business; Business, Finance; Economics; Management
SC Business & Economics
GA BKP51
UT WOS:000268879300027
ER
PT J
AU Biddie, SC
Hager, GL
AF Biddie, Simon C.
Hager, Gordon L.
TI Glucocorticoid receptor dynamics and gene regulation
SO STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS
LA English
DT Review
DE Glucocorticoid receptor; chromatin; dynamics; gene expression
ID MAMMARY-TUMOR VIRUS; NF-KAPPA-B; LONG TERMINAL REPEAT; IN-VIVO;
ESTROGEN-RECEPTOR; LIVING CELLS; TRANSCRIPTIONAL ACTIVATION; MOLECULAR
CHAPERONES; TRANSACTIVATION DOMAIN; CHROMATIN DYNAMICS
AB The glucocorticoid receptor regulates the expression of a large number of genes in mammalian cells. The interaction of this receptor with regulatory elements has been discovered to be highly dynamic, with occupancy states measured in seconds, rather than minutes or hours. This finding has led to a paradigm shift in our understanding of receptor function throughout the genome. The mechanisms involved in these rapid exchange events, as well as the implications for receptor function, are discussed.
C1 [Biddie, Simon C.; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
[Biddie, Simon C.] Univ Bristol, Dept Med, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol BS1 3NY, Avon, England.
RP Hager, GL (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bldg 41,B602,41 Lib Dr, Bethesda, MD 20892 USA.
EM hagerg@exchange.nih.gov
OI Biddie, Simon/0000-0002-8253-0253
FU Intramural Research Program; NIH, National Cancer Institute; Center for
Cancer Research
FX S. C. B was supported, in part, by The Needham Cooper Postgraduate
Medicine Scholarship held by Stafford L. Lightman and the Faculty of
Medicine, University of Bristol. This research was supported by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 109
TC 37
Z9 38
U1 1
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1025-3890
J9 STRESS
JI Stress
PY 2009
VL 12
IS 3
BP 193
EP 205
AR PII 906263195
DI 10.1080/10253890802506409
PG 13
WC Behavioral Sciences; Endocrinology & Metabolism; Neurosciences
SC Behavioral Sciences; Endocrinology & Metabolism; Neurosciences &
Neurology
GA 438VK
UT WOS:000265583600001
PM 19051126
ER
PT J
AU Ali, M
Atula, S
Bath, PMW
Grotta, J
Hacke, W
Lyden, P
Marler, JR
Sacco, RL
Lees, KR
AF Ali, Myzoon
Atula, Sari
Bath, Philip M. W.
Grotta, James
Hacke, Werner
Lyden, Patrick
Marler, John R.
Sacco, Ralph L.
Lees, Kennedy R.
CA VISTA Investigators
TI Stroke Outcome in Clinical Trial Patients Deriving From Different
Countries
SO STROKE
LA English
DT Article
DE acute care; clinical trials; database; epidemiology; outcomes
ID ACUTE ISCHEMIC-STROKE; CASE-FATALITY; RISK-FACTORS; MONICA PROJECT;
EUROPEAN PERSPECTIVE; SOCIOECONOMIC-STATUS; NORTHERN MANHATTAN; WIDENING
GAP; MORTALITY; CARE
AB Background and Purpose-Stroke incidence and outcome vary widely within and across geographical locations. We examined whether differences in index stroke severity, stroke risk factors, mortality, and stroke outcome across geographical locations remain after adjusting for case mix.
Methods-We analyzed 3284 patients from the Virtual International Stroke Trials Archive (VISTA). We used logistic regression to examine the incidence of mild index stroke, functional, and neurological outcomes after accounting for age, medical history, year of trial recruitment, and initial stroke severity in the functional and neurological outcome analyses. We examined mortality between geographical regions using a Cox proportional hazards model, accounting for age, initial stroke severity, medical history, and year of trial recruitment.
Results-Patients enrolled in the USA and Canada had the most severe index strokes. Those recruited in Austria and Switzerland had the best functional and neurological outcomes at 90 days (P<0.05), whereas those enrolled in Germany had the worst functional outcome at 90 days (P=0.013). Patients enrolled in Austria, Switzerland, Belgium, Netherlands, Finland, Germany, Greece, Israel, Spain, and Portugal had a significantly better survival rate when compared with those enrolled in USA and Canada. Patients enrolled in trials after 1998 had more severe index strokes, with no significant difference in outcome compared with those enrolled before 1998.
Conclusion-We identified regional variations in index stroke severity, outcome, and mortality for patients enrolled in ischemic stroke clinical trials over the past 13 years that were not fully explained by case mix. Index stroke severity was greater in patients enrolled after 1998, with no significant improvement in outcomes compared to those enrolled before 1998. (Stroke. 2009;40:35-40.)
C1 [Ali, Myzoon; Atula, Sari; Lees, Kennedy R.] Univ Glasgow, Western Infirm, Gardiner Inst, Dept Med & Therapeut, Glasgow G11 6NT, Lanark, Scotland.
[Bath, Philip M. W.] Univ Nottingham, Div Stroke Med, Nottingham NG7 2RD, England.
[Grotta, James] Univ Texas Houston, Houston Med Sch, Dept Neurol, Houston, TX USA.
[Hacke, Werner] Univ Heidelberg, Dept Neurol, D-6900 Heidelberg, Germany.
[Lyden, Patrick] Univ Calif San Diego, San Diego, CA 92103 USA.
[Lyden, Patrick] VA Stroke Ctr, San Diego, CA USA.
[Marler, John R.] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
[Sacco, Ralph L.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
RP Ali, M (reprint author), Univ Glasgow, Western Infirm, Gardiner Inst, Univ Dept Med & Therapeut,Div Cardiovasc & Med Sc, 44 Church St, Glasgow G11 6NT, Lanark, Scotland.
EM myzoonali@clinmed.gla.ac.uk
RI Bath, Philip/F-9020-2011; Davis, Stephen/L-5260-2013;
OI Bath, Philip/0000-0003-2734-5132; Davis, Stephen/0000-0003-0962-2300;
Gregson, Barbara/0000-0003-4868-9137; Kaste, Markku/0000-0001-6557-6412
NR 43
TC 23
Z9 25
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2009
VL 40
IS 1
BP 35
EP 40
DI 10.1161/STROKEAHA.108.518035
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 388ZN
UT WOS:000262059400009
PM 18927457
ER
PT J
AU Ay, H
Arsava, EM
Johnston, SC
Vangel, M
Schwamm, LH
Furie, KL
Koroshetz, WJ
Sorensen, AG
AF Ay, Hakan
Arsava, E. Murat
Johnston, S. Claiborne
Vangel, Mark
Schwamm, Lee H.
Furie, Karen L.
Koroshetz, Walter J.
Sorensen, A. Gregory
TI Clinical- and Imaging-Based Prediction of Stroke Risk After Transient
Ischemic Attack The CIP Model
SO STROKE
LA English
DT Article
DE diffusion-weighted imaging; stroke risk; transient ischemic attack
ID DIFFUSION-WEIGHTED MRI; MINOR STROKE; TIA PATIENTS; ABCD SCORE;
EMERGENCY; PREVALENCE; LESIONS; VALIDATION
AB Background and Purpose-Predictive instruments based on clinical features for early stroke risk after transient ischemic attack suffer from limited specificity. We sought to combine imaging and clinical features to improve predictions for 7-day stroke risk after transient ischemic attack.
Methods-We studied 601 consecutive patients with transient ischemic attack who had MRI within 24 hours of symptom onset. A logistic regression model was developed using stroke within 7 days as the response criterion and diffusion-weighted imaging findings and dichotomized ABCD(2) score (ABCD(2) >= 4) as covariates.
Results-Subsequent stroke occurred in 25 patients (5.2%). Dichotomized ABCD(2) score and acute infarct on diffusion-weighted imaging were each independent predictors of stroke risk. The 7-day risk was 0.0% with no predictor, 2.0% with ABCD(2) score >= 4 alone, 4.9% with acute infarct on diffusion-weighted imaging alone, and 14.9% with both predictors (an automated calculator is available at http://cip. martinos. org). Adding imaging increased the area under the receiver operating characteristic curve from 0.66 (95% CI, 0.57 to 0.76) using the ABCD(2) score to 0.81 (95% CI, 0.74 to 0.88; P = 0.003). The sensitivity of 80% on the receiver operating characteristic curve corresponded to a specificity of 73% for the CIP model and 47% for the ABCD(2) score.
Conclusions-Combining acute imaging findings with clinical transient ischemic attack features causes a dramatic boost in the accuracy of predictions with clinical features alone for early risk of stroke after transient ischemic attack. If validated in relevant clinical settings, risk stratification by the CIP model may assist in early implementation of therapeutic measures and effective use of hospital resources. (Stroke. 2009; 40: 181-186.)
C1 [Ay, Hakan; Schwamm, Lee H.; Furie, Karen L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Stroke Serv, Charlestown, MA 02129 USA.
[Ay, Hakan; Arsava, E. Murat; Vangel, Mark; Sorensen, A. Gregory] Harvard Univ, Massachusetts Gen Hosp, Sch Med, AA Martinos Ctr Biomed Imaging,Dept Radiol, Charlestown, MA 02129 USA.
[Johnston, S. Claiborne] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Johnston, S. Claiborne] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Koroshetz, Walter J.] NINDS, NIH, Bethesda, MD USA.
RP Ay, H (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Stroke Serv, 149 13th St,Room 2301, Charlestown, MA 02129 USA.
EM hay@partners.org
RI Arsava, Ethem Murat/I-9197-2013;
OI Arsava, Ethem Murat/0000-0002-6527-4139; Schwamm,
Lee/0000-0003-0592-9145
FU NIH [R01-NS38477-04, P41-RR14075]; [USPHSNS38477]
FX This work was supported by USPHSNS38477 and NIH grants R01-NS38477-04
and P41-RR14075.
NR 34
TC 78
Z9 91
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2009
VL 40
IS 1
BP 181
EP 186
DI 10.1161/STROKEAHA.108.521476
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 388ZN
UT WOS:000262059400032
PM 18948609
ER
PT J
AU Schoch, CL
Crous, PW
Groenewald, JZ
Boehm, EWA
Burgess, TI
de Gruyter, J
de Hoog, GS
Dixon, LJ
Grube, M
Gueidan, C
Harada, Y
Hatakeyama, S
Hirayama, K
Hosoya, T
Huhndorf, SM
Hyde, KD
Jones, EBG
Kohlmeyer, J
Kruys, A
Li, YM
Lucking, R
Lumbsch, HT
Marvanova, L
Mbatchou, JS
Mcvay, AH
Miller, AN
Mugambi, GK
Muggia, L
Nelsen, MP
Nelson, P
Owensby, CA
Phillips, AJL
Phongpaichit, S
Pointing, SB
Pujade-Renaud, V
Raja, HA
Plata, ER
Robbertse, B
Ruibal, C
Sakayaroj, J
Sano, T
Selbmann, L
Shearer, CA
Shirouzu, T
Slippers, B
Suetrong, S
Tanaka, K
Volkmann-Kohlmeyer, B
Wingfield, MJ
Wood, AR
Woudenberg, JHC
Yonezawa, H
Zhang, Y
Spatafora, JW
AF Schoch, C. L.
Crous, P. W.
Groenewald, J. Z.
Boehm, E. W. A.
Burgess, T. I.
de Gruyter, J.
de Hoog, G. S.
Dixon, L. J.
Grube, M.
Gueidan, C.
Harada, Y.
Hatakeyama, S.
Hirayama, K.
Hosoya, T.
Huhndorf, S. M.
Hyde, K. D.
Jones, E. B. G.
Kohlmeyer, J.
Kruys, A.
Li, Y. M.
Lucking, R.
Lumbsch, H. T.
Marvanova, L.
Mbatchou, J. S.
McVay, A. H.
Miller, A. N.
Mugambi, G. K.
Muggia, L.
Nelsen, M. P.
Nelson, P.
Owensby, C. A.
Phillips, A. J. L.
Phongpaichit, S.
Pointing, S. B.
Pujade-Renaud, V.
Raja, H. A.
Plata, E. Rivas
Robbertse, B.
Ruibal, C.
Sakayaroj, J.
Sano, T.
Selbmann, L.
Shearer, C. A.
Shirouzu, T.
Slippers, B.
Suetrong, S.
Tanaka, K.
Volkmann-Kohlmeyer, B.
Wingfield, M. J.
Wood, A. R.
Woudenberg, J. H. C.
Yonezawa, H.
Zhang, Y.
Spatafora, J. W.
TI A class-wide phylogenetic assessment of Dothideomycetes
SO STUDIES IN MYCOLOGY
LA English
DT Review
DE Ascomycota; Pezizomycotina; Dothideomyceta; fungal evolution; lichens;
multigene phylogeny; phylogenomics; plant pathogens; saprobes; Tree of
Life
ID RIBOSOMAL DNA-SEQUENCES; MULTIGENE PHYLOGENIES; MOLECULAR PHYLOGENY;
MAXIMUM-LIKELIHOOD; MULTIPLE ALIGNMENT; MARINE ASCOMYCOTA; RDNA
SEQUENCES; FUNGI; EVOLUTION; CLASSIFICATION
AB We present a comprehensive phylogeny derived from 5 genes, nucSSU, nucLSU rDNA, TEF1, RPB1 and RPB2, for 356 isolates and 41 families (six newly described in this volume) in Dothideomycetes. All currently accepted orders in the class are represented for the first time in addition to numerous previously unplaced lineages. Subclass Pleosporomycelidae is expanded to include the aquatic order Jahnulales. An ancestral reconstruction of basic nutritional modes supports numerous transitions from saprobic life histories to plant associated and lichenised modes and a transition from terrestrial to aquatic habitats are confirmed. Finally, a genomic comparison of 6 dothideomycete genomes with other fungi finds a high level of unique protein associated with the class, supporting its delineation as a separate taxon.
C1 [Schoch, C. L.; Robbertse, B.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Crous, P. W.; Groenewald, J. Z.; de Gruyter, J.; de Hoog, G. S.; Gueidan, C.; Woudenberg, J. H. C.] CBS KNAW Fungal Biodivers Ctr, NL-3508 AD Utrecht, Netherlands.
[Boehm, E. W. A.] Kean Univ, Dept Biol Sci, Union, NJ 07083 USA.
[Burgess, T. I.] Murdoch Univ, Murdoch, WA 6150, Australia.
[de Gruyter, J.] Plant Protect Serv, NL-6700 HC Wageningen, Netherlands.
[Dixon, L. J.] USDA ARS, Systemat Mycol & Microbiol Lab, Beltsville, MD 20705 USA.
[Grube, M.; Muggia, L.] Karl Franzens Univ Graz, Inst Plant Sci, Graz, Austria.
[Harada, Y.; Hatakeyama, S.; Hirayama, K.; Sano, T.; Tanaka, K.; Yonezawa, H.] Hirosaki Univ, Fac Agr & Life Sci, Aomori 0368561, Japan.
[Hosoya, T.] Natl Museum Nat & Sci, Tsukuba, Ibaraki 3050005, Japan.
[Huhndorf, S. M.; Lucking, R.; Lumbsch, H. T.; Mbatchou, J. S.; Mugambi, G. K.; Nelsen, M. P.; Plata, E. Rivas] Field Museum, Dept Bot, Chicago, IL 60605 USA.
[Hyde, K. D.] Mae Fah Luang Univ, Sch Sci 17, Muang 57100, Chiang Rai, Thailand.
[Jones, E. B. G.; Sakayaroj, J.; Suetrong, S.] Natl Ctr Genet Engn & Biotechnol BIOTEC, Bioresources Technol Unit, Khlong Luang 12120, Pathum Thani, Thailand.
[Kohlmeyer, J.; Volkmann-Kohlmeyer, B.] Univ N Carolina Chapel Hill, Inst Marine Sci, Morehead City, NC 28557 USA.
[Kruys, A.] Uppsala Univ, Evolutionary Biol Ctr, Dept Systemat Biol, SE-75236 Uppsala, Sweden.
[Marvanova, L.] Masaryk Univ, Fac Sci, Inst Expt Biol, CZ-60200 Brno, Czech Republic.
[Mbatchou, J. S.] Depaul Univ, Coll Liberal Arts & Sci, Chicago, IL 60604 USA.
[McVay, A. H.; Owensby, C. A.; Spatafora, J. W.] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA.
[Miller, A. N.] Univ Illinois, Illinois Nat Hist Survey, Champaign, IL 61820 USA.
[Mugambi, G. K.] Natl Museums Kenya, Dept Bot, Nairobi 00100, Kenya.
[Nelsen, M. P.] Univ Chicago, Comm Evolutionary Biol, Chicago, IL 60637 USA.
[Nelson, P.] Univ Minnesota, St Paul, MN 55108 USA.
[Phillips, A. J. L.] Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Ciencias Vida, Ctr Recursos Microbiol, P-2829516 Quinta Da Torre, Caparica, Portugal.
[Phongpaichit, S.; Suetrong, S.] Prince Songkia Univ, Fac Sci, Dept Microbiol, Hat Yai 90112, Songkhla, Thailand.
[Pointing, S. B.; Zhang, Y.] Univ Hong Kong, Sch Biol Sci, Div Microbiol, Hong Kong, Hong Kong, Peoples R China.
[Pujade-Renaud, V.] Univ Clermont Ferrand, CIRAD PIAF, F-63177 Aubiere, France.
[Raja, H. A.; Shearer, C. A.] Univ Illinois, Dept Plant Biol, Urbana, IL 61801 USA.
[Mugambi, G. K.; Plata, E. Rivas] Univ Illinois, Dept Biol Sci, Chicago, IL 60607 USA.
[Ruibal, C.] Univ Politecn Madrid, Escuela Tecn Super Ingenieros Ind, Dept Ingn & Ciencia Mat, E-28006 Madrid, Spain.
[Selbmann, L.] Largo Univ, Univ Tuscia, DECOS, Viterbo, Italy.
[Shirouzu, T.] Tottori Univ, Fungus Mushroom Resource & Res Ctr, Tottori 6808553, Japan.
[Slippers, B.; Wingfield, M. J.] Univ Pretoria, Fac Nat & Agr Sci, Dept Genet, Ctr Excellence Tree Hlth Biotechnol,FABI, ZA-0002 Pretoria, South Africa.
[Wood, A. R.] ARC Plant Protect Res Inst, ZA-7599 Stellenbosch, South Africa.
[Hyde, K. D.; Li, Y. M.] Chinese Acad Forestry, Res Inst Resource Insects, Int Fungal Res Dev Ctr, Kunming, Yunnan, Peoples R China.
RP Schoch, CL (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, 45 Ctr Dr,MSC 6510, Bethesda, MD 20892 USA.
EM schoch2@ncbi.nlm.nih.gov
RI REQUIMTE, MM/M-6160-2013; REQUIMTE, UCIBIO/N-9846-2013; Gueidan,
Cecile/C-8803-2014; Phillips, Alan/C-6102-2011; Slippers,
Bernard/A-9351-2008; Groenewald, Johannes/F-4667-2011; Sakayaroj,
Jariya/D-1845-2012; Crous, Pedro/H-1489-2012; Schoch,
Conrad/J-4825-2012; Lumbsch, Thorsten/K-3573-2012; Wingfield,
Michael/A-9473-2008; Jones, Gareth/C-5137-2013; Woudenberg, Joyce
H.C./C-9384-2013; Tanaka, Kazuaki/F-1924-2013; Burgess,
Treena/G-4770-2011; Selbmann, Laura/L-3056-2013
OI Raja, Huzefa/0000-0002-0824-9463; Ruibal Villasenor,
Constantino/0000-0003-3494-7051; Grube, Martin/0000-0001-6940-5282;
Phillips, Alan/0000-0001-6367-9784; Slippers,
Bernard/0000-0003-1491-3858; Crous, Pedro/0000-0001-9085-8825; Lumbsch,
Thorsten/0000-0003-1512-835X; Woudenberg, Joyce
H.C./0000-0002-7337-6864; Burgess, Treena/0000-0002-7962-219X;
FU NIH; National Library of Medicine; NSF [DEB-0717476, DEB-0732993]
FX Authors from individual papers in this volume contributed to this work
and specific acknowledgements to that regard can be found in individual
papers. Work performed for this paper by the first author after 2008 was
supported in part by the Intramural Research Program of the NIH,
National Library of Medicine. Part of this work was also funded by
grants from NSF (DEB-0717476) to J. W. Spatafora (and C.L. Schoch until
2008) and (DEB-0732993) to J.W. Spatafora and B. Robbertse.
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SN 0166-0616
J9 STUD MYCOL
JI Stud. Mycol.
PY 2009
IS 64
BP 1
EP 15
DI 10.3114/sim.2009.64.01
PG 15
WC Mycology
SC Mycology
GA 553KQ
UT WOS:000274365900002
ER
PT J
AU Crous, PW
Schoch, CL
Hyde, KD
Wood, AR
Gueidan, C
de Hoog, GS
Groenewald, JZ
AF Crous, P. W.
Schoch, C. L.
Hyde, K. D.
Wood, A. R.
Gueidan, C.
de Hoog, G. S.
Groenewald, J. Z.
TI Phylogenetic lineages in the Capnodiales
SO STUDIES IN MYCOLOGY
LA English
DT Review
DE Ascomycetes; Brunneosphaerella; Capnodiales; DNA sequence comparisons;
Mycosphaerella; novel primers; systematics
ID RIBOSOMAL DNA-SEQUENCES; LEAF SPOTS; GEN-NOV; FUNGAL PATHOGENS;
LICHENIZED FUNGI; BLOTCH-DISEASE; CROFTON WEED; SOUTH-AFRICA;
MYCOSPHAERELLA; EUCALYPTUS
AB The Capnodiales incorporates plant and human pathogens, endophytes, saprobes and epiphytes, with a wide range of nutritional modes. Several species are lichenised, or occur as parasites on fungi, or animals. The aim of the present study was to use DNA sequence data of the nuclear ribosomal small and large subunit RNA genes to test the monophyly of the Capnodiales, and resolve families within the order. We designed primers to allow the amplification and sequencing of almost the complete nuclear ribosomal small and large subunit RNA genes. Other than the Capnodiaceae (sooty moulds), and the Davidiellaceae, which contains saprobes and plant pathogens, the order presently incorporates families of major plant pathological importance such as the Mycosphaerellaceae, Teratosphaeriaceae and Schizothyriaceae. The Piedraiaceae was not supported, but resolves in the Teratosphaeriaceae. The Dissoconiaceae is introduced as a new family to accommodate Dissoconium and Ramichloridium. Lichenisation, as well as the ability to be saprobic or plant pathogenic evolved more than once in several families, though the taxa in the upper clades of the tree lead us to conclude that the strictly plant pathogenic, nectrotrophic families evolved from saprobic ancestors (Capnodiaceae), which is the more primitive state.
C1 [Crous, P. W.; Gueidan, C.; de Hoog, G. S.; Groenewald, J. Z.] CBS KNAW Fungal Biodivers Ctr, NL-3508 AD Utrecht, Netherlands.
[Crous, P. W.] Univ Wageningen & Res Ctr, Phytopathol Lab, NL-6708 PB Wageningen, Netherlands.
[Schoch, C. L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Wood, A. R.] ARC Plant Protect Res Inst, ZA-7599 Stellenbosch, South Africa.
[Hyde, K. D.] Mae Fah Luang Univ, Sch Sci, Muang 57100, Chiang Rai, Thailand.
RP Crous, PW (reprint author), CBS KNAW Fungal Biodivers Ctr, POB 85167, NL-3508 AD Utrecht, Netherlands.
EM p.crous@cbs.knaw.nl
RI Groenewald, Johannes/F-4667-2011; Crous, Pedro/H-1489-2012; Schoch,
Conrad/J-4825-2012; Gueidan, Cecile/C-8803-2014
OI Crous, Pedro/0000-0001-9085-8825;
FU NIH; National Library of Medicine; NSF [DEB-0717476]
FX Several colleagues have helped to collect material studied here, without
which this work would not have been possible. Drs E.H.C. Mckenzie and
S.R. Pennycook (Landcare New Zealand) are specifically thanked for
recollecting Phaeophleospora atkinsonfi. We are grateful to BIOTEC and
Dr Lily Eurwilaichitr (Director, Bioresources unit, BIOTEC) for
assisting with a collection trip in Thailand under the collaborative
BIOTEC-CBS memorandum of understanding. We thank Miss Marjan Vermaas for
preparing the photographic plates, and M. Starink-Willemse, and A. van
lperen, for assistance with DNA sequencing and fungal cultures. Work
performed for this paper by the second author after 2008 was supported
in part by the Intramural Research Program of the NIH, National Library
of Medicine. Before 2008 work was funded by a grant from NSF
(DEB-0717476). We are grateful to Drs Roland Kirschner, Alan J. Phillips
and Treena I. Burgess for their critical comments on this script. The
views expressed, however, are those of the authors.
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SC Mycology
GA 553KQ
UT WOS:000274365900003
PM 20169022
ER
PT J
AU Boehm, EWA
Mugambi, GK
Miller, AN
Huhndorf, SM
Marincowitz, S
Spatafora, JW
Schoch, CL
AF Boehm, E. W. A.
Mugambi, G. K.
Miller, A. N.
Huhndorf, S. M.
Marincowitz, S.
Spatafora, J. W.
Schoch, C. L.
TI A molecular phylogenetic reappraisal of the Hysteriaceae,
Mytilinidiaceae and Gloniaceae (Pleosporomycetidae, Dothideomycetes)
with keys to world species
SO STUDIES IN MYCOLOGY
LA English
DT Review
DE Evolution; fungi; Hysteriales; Mytilinidiales; Patellariales; phylogeny;
speciation; taxonomy
ID RUSSIAN FAR-EAST; RIBOSOMAL DNA-SEQUENCES; SOUTHERN SOUTH-AMERICA; GENUS
HYSTEROGRAPHIUM; MULTIPLE ALIGNMENT; FUNGI; ASCOMYCOTA; NUCLEAR;
EVOLUTION; TAXONOMY
AB A reappraisal of the phylogenetic integrity of bitunicate ascomycete fungi belonging to or previously affiliated with the Hysteriaceae, Mytilinidiaceae, Gloniaceae and Patellariaceae is presented, based on an analysis of 121 isolates and four nuclear genes, the ribosomal large and small subunits, transcription elongation factor I and the second largest RNA polymerase 11 subunit. A geographically diverse and high density taxon sampling strategy was employed, including multiple isolates/species from the following genera: Anteaglonium (6/4), Encephalographa (1/1), Farlowiella (3/1), Gloniopsis (8/4), Glonium (4/2), Hysterium (12/5), Hysterabrevium (14/3), Hysterographium (2/1), Hysteropatella (2/2), Lophium (4/2), Mytilinidion (13/10), Oedohysterium (5/3), Ostreichnion (212), Patellaria (1/1), Psiloglonium (11/3), Quasiconcha (1/1), Rhytidhysteron (8/3), and 24 outgroup taxa. Sequence data indicate that although the Hysteriales are closely related to the Pleosporales, sufficient branch support exists for their separation into separate orders within the Pleosporomycetidae. The Mytilinidiales are more distantly related within the subclass and show a dose association with the Gloniaceae. Although there are examples of concordance between morphological and molecular data, these are few. Molecular data instead support the premise of a large number of convergent evolutionary lineages, which do not correspond to previously held assumptions of synapomorphy relating to spore morphology. Thus, within the Hysteriaceae, the genera Gloniopsis, Glonium, Hysterium and Hysterographium are highly polyphyletic. This necessitated the transfer of two species of Hysterium to Oedohysterium gen. nov (Od. insidens comb. nov. and Od. sinense comb. nov), the description of a new species, Hysterium barrianum sp. nov, and the transfer of two species of Gloniopsis to Hysterobrevium gen. nov. (Hb. smilacis comb. nov. and Hb. constrictum comb. nov). While Hysterographium, with the type Hg. fraxini, is removed from the Hysteriaceae, some of its species remain within the family, transferred here to Oedohysterium (Od. pulchrum comb. nov.), Hysterobrevium (Hb. mori comb. nov) and Gloniopsis (Gp. subrugosa comb. nov.); the latter genus, in addition to the type, Gp. praelonga, with two new species, Gp. arciformis sp. nov. and Gp. kenyensis sp. nov. The genus Glonium is now divided into Anteaglonium (Pleosporales), Glonium (Gloniaceae), and Psiloglonium, (Hysteriaceae). The hysterothecium has evolved convergently no less than five times within the Pleosporomycetidae (e.g., Anteaglonium, Farlowiella, Glonium, Hysterographium and the Hysteriaceae). Similarly, thin-walled mytilinidioid (e.g., Ostreichnion) and patellarioid (e.g., Rhytidhysteron) genera, previously in the Mytilinidiaceae and Patellariaceae, respectively, transferred here to the Hysteriaceae, have also evolved at least twice within the subclass. As such, character states traditionally considered to represent synapomorphies among these fungi, whether they relate to spore septation or the ascomata, in fact, represent symplesiomorphies, and most likely have arisen multiple times through convergent evolutionary processes in response to common selective pressures.
C1 [Boehm, E. W. A.] Kean Univ, Dept Biol Sci, Union, NJ 07083 USA.
[Mugambi, G. K.] Natl Museums Kenya, Dept Bot, Nairobi 00100, Kenya.
[Miller, A. N.] Univ Illinois, Illinois Nat Hist Survey, Champaign, IL USA.
[Huhndorf, S. M.] Field Museum, Chicago, IL 60605 USA.
[Marincowitz, S.] Univ Pretoria, Forestry & Agr Biotechnol Inst, ZA-0002 Pretoria, South Africa.
[Spatafora, J. W.] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR USA.
[Schoch, C. L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, GenBank, Bethesda, MD 20892 USA.
RP Boehm, EWA (reprint author), Kean Univ, Dept Biol Sci, 1000 Morris Ave, Union, NJ 07083 USA.
EM eboehm@kean.edu
RI Marincowitz, Seonju/A-9185-2008; Schoch, Conrad/J-4825-2012
FU National Science Foundation (NSF) [DBI 0922603, DEB0515558,
DEB-0717476]; Discover Life in America [DLIA 2005-15]; NIH; National
Library of Medicine
FX The authors wish to thank Alain Gardiennet (Veronnes, France), Gintaras
Kantvilas (Tasmanian Herbarium, Hobart, Tasmania), Marieka Gryzenhout
(Dept. Microbiology and Plant Pathology, Forestry and Agricultural
Biotechnology Institute, University of Pretoria, South Africa), Maria
Inez Messuti and Laura Emma Lorenzo (Departamento de Botanica, Centro
Regional Universitario Bariloche, Universidad Nacional del Comahue,
Quintral, Bariloche, Rio Negro, Argentina), Eunice Nkansah (Kean
University, Union, NJ, U.S.A.), and Meredith Blackwell (Dept. Biological
Sciences, Louisiana State University, Baton Rouge, Louisiana, U.S.A.)
for kindly supplying some of the isolates used in this study (Table 1).
The authors wish to thank Walter Gams (Baam, The Netherlands) for the
Latin translations, and for his numerous helpful insights into the
taxonomic and nomenclatural issues raised by this work. We also wish to
acknowledge Scott Redhead (National Mycological Herbarium, Agriculture
and Agri-Food Canada, Ottawa, Canada) who provided helpful suggestions
on the manuscript prior to submission. E.W.A. Boehm wishes to
acknowledge support from the National Science Foundation (NSF) Major
Research Instrumentation Grant DBI 0922603. A.N. Miller acknowledges
funding from the NSF through a BS&I award (DEB0515558) and from Discover
Life in America (DLIA 2005-15). Part of this work was also funded by a
grant from NSF (DEB-0717476) to J.W. Spatafora (and C.L. Schoch until
2008). Work performed by C.L. Schoch after 2008 was supported in part by
the Intramural Research Program of the NIH, National Library of
Medicine.
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JI Stud. Mycol.
PY 2009
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SC Mycology
GA 553KQ
UT WOS:000274365900004
ER
PT J
AU Zhang, Y
Schoch, CL
Fournier, J
Crous, PW
de Gruyter, J
Woudenberg, JHC
Hirayama, K
Tanaka, K
Pointing, SB
Spatafora, JW
Hyde, KD
AF Zhang, Y.
Schoch, C. L.
Fournier, J.
Crous, P. W.
de Gruyter, J.
Woudenberg, J. H. C.
Hirayama, K.
Tanaka, K.
Pointing, S. B.
Spatafora, J. W.
Hyde, K. D.
TI Multi-locus phylogeny of Pleosporales: a taxonomic, ecological and
evolutionary re-evaluation
SO STUDIES IN MYCOLOGY
LA English
DT Review
DE Environmental habit; evolution; molecular phylogeny; nutritional mode;
taxonomy
ID RIBOSOMAL DNA-SEQUENCES; STAGONOSPORA-NODORUM; MOLECULAR PHYLOGENY;
LEPTOSPHAERIA-MACULANS; PHAEOSPHAERIA-NODORUM; MULTIGENE PHYLOGENY;
MULTIPLE ALIGNMENT; ENDOPHYTIC FUNGI; SP-NOV; ASCOMYCOTA
AB Five loci, nucSSU, nucLSU rDNA, TEF1, RPB1 and RPB2, are used for analysing 129 pleosporalean taxa representing 59 genera and 15 families in the current classification of Pleosporales. The suborder Pleosporineae is emended to include four families, viz. Didymellaceae, Leptosphaeriaceae, Phaeosphaeriaceae and Pleosporaceae. In addition, two new families are introduced, i.e. Amniculicolaceae and Lentitheciaceae. Pleomassariaceae is treated as a synonym of Melanommataceae, and new circumscriptions of Lophiostomataceae s. str, Massarinaceae and Lophiotrema are proposed. Familial positions of Entodesmium and Setomelanomma in Phaeosphaeriaceae, Neophaeosphaeria in Leptosphaeriaceae, Leptosphaerulina, Macroventuria and Platychora in Didymellaceae, Pleomassaria in Melanommataceae and Bimuria, Didymocrea, Karstenula and Paraphaeosphaeria in Montagnulaceae are clarified. Both ecological and morphological characters show varying degrees of phylogenetic significance. Pleosporales is most likely derived from a saprobic ancestor with fissitunicate asci containing conspicuous ocular chambers and apical rings. Nutritional shifts in Pleosporales likely occured from saprotrophic to hemibiotrophic or biotrophic.
C1 [Hyde, K. D.] Mae Fah Luang Univ, Sch Sci, Muang 57100, Chiang Rai, Thailand.
[Zhang, Y.; Pointing, S. B.] Univ Hong Kong, Sch Biol Sci, Div Microbiol, Hong Kong, Hong Kong, Peoples R China.
[Schoch, C. L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Crous, P. W.; de Gruyter, J.; Woudenberg, J. H. C.] CBS KNAW Fungal Biodivers Ctr, NL-3508 AD Utrecht, Netherlands.
[Fournier, J.] Las Muros, F-09420 Rimont, Ariege, France.
[de Gruyter, J.] Plant Protect Serv, NL-6700 HC Wageningen, Netherlands.
[Hirayama, K.; Tanaka, K.] Hirosaki Univ, Fac Agr & Life Sci, Aomori 0368561, Japan.
[Spatafora, J. W.] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR USA.
[Hyde, K. D.] Chinese Acad Forestry, Res Inst Resource Insects, Int Fungal Res & Dev Ctr, Kunming 650034, Yunnan, Peoples R China.
RP Hyde, KD (reprint author), Mae Fah Luang Univ, Sch Sci, Muang 57100, Chiang Rai, Thailand.
EM kdhyde2@gmail.com
RI Crous, Pedro/H-1489-2012; Schoch, Conrad/J-4825-2012; Woudenberg, Joyce
H.C./C-9384-2013; Tanaka, Kazuaki/F-1924-2013
OI Crous, Pedro/0000-0001-9085-8825; Woudenberg, Joyce
H.C./0000-0002-7337-6864;
FU NIH; National Library of Medicine; NSF [DEB 0717476]
FX The authors thank O.E. Eriksson for his comments on a draft version of
this script, as well as two other anonymous reviewers. Dr Shaun
Pennycook is thanked for his valuable suggestions on nomenclature. The
University of Hong Kong is thanked for providing YZ with a postgraduate
studentship. Work performed by CLS after 2008 was supported in part by
the Intramural Research Program of the NIH, National Library of
Medicine. This work was funded by a grant from NSF to JWS and to CLS
until 2008 (DEB 0717476).
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JI Stud. Mycol.
PY 2009
IS 64
BP 85
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DI 10.3114/sim.2009.64.04
PG 18
WC Mycology
SC Mycology
GA 553KQ
UT WOS:000274365900005
PM 20169024
ER
PT J
AU Ruibal, C
Gueidan, C
Selbmann, L
Gorbushina, AA
Crous, PW
Groenewald, JZ
Muggia, L
Grube, M
Isola, D
Schoch, CL
Staley, JT
Lutzoni, F
de Hoog, GS
AF Ruibal, C.
Gueidan, C.
Selbmann, L.
Gorbushina, A. A.
Crous, P. W.
Groenewald, J. Z.
Muggia, L.
Grube, M.
Isola, D.
Schoch, C. L.
Staley, J. T.
Lutzoni, F.
de Hoog, G. S.
TI Phylogeny of rock-inhabiting fungi related to Dothideomycetes
SO STUDIES IN MYCOLOGY
LA English
DT Article
DE Arthoniomycetes; Capnodiales; Dothideomycetes; evolution;
extremotolerance; multigene phylogeny; rock-inhabiting fungi
ID SUBUNIT RIBOSOMAL DNA; MICROCOLONIAL FUNGI; MERISTEMATIC FUNGI;
LICHENIZED FUNGI; ANTIQUE MARBLES; BLACK YEASTS; PCR PRIMERS; EVOLUTION;
ASCOMYCOTA; LIFE
AB The class Dothideomycetes (along with Eurotiomycetes) includes numerous rock-inhabiting fungi (RIF), a group of ascomycetes that tolerates surprisingly well harsh conditions prevailing on rock surfaces. Despite their convergent morphology and physiology, RIF are phylogenetically highly diverse in Dothideomycetes. However, the positions of main groups of RIF in this Class remain unclear due to the lack of a strong phylogenetic framework. Moreover, connections between rock-dwelling habit and other lifestyles found in Dothideomycetes such as plant pathogens, saprobes and lichen-forming fungi are still unexplored. Based on multigene phylogenetic analyses, we report that RIF belong to Capnodiales (particularly to the family Teratosphaeriaceae s.l.), Dothideales, Pleosporales, and Myriangiales, as well as some uncharacterised groups with affinities to Dothideomycetes. Moreover, one lineage consisting exclusively of RIF proved to be closely related to Arthoniomycetes, the sister class of Dothideomycetes. The broad phylogenetic amplitude of RIF in Dothideomycetes suggests that total species richness in this class remains underestimated. Composition of some RIF-rich lineages suggests that rock surfaces are reservoirs for plant-associated fungi or saprobes, although other data also agree with rocks as a primary substrate for ancient fungal lineages. According to the current sampling, long distance dispersal seems to be common for RIF. Dothideomycetes lineages comprising lichens also include RIF, suggesting a possible link between rock-dwelling habit and lichenisation.
C1 [Ruibal, C.] Univ Politecn Madrid, Escuela Tecn Super Ingenieros Ind, Dept Ingn & Ciencia Mat, E-28006 Madrid, Spain.
[Gueidan, C.; Crous, P. W.; Groenewald, J. Z.; de Hoog, G. S.] CBS KNAW Fungal Biodivers Ctr, NL-3508 AD Utrecht, Netherlands.
[Selbmann, L.; Isola, D.] Largo Univ, Univ Tuscia, DECOS, Viterbo, Italy.
[Gorbushina, A. A.] Free Univ Berlin, D-12205 Berlin, Germany.
[Gorbushina, A. A.] BAM Fed Inst Mat Res & Testing, Dept Mat & Environm 4, D-12205 Berlin, Germany.
[Muggia, L.; Grube, M.] Karl Franzens Univ Graz, Inst Pflanzenwissensch, A-8010 Graz, Austria.
[Schoch, C. L.] NIH, NCBI, Natl Lib Med, Bethesda, MD 20892 USA.
[Staley, J. T.] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Lutzoni, F.] Duke Univ, Dept Biol, Durham, NC 27708 USA.
RP Ruibal, C (reprint author), Univ Politecn Madrid, Escuela Tecn Super Ingenieros Ind, Dept Ingn & Ciencia Mat, Jose Gutierrez Abascal 2, E-28006 Madrid, Spain.
EM tinoruibal@yahoo.com
RI Groenewald, Johannes/F-4667-2011; Crous, Pedro/H-1489-2012; Schoch,
Conrad/J-4825-2012; Selbmann, Laura/L-3056-2013; Gueidan,
Cecile/C-8803-2014;
OI Crous, Pedro/0000-0001-9085-8825; Ruibal Villasenor,
Constantino/0000-0003-3494-7051; Grube, Martin/0000-0001-6940-5282
FU NSF AToL [DEB-0228725, DEB-0717476]; National Institutes of Health
(National Library of Medicine); National Swiss Foundation
[31003A-122513]; Deutsche Forschungsgerneinschaft [Go 897/3]; Synthesys
grant
FX Work performed by C.R. at Duke University was supported by a NSF AToL
grant (AFTOL, DEB-0228725) to F.L. Work performed by C.L.S. after 2008
was supported in part by the Intramural Research Program of the National
Institutes of Health (National Library of Medicine), and until 2008 by a
grant from NSF (DEB-0717476). Work performed by A.A.G. was funded by
grants from the National Swiss Foundation (31003A-122513) and the
Deutsche Forschungsgerneinschaft (DFG Go 897/3). Work performed by L.S.
at the CBS was funded by a Synthesys grant. The authors would like to
acknowledge the Italian National Program for Antarctic Research (PNRA)
for supporting the collection of samples, the Italian National Antarctic
Museum 'Felice Ippolito" for supporting the Culture Collection of Fungi'
From Extreme Environments (CCFEE) and the Alpine guides A. Serafini and
M. Heltai for collecting rock samples in the Alps and Aconcagua,
respectively. Thanks to William Broughton for his editorial help and to
the technical staff of the CBS for their assistance with the cultures.
NR 85
TC 66
Z9 68
U1 2
U2 13
PU CENTRAALBUREAU SCHIMMELCULTURE
PI UTRECHT
PA PO BOX 85167, 3508 AD UTRECHT, NETHERLANDS
SN 0166-0616
EI 1872-9797
J9 STUD MYCOL
JI Stud. Mycol.
PY 2009
IS 64
BP 123
EP 133
DI 10.3114/sim.2009.64.06
PG 11
WC Mycology
SC Mycology
GA 553KQ
UT WOS:000274365900007
ER
PT J
AU Suetrong, S
Schoch, CL
Spatafora, JW
Kohlmeyer, J
Volkmann-Kohlmeyer, B
Sakayaroj, J
Phongpaichit, S
Tanaka, K
Hirayama, K
Jones, EBG
AF Suetrong, S.
Schoch, C. L.
Spatafora, J. W.
Kohlmeyer, J.
Volkmann-Kohlmeyer, B.
Sakayaroj, J.
Phongpaichit, S.
Tanaka, K.
Hirayama, K.
Jones, E. B. G.
TI Molecular systematics of the marine Dothideomycetes
SO STUDIES IN MYCOLOGY
LA English
DT Review
DE Dothideomycetes; ecology; marine fungi; multi-locus; new genera;
systematics
ID MULTIPLE SEQUENCE ALIGNMENT; INTERTIDAL MANGROVE WOOD; RIBOSOMAL
DNA-SEQUENCES; MORPHOLOGICALLY SIMILAR GENERA; SP-NOV;
PHYLOGENETIC-RELATIONSHIPS; JUNCUS-ROEMERIANUS; FRESH-WATER; RDNA
SEQUENCES; NYPA-FRUTICANS
AB Phylogenetic analyses of four nuclear genes, namely the large and small subunits of the nuclear ribosomal RNA, transcription elongation factor I-alpha and the second largest RNA polymerase 11 subunit, established that the ecological group of marine bitunicate ascomycetes has representatives in the orders Capnodiales, Hysteriales, Jahnulales, Mytilinidiales, Patellariales and Pleosporales. Most of the fungi sequenced were intertidal mangrove taxa and belong to members of 12 families in the Pleosporales: Aigialaceae, Didymellaceae, Leptosphaeriaceae, Lenthitheciaceae, Lophiostomataceae, Massarinaceae, Montagnulaceae, Morosphaeriaceae, Phaeosphaeriaceae, Pleosporaceae, Testudinaceae and Trematosphaeriaceae. Two new families are described: Aigialaceae and Morosphaeriaceae, and three new genera proposed: Halomassarina, Morosphaerial and Rimora. Few marine species are reported from the Dothideomycetidae (e.g. Mycosphaerellaceae, Capnodiales), a group poorly studied at the molecular level. New marine lineages include the Testudinaceae and Manglicola guatemalensis in the Jahnulales. Significantly, most marine Dothideomycetes are intertidal tropical species with only a few from temperate regions on salt marsh plants (Spartina species and Juncus roemerianus), and rarely totally submerged (e.g. Halotthia posidoniae and Pontoporeia biturbinata on the seagrasses Posidonia oceanica and Cymodocea nodosum). Specific attention is given to the adaptation of the Dothideomycetes to the marine milieu, new lineages of marine fungi and their host specificity.
C1 [Suetrong, S.; Sakayaroj, J.; Jones, E. B. G.] Natl Ctr Genet Engn & Biotechnol BIOTEC, Bioresources Technol Unit, Khlong Luang 12120, Pathum Thani, Thailand.
[Suetrong, S.; Phongpaichit, S.] Prince Songkla Univ, Fac Sci, Dept Microbiol, Hat Yai 90112, Songkhla, Thailand.
[Schoch, C. L.] NIH, Natl Ctr Biothechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Spatafora, J. W.] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA.
[Kohlmeyer, J.; Volkmann-Kohlmeyer, B.] Univ N Carolina Chapel Hill, Inst Marine Sci, Morehead City, NC 28557 USA.
[Tanaka, K.; Hirayama, K.] Hirosaki Univ, Fac Agr & Life Sci, Aomori 0368561, Japan.
RP Jones, EBG (reprint author), Natl Ctr Genet Engn & Biotechnol BIOTEC, Bioresources Technol Unit, 113 Thailand Sci Pk,Paholyothin Rd,Khlong 1, Khlong Luang 12120, Pathum Thani, Thailand.
EM remispora@gmail.com
RI Sakayaroj, Jariya/D-1845-2012; Schoch, Conrad/J-4825-2012; Jones,
Gareth/C-5137-2013; Tanaka, Kazuaki/F-1924-2013
FU TRF/BIOTEC Special Program for Biodiversity Research and Training [BRT
R251006, BRT R351004, BRT R352015]; TOTAL Corporate Foundation; TOTAL E
P Thailand; Prince of Songkla University; NIH; National Library of
Medicine; NSF [DEB-0717476]
FX This work was supported by TRF/BIOTEC Special Program for Biodiversity
Research and Training Grant BRT R251006, BRT R351004 BRT R352015, and a
TOTAL Corporate Foundation, TOTAL E & P Thailand. We thank Y. Zhang and
Dr K.D. Hyde for exchange of data and useful discussions. SS
acknowledges the Songklanagarind Scholarship for Graduate Studies from
the Prince of Songkla University. We thank Prof. M. Tanticharoen, Dr K.
Kirtikara and Dr L. Eurwilaichitr for continued support. We thank A.
Klaysuban for technical assistance, and U. Pinruan, N. Rungjindamai, R.
Choeyklin, A. Loilong, S. Preedanon and O. Supaphon for assistance with
the field work. Work performed by CLS after 2008 was supported in part
by the Intramural Research Program of the NIH, National Library of
Medicine. Part of this work was also funded by a grant from NSF
(DEB-0717476) to JWS and CLS (until 2008).
NR 175
TC 88
Z9 91
U1 10
U2 23
PU CENTRAALBUREAU SCHIMMELCULTURE
PI UTRECHT
PA UPPSALALAAN 8, 3584 CT UTRECHT, NETHERLANDS
SN 0166-0616
J9 STUD MYCOL
JI Stud. Mycol.
PY 2009
IS 64
BP 155
EP 173
DI 10.3114/sim.2009.64.09
PG 19
WC Mycology
SC Mycology
GA 553KQ
UT WOS:000274365900010
ER
PT J
AU Phillips, KA
Chaudhry, A
Nahvi, S
Kunins, H
Gourevitch, M
Alford, DP
AF Phillips, K. A.
Chaudhry, A.
Nahvi, S.
Kunins, H.
Gourevitch, M.
Alford, D. P.
TI Impact of an Office-Based Opioid Treatment (OBOT) Workshop
SO SUBSTANCE ABUSE
LA English
DT Meeting Abstract
C1 [Phillips, K. A.] NIDA, Bethesda, MD USA.
[Chaudhry, A.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
[Nahvi, S.; Kunins, H.] Albert Einstein Coll Med, Bronx, NY USA.
[Gourevitch, M.] NYU, Sch Med, New York, NY 10003 USA.
[Alford, D. P.] Boston Univ, Sch Med, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0889-7077
J9 SUBST ABUS
JI Subst. Abus.
PY 2009
VL 30
IS 1
BP 92
EP 93
PG 2
WC Substance Abuse
SC Substance Abuse
GA 668WO
UT WOS:000283304800030
ER
PT J
AU Phillips, KA
Walley, AY
Gordon, AJ
AF Phillips, K. A.
Walley, A. Y.
Gordon, A. J.
TI Patients in Recovery (PIR): Success at Teaching Opioid Addiction
Treatments to Physicians
SO SUBSTANCE ABUSE
LA English
DT Meeting Abstract
C1 [Phillips, K. A.] NIDA, NIH, Bethesda, MD USA.
[Walley, A. Y.] Boston Univ, Sch Med, Boston, MA 02215 USA.
[Gordon, A. J.] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0889-7077
J9 SUBST ABUS
JI Subst. Abus.
PY 2009
VL 30
IS 1
BP 96
EP 97
PG 2
WC Substance Abuse
SC Substance Abuse
GA 668WO
UT WOS:000283304800037
ER
PT J
AU Hermos, J
Winter, M
Heeren, T
Hingson, R
AF Hermos, J.
Winter, M.
Heeren, T.
Hingson, R.
TI Alcohol-Related Problems Among Younger Drinkers Who Misuse Prescription
Drugs: Results from the National Epidemiologic Survey of Alcohol and
Related Conditions (NESARC)
SO SUBSTANCE ABUSE
LA English
DT Article
DE Alcohol-related problems; prescription drug misuse; young drinkers
ID DSM-IV ALCOHOL; AGE-OF-ONSET; USE DISORDERS; SUBSTANCE USE;
NATURAL-HISTORY; NONMEDICAL USE; UNITED-STATES; PREVALENCE; DRINKING;
COOCCURRENCE
AB The authors determined whether lifetime prescription drug misuse ( PDM) associated with increased risks for alcohol-related problems among 18- to 34-year-old, NESARC respondents. Among 8222 "ever-drinkers," 15.4% reported ever "misusing sedatives, tranquilizers, painkillers or stimulants ... as prescriptions or from indirect sources." Outcomes were within two alcohol-related problem domains, "risk-taking behaviors," including driving while drinking, fights, injuries, and arrests, and "interpersonal troubles," including problems with jobs, family, or friends. Among all drinkers and among alcohol-dependent and cannabis-using subsamples, those reporting PDM were significantly more likely to report alcohol-related "risk-taking behaviors" or "interpersonal troubles" than were those without PDM. In adjusted analysis, young age drinking onsets, and heavy and dependent drinking independently increased these risks. Results of this cross-sectional analysis support the need for longitudinal data to more clearly define the association between drinking problems and PDM, and which can support prevention, treatment, and harm-reduction efforts for younger, multisubstance users.
C1 [Hermos, J.; Winter, M.; Heeren, T.; Hingson, R.] Boston Univ, Sch Publ Hlth, Youth Alcohol Prevent Ctr, Boston, MA USA.
[Hermos, J.; Hingson, R.] Boston Univ, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA USA.
[Winter, M.; Heeren, T.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Hingson, R.] NIAAA, Div Epidemiol & Prevent, NIH, Bethesda, MD USA.
RP Hermos, J (reprint author), VA Boston Healthcare Syst 151MAV, 150 S Huntington Ave, Boston, MA 02130 USA.
EM jhermos@bu.edu
OI Heeren, Timothy/0000-0001-5643-3559
FU National Institute on Alcohol Abuse and Alcoholism for the Youth Alcohol
Prevention Center, Boston University School of Public Health;
Statistical Coordinating Center, Boston University School of Public
Health
FX This work was supported by Core Funds from the National Institute on
Alcohol Abuse and Alcoholism for the Youth Alcohol Prevention Center,
Boston University School of Public Health, and Core Funds from the
Statistical Coordinating Center, Boston University School of Public
Health.
NR 22
TC 9
Z9 9
U1 2
U2 5
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0889-7077
J9 SUBST ABUS
JI Subst. Abus.
PY 2009
VL 30
IS 2
BP 118
EP 126
DI 10.1080/08897070902802034
PG 9
WC Substance Abuse
SC Substance Abuse
GA 668WZ
UT WOS:000283306600002
PM 19347751
ER
PT B
AU Mukhopadhyay, D
Dasso, M
AF Mukhopadhyay, Debaditya
Dasso, Mary
BE Wilson, VG
TI The SUMO Pathway in Mitosis
SO SUMO REGULATION OF CELLULAR PROCESSES
LA English
DT Article; Book Chapter
DE Mitosis; SUMO; Condensin; Topoisomerase; Kinetochore
ID SEPTIN-INTERACTING PROTEINS; DNA TOPOISOMERASE-II; E3 LIGASE ACTIVITY;
SACCHAROMYCES-CEREVISIAE; CENP-E; IN-VIVO; CHROMOSOME SEGREGATION;
SUMOYLATED PROTEINS; CENTROMERE PROTEIN; SISTER CHROMATIDS
AB Mitosis is the stage of the cell cycle during which replicated chromosomes must be precisely divided to allow the formation of two daughter cells possessing equal genetic material. Much of the careful spatial and temporal organization of mitosis is maintained through post-translational modifications, such as phosphorylation and ubiquitination, of key cellular proteins. Here, we will review evidence that sumoylation, conjugation to the SUMO family of small ubiquitin-like modifiers, also serves essential regulatory roles during mitosis. We will discuss the basic biology of sumoylation, how the SUMO pathway has been implicated in particular mitotic functions, including chromosome condensation, centromere/kinetochore organization and cytokinesis, and what cellular proteins may be the targets underlying these phenomena.
C1 [Mukhopadhyay, Debaditya; Dasso, Mary] Natl Inst Child Hlth & Dev, Sect Cell Cycle Regulat, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Dasso, M (reprint author), Natl Inst Child Hlth & Dev, Sect Cell Cycle Regulat, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
EM mukhopad@mail.nih.gov; mdasso@helix.nih.gov
OI Dasso, Mary/0000-0002-5410-1371
NR 96
TC 1
Z9 1
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-90-481-2648-4
PY 2009
BP 153
EP 169
DI 10.1007/978-90-481-2649-1_9
D2 10.1007/978-90-481-2649-1
PG 17
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA BNH44
UT WOS:000274564200009
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI A SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES A Collaborative Effort of the National Research Council and the
American Association for the Advancement of Science Summary
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Editorial Material; Book Chapter
ID BIOLOGICAL WEAPONS; ETHICAL-ISSUES; SCIENTIFIC-RESEARCH; RESEARCH NORMS;
1918 FLU; VIRUS; GENETICS; CODES; INDUSTRY; FACULTY
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 168
TC 1
Z9 1
U1 1
U2 1
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP 1
EP +
PG 20
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100002
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI A SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES A Collaborative Effort of the National Research Council and the
American Association for the Advancement of Science Preface and
Acknowledgments
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Editorial Material; Book Chapter
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP VII
EP IX
PG 3
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100001
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI A SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES A Collaborative Effort of the National Research Council and the
American Association for the Advancement of Science Overview
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Editorial Material; Book Chapter
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP 11
EP 41
PG 31
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100003
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI Approach
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Article; Book Chapter
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP 43
EP 61
PG 19
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100004
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI Results of the Survey
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Article; Book Chapter
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP 63
EP 113
PG 51
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100005
ER
PT J
AU Atlas, RM
AF Atlas, Ronald M.
GP Natl Res Council
TI A SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES A Collaborative Effort of the National Research Council and the
American Association for the Advancement of Science Conclusions and
Recommendations
SO SURVEY OF ATTITUDES AND ACTIONS ON DUAL USE RESEARCH IN THE LIFE
SCIENCES: A COLLABORATIVE EFFORT OF THE NATIONAL RESEARCH COUNCIL AND
THE AMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE
LA English
DT Editorial Material; Book Chapter
C1 [Atlas, Ronald M.] Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
[Atlas, Ronald M.] Univ Louisville, Ctr Hlth Hazards Preparedness, Louisville, KY 40292 USA.
[Atlas, Ronald M.] NASA, Planetary Protect Board, Washington, DC USA.
[Atlas, Ronald M.] Wellcome Trust Infect Immunol & Populat Hlth Stra, Baltimore, MD USA.
[Atlas, Ronald M.] ASM Task Force Biodef, Boston, MA USA.
[Atlas, Ronald M.] ASM, Madison, WI USA.
[Atlas, Ronald M.] NIH, Recombinant DNA Advisory Comm, Baltimore, MD USA.
[Atlas, Ronald M.] Dept Homeland Secur Sci & Technol Advisory Comm, Oslo, Norway.
[Atlas, Ronald M.] Fed Bur Invest Sci Working Grp Bioforens, London, England.
RP Atlas, RM (reprint author), Univ Louisville, Biol & Publ Hlth, Louisville, KY 40292 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 978-0-309-12510-9
PY 2009
BP 115
EP 122
PG 8
WC Education & Educational Research
SC Education & Educational Research
GA BC4IZ
UT WOS:000352554100006
ER
PT J
AU Finnema, SJ
Donohue, SR
Zoghbi, SS
Brown, AK
Gulyas, B
Innis, RB
Halldin, C
Pike, VW
AF Finnema, Sjoerd J.
Donohue, Sean R.
Zoghbi, Sami S.
Brown, Amira K.
Gulyas, Balazs
Innis, Robert B.
Halldin, Christer
Pike, Victor W.
TI Evaluation of [C-11]PipISB and [F-18]PipISB in Monkey as Candidate
Radioligands for Imaging Brain Cannabinoid Type-1 Receptors In Vivo
SO SYNAPSE
LA English
DT Article
DE positron emission tomography; carbon-11; fluorine-18; radiotracer
ID INVERSE AGONIST; RAT-BRAIN; DRUG DEVELOPMENT; PET; LOCALIZATION;
SR141716A; BINDS; DRONABINOL; ANOREXIA; OBESITY
AB N-(4-Fluorobenzyl)-4-[3-(piperidin-1-yl)indole-1-sulfonyl]benzamide] (PipISB, 3) is a selective and high-potency cannabinoid subtype-1 (CBI) receptor inverse agonist. We have previously reported radiosyntheses of [C-11]3 and [F-18]3. Here, we aimed to evaluate the uptake and CB, receptor-specific binding of each radioligand in monkey brain in vivo with positron emission tomography (PET). [C-11]3 or [F-18]3 was injected intravenously into rhesus or cynomolgus monkey, respectively, and examined with PET at baseline or after pretreatment with a receptor-saturating dose of CB1 receptor-selective ligand (3 for [C-11]3 or 8 for [F-18](3)). In one PET experiment, the dose of 3 was administered at 100 min after [C-11]3. Relative plasma concentrations of radioligand and radiometabolites were concurrently measured in baseline experiments with high-performance liquid chromatography. Brain radioactivity uptake was highest in striatum and cerebellum, and it reached 170-270% standardized uptake value (SUV) at 120 min after injection of [C-11](3) and 180% SUV at 240 min after injection of [F-18](3). Radioactivity was well retained in all CBI receptor-rich regions. No reference region could be identified for nonspecifically bound radioligand. Under CB1 receptor pretreatment and displacement conditions, initial brain uptakes of radioactivity were similar to those at baseline. Regional brain radioactivity concentrations then became homogeneous and diminished to between 70 and 80% SUV at 120 min after injection of [C-11]3 and to 25% SUV at 240 min after injection of [F-18]3. [F-18]3 was not defluorinated but was metabolized to less lipophilic radiometabolites, as was [C-11]3. Hence, [C-11]3 and [F-18]3 showed high CBI receptor-specific binding in monkey brain in vivo and merit further investigation as prospective PET radioligands in humans. Synapse 63:22-30, 2009. Published 2008 Wiley-Liss, Inc.
C1 [Donohue, Sean R.; Zoghbi, Sami S.; Brown, Amira K.; Innis, Robert B.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Finnema, Sjoerd J.; Donohue, Sean R.; Gulyas, Balazs; Halldin, Christer] Karolinska Hosp, Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
RP Pike, VW (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Rm B3 C346A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pikev@mail.nih.gov
RI Gulyas, Balazs/F-9508-2015
FU National Institute of Mental Health [Z01-MH-002795]
FX Contract grant sponsor: National Institute of Mental Health; Contract
grant number: Z01-MH-002795
NR 39
TC 7
Z9 7
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0887-4476
J9 SYNAPSE
JI Synapse
PD JAN
PY 2009
VL 63
IS 1
BP 22
EP 30
DI 10.1002/syn.20578
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 383FB
UT WOS:000261658400004
PM 18925657
ER
PT B
AU Galperin, MY
AF Galperin, Michael Y.
BE Lee, SY
TI Sensory Transduction Network of E. coli
SO SYSTEMS BIOLOGY AND BIOTECHNOLOGY OF ESCHERICHIA COLI
LA English
DT Article; Book Chapter
ID COMPLETE GENOME SEQUENCE; 2-COMPONENT SIGNAL-TRANSDUCTION; BACTERIAL
RESPONSE REGULATORS; C-DI-GMP; ESCHERICHIA-COLI;
PROTEIN-PHOSPHORYLATION; CYCLIC DIGUANYLATE; RNA-POLYMERASE; IN-VITRO;
DOMAIN
AB The genome of Escherichia coli K12 encodes at least 6 classes of sensor proteins: 30 histidine protein kinases, 5 methyl-accepting chemotaxis proteins, 23 membrane components of the sugar: phosphotransferase system (PTS), 29 proteins with diguanylate cyclase and/or c-di-GMP-specific phosphodiesterase activity and two predicted serine/threonine protein kinases. The full signal transduction network additionally includes 32 response regulators, numerous chemotaxis proteins, PTS components, adenylate cyclase, CRP, and uncharacterized c-di-GMP-responsive components. Bacterial response to environmental signals can occur on several levels: the level of individual genes and proteins (changes in gene expression, post-translational regulation), the whole-cell level (chemotaxis), and the multicellular level (biofilm formation). All signal transduction systems are energy-dependent but their energy expenditure is miniscule compared to that of the processes they regulate. A better understanding of the signal transduction mechanisms and integration of these mechanisms into the metabolic pathway model of the E. coli cell will remain major challenges for systems biology.
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Galperin, MY (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM galperin@ncbi.nlm.nih.gov
OI Galperin, Michael/0000-0002-2265-5572
NR 46
TC 1
Z9 1
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
BN 978-1-4020-9393-7
PY 2009
BP 133
EP 148
DI 10.1007/978-1-4020-9394-4_8
D2 10.1007/978-1-4020-9394-4
PG 16
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Microbiology
GA BKK54
UT WOS:000268388500008
ER
PT B
AU Shiloach, J
Rinas, U
AF Shiloach, Joseph
Rinas, Ursula
BE Lee, SY
TI Glucose and Acetate Metabolism in E. coli - System Level Analysis and
Biotechnological Applications in Protein Production Processes
SO SYSTEMS BIOLOGY AND BIOTECHNOLOGY OF ESCHERICHIA COLI
LA English
DT Article; Book Chapter
ID HIGH-CELL-DENSITY; RECOMBINANT ESCHERICHIA-COLI; CARBOHYDRATE
PHOSPHOTRANSFERASE SYSTEM; LIMITED CONTINUOUS-CULTURE; FED-BATCH
FERMENTATIONS; GLOBAL GENE-EXPRESSION; GROWTH-RATE; REGULATORY PROTEIN;
FLUX ANALYSIS; ENZYME-ACTIVITIES
AB Escherichia coli is the main bacterial producer of heterologous proteins. The current production strategies aim at growing the bacteria to high density in order to achieve high levels of desired proteins. The major obstacle for reaching high cell densities with high product titers is the tendency of the bacteria to accumulate acetate during the unrestricted growth on glucose. Moreover, the high demand for precursors and energy required for the biosynthesis of the heterologous protein causes the cells to readjust their anabolic and catabolic reactions which, most often, aggravate the acetate problem. Implementing fed-batch protocols and employing more robust strains, such as E. coli B instead of K, can reduce acetate formation. Another approach is to implement metabolic engineering to minimize acetate formation by: (a) turning off genes which directly lead to the formation of acetate, (b) introducing genes that channel the carbon flow away from acetate towards other pathways, and (c) by reducing the glucose uptake through deleting or replacing genes of the sugar uptake system. Results show that a more general approach that focuses on global regulators and/or gene sets, encoding multiple pathways will be required to construct a robust strain capable of efficiently executing the production of recombinant proteins at high growth rates without the formation of toxic byproducts such as acetic acid.
C1 [Shiloach, Joseph] NIH, Biotechnol Unit, NIDDK, Bethesda, MD 20892 USA.
[Rinas, Ursula] Helmholtz Ctr Infect Res, D-38124 Braunschweig, Germany.
RP Shiloach, J (reprint author), NIH, Biotechnol Unit, NIDDK, Bldg 14A,Room 173, Bethesda, MD 20892 USA.
EM ljs@helix.nih.gov; uri@helmholtz-hzi.de
NR 133
TC 11
Z9 11
U1 1
U2 11
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
BN 978-1-4020-9393-7
PY 2009
BP 377
EP 400
DI 10.1007/978-1-4020-9394-4_18
D2 10.1007/978-1-4020-9394-4
PG 24
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Microbiology
GA BKK54
UT WOS:000268388500018
ER
PT J
AU Slaughter, AJ
Yu, JN
Koehly, LM
AF Slaughter, Andrew J.
Yu, Janie
Koehly, Laura M.
BE Salas, E
Goodwin, GF
Burke, CS
TI Social Network Analysis: Understanding the Role of Context in Small
Groups and Organizations
SO TEAM EFFECTIVENESS IN COMPLEX ORGANIZATIONS: CROSS-DISCIPLINARY
PERSPECTIVES AND APPROACHES
SE SIOP Organizational Frontiers Series
LA English
DT Article; Book Chapter
ID DECISION DEVELOPMENT; LOGIT-MODELS; CENTRALITY; GRAPH; PERFORMANCE;
SEQUENCE; MATRIX; INDEX; TEAMS
C1 [Yu, Janie] Texas A&M Univ, College Stn, TX 77843 USA.
[Koehly, Laura M.] NHGRI, Social Network Methods Sect, Social & Behav Res Branch, NIH, Bethesda, MD USA.
RP Slaughter, AJ (reprint author), Texas A&M Univ, College Stn, TX 77843 USA.
NR 61
TC 2
Z9 2
U1 1
U2 2
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH ROAD, HOVE BN3 2FA, E SUSSEX, ENGLAND
BN 978-0-8058-5881-5
J9 SIOP ORGAN FRONT SER
PY 2009
BP 433
EP 459
PG 27
WC Psychology, Applied; Management
SC Psychology; Business & Economics
GA BUY94
UT WOS:000290753500018
ER
PT J
AU Ivanova, EV
Bogatyreva, ZI
Isayeva, MA
Suchkova, EN
Baisugurov, MA
Andreyeva, AV
Korotkova, AA
Notkins, A
Paltsev, MA
Suchkov, SV
AF Ivanova, E. V.
Bogatyreva, Z. I.
Isayeva, M. A.
Suchkova, E. N.
Baisugurov, M. A.
Andreyeva, A. V.
Korotkova, A. A.
Notkins, A.
Paltsev, M. A.
Suchkov, S. V.
TI ANTITHYROID ANTIBODIES OF VARYING SPECIFICITY IN THE PATHOGENESIS AND
DIAGNOSIS OF AUTOIMMUNE THYROID DISEASES
SO TERAPEVTICHESKII ARKHIV
LA Russian
DT Article
DE antithyroid autoantibodies (autoAB); specificity of autoAB; anti-TG
autoAB; anti-TPO autoAB; anti-TGPO autoAB
ID AUTOANTIBODIES; THYROGLOBULIN; PEROXIDASE; CYTOTOXICITY; HORMONES;
GRAVES; HEALTH; ASSAY
AB Aim. To compare the possible pathogenetic and clinicodiagnostic value of antithyroid autoantibodies (autoAB) different in specificity, such as monospecific ones to thyroglobulin and thyroid peroxidase (anti-TG and anti-TPO autoAB) and bispecific ones to thyroglobulin and thyroid peroxidase simultaneously (anti-TGPO autoAB), in patients with autoimmune thyroid diseases.
Materials and methods. ne sera from 240 patients with autoimmune thyroiditis (AIT) and from 124 with diffuse toxic goiter (DTG) were examined. The sera from 40 healthy donors served as a control. The sera were screened for anti-TG and anti-TPO autoAB, anti-TGPO autoAB, by employing enzyme immunoassay and/or radioimmunoassay. The results were statistically processed using the variation statistics-based programs.
Results. The specific features of an autoantigenic component to thyroid tissues were found in the sera of patients with AIT and DTG. An association was established between the progression of disease and the phasic change of autoAB populations or their combinations.
Conclusion. The procedure for evaluating seropositivity for antithyroid autoAB, which is referred to as non-invasive studies, can be considered as a criterion test in the diagnosis and prediction of the course of AIT and DTG.
C1 [Ivanova, E. V.; Bogatyreva, Z. I.; Andreyeva, A. V.] City Clin Hosp Eighty One, Unit Endocrinol, Moscow, Russia.
[Korotkova, A. A.; Paltsev, M. A.; Suchkov, S. V.] IM Sechenov Moscow Med Acad, Moscow, Russia.
[Isayeva, M. A.] MedStyle Effect Med Ctr, Dept Endocrinol, Moscow, Russia.
[Suchkova, E. N.; Baisugurov, M. A.] AV Lunacharsky Astrakhan State Med Acad, Clin Endocrinol, Astrakhan, Russia.
[Notkins, A.] Natl Inst Maxillofacial Surg, Immunol Lab, NIH, Bethesda, MD USA.
RP Ivanova, EV (reprint author), City Clin Hosp Eighty One, Unit Endocrinol, Moscow, Russia.
EM iva0577@mail.ru; isaeva_marina@bk.ru; _1410_@rambler.ru;
fleur@andyone.in; anotkins@mail.nih.gov; stepanova@mmascience.ru;
ssuchkov@online.ru
NR 23
TC 0
Z9 0
U1 0
U2 1
PU IZDATELSTVO MEDITSINA
PI MOSCOW
PA PETROVERIGSKII PER 6-8, K-142 MOSCOW, RUSSIA
SN 0040-3660
J9 TERAPEVT ARKH
JI Ter. Arkhiv
PY 2009
VL 81
IS 10
BP 39
EP 45
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 531EN
UT WOS:000272646400007
PM 19947439
ER
PT J
AU Lenfant, C
AF Lenfant, Claude
TI CONTROLLING BLOOD PRESSURE: HOW WELL ARE WE DOING?
SO TERAPEVTICHESKII ARKHIV
LA Russian
DT Article
DE review; arterial pressure; prevalence; treatment
ID CORONARY-HEART-DISEASE; CLINICAL-PRACTICE; GLOBAL BURDEN; PRIMARY-CARE;
HYPERTENSION; MANAGEMENT; GUIDELINES; SOCIETY; IMPROVEMENT; POPULATION
AB The author analyses global prevalence of arterial pressure and its impact on population mortality and disability, draws attention to insufficient efficacy of this disease treatment, low awareness of the population about this disease and compliance of the patients. To achieve target arterial pressure, cooperation is necessary between the physician and the patient.
C1 NHLBI, NIH, Vancouver, WA USA.
RP Lenfant, C (reprint author), NHLBI, NIH, Vancouver, WA USA.
EM lenfantc@prodigy.net
NR 28
TC 0
Z9 0
U1 1
U2 1
PU IZDATELSTVO MEDITSINA
PI MOSCOW
PA PETROVERIGSKII PER 6-8, K-142 MOSCOW, RUSSIA
SN 0040-3660
J9 TERAPEVT ARKH
JI Ter. Arkhiv
PY 2009
VL 81
IS 5
BP 47
EP +
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 462NP
UT WOS:000267361100008
PM 19537586
ER
PT S
AU Chaudret, R
Ulmer, S
van Severen, MC
Gresh, N
Parisel, O
Cisneros, GA
Darden, TA
Piquemal, JP
AF Chaudret, R.
Ulmer, S.
van Severen, M. C.
Gresh, N.
Parisel, O.
Cisneros, G. A.
Darden, T. A.
Piquemal, J. -P
BE Wei, DQ
Wang, XJ
TI Progress Towards Accurate Molecular Modeling of Metal Complexes Using
Polarizable Force Fields
SO THEORY AND APPLICATIONS OF COMPUTATIONAL CHEMISTRY - 2008
SE AIP Conference Proceedings
LA English
DT Proceedings Paper
CT Conference on Theory and Applications of Computational Chemistry
CY SEP 23-27, 2008
CL Shanghai, PEOPLES R CHINA
SP Shanghai Jiao Tong Univ, Int Assoc Scientists Interdisciplinary Areas, Natl Sci Fdn China, Res Councils UK, Chinese Chem Soc, Canadian Hongcam Int Trade Corp, Tri Biotech, Shanghai Ctr Bioinformat Technol, KC Wong Educ Fdn, Interdisciplinary Sci, Computat Life Sci, Mol Simulat, Chem Phys & Biophys Chem, Acta Physico Chem Sinica, Journal Mol Graph & Modelling
DE metals; cations; molecular mechanics; density fitting; multiscale
approaches
ID INTERMOLECULAR INTERACTION ENERGY; CHARGE-TRANSFER CONTRIBUTION;
MECHANICS
AB We present refinements of the SIBFA (Sum of Interaction Between Fragments ab initio) and GEM (Gaussian electrostatic Model) polarizable molecular mechanics procedure to represent the intermolecular interaction energies of metal cations. Improved forces fields for closed-shell, open-shell and heavy metals are discussed. Some perspectives towards a multiscale SIBFA-GEM approach using density fitting techniques are presented.
C1 [Chaudret, R.; Ulmer, S.; van Severen, M. C.; Parisel, O.; Piquemal, J. -P] Univ Paris 06, UPMC, Chim Theor Lab, UMR 7616, Case Courrier 137,4 Pl Jussieu, F-75005 Paris, France.
[Chaudret, R.; Ulmer, S.; van Severen, M. C.; Parisel, O.; Piquemal, J. -P] CNRS, Chim Theor Lab, UMR 7616, F-75005 Paris, France.
[Gresh, N.] Univ Paris 05, UFR Biomed, Lab Pharmcochim Mol & Cellularie, U648 INSERM, F-75006 Paris, France.
[Cisneros, G. A.; Darden, T. A.] NIEHS, Lab Struct Biol, Res Triangle Pk, NC 27709 USA.
RP Chaudret, R (reprint author), Univ Paris 06, UPMC, Chim Theor Lab, UMR 7616, Case Courrier 137,4 Pl Jussieu, F-75005 Paris, France.
RI Chaudret, Robin/C-3431-2009; Van Severen, Marie-Celine/C-3514-2009;
vanseveren, marie-celine/D-2588-2009; Piquemal, Jean-Philip/B-9901-2009;
Chaudret, Robin/D-6950-2012
OI Piquemal, Jean-Philip/0000-0001-6615-9426;
FU French ANR (project Lasihmodo); CNRS (France); Ligue Nationale contre le
Cancer (Comite Ile-de-France); Intramural Research Program of the NIH;
NIEHS (USA)
FX This research was supported in part by the French ANR (project
Lasihmodo), CNRS (France), the Ligue Nationale contre le Cancer (Comite
Ile-de-France) and by the Intramural Research Program of the NIH and
NIEHS (USA).
NR 25
TC 6
Z9 6
U1 0
U2 3
PU AMER INST PHYSICS
PI MELVILLE
PA 2 HUNTINGTON QUADRANGLE, STE 1NO1, MELVILLE, NY 11747-4501 USA
SN 0094-243X
BN 978-0-7354-0637-7
J9 AIP CONF PROC
PY 2009
VL 1102
BP 185
EP +
PG 2
WC Chemistry, Multidisciplinary; Mathematical & Computational Biology;
Physics, Applied
SC Chemistry; Mathematical & Computational Biology; Physics
GA BJE20
UT WOS:000265089800015
ER
PT J
AU Nie, ZG
Zorrilla, EP
Madamba, SG
Rice, KC
Roberto, M
Siggins, GR
AF Nie, Zhiguo
Zorrilla, Eric P.
Madamba, Samuel G.
Rice, Kenner C.
Roberto, Marisa
Siggins, George Robert
TI Presynaptic CRF1 Receptors Mediate the Ethanol Enhancement of GABAergic
Transmission in the Mouse Central Amygdala
SO THESCIENTIFICWORLDJOURNAL
LA English
DT Article
DE electrophysiology; alcohol; gamma aminobutyric acid;
corticotrophin-releasing factor; corticotropin-releasing hormone; CRH;
urocortin; stresscopin; whole-cell patch; IPSC
ID CORTICOTROPIN-RELEASING-FACTOR; ANXIETY-LIKE BEHAVIOR; FACTOR-LIKE
IMMUNOREACTIVITY; IMPAIRED STRESS-RESPONSE; CENTRAL-NERVOUS-SYSTEM;
DEPENDENT RATS; MONOAMINERGIC AFFERENTS; CENTRAL NUCLEUS;
DRUG-ADDICTION; HIGH-AFFINITY
AB Corticotropin-releasing factor (CRF) is a 41-amino-acid neuropeptide involved in stress responses initiated from several brain areas, including the amygdala formation. Research shows a strong relationship between stress, brain CRF, and excessive alcohol consumption. Behavioral studies suggest that the central amygdala (CeA) is significantly involved in alcohol reward and dependence. We recently reported that the ethanol augmentation of GABAergic synaptic transmission in rat CeA involves CRF1 receptors, because both CRF and ethanol significantly enhanced the amplitude of evoked GABAergic inhibitory postsynaptic currents (IPSCs) in CeA neurons from wild-type (WT) and CRF2 knockout (KO) mice, but not in neurons of CRF1 KO mice. The present study extends these findings using selective CRF receptor ligands, gene KO models, and miniature IPSC (mIPSC) analysis to assess further a presynaptic role for the CRF receptors in mediating ethanol effects in the CeA. In whole-cell patch recordings of pharmacologically isolated GABA(A)ergic IPSCs from slices of mouse CeA, both CRF and ethanol augmented evoked IPSCs in a concentration-dependent manner, with low EC(50)s. A CRF1 (but not CRF2) KO construct and the CRF1-selective nonpeptide antagonist NIH-3 (LWH-63) blocked the augmenting effect of both CRF and ethanol on evoked IPSCs. Furthermore, the new selective CRF1 agonist stressin(1), but not the CRF2 agonist urocortin 3, also increased evoked IPSC amplitudes. Both CRF and ethanol decreased paired-pulse facilitation (PPF) of evoked IPSCs and significantly enhanced the frequency, but not the amplitude, of spontaneous miniature GABAergic mIPSCs in CeA neurons of WT mice, suggesting a presynaptic site of action. The PPF effect of ethanol was abolished in CeA neurons of CRF1 KO mice. The CRF1 antagonist NIH-3 blocked the CRF- and ethanol-induced enhancement of mIPSC frequency in CeA neurons. These data indicate that presynaptic CRF1 receptors play a critical role in permitting or mediating ethanol enhancement of GABAergic synaptic transmission in CeA, via increased vesicular GABA release, and thus may be a rational target for the treatment of alcohol abuse and alcoholism.
C1 [Madamba, Samuel G.; Siggins, George Robert] Scripps Res Inst, Dept Mol & Integrat Neurosci, La Jolla, CA 92037 USA.
[Madamba, Samuel G.; Siggins, George Robert] Scripps Res Inst, Alcohol Res Ctr, La Jolla, CA 92037 USA.
[Nie, Zhiguo] Burnham Inst Med Res, La Jolla, CA USA.
[Zorrilla, Eric P.; Roberto, Marisa] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, NIH, Bethesda, MD USA.
RP Siggins, GR (reprint author), Scripps Res Inst, Dept Mol & Integrat Neurosci, La Jolla, CA 92037 USA.
EM geobob@scripps.edu
FU (Novartis Pharma) [CGP-55845A]; NIH [U01-AA10994]; NIAAA [AA06420,
DA03665, NS38633]; National Institute on Drug Abuse; National Institute
of Alcohol Abuse and Alcoholism; National Institute of Diabetes and
Digestive and Kidney Diseases
FX We thank Drs. G. Koob, P. Schweitzer, and S. Moore for helpful comments;
T. Acosta for technical support; Drs. J. Rivier and W. Vale (Salk
Institute) for the gift of stressin1 and Ucn 3; Drs. K.-F.
Lee and W. Vale (Salk Institute) for the receptor null mice; and Drs. W.
Frstl and A. Suter (Novartis Pharma) for the gift of CGP-55845A. This
work was supported by NIH grants U01-AA10994 (under the INIA Consortium
of the NIAAA), AA06420, DA03665, and NS38633. This work also was
partially supported by the NIH Intramural Research Programs of the
National Institute on Drug Abuse, the National Institute of Alcohol
Abuse and Alcoholism, and the National Institute of Diabetes and
Digestive and Kidney Diseases.
NR 64
TC 27
Z9 27
U1 0
U2 4
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1537-744X
J9 THESCIENTIFICWORLDJO
JI TheScientificWorldJOURNAL
PY 2009
VL 9
BP 68
EP 85
DI 10.1100/tsw.2009.1
PG 18
WC Environmental Sciences; Multidisciplinary Sciences
SC Environmental Sciences & Ecology; Science & Technology - Other Topics
GA 395RW
UT WOS:000262542200009
PM 19151899
ER
PT J
AU Quiroz, C
Lujan, R
Uchigashima, M
Simoes, AP
Lerner, TN
Borycz, J
Kachroo, A
Canas, PM
Orru, M
Schwarzschild, MA
Rosin, DL
Kreitzer, AC
Cunha, RA
Watanabe, M
Ferre, S
AF Quiroz, Cesar
Lujan, Rafael
Uchigashima, Motokazu
Simoes, Ana Patricia
Lerner, Talia N.
Borycz, Janusz
Kachroo, Anil
Canas, Paula M.
Orru, Marco
Schwarzschild, Michael A.
Rosin, Diane L.
Kreitzer, Anatol C.
Cunha, Rodrigo A.
Watanabe, Masahiko
Ferre, Sergi
TI Key Modulatory Role of Presynaptic Adenosine A(2A) Receptors in Cortical
Neurotransmission to the Striatal Direct Pathway
SO THESCIENTIFICWORLDJOURNAL
LA English
DT Article
DE adenosine A(2A) receptor; striatum; basal ganglia; medium spiny neuron;
glutamatergic neurotransmission; presynaptic receptors
ID CENTRAL-NERVOUS-SYSTEM; MEDIUM SPINY NEURONS; LONG-TERM POTENTIATION;
BASAL GANGLIA; NUCLEUS-ACCUMBENS; DOPAMINE RELEASE; RAT STRIATUM;
ULTRASTRUCTURAL-LOCALIZATION; PARKINSONS-DISEASE; DORSAL STRIATUM
AB Basal ganglia processing results from a balanced activation of direct and indirect striatal efferent pathways, which are controlled by dopamine D-1 and D-2 receptors, respectively. Adenosine A(2A) receptors are considered novel antiparkinsonian targets, based on their selective postsynaptic localization in the indirect pathway, where they modulate D-2 receptor function. The present study provides evidence for the existence of an additional, functionally significant, segregation of A(2A) receptors at the presynaptic level. Using integrated anatomical, electrophysiological, and biochemical approaches, we demonstrate that presynaptic A(2A) receptors are preferentially localized in cortical glutamatergic terminals that contact striatal neurons of the direct pathway, where they exert a selective modulation of corticostriatal neurotransmission. Presynaptic striatal A(2A) receptors could provide a new target for the treatment of neuropsychiatric disorders.
C1 [Quiroz, Cesar; Borycz, Janusz; Orru, Marco; Ferre, Sergi] Natl Inst Drug Abuse, IRP, NIH, DHHS, Baltimore, MD USA.
[Lujan, Rafael] Univ Castilla La Mancha, Fac Med, Dept Ciencias Med, Albacete, Spain.
[Uchigashima, Motokazu] Hokkaido Univ, Sch Med, Dept Anat, Sapporo, Hokkaido 060, Japan.
[Simoes, Ana Patricia; Canas, Paula M.; Cunha, Rodrigo A.] Univ Coimbra, Inst Biochem, Fac Med, CNC, Coimbra, Portugal.
[Lerner, Talia N.; Kreitzer, Anatol C.] Univ Calif San Francisco, Gladstone Inst Neurol Dis, San Francisco, CA 94143 USA.
[Lerner, Talia N.; Kreitzer, Anatol C.] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA.
[Kachroo, Anil; Schwarzschild, Michael A.] MassGen Inst Neurodegenerat Dis, Dept Neurol, Charlestown, MA USA.
[Rosin, Diane L.] Univ Virginia, Hlth Sci Ctr, Dept Pharmacol, Charlottesville, VA 22908 USA.
RP Ferre, S (reprint author), Natl Inst Drug Abuse, IRP, NIH, DHHS, Baltimore, MD USA.
EM sferre@intra.nida.nih.gov
RI WATANABE, Masahiko/A-4055-2012; Uchigashima, Motokazu/C-5715-2012;
Ferre, Sergi/K-6115-2014; Canas, Paula/Q-2101-2015; Cunha,
Rodrigo/E-7475-2015;
OI Ferre, Sergi/0000-0002-1747-1779; Canas, Paula/0000-0002-4091-6406;
Cunha, Rodrigo/0000-0003-2550-6422; Simoes, Ana
Patricia/0000-0003-2937-7015
FU National Institute on Drug Abuse; CHDI Foundation; Consejeria de
Educacion y Ciencia de la Junta de Comunidades de Castilla-La Mancha
[PAI08-0174-6967]; Fundacao para a Ciencia e Tecnologia
[FCT-PTDC/SAU-NEU/81064/2006]; National Institutes of Health [RO1
NS054978]
FX The authors would like to thank Mrs. Mar a Jose Cabanero for the
excellent technical assistance and Dr. Robert H. Edwards, UCSF, San
Francisco, for kindly providing the vGluT1 receptor antibody. Work
supported by the intramural funds of the National Institute on Drug
Abuse, CHDI Foundation, the "Consejeria de Educacion y Ciencia de la
Junta de Comunidades de Castilla-La Mancha" (PAI08-0174-6967) to RL,
Fundacao para a Ciencia e Tecnologia (FCT-PTDC/SAU-NEU/81064/2006) to
RAC, National Institutes of Health RO1 NS054978.
NR 55
TC 45
Z9 45
U1 0
U2 6
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1537-744X
J9 THESCIENTIFICWORLDJO
JI TheScientificWorldJOURNAL
PY 2009
VL 9
BP 1321
EP 1344
DI 10.1100/tsw.2009.143
PG 24
WC Environmental Sciences; Multidisciplinary Sciences
SC Environmental Sciences & Ecology; Science & Technology - Other Topics
GA 544SJ
UT WOS:000273679300059
PM 19936569
ER
PT S
AU Smirnov, AV
Combs, CA
Balaban, RS
Tang, K
Knutson, JR
AF Smirnov, Aleksandr V.
Combs, Christian A.
Balaban, Robert S.
Tang, Kevin
Knutson, Jay R.
BE Conchello, JA
Cogswell, CJ
Wilson, T
TI A hybrid global fitting algorithm for decay-associated images from
fluorescence lifetime image microscopy data
SO THREE-DIMENSIONAL AND MULTIDIMENSIONAL MICROSCOPY: IMAGE ACQUISITION AND
PROCESSING XVI
SE Proceedings of SPIE-The International Society for Optical Engineering
LA English
DT Proceedings Paper
CT Conference on Three-Dimensional and Multidimensional Microscopy - Image
Acquisition and Processing XVI
CY JAN 26-29, 2009
CL San Jose, CA
SP SPIE
DE deconvolution; global fitting; FLIM; DAS; DAI; NADH; free-to-bound ratio
ID ANISOTROPY; SPECTRA; NADH
AB Fluorescence lifetime imaging microscopy ("FLIM") is a technique for measuring fluorescence lifetime(s) at each pixel of a microscope image. Imaging of fluorescence lifetimes enables biochemical reactions to be followed at each microscopically resolvable location within the cell. FLIM has thus become very useful for biomedical tissue imaging. Global analysis [1] is a method of recovering fluorescence decay parameters from either time-resolved emission spectra to yield Decay-Associated Spectra [2], or equivalently, from FLIM datasets to yield Decay-Associated Images ("DAI"). Global analysis enables a sensitive and non-invasive probe of metabolic state of intracellular molecules such as NADH. Using linkage information, such as the spatial invariance of the lifetime of each fluorescent species in the image, global analysis can recover lifetimes and amplitudes more accurately than traditional pixel-by-pixel analysis. Here, we explain a method to analyze FLIM data so that more accurate lifetimes and DAIs can be computed in a reasonable time. This approach involves coupling an iterative global analysis with linear algebraic operations.
C1 [Smirnov, Aleksandr V.; Combs, Christian A.; Balaban, Robert S.; Knutson, Jay R.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Smirnov, AV (reprint author), NHLBI, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU SPIE-INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA
SN 0277-786X
BN 978-0-8194-7430-8
J9 P SOC PHOTO-OPT INS
PY 2009
VL 7184
AR 71841D
DI 10.1117/12.809844
PG 6
WC Microscopy; Optics; Imaging Science & Photographic Technology
SC Microscopy; Optics; Imaging Science & Photographic Technology
GA BSL65
UT WOS:000284868100023
ER
PT B
AU Shields, AE
Fullerton, SM
Olden, K
AF Shields, Alexandra E.
Fullerton, Stephanie M.
Olden, Kenneth
BE Koh, HK
TI Genes, Environment, and Cancer Disparities
SO TOWARD THE ELIMINATION OF CANCER DISPARITIES: CLINICAL AND PUBLIC HEALTH
PERSPECTIVES
LA English
DT Article; Book Chapter
ID MICROSOMAL EPOXIDE HYDROLASE; NONPOLYPOSIS COLORECTAL-CANCER; CUMULATIVE
CIGARETTE-SMOKING; GENOME-WIDE ASSOCIATION; DNA-REPAIR GENES;
S-TRANSFERASE M1; BREAST-CANCER; LUNG-CANCER; HEALTH DISPARITIES;
PROSTATE-CANCER
C1 [Shields, Alexandra E.] Harvard MGH Ctr Genom Vulnerable Populat & Hlth D, Boston, MA 02115 USA.
[Fullerton, Stephanie M.] Univ Washington, Dept Med Hist & Eth, Seattle, WA 98195 USA.
[Fullerton, Stephanie M.] Univ Washington, Ctr Genom & Healthcare Equal, Seattle, WA 98195 USA.
[Olden, Kenneth] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Shields, Alexandra E.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Shields, Alexandra E.] Massachusetts Gen Hosp Partners HealthCare, Inst Hlth Policy, Boston, MA USA.
RP Shields, AE (reprint author), Harvard MGH Ctr Genom Vulnerable Populat & Hlth D, Boston, MA 02115 USA.
OI Fullerton, Stephanie/0000-0002-0938-6048
NR 116
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-0-387-89442-3
PY 2009
BP 49
EP 82
DI 10.1007/978-0-387-89443-0_3
D2 10.1007/978-0-387-89443-0
PG 34
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA BKN85
UT WOS:000268727300003
ER
PT J
AU Renne, R
Brix, A
Harkema, J
Herbert, R
Kittel, B
Lewis, D
March, T
Nagano, K
Pino, M
Rittinghausen, S
Rosenbruch, M
Tellier, P
Wohrmann, T
AF Renne, Roger
Brix, Amy
Harkema, Jack
Herbert, Ron
Kittel, Birgit
Lewis, David
March, Thomas
Nagano, Kasuke
Pino, Michael
Rittinghausen, Susanne
Rosenbruch, Martin
Tellier, Pierre
Wohrmann, Thomas
TI Proliferative and Nonproliferative Lesions of the Rat and Mouse
Respiratory Tract
SO TOXICOLOGIC PATHOLOGY
LA English
DT Review
DE respiratory system; lesions of the rat respiratory system; lesions of
the mouse respiratory system
ID GENE-RELATED PEPTIDE; SPRAGUE-DAWLEY RATS; FISCHER 344 RATS;
BETA-OXIDIZED DIPROPYLNITROSAMINE; CYTOKERATIN EXPRESSION PATTERNS;
TOBACCO-SPECIFIC NITROSAMINE; TITANIUM-DIOXIDE PARTICLES; LONG-TERM
INHALATION; NASAL CAVITY TUMORS; CLARA CELL ADENOMAS
AB The INHAND Project (International Harmonization of and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of the Societies of Toxicologic Pathology from Europe (ESTP). Great Britain (BSTP). Japan (JSPT) and North America (STP) to develop an internationally-accepted nomenclature for proliferative and non-proliferative lesions in laboratory animals. The purpose of this publication is to provide a standardized nomenclature for classifying microscopic lesions observed in the respiratory tract of laboratory rats and mice, with color photomicrographs illustrating examples of some lesions. The standardized nomenclature presented in this document is also available electronically on the internet (http.//www gorem org/) Sources of material included histopathology databases from government, academia, and industrial laboratories throughout the world. Content includes spontaneous developmental and aging lesions as well as lesions induced by exposure to test materials. A widely accepted and utilized international harmonization of nomenclature for respiratory tract lesions in laboratory animals will decrease confusion among regulatory and scientific research organizations in different countries and provide a common language to increase and enrich international exchanges of information among toxicologists and pathologists.
C1 [Renne, Roger] Roger Renne ToxPath Consulting, Sumner, WA USA.
[Brix, Amy] Expt Pathol Labs, Res Triangle Pk, NC USA.
[Harkema, Jack] Michigan State Univ, Coll Vet Med, E Lansing, MI 48824 USA.
[Herbert, Ron] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Kittel, Birgit] Novartis Inst BioMed Res, Basel, Switzerland.
[Lewis, David] GlaxoSmithKline Inc, Ware, Herts, England.
[March, Thomas] Lovelace Resp Res Inst, Albuquerque, NM USA.
[Nagano, Kasuke] Japan Ind Safety & Hlth Assoc, Japan Bioassay Res Ctr, Kanagawa, Japan.
[Pino, Michael] Sanofi Aventis, Bridgewater, NJ USA.
[Rittinghausen, Susanne] Fraunhofer Inst Toxicol & Expt Med, Hannover, Germany.
[Rosenbruch, Martin] Bayer Schering Pharma AG, Wuppertal, Germany.
[Tellier, Pierre] Charles River Labs, Montreal, PQ, Canada.
[Wohrmann, Thomas] Nycomed GmbH, Inst Pharmacol & Preclin Drug Safety Haidkrugsweg, Barsbuttel, Germany.
RP Renne, R (reprint author), Roger Renne ToxPath Consulting, Sumner, WA USA.
NR 275
TC 52
Z9 54
U1 1
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PY 2009
VL 37
IS 7
BP 5S
EP 73S
DI 10.1177/0192623309353423
PG 69
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 529YS
UT WOS:000272556100001
PM 20032296
ER
PT J
AU Wang, NN
Symons, JD
Zhang, H
Jia, ZJ
Gonzalez, FJ
Yang, TX
AF Wang, Ningning
Symons, J. David
Zhang, Hui
Jia, Zhanjun
Gonzalez, Frank J.
Yang, Tianxin
TI Distinct Functions of Vascular Endothelial and Smooth Muscle PPAR gamma
in Regulation of Blood Pressure and Vascular Tone
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE PPAR gamma; rosiglitazone; endothelial cells; smooth muscle cells; blood
pressure
ID ACTIVATED-RECEPTOR-GAMMA; CELL-GROWTH; INSULIN-RESISTANCE;
GENE-EXPRESSION; DEFICIENT MICE; C57BL/6J MICE; THIAZOLIDINEDIONES;
HYPERTENSION; DELETION; OBESITY
AB Thiazolidinediones (TZDs) are peroxisome proliferators-activated receptor gamma ( PPAR.) activators that exhibit antihypertensive and vasculo-protective effects. Here we describe the use of Tie2Cre/flox and SM22Cre/flox mice, which respectively lacked PPAR gamma in the endothelium and the smooth muscle, to study vascular function of PPAR gamma. Rosiglitazone (RGZ) induced a similar blood pressure (BP)-lowering effect in deoxycorticosterone acetate ( DOCA) salt-treated PPAR gamma(f/f) and SM22Cre/flox mice, whereas Tie2Cre/flox mice were completely resistant to this effect. The femoral arteries lacking endothelial PPAR gamma exhibited increased reactivity to various vasoconstrictors without a significant alteration in acetylcholine-induced relaxation. In sharp contrast, the vasculature lacking smooth muscle PPAR gamma had blunted sensitivity to alpha 1-adrenergic agents but enhanced sensitivity to acetylcholine. Our results demonstrated endothelium but not smooth muscle as the site for TZD-induced BP-lowering effect and also uncovered distinct functions of endothelial and smooth muscle PPAR gamma in regulation of vascular tone.
C1 [Wang, Ningning; Zhang, Hui; Jia, Zhanjun; Yang, Tianxin] Univ Utah, Dept Internal Med, Salt Lake City, UT 84132 USA.
[Wang, Ningning; Zhang, Hui; Jia, Zhanjun; Yang, Tianxin] Salt Lake Vet Affairs Med Ctr, Salt Lake City, UT USA.
[Symons, J. David] Univ Utah, Coll Hlth, Salt Lake City, UT 84132 USA.
[Symons, J. David] Univ Utah, Div Endocrinol Diabet & Metab, Salt Lake City, UT 84132 USA.
[Gonzalez, Frank J.] NCI, NIH, Bethesda, MD 20892 USA.
RP Yang, TX (reprint author), Univ Utah, Dept Internal Med, 30 N 1900 E,Rm 4R312, Salt Lake City, UT 84132 USA.
EM Tianxin.Yang@hsc.utah.edu
FU Merit Review from the Department of Veterans Affairs [RO-1 HL079453];
National Institute of Health
FX This work was supported by Merit Review from the Department of Veterans
Affairs as well as RO-1 HL079453 from National Institute of Health ( to
T. Yang).
NR 37
TC 17
Z9 18
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD JAN
PY 2009
VL 37
IS 1
BP 21
EP 27
DI 10.1177/0192623308328545
PG 7
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 463XE
UT WOS:000267466500004
PM 19075043
ER
PT J
AU Singh, BP
Nyska, A
Johansson, SL
Malarkey, DE
Hooth, MJ
AF Singh, B. P.
Nyska, A.
Johansson, S. L.
Malarkey, D. E.
Hooth, M. J.
TI Urethral Transitional Carcinoma and Hyperplasia in Male B6c3f1 Mice
Treated with Tetrachloroazobenzene (TCAB)
SO TOXICOLOGIC PATHOLOGY
LA English
DT Meeting Abstract
C1 [Singh, B. P.; Malarkey, D. E.; Hooth, M. J.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Johansson, S. L.] Univ Nebraska Med Ctr, Eppley Canc Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD JAN
PY 2009
VL 37
IS 1
MA P10
BP 126
EP 126
PG 1
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 463XE
UT WOS:000267466500024
ER
PT J
AU Ramot, Y
Nyska, A
Lieuallen, W
Maly, A
Zlotogorski, A
Flake, G
Kissling, G
Brix, A
Malarkey, D
Hooth, M
AF Ramot, Yuval
Nyska, Abraham
Lieuallen, Warren
Maly, Alex
Zlotogorski, Abraham
Flake, Gordon
Kissling, Grace
Brix, Amy
Malarkey, David
Hooth, Michelle
TI Inflammatory and Chloracne-Like Skin Lesions in B6C3F1 Mice Exposed to
Tetrachloroazobenzene (TCAB) for Two Years
SO TOXICOLOGIC PATHOLOGY
LA English
DT Meeting Abstract
C1 [Ramot, Yuval; Maly, Alex; Zlotogorski, Abraham] Hadassah Hebrew Univ, Med Ctr, Jerusalem, Israel.
[Nyska, Abraham] Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
[Lieuallen, Warren] Pathol Associates Inc, Charles River Labs, Durham, NC USA.
[Flake, Gordon; Brix, Amy; Malarkey, David] Natl Inst Environm Hlth Sci, Lab Expt Pathol, Res Triangle Pk, NC USA.
[Kissling, Grace] Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC USA.
[Hooth, Michelle] Natl Inst Environm Hlth Sci, Toxicol Operat Branch, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD JAN
PY 2009
VL 37
IS 1
MA P44
BP 137
EP 137
PG 1
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 463XE
UT WOS:000267466500058
ER
PT J
AU Brin, YS
Nyska, M
Mizrahi, B
Golenser, J
Maoz, G
Domb, AJ
Peddada, S
Nyska, A
AF Brin, Yaron S.
Nyska, Meir
Mizrahi, Boaz
Golenser, Jacob
Maoz, Guy
Domb, Avi J.
Peddada, Shyamal
Nyska, Abraham
TI Treatment of Osteomyelitis in Rats by Injection of Degradable
Polymer-Releasing Gentamicin
SO TOXICOLOGIC PATHOLOGY
LA English
DT Meeting Abstract
C1 [Brin, Yaron S.; Nyska, Meir; Maoz, Guy] Meir Med Ctr, Dept Orthopaed Surg, Kefar Sava, Israel.
[Mizrahi, Boaz; Domb, Avi J.] Hebrew Univ Jerusalem, Sch Pharm, Dept Med Chem & Nat Prod, IL-91120 Jerusalem, Israel.
[Golenser, Jacob] Hebrew Univ Jerusalem, Kuvin Ctr Study Infect & Trop Dis, Dept Parasitol, IL-91120 Jerusalem, Israel.
[Peddada, Shyamal] NIEHS, Biostat Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
[Nyska, Abraham] Tel Aviv Univ, Israel Sackler Sch Med, IL-69978 Tel Aviv, Israel.
RI Peddada, Shyamal/D-1278-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD JAN
PY 2009
VL 37
IS 1
MA P63
BP 142
EP 143
PG 2
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 463XE
UT WOS:000267466500076
ER
PT J
AU Kissling, GE
Malarkey, DE
Vallant, MK
Johnson, JD
Hejtmancik, MR
Herbert, RA
Boorman, GA
AF Kissling, Grace E.
Malarkey, David E.
Vallant, Molly K.
Johnson, Jerry D.
Hejtmancik, Milton R.
Herbert, Ronald A.
Boorman, Gary A.
TI Evaluation of Dichloroacetic Acid for Carcinogenicity in Genetically
Modified Tg.AC Hemizygous and p53 Haploinsufficient Mice
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
ID TRANSGENIC MOUSE MODELS; LIVER-TUMOR INDUCTION; MALE B6C3F(1) MOUSE;
DRINKING-WATER; DOSE-RESPONSE; TRICHLOROACETIC-ACID;
HEPATOCARCINOGENICITY; TRICHLOROETHYLENE; EXPRESSION; BIOASSAYS
AB There has been considerable interest in the use of genetically modified mice for detecting potential environmental carcinogens. For this reason, the National Toxicology Program has been evaluating Tg.AC hemizygous and p53 haploinsufficient mice as models to detect potential carcinogens. It was reasoned that these mouse models might also prove more effective than standard rodent models in evaluating the numerous disinfection byproducts that are found in low concentrations in drinking water. Dichloroacetic acid (DCA) is one of the most frequently found disinfection byproducts and DCA has been consistently shown to cause hepatocellular tumors in rats and mice in standard rodent studies. Tg.AC hemizygous and p53 haploinsufficient mice were exposed in the drinking water to DCA for up to 41 weeks. In a second study Tg.AC mice were subjected to dermal DCA exposure for up to 39 weeks. Increased incidences and severity of cytoplasmic vacuolization of hepatocytes were seen in the p53 mice, but there was no evidence of carcinogenic activity at exposures of up to 2000 mg/l in the drinking water. Increased incidences and severity of cytoplasmic vacuolization of hepatocytes were seen in the drinking water study with Tg.AC mice and a modest non-dose-related increase in pulmonary adenomas was observed in males exposed to 1000 mg/l in the drinking water. Dermal exposure up to 500 mg/kg for 39 weeks resulted in increased dermal papillomas at the site of application in Tg.AC mice. No significant increase in papillomas under the same study conditions was seen in the 26-week study. For DCA under these study conditions, the p53 and Tg.AC mice appear less sensitive to hepatocarcinogenesis than standard rodent models. These results suggest caution for the use of Tg.AC and p53 mice to screen unknown chemicals in drinking water for potential carcinogenicity.
C1 [Kissling, Grace E.] NIEHS, Environm Dis & Med Program, Res Triangle Pk, NC 27709 USA.
[Malarkey, David E.; Vallant, Molly K.; Herbert, Ronald A.; Boorman, Gary A.] NIEHS, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Johnson, Jerry D.; Hejtmancik, Milton R.] Battelle Columbus Operat, Hlth Div, Columbus, OH 43201 USA.
RP Kissling, GE (reprint author), NIEHS, Environm Dis & Med Program, MD A3-03,POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM kissling@niehs.nih.gov
FU National Institutes of Health; National Institute of Environmental
Health Sciences (NIEHS) [NO1-ES-65406]
FX Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences (NIEHS); and NIEHS
contract (NO1-ES-65406) to Battelle Laboratories, Columbus, OH 43201,
conducted the in-life portion of the study.
NR 27
TC 3
Z9 3
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD JAN
PY 2009
VL 107
IS 1
BP 19
EP 26
DI 10.1093/toxsci/kfn228
PG 8
WC Toxicology
SC Toxicology
GA 386NM
UT WOS:000261889900003
PM 18974089
ER
PT J
AU Marchetti, F
Bishop, J
Xiu, LW
Wyrobek, AJ
AF Marchetti, Francesco
Bishop, Jack
Xiu Lowe
Wyrobek, Andrew J.
TI Chromosomal Mosaicism in Mouse Two-Cell Embryos after Paternal Exposure
to Acrylamide
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
ID UNSCHEDULED DNA-SYNTHESIS; HUMAN PREIMPLANTATION EMBRYOS; CONFINED
PLACENTAL MOSAICISM; INDUCED CELL DEATH; MALE GERM-CELLS; MALE-MICE;
HERITABLE TRANSLOCATIONS; CLEAVAGE DIVISIONS; MAILLARD REACTION; LOCUS
MUTATIONS
AB Chromosomal mosaicism in human preimplantation embryos is a common cause of spontaneous abortions, however, our knowledge of its etiology is limited. We used multicolor fluorescence in situ hybridization painting to investigate whether paternally transmitted chromosomal aberrations result in mosaicism in mouse two-cell embryos. Paternal exposure to acrylamide, an important industrial chemical also found in tobacco smoke and generated during the cooking process of starchy foods, produced significant increases in chromosomally defective two-cell embryos, however, the effects were transient primarily affecting the postmeiotic stages of spermatogenesis. Comparisons with our previous study of zygotes demonstrated similar frequencies of chromosomally abnormal zygotes and two-cell embryos suggesting that there was no apparent selection against numerical or structural chromosomal aberrations. However, the majority of affected two-cell embryos were mosaics showing different chromosomal abnormalities in the two blastomeric metaphases. Analyses of chromosomal aberrations in zygotes and two-cell embryos showed a tendency for loss of acentric fragments during the first mitotic division of embryogenesis, whereas both dicentrics and translocations apparently underwent proper segregation. These results suggest that embryonic development can proceed up to the end of the second cell cycle of development in the presence of abnormal paternal chromosomes and that even dicentrics can persist through cell division. The high incidence of chromosomally mosaic two-cell embryos suggests that the first mitotic division of embryogenesis is prone to missegregation errors and that paternally transmitted chromosomal abnormalities increase the risk of missegregation leading to embryonic mosaicism.
C1 [Marchetti, Francesco; Xiu Lowe; Wyrobek, Andrew J.] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA.
[Marchetti, Francesco; Xiu Lowe; Wyrobek, Andrew J.] Lawrence Livermore Natl Lab, Biosci Directorate, Livermore, CA 94550 USA.
[Bishop, Jack] NIEHS, Res Triangle Pk, NC 27709 USA.
[Xiu Lowe] Kaiser Permanente Med Grp Inc, Dept Psychiat, Hayward, CA 94545 USA.
RP Marchetti, F (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, 1 Cyclotron Rd, Berkeley, CA 94720 USA.
EM fmarchetti@lbl.gov
OI Marchetti, Francesco/0000-0002-9435-4867
FU National Institute of Environmental Health Sciences through an NIEHS/DOE
Interagency Agreement [Y01ES-10203-00]; California Tobacco Related
Disease Research Program [13RT-140A]
FX National Institute of Environmental Health Sciences through an NIEHS/DOE
Interagency Agreement (grant number Y01ES-10203-00) to A. W. J. and F.
M.; and California Tobacco Related Disease Research Program (grant
number 13RT-140A) to F. M.
NR 69
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Z9 8
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD JAN
PY 2009
VL 107
IS 1
BP 194
EP 205
DI 10.1093/toxsci/kfn209
PG 12
WC Toxicology
SC Toxicology
GA 386NM
UT WOS:000261889900019
PM 18930949
ER
PT J
AU Brimfield, AA
Mancebo, AM
Mason, RP
Jiang, JJ
Siraki, AG
Novak, MJ
AF Brimfield, A. A.
Mancebo, A. M.
Mason, R. P.
Jiang, J. J.
Siraki, A. G.
Novak, M. J.
TI Free radical production from the interaction of 2-chloroethyl vesicants
(mustard gas) with pyridine nucleotide-driven flavoprotein electron
transport systems
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Chemical warfare; Flavoenzyme; Chloroethyl mustards; Onium ion;
Enzymatic reduction; Electron transport; Free radical; EPR
ID NITRIC-OXIDE SYNTHASE; SULFUR MUSTARD; THIOREDOXIN REDUCTASE; SULFONIUM
SALTS; IN-VITRO; MECHANISM; TOXICITY; DRUG; IDENTIFICATION; PROCARBAZINE
AB The biochemical sequelae to chloroethyl mustard exposure correspond very well to toxic processes initiated by free radicals. Additionally, mustard solutions contain spontaneously formed cyclic onium ions which produce carbon free radicals when reduced electrochemically. Therefore, we hypothesized that the onium ions of sulfur or nitrogen mustards might produce carbon free radicals upon being reduced enzymatically, and that these radicals might constitute a metabolic activation. We set out to document radical production using an in vitro metabolic system and electron paramagnetic resonance (EPR). Our system consisted of NADPH, one of several pyridine nucleotide-driven flavoprotein reductases, cytochrome c as a terminal electron acceptor, various sulfur or nitrogen mustards and the spin trap alpha-[4-pyridyl-1-oxide]-N-tertbutylnitrone in buffer. Reactions were started by adding the reductase to the other materials, vortexing and immediately transferring the mixture to a 10 mm EPR flat cell. Repeated scans on a Bruker ESP 300E EPR spectrometer produced a triplet of doublets with hyperfine splitting constants of a(N) = 15.483 G and a(H)=2.512 G. The outcome supported our hypothesis that carbon-centered free radicals are produced when mustard-related onium ions are enzymatically reduced. The EPR results varied little with the chloroethyl compound used or with porcine or human cytochrome P450 reductase, the reductase domain of rat brain neuronal nitric oxide synthase or rat liver thioredoxin reductase. Our results offer new insight into the basis for mustard-induced vesication and the outcome of exposure to different mustards. The free radical model provides an explanation for similarities in the lesions arising from mustard exposure and energy-based lesions such as those from heat, ultraviolet and nuclear radiation as well as damage across tissue types such as skin, eyes or airway epithelium. Published by Elsevier Inc.
C1 [Brimfield, A. A.; Mancebo, A. M.] USA, Med Res Inst Chem Def, Aberdeen Proving Ground, MD 21010 USA.
[Mason, R. P.; Jiang, J. J.; Siraki, A. G.] NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA.
[Novak, M. J.] Florida Inst Technol, Dept Chem, Melbourne, FL 32901 USA.
RP Brimfield, AA (reprint author), USA, Med Res Inst Chem Def, Aberdeen Proving Ground, MD 21010 USA.
EM alan.a.brimfield@us.army.mil
FU Defense Threat Reduction Agency; Joint Science and Technology Office;
U.S. Army Medical Research and Materiel Command; Intramural Research
Program of the NIH; [17-00-2-008]
FX This work was supported by the Defense Threat Reduction Agency - Joint
Science and Technology Office, Medical S and T Division and, in part, by
award number DAMD 17-00-2-008 from the U.S. Army Medical Research and
Materiel Command. This research was also Supported in part by the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences. Thanks are due to Dr. Carmen Arroyo and
Mr. Brendon Gallagher of USAMRICD for helping to get this work started.
We are grateful to Professor Bettie Sue Masters of the Department of
Biochemistry, University of Texas Health Sciences Center, San Antonio,
for the kind gift of recombinant rat brain nNOS reductase domain and
recombinant porcine liver NADPHcytochrome P450 redUctase and to Dr.
Thomas M. Shea of that laboratory for generous advice. And finally, we
would like to express our thanks to Dr. MarkA. Zottola and Dr. Sunil D.
Soni of USAMRICD for discussions that were inevitably helpful and
enlightening.
NR 43
TC 16
Z9 17
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JAN 1
PY 2009
VL 234
IS 1
BP 128
EP 134
DI 10.1016/j.taap.2008.10.002
PG 7
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 397SL
UT WOS:000262682300014
PM 18977373
ER
PT S
AU Preuss, ML
Weidman, P
Nielsen, E
AF Preuss, Mary L.
Weidman, Peggy
Nielsen, Erik
BA Segev, N
BF Segev, N
TI How We Study Protein Transport
SO TRAFFICKING INSIDE CELLS: PATHWAYS, MECHANISMS AND REGULATION
SE Molecular Biology Intelligence Unit
LA English
DT Article; Book Chapter
ID GREEN-FLUORESCENT PROTEIN; CELL-FREE SYSTEM; VESICULAR STOMATITIS-VIRUS;
RECEPTOR-MEDIATED ENDOCYTOSIS; DENSITY-LIPOPROTEIN RECEPTOR; RESONANCE
ENERGY-TRANSFER; YEAST SECRETORY PATHWAY; PERFORATED MDCK CELLS;
TO-GOLGI TRANSPORT; IN-VITRO
AB For the greater part of the last century, research in the field of protein transport was synonymous with microscopy. Before the end of the century, this view was dramatically changed by the emergence of innovative genetic, molecular and biochemical approaches that revolutionized and invigorated the field. Far from being displaced as an essential tool, microscopy techniques have also evolved. What was once largely a science of "dead cells" has been transformed into a window on the inner workings of living cells. The objective of this chapter is to provide an overview of the major approaches that are employed in the analysis of protein transport within the membrane trafficking system of eukaryotic cells. In particular, we discuss the identification of several of the common model cargo proteins for studying both secretory and endocytic membrane trafficking in both mammalian and yeast systems. We then discuss the development of both in vivo and in vitro techniques to study the transport of these model cargo proteins within cells, and explain some of the common principles involved in these assays. Finally, we discuss some of the recent advances in imaging techniques and technology that have driven the recent "renaissance" in the use of microscopic techniques in the investigation of membrane trafficking events in living cells.
C1 [Nielsen, Erik] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA.
[Weidman, Peggy] NIGMS, Off Sci Review, Bethesda, MD USA.
[Preuss, Mary L.] Donald Danforth Plant Sci Ctr, St Louis, MO USA.
RP Nielsen, E (reprint author), Univ Michigan, Dept Mol Cellular & Dev Biol, 830 N Univ Ave, Ann Arbor, MI 48109 USA.
EM nielsene@umich.edu
RI Nielsen, Erik/G-5843-2013
NR 182
TC 0
Z9 0
U1 0
U2 3
PU LANDES BIOSCIENCE
PI GEORGETOWN
PA 810 S CHURCH ST, GEORGETOWN, TX 78626 USA
SN 1431-0414
BN 978-0-387-93876-9
J9 MOL BIOL INTELL UNIT
JI Mol. Biol. Intell. Unit
PY 2009
BP 15
EP 41
DI 10.1007/978-0-387-93877-6_2
D2 10.1007/978-0-387-93877-6
PG 27
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BLT03
UT WOS:000270966400002
ER
PT S
AU Donaldson, J
Segev, N
AF Donaldson, Julic
Segev, Nava
BA Segev, N
BF Segev, N
TI Regulation and Coordination of Intracellular Trafficking: An Overview
SO TRAFFICKING INSIDE CELLS: PATHWAYS, MECHANISMS AND REGULATION
SE Molecular Biology Intelligence Unit
LA English
DT Article; Book Chapter
ID NUCLEOTIDE-EXCHANGE FACTOR; TRANS-GOLGI; RAB GTPASES; ENDOCYTIC
TRAFFICKING; COATED VESICLES; CELL-MIGRATION; YPT GTPASES; PROTEIN;
YEAST; ARF
AB During the last two decades, efforts in the protein trafficking field have focused primarily on the identification of the machinery components of vesicular transport and mechanisms that underlie it. In addition, research has started to reveal how intracellular trafficking is regulated. Here, we summarize the current state of our knowledge about the regulation of vesicular transport and its coordination with other cellular processes. At the most basic level, individual transport steps are regulated spatially and temporally in two different ways. First, molecular switches of the Arf, Rab and Rho GTPase families regulate the assembly of components of the vesicular transport machinery on membranes, mediating the formation, targeting and fusion of vesicles that shuttle cargo between intracellular compartments. Second, reversible posttranslational modifications, like phosphorylation and abiquitination, allow efficient cargo sorting and machinery component recycling. At a higher level, individual transport steps are integrated into whole pathways, with GTPases as a mechanism for this integration. Finally, intracellular trafficking pathways are coordinated with other cellular processes. Here too, GTPases appear to play a role by orchestrating coordination.
C1 [Segev, Nava] Univ Illinois, Dept Biol Sci, Chicago, IL 60607 USA.
[Donaldson, Julic] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Segev, N (reprint author), Univ Illinois, Dept Biol Sci, Chicago, IL 60607 USA.
EM nava@uic.edu; nava@uic.edu
NR 63
TC 4
Z9 4
U1 0
U2 1
PU LANDES BIOSCIENCE
PI GEORGETOWN
PA 810 S CHURCH ST, GEORGETOWN, TX 78626 USA
SN 1431-0414
BN 978-0-387-93876-9
J9 MOL BIOL INTELL UNIT
JI Mol. Biol. Intell. Unit
PY 2009
BP 329
EP 341
DI 10.1007/978-0-387-93877-6_15
D2 10.1007/978-0-387-93877-6
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BLT03
UT WOS:000270966400015
ER
PT J
AU Singh, AK
Horvath, KA
Mohiuddin, MM
AF Singh, A. K.
Horvath, K. A.
Mohiuddin, M. M.
TI Rapamycin Promotes the Enrichment of CD4(+)CD25(hi)FoxP3(+) T Regulatory
Cells From Naive CD4(+) T Cells of Baboon That Suppress Antiporcine
Xenogenic Response In Vitro
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 22nd International Congress of the Transplantation-Society
CY AUG 10-14, 2008
CL Sydney, AUSTRALIA
SP Transplantat Soc, Transplantat Soc Australia & New Zealand
ID VERSUS-HOST-DISEASE; BONE-MARROW-TRANSPLANTATION
AB The CD4(+)CD25(+)FoxP3(+) regulatory T (Treg) cells play an important role in regulating the immune response. These Treg cells are present in peripheral blood and lymphoid organs and have a high potential for immunotherapy in clinics. Adoptive cell transfer therapy using CD4(+)CD25(+) cells has been shown to prevent autoimmune diseases and has also induced transplant tolerance in mice. Treg cells low frequency in peripheral blood will necessitate its ex vivo expansion to enable adaptive immunotherapy. Recently, it has been reported that rapamycin, an immunosuppressive agent, inhibits T-cell proliferation while selectively increasing the number of Treg cells. Based on this additional mode of action, rapamycin can be used to expand Treg cells for ex vivo cellular therapy in T-cell-mediated diseases and in transplantation. We have reported the ex vivo expansion of baboon Treg cells, using irradiated pig peripheral blood mononuclear cell (PBMC) and interleukin (IL)-2, and have demonstrated the suppression of autologus CD4(+)CD25(neg) T-cell proliferation in response to pig PBMCs. In the present study, we have expanded baboon CD4(+) T cells in the presence or absence of rapamycin (0.1-10 nmol/L) using irradiated pig PBMCs and IL-2 to enrich the regulatory T cells. CD4(+)CD25(+)FoxP3(+) Treg cells were increased up to 2 times in the presence of rapamycin versus without rapamycin in vitro. However, a higher dose of rapamycin (>= 10 nmol/L) considerably decreases the number of Treg cells. Furthermore, purified CD4(+)CD25(+) Treg cells enriched from CD4(+) cells in the presence of rapamycin were able to suppress the baboon anti-porcine xenogeneic immune responses in vitro up to 93% at a 1:1 ratio (Treg cells:T effector cells) and suppression ability exists even at a 1:256 ratio, whereas freshly isolated natural Treg cells suppress only 70% at 1:1 and lose their suppressive ability (>50%) at 1:16. Our results demonstrate that the addition of rapamycin to the culture enriches the Treg phenotype and induces functional regulatory T cells. This method may allow the production of large numbers of regulatory cells for the preclinical testing of Treg cell therapy in a non-human primate model.
C1 [Mohiuddin, M. M.] NHLBI, Cardiothorac Surg Res Program, NIH, Bethesda, MD 20850 USA.
RP Mohiuddin, MM (reprint author), NHLBI, Cardiothorac Surg Res Program, NIH, 10 Ctr Dr,Bldg 10,Rm 2N246, Bethesda, MD 20850 USA.
RI Mohiuddin, Muhammad/M-4642-2013
OI Mohiuddin, Muhammad/0000-0003-4654-783X
FU Intramural NIH HHS [Z99 HL999999]
NR 8
TC 12
Z9 14
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
J9 TRANSPL P
JI Transplant. Proc.
PD JAN-FEB
PY 2009
VL 41
IS 1
BP 418
EP 421
DI 10.1016/j.transproceed.2008.10.079
PG 4
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 412UG
UT WOS:000263749100109
PM 19249569
ER
PT S
AU Newman, AH
Katz, JL
AF Newman, Amy Hauck
Katz, Jonathan L.
BE Napier, S
Bingham, M
TI Atypical Dopamine Uptake Inhibitors that Provide Clues About Cocaine's
Mechanism at the Dopamine Transporter
SO TRANSPORTERS AS TARGETS FOR DRUGS
SE Topics in Medicinal Chemistry Series
LA English
DT Article; Book Chapter
DE Addiction medication discovery; Benztropine; Cocaine; Dopamine
transporter; Dopamine uptake inhibitor
ID HISTAMINE H-1 ANTAGONISTS; MOLECULAR-FIELD ANALYSIS; NON-NITROGEN
INHIBITORS; MONOAMINE TRANSPORTERS; RHESUS-MONKEYS; BENZTROPINE ANALOGS;
IN-VIVO; 3-ALPHA-DIPHENYLMETHOXYTROPANE ANALOGS; POPULATION
PHARMACOKINETICS; RIMCAZOLE ANALOGS
AB The dopamine transporter (DAT) has been a primary target for cocaine abuse/adwdiction medication discovery. However predicted addiction liability and limited clinical evaluation has provided a formidable challenge for development of these agents for human use. The unique and atypical pharmacological profile of the benztropine (BZT) class of dopamine uptake inhibitors, in preclinical models of cocaine effects and abuse, has encouraged further development of these agents. Moreover, in vivo studies have challenged the original DAT hypothesis and demonstrated that DAT occupancy and subsequent increases in dopamine produced by BZT analogues are significantly delayed and long lasting, as compared to cocaine. These important and distinctive elements are critical to the lack of abuse liability among BZT analogues, and improve their potential for development as treatments for cocaine abuse and possibly other neuropsychiatric disorders.
C1 [Newman, Amy Hauck; Katz, Jonathan L.] Natl Inst Drug Abuse, Medicat Discovery Res Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Newman, Amy Hauck] NIDA, Med Chem Sect, IRP, NIH, Baltimore, MD 21224 USA.
[Katz, Jonathan L.] NIDA, Psychobiol Sect, IRP, NIH, Baltimore, MD 21224 USA.
RP Newman, AH (reprint author), Natl Inst Drug Abuse, Medicat Discovery Res Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM anewman@intra.nida.nih.gov
OI Katz, Jonathan/0000-0002-1068-1159
NR 78
TC 12
Z9 12
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
SN 1862-2461
BN 978-3-540-87911-4
J9 TOP MED CHEM SER
JI Top. Med. Chem.
PY 2009
VL 4
BP 95
EP 129
DI 10.1007/7355_2008_027
D2 10.1007/978-3-540-87912-1
PG 35
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA BKL76
UT WOS:000268445900004
ER
PT J
AU Mattson, MP
Ashery, U
AF Mattson, Mark P.
Ashery, Uri
TI No more brain tangles with Delta Np73
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Article
ID ALZHEIMERS-DISEASE; NEURONAL DIFFERENTIATION; EXCITOTOXIC INSULTS; P53;
P73; NEURODEGENERATION; APOPTOSIS; SURVIVAL; MICE; BAX
AB In Alzheimer's disease (AD), neurons suffer dysfunction and death associated with aberrant tau phosphorylation and subsequent neurofibrillary tangles. A new study reveals a surprising neuroprotective role for a truncated p73 isoform (Delta Np73). Aged mice with reduced Delta Np73 levels exhibit tau pathology and cognitive deficits, and Delta Np73 reduction in mice with amyloid pathology causes extensive tangle formation and neuron death. These findings provide a novel animal model of AD and a potential therapeutic role for Delta Np73 inducers.
C1 [Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Ashery, Uri] Tel Aviv Univ, Dept Neurobiol, George S Wise Fac Life Sci, IL-69978 Tel Aviv, Israel.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Mattson, Mark/F-6038-2012
FU Intramural NIH HHS [Z01 AG000313-07]
NR 24
TC 4
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD JAN
PY 2009
VL 34
IS 1
BP 6
EP 8
DI 10.1016/j.tibs.2008.10.004
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 402HY
UT WOS:000263006000005
PM 19008105
ER
PT J
AU Doyle, SM
Wickner, S
AF Doyle, Shannon M.
Wickner, Sue
TI Hsp104 and ClpB: protein disaggregating machines
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
ID PLUS CHAPERONE CLPB; SACCHAROMYCES-CEREVISIAE HSP104; TERMINAL ATPASE
DOMAIN; ESCHERICHIA-COLI; MOLECULAR CHAPERONE; DEGRADATION MACHINE;
SUBSTRATE RECOGNITION; AGGREGATED PROTEINS; NUCLEOTIDE-BINDING; PRION
PROPAGATION
AB Heat-shock protein 104 (Hsp104) and caseinolytic peptidase B (ClpB), members of the AAA+ superfamily, are molecular machines involved in disaggregating insoluble protein aggregates, a process not long ago thought to be impossible. During extreme stress they are essential for cell survival. In addition, Hsp104 regulates prion assembly and disassembly. For most of their protein remodeling activities Hsp104 and ClpB work in collaboration with the Hsp70 or DnaK chaperone systems. Together, the two chaperones catalyze protein disaggregation and reactivation by a mechanism probably involving the extraction of polypeptides from aggregates by forced unfolding and translocation through the Hsp104/ClpB central cavity. The polypeptides are then released back into the cellular milieu for spontaneous or chaperone-mediated refolding.
C1 [Doyle, Shannon M.; Wickner, Sue] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Wickner, S (reprint author), NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM wickners@mail.nih.gov
FU National Institutes of Health National Cancer Institute Center for
Cancer Research
FX We thank Joel Hoskins, Jodi Camberg and Danielle Johnston for their
helpful discussions and critical reading of the manuscript. Work in our
laboratory is supported by the Intramural Research Program of the
National Institutes of Health National Cancer Institute Center for
Cancer Research (http://ccr.cancer.gov).
NR 81
TC 138
Z9 139
U1 4
U2 16
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD JAN
PY 2009
VL 34
IS 1
BP 40
EP 48
DI 10.1016/j.tibs.2008.09.010
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 402HY
UT WOS:000263006000010
PM 19008106
ER
PT J
AU Hamburg, NM
Benjamin, EJ
AF Hamburg, Naomi M.
Benjamin, Emelia J.
TI Assessment of Endothelial Function Using Digital Pulse Amplitude
Tonometry
SO TRENDS IN CARDIOVASCULAR MEDICINE
LA English
DT Review
ID OXIDE-DEPENDENT VASODILATION; OBSTRUCTIVE SLEEP-APNEA; FLOW-MEDIATED
DILATION; FLAVANOL-RICH COCOA; NITRIC-OXIDE; VASCULAR FUNCTION;
FALCIPARUM-MALARIA; REACTIVE HYPEREMIA; DYSFUNCTION; HUMANS
AB The importance of endothelial dysfunction in the development and clinical expression of cardiovascular disease is well recognized. Impaired endothelial function has been associated with an increased risk of cardiovascular events. Endothelial function may be evaluated in humans by assessing vasodilation in response to stimuli known to induce the release of nitric oxide. A novel pulse amplitude tonometry device noninvasively measures vasodilator function in the microcirculation of the finger. This article reviews the recent studies that support the utility of digital pulse amplitude tonometry as a relevant test of peripheral endothelial function. (Trends Cardiovasc Med 2009; 19:6-11) (C) 2009, Elsevier Inc.
C1 [Hamburg, Naomi M.] Boston Univ, Whitaker Cardiovasc Inst, Dept Med, Sch Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Whitaker Cardiovasc Inst, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02118 USA.
[Benjamin, Emelia J.] NHLBI, Framingham, MA 01702 USA.
[Benjamin, Emelia J.] Boston Univ Framingham Heart Study, Framingham, MA 01702 USA.
RP Hamburg, NM (reprint author), Boston Univ, Whitaker Cardiovasc Inst, Dept Med, Sch Med, 88 E Newton St C818, Boston, MA 02118 USA.
EM naomi.hamburg@bmc.org
OI Benjamin, Emelia/0000-0003-4076-2336
FU National Institutes of Health [HL083781]; [RO1 HL076784]; [1R01
AG028321]; [RO1 HL70100]; [N01-HC 25195]
FX Dr Hamburg is supported by National Institutes of Health grant HL083781.
Dr Benjamin receives support from RO1 HL076784, 1R01 AG028321, RO1
HL70100, and N01-HC 25195.
NR 32
TC 76
Z9 82
U1 1
U2 6
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1050-1738
J9 TRENDS CARDIOVAS MED
JI Trends Cardiovasc. Med.
PD JAN
PY 2009
VL 19
IS 1
BP 6
EP 11
AR PII S1050-1738(09)00051-6
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 462NQ
UT WOS:000267361200002
PM 19467447
ER
PT J
AU Morrison, DK
AF Morrison, Deborah K.
TI The 14-3-3 proteins: integrators of diverse signaling cues that impact
cell fate and cancer development
SO TRENDS IN CELL BIOLOGY
LA English
DT Review
ID ORGAN SIZE CONTROL; HIPPO PATHWAY; JNK PHOSPHORYLATION; CONTACT
INHIBITION; GROWTH-CONTROL; GENE-PRODUCT; DNA-DAMAGE; B-RAF; MTOR; TSC2
AB The highly conserved 14-3-3 protein family has risen to a position of importance in cell biology owing to its involvement in vital cellular processes, such as metabolism, protein trafficking, signal transduction, apoptosis and cell-cycle regulation. The 14-3-3 proteins are phosphoserine/phospho-threonine binding proteins that interact with a diverse array of binding partners. Because many 14-3-3 interactions are phosphorylation-dependent, 14-3-3 has been tightly integrated into the core phosphoregulatory pathways that are crucial for normal growth and development and that often become dysregulated in human disease states such as cancer. This review examines the recent advances that further elucidate the role of 14-3-3 proteins as integrators of diverse signaling cues that influence cell fate decisions and tumorigenesis.
C1 NCI Frederick, Lab Cell & Dev Signaling, Frederick, MD 21702 USA.
RP Morrison, DK (reprint author), NCI Frederick, Lab Cell & Dev Signaling, Frederick, MD 21702 USA.
EM dmorrison@nciferf.gov
FU Intramural NIH HHS [ZIA BC010329-11]
NR 66
TC 293
Z9 306
U1 4
U2 39
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0962-8924
J9 TRENDS CELL BIOL
JI Trends Cell Biol.
PD JAN
PY 2009
VL 19
IS 1
BP 16
EP 23
DI 10.1016/j.tcb.2008.10.003
PG 8
WC Cell Biology
SC Cell Biology
GA 402HP
UT WOS:000263005100003
PM 19027299
ER
PT J
AU Kunos, G
Osei-Hyiaman, D
Batkai, S
Sharkey, KA
Makriyannis, A
AF Kunos, George
Osei-Hyiaman, Douglas
Batkai, Sandor
Sharkey, Keith A.
Makriyannis, Alexandros
TI Should peripheral CB1 cannabinoid receptors be selectively targeted for
therapeutic gain?
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID DIET-INDUCED OBESITY; ENDOCANNABINOID SYSTEM; ANTAGONIST SR141716;
INSULIN-RESISTANCE; NEUROPATHIC PAIN; ENERGY-BALANCE; RISK-FACTORS;
OVERWEIGHT PATIENTS; METABOLIC SYNDROME; LEPTIN RESISTANCE
AB Endocannabinoids, endogenous lipid ligands of cannabinoid receptors, mediate a variety of effects similar to those of marijuana. Cannabinoid CB1 receptors are highly abundant in the brain and mediate psychotropic effects, which limits their value as a potential therapeutic target. There is growing evidence for CB1 receptors in peripheral tissues that modulate a variety of functions, including pain sensitivity and obesity-related hormonal and metabolic abnormalities. In this review we propose that selective targeting of peripheral CB1 receptors has potential therapeutic value because it would help to minimize addictive, psychoactive effects in the case of CB1 agonists used as analgesics, or depression and anxiety in the case of CB1 antagonists used in the management of cardiometabolic risk factors associated with the metabolic syndrome.
C1 [Kunos, George; Osei-Hyiaman, Douglas; Batkai, Sandor] NIAAA, Lab Physiol Studies, Bethesda, MD 20892 USA.
[Sharkey, Keith A.] Univ Calgary, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada.
[Makriyannis, Alexandros] Northeastern Univ, Ctr Drug Discovery, Boston, MA 02115 USA.
RP Kunos, G (reprint author), NIAAA, Lab Physiol Studies, Bethesda, MD 20892 USA.
EM gkunos@mail.nih.gov
RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014
FU National Institutes of Health
FX The work of G.K., D. O-H. and S.B. is supported by intramural funds of
the National Institutes of Health.
NR 65
TC 74
Z9 76
U1 1
U2 5
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD JAN
PY 2009
VL 30
IS 1
BP 1
EP 7
DI 10.1016/j.tips.2008.10.001
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 400VY
UT WOS:000262898700001
PM 19042036
ER
PT J
AU O'Meara, WP
Noor, A
Gatakaa, H
Tsofa, B
McKenzie, FE
Marsh, K
AF O'Meara, W. P.
Noor, A.
Gatakaa, H.
Tsofa, B.
McKenzie, F. E.
Marsh, K.
TI The impact of primary health care on malaria morbidity - defining access
by disease burden
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Article
DE primary health care; malaria morbidity; access; travel time; Kenya
ID KENYA; CHILDREN; SERVICES; COAST; TRANSMISSION; VACCINE; EQUITY; FEVERS
AB Primary care facilities are increasingly becoming the focal point for distribution of malaria intervention strategies, but physical access to these facilities may limit the extent to which communities can be reached. To investigate the impact of travel time to primary care on the incidence of hospitalized malaria episodes in a rural district in Kenya.
The incidence of hospitalized malaria in a population under continuous demographic surveillance was recorded over 3 years. The time to travel to the nearest primary health care facility was calculated for every child between birth and 5 years of age and trends in incidence of hospitalized malaria as a function of travel time were evaluated.
The incidence of hospitalized malaria more than doubled as travel time to the nearest primary care facility increased from 10 min to 2 h. Good access to primary health facilities may reduce the burden of disease by as much as 66%.
Our results highlight both the potential of the primary health care system in reaching those most at risk and reducing the disease burden. Insufficient access is an important risk factor, one that may be inequitably distributed to the poorest households.
C1 [O'Meara, W. P.; McKenzie, F. E.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Noor, A.] Wellcome Trust Collaborat Program, KEMRI, Nairobi, Kenya.
[Gatakaa, H.] Kenya Govt Med Res Ctr, CGMRC, Wellcome Trust Collaborat Program, Kilifi, Kenya.
[Tsofa, B.; Marsh, K.] Minist Hlth, Kilifi, Kenya.
RP O'Meara, WP (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM prudhomw@mail.nih.gov
FU Fogarty International Center of the National Institutes of Health; The
Wellcome Trust; Kenya Medical Research Institute
FX WPO gratefully acknowledges the Fogarty International Center of the
National Institutes of Health for funding and support. This
investigation received financial support from The Wellcome Trust and the
Kenya Medical Research Institute.
NR 24
TC 24
Z9 24
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD JAN
PY 2009
VL 14
IS 1
BP 29
EP 35
DI 10.1111/j.1365-3156.2008.02194.x
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 395IN
UT WOS:000262517900005
PM 19121148
ER
PT J
AU Bermudez-Morales, VH
Peralta-Zaragoza, O
Guzman-Olea, E
Garcia-Carranca, A
Bahena-Roman, M
Alcocer-Gonzalez, JM
Madrid-Marina, V
AF Bermudez-Morales, V. H.
Peralta-Zaragoza, O.
Guzman-Olea, E.
Garcia-Carranca, A.
Bahena-Roman, M.
Alcocer-Gonzalez, J. M.
Madrid-Marina, V.
TI HPV 16 E2 Protein Induces Apoptosis in Human and Murine HPV 16
Transformed Epithelial Cells and Has Antitumoral Effects in vivo
SO TUMOR BIOLOGY
LA English
DT Article
DE HPV 16 E2; Apoptosis; Cell death; Epithelial cells
ID HUMAN-PAPILLOMAVIRUS TYPE-16; CERVICAL-CARCINOMA CELLS; BOVINE
PAPILLOMAVIRUS; REGULATORY REGION; DNA IMMUNIZATION; PHYSICAL STATUS;
VACCINIA VIRUS; HELA-CELLS; HIGH-RISK; GENE
AB Objective: Our aims were to examine the ability of the human papillomaviruse (HPV) 16 E2 protein to induce apoptosis in a murine HPV-transformed cell line, and to evaluate its antitumor properties on HPV-associated tumors in vivo in immunocompetent mice. Methods: HPV-transformed murine BMK-16/myc cells and human SiHa cells were transfected with the HPV 16 E2 gene to examine the effects of the E2 protein on cell growth and on the E6 and E7 oncogenes as well as DNA fragmentation and activation of the extrinsic pathway of apoptosis. Finally, to test the antitumor effect of the E2 protein on an experimental mouse tumor model, we generated a recombinant adenovirus expressing the E2 protein. Results: The E2 protein inhibited the growth of SiHa and BMK-16/myc cell lines, and repressed the E6 and E7 oncogenes. Moreover, the E2 protein induced DNA fragmentation and apoptosis through activation of caspases 8 and 3 in BMK-16/myc cells. On the other hand, E2 also showed antitumor effects in vivo. Conclusions: Our findings indicate that E2 exerts pro-apoptotic activity in a murine HPV-transformed cell line as well as an antitumor effect in vivo. Copyright (C) 2009 S. Karger AG, Basel
C1 [Bermudez-Morales, V. H.; Peralta-Zaragoza, O.; Bahena-Roman, M.; Madrid-Marina, V.] Natl Inst Publ Hlth, Cuernavaca 62508, Morelos, Mexico.
[Guzman-Olea, E.] Natl Canc Inst, Biomed Res Inst, Unit Biomed Res Canc, Bethesda, MD 20892 USA.
[Bermudez-Morales, V. H.] Univ Nacl Autonoma Mexico, Sch Med, Mexico City 04510, DF, Mexico.
[Alcocer-Gonzalez, J. M.] Autonomous Univ Nuevo Leon, Sch Biol Sci, Monterrey, Mexico.
RP Madrid-Marina, V (reprint author), Natl Inst Publ Hlth, Av Univ 655, Cuernavaca 62508, Morelos, Mexico.
EM vmarina@correo.insp.mx
FU CONACYT [125098]; Mexican government through a grant from CONACYT-SEP
[46151]; Universidad Nacional Autonoma de Mexico [501036762]
FX This work was submitted in partial fulfillment of the requirements for
the DSc degree by Victor Hugo Bermudez-Morales at the Doctorado en
Ciencias Biomedicas, Universidad Nacional Autonoma de Mexico. Number:
501036762.
NR 48
TC 5
Z9 8
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1010-4283
J9 TUMOR BIOL
JI Tumor Biol.
PY 2009
VL 30
IS 2
BP 61
EP 72
DI 10.1159/000214438
PG 12
WC Oncology
SC Oncology
GA 446CM
UT WOS:000266098000002
PM 19390235
ER
PT S
AU Weissman, AM
Yang, Y
Kitagaki, J
Sasiela, CA
Beutler, JA
O'Keefe, BR
AF Weissman, A. M.
Yang, Y.
Kitagaki, J.
Sasiela, C. A.
Beutler, J. A.
O'Keefe, B. R.
BE Jentsch, S
Haendler, B
TI Inhibiting Hdm2 and Ubiquitin-Activating Enzyme: Targeting the Ubiquitin
Conjugating System in Cancer
SO Ubiquitin System in Health and Disease
SE Ernst Schering Foundation Symposium Proceedings
LA English
DT Proceedings Paper
CT Ernst-Schering-Foundation Symposium on Ubiquitin System in Health and
Disease
CY APR 09-11, 2008
CL Berlin, GERMANY
SP Ernst Schering Fdn
ID LIGASE ACTIVITY; P53 PATHWAY; MDM2; PROTEINS; CELLS; BORTEZOMIB;
MECHANISM; SCREEN; ITSELF; GENE
AB The ubiquitin conjugating system represents a rich source of potential molecular targets for cancer and other diseases. One target of great interest is the RING finger ubiquitin ligase (B) Hdm2/Mdm2, which is frequently overexpressed in cancer and is a critical E3 for the tumor suppressor p53. For those 50% of tumors that express wild-type p53, agents that inhibit Hdm2 have great potential clinical utility. We summarize our ongoing efforts to identify inhibitors of Hdm2 E3 activity by high-throughput screening of both defined small molecules and natural product extracts. Employing a strategy using both enzymatic and cell-based assays, we have identified inhibitors that block the E3 activity of Hdm2, activate a p53 response, preferentially kill p53-expressing cells, and have the capacity to differentially cause death of transformed cells. Therefore, screening for inhibitors of Hdm2 ubiquitin ligase activity through in vitro assays represents a powerful means of identifying molecules that activate p53 in cancer cells to induce apoptosis. We also discuss the potential of inhibitors Of Ubiquitin-activating enzyme (El) that were discovered during these screens. El inhibitors may similarly serve its the basis for novel therapeutics. Additionally, they represent unique tools for providing new insights into the ubiquitin conjugating system.
C1 [Weissman, A. M.; Yang, Y.; Kitagaki, J.; Sasiela, C. A.; Beutler, J. A.; O'Keefe, B. R.] NCI, Lab Prot Dynam & Signaling, Frederick, MD 21702 USA.
RP Weissman, AM (reprint author), NCI, Lab Prot Dynam & Signaling, Rm 22-103,POB Bldg 560, Frederick, MD 21702 USA.
EM amw@nih.gov
NR 40
TC 0
Z9 0
U1 0
U2 3
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0947-6075
BN 978-3-540-85106-6
J9 ERNST SCHERING FOUND
PY 2009
VL 1
BP 171
EP 190
DI 10.1007/2789_2008_108
PG 20
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA BIS93
UT WOS:000262475400011
ER
PT B
AU Jakobsson, E
AF Jakobsson, Eric
BE Cope, B
Kalantzis, M
TI Biology Using a Ubiquitous Knowledge Environment to Integrate Teaching,
Learning, and Research in Biology and Chemistry
SO UBIQUITOUS LEARNING
LA English
DT Article; Book Chapter
ID EVOLUTION; DATABASE
C1 [Jakobsson, Eric] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
[Jakobsson, Eric] Univ Illinois, Natl Ctr Supercomp Applicat, Urbana, IL 61801 USA.
[Jakobsson, Eric] NIH, Biomed Informat Sci & Technol Initiat Consortium, Bethesda, MD 20892 USA.
[Jakobsson, Eric] NIH, Natl Ctr Design Biomimet Nanoconductors, Bethesda, MD 20892 USA.
[Jakobsson, Eric] Amer Phys Soc, College Pk, MD USA.
RP Jakobsson, E (reprint author), Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
NR 17
TC 0
Z9 0
U1 0
U2 0
PU UNIV ILLINOIS PRESS
PI URBANA
PA URBANA, IL 61801 USA
BN 978-0-252-07680-0
PY 2009
BP 216
EP 229
PG 14
WC Education & Educational Research
SC Education & Educational Research
GA BCI38
UT WOS:000310243800020
ER
PT J
AU Kagiya, G
Ogawa, R
Ito, S
Fukuda, S
Hatashita, M
Tanaka, Y
Yamamoto, K
Kondo, T
AF Kagiya, Go
Ogawa, Ryohei
Ito, Shinji
Fukuda, Shigekazu
Hatashita, Masanori
Tanaka, Yoshikazu
Yamamoto, Kazutaka
Kondo, Takashi
TI IDENTIFICATION OF A CIS-ACTING ELEMENT RESPONSIVE TO ULTRASOUND IN THE 5
'-FLANKING REGION OF THE HUMAN HEME OXYGENASE-1 GENE
SO ULTRASOUND IN MEDICINE AND BIOLOGY
LA English
DT Article
DE Ultrasound; Heme oxygenase-1; Reactive oxygen species; Stress-responsive
element
ID TRANSCRIPTIONAL ACTIVATION; NITRIC-OXIDE; CELLS; EXPRESSION; INDUCTION;
CADMIUM; MECHANISM; NRF2; SONOCHEMISTRY; ARSENITE
AB We previously found that the heme oxygenase-1 gene (hmox-1) was the most upregulated gene among 9,182 genes in human lymphoma U937 cells exposed to 1-MHz continuous ultrasound using the cDNA microarray technique. However, little is known about the molecular mechanisms of the induction of hmox-1 expression by ultrasound. We investigated the mechanism using human prostate cancer DU145 cells in which expression of hmox-1 increased with sonication in a time and an intensity-dependent manner. When N-acetyl-L-cysteine or glutathione-monoethyl ester, a potent antioxidant, was added to cell culture, hmox-1 upregulation was attenuated, suggesting that oxidative stress caused by sonication is involved in this process. To identify cis-acting elements required for the ultrasound-mediated induction, we carried out transient expression assays with plasmids carrying the luciferase gene under control of deletion mutants of the 5'-flanking region of hmox-1. The results revealed that the upregulations by sonication were observed with deletion mutants carrying the El or E2 enhancer of the 5'-flanking region, suggesting stress-responsive elements (StRE) were involved in the induction because either enhancer contains a number of the element. Indeed, site-directed mutations within StRE decreased the reactivity of deletion mutants to sonication. A transcription factor NF-E2-related Factor 2 that binds to StRE would therefore be activated by oxidative stress induced by sonication.
C1 [Ogawa, Ryohei; Kondo, Takashi] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Radiol Sci, Toyama 9300194, Japan.
[Kagiya, Go; Ito, Shinji] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
[Kagiya, Go] Kitasato Univ, Sch Allied Hlth Sci, Kanagawa, Japan.
[Fukuda, Shigekazu; Yamamoto, Kazutaka] Wakasa Wan Energy Res Ctr, Div Med, Fukui, Japan.
[Hatashita, Masanori; Tanaka, Yoshikazu] Wakasa Wan Energy Res Ctr, Biol Grp, Fukui, Japan.
RP Ogawa, R (reprint author), Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Radiol Sci, Toyama 9300194, Japan.
EM ogawa@med.u-toyama.ac.jp
NR 30
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-5629
J9 ULTRASOUND MED BIOL
JI Ultrasound Med. Biol.
PD JAN
PY 2009
VL 35
IS 1
BP 155
EP 164
DI 10.1016/j.ultrasmedbio.2008.07.012
PG 10
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 390DN
UT WOS:000262144600019
PM 18829152
ER
PT J
AU Vaughn, DW
Whitehead, SS
Durbin, AP
AF Vaughn, David W.
Whitehead, Stephen S.
Durbin, Anna P.
BE Barrett, ADT
Stanberry, LR
TI Dengue
SO VACCINES FOR BIODEFENSE AND EMERGING AND NEGLECTED DISEASES
LA English
DT Article; Book Chapter
ID T-CELL RESPONSES; NEUTRALIZING ANTIBODY-RESPONSE; RECOMBINANT VACCINIA
VIRUS; HUMAN ENDOTHELIAL-CELLS; DISSEMINATED INTRAVASCULAR COAGULATION;
CLINICAL LABORATORY RESPONSES; RESPIRATORY SYNCYTIAL VIRUS;
JAPANESE-ENCEPHALITIS-VIRUS; PERIPHERAL-BLOOD LEUKOCYTES; INTERFERON
GAMMA-PRODUCTION
AB Molecular evolution studies suggest that dengue virus (DENV) evolved 1000 years ago and entered a sustained human-mosquito cycle between 125 and 320 years ago. While it is unlikely that DENV would be used as a biothreat agent, DENV has emerged since World War II as the most important mosquito-borne viral pathogen infecting an estimated 100 million persons each year. Infection with any of the four DENV serotypes (DENV-1, 2, 3, and 4) can be inapparent, result in classic dengue fever with high fever, headache, eye pain and muscle ache, or progress at the time of defervescence to dengue hemorrhagic fever (DHF) characterized by hemorrhagic manifestations and plasma leakage that can lead to shock and death. The immunopathological mechanisms by which DENV causes the clinical features of DHF are intricate and include aberrant humoral and cellular immune responses. Previous DENV infections may predispose to more severe disease by the induction of enhancing antibody and cross-reactive T cells. Treatment is supportive relying upon careful fluid management which can be lifesaving. Prevention currently depends on vector control which has been largely unsuccessful. Several dengue vaccine candidates have advanced to clinical trials to include classically and molecularly attenuated live virus vaccines, chimeric vaccines using dengue and yellow fever virus backbones, and DNA vaccines. Whole virus inactivated and recombinant subunit vaccine candidates should soon enter into clinical testing. Live attenuated DENV vaccines offer the most promise in terms of broad, long-lasting protection, and although they are economical to produce, they may carry the risks of enhanced reactogenicity in recipients with preexisting flavivirus antibodies, adverse events among the immunocompromised, vaccine virus transmission by vector mosquitoes, and the risk of adventitious agents. Chimeric vaccine approaches use the same gene sequence for the nonstructural proteins for each of the four DENV serotypes avoiding the need for attenuating mutations in the structural genes and potentially reducing interference in the replication of the four virus vaccine components within the multivalent vaccine recipient. DNA vaccines, in combination with other approaches, may increase the complexity and effectiveness of the immune response. Whole inactivated virus approaches have been used successfully for other viral diseases, reduce interference issues in multivalent vaccines, and have protected nonhuman primates from viremia following challenge with wild-type virus. Recombinant subunit vaccines have also protected nonhuman primates from viremia and offer a more focused approach in an attempt to tailor antibody and cell-mediated immure responses. While pathogenesis studies seek to dissect immune responses in an attempt to avoid vaccine-related disease enhancement, these risks, which apply to all vaccine approaches, may need to be evaluated empirically.
C1 [Vaughn, David W.] USA, Mil Infect Dis Res Program, Med Res & Dev Command, Ft Detrick, MD USA.
[Whitehead, Stephen S.] NIAID, Infect Dis Lab, Bethesda, MD 20892 USA.
[Durbin, Anna P.] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Immunizat Res, Dept Int Hlth, Baltimore, MD USA.
RP Vaughn, DW (reprint author), USA, Mil Infect Dis Res Program, Med Res & Dev Command, Ft Detrick, MD USA.
NR 356
TC 1
Z9 1
U1 1
U2 3
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
BN 978-0-08-091902-7
PY 2009
BP 287
EP 324
PG 38
WC Public, Environmental & Occupational Health; Immunology; Infectious
Diseases
SC Public, Environmental & Occupational Health; Immunology; Infectious
Diseases
GA BCR60
UT WOS:000311106000021
ER
PT S
AU Chen, GL
Subbarao, K
AF Chen, Grace L.
Subbarao, Kanta
BE Compans, RW
Orenstein, WA
TI Live Attenuated Vaccines for Pandemic Influenza
SO VACCINES FOR PANDEMIC INFLUENZA
SE Current Topics in Microbiology and Immunology
LA English
DT Article; Book Chapter
DE live attenuated influenza vaccines pandemic; Plasmid-based reverse
genetics techniques
ID COLD-ADAPTED INFLUENZA; A VIRUS-VACCINES; RANDOMIZED CONTROLLED-TRIAL;
YOUNG-CHILDREN; HONG-KONG; TEMPERATURE SENSITIVITY; INACTIVATED
VACCINES; GENOTYPIC STABILITY; ANTIBODY-RESPONSES; REVERSE GENETICS
AB In this chapter, we will review the development of and clinical experience with the currently licensed seasonal live attenuated influenza vaccines (LAIV) and preclinical studies of H5, H7, and H9 live attenuated pandemic influenza vaccine candidates. Vectored vaccine approaches will not be reviewed in this chapter. Experience with seasonal influenza vaccination has demonstrated the safety and efficacy of LAIV in both children and adults; moreover, cross-protection among antigenically distinct viruses within the same subtype may be induced by LAIV. While clinical studies and further characterization of the immunologic response to avian influenza viruses are still needed, the experience with seasonal LAIV underscores the potential of live attenuated vaccines to play an important role in the event of a pandemic.
C1 [Subbarao, Kanta] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Subbarao, K (reprint author), NIAID, Infect Dis Lab, NIH, Bldg 33,Room 3E13C-1,33 N Dr,MSC 3203, Bethesda, MD 20892 USA.
EM chengra@niaid.nih.gov; ksubbarao@niaid.nih.gov
FU Intramural NIH HHS
NR 82
TC 16
Z9 17
U1 0
U2 3
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0070-217X
BN 978-3-540-92164-6
J9 CURR TOP MICROBIOL
JI Curr.Top.Microbiol.Immunol.
PY 2009
VL 333
BP 109
EP 132
DI 10.1007/978-3-540-92165-3_5
D2 10.1007/978-3-540-92165-3
PG 24
WC Biotechnology & Applied Microbiology; Immunology; Microbiology
SC Biotechnology & Applied Microbiology; Immunology; Microbiology
GA BKY26
UT WOS:000269608300005
PM 19768402
ER
PT J
AU Jefferson, AL
Benjamin, EJ
AF Jefferson, Angela L.
Benjamin, Emelia J.
BE Wahlund, LO
Erkinjuntti, T
Gauthier, S
TI Cardiovascular disease, cognitive decline, and dementia
SO VASCULAR COGNITIVE IMPAIRMENT IN CLINICAL PRACTICE
LA English
DT Article; Book Chapter
ID VASCULAR RISK-FACTORS; ARTERY-BYPASS GRAFT; INCIDENT ALZHEIMER-DISEASE;
NONVALVULAR ATRIAL-FIBRILLATION; LEFT-VENTRICULAR DYSFUNCTION; HOSPITAL
CARDIAC-ARREST; CEREBRAL BLOOD-FLOW; HEART-FAILURE; APOLIPOPROTEIN-E;
MYOCARDIAL-INFARCTION
C1 [Jefferson, Angela L.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Jefferson, Angela L.] Boston Univ, Sch Med, Alzheimers Dis Ctr, Boston, MA 02118 USA.
[Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Prevent Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
RP Jefferson, AL (reprint author), Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
OI Benjamin, Emelia/0000-0003-4076-2336
NR 80
TC 2
Z9 2
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-0-521-87537-0
PY 2009
BP 166
EP 177
DI 10.1017/CBO9780511575976.014
D2 10.1017/CBO9780511575976
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA BDM65
UT WOS:000313873000014
ER
PT J
AU Reynolds, TL
Barnes, HJ
Wolfe, B
Lu, L
Camp, DM
Malarkey, DE
AF Reynolds, T. L.
Barnes, H. J.
Wolfe, B.
Lu, L.
Camp, D. M.
Malarkey, D. E.
TI Bilateral Nocardial Endophthalmitis in a Prothonotary Warbler
(Protonotaria citrea)
SO VETERINARY PATHOLOGY
LA English
DT Article
DE Acid-fast stain; avian; eye; Fite's acid-fast stain; Nocardia;
Passeriformes; prothonotary warbler; Protonotaria citrea;
pyogranulomatous endophthalmitis
AB A 7-year-old captive female prothonotary warbler (Protonotaria citrea) died following chronic feather and weight loss. At necropsy, the right eye had a 2 x 2 x 1 mm corneal plaque Of inspissated yellow-tan material and edema of the lower eyelid. Microscopically, both eyes exhibited diffuse, severe pyogranulomatous endophthalmitis with retinal necrosis and detachment. Numerous intralesional branching, gram-positive. beaded, filamentous bacteria formed a thick mat attached to the retinal pigmented epithelium and extending into the pecten. Bacteria were strongly acid-fast positive by Fite's stain but only occasionally acid-fast positive by Ziehl-Neelsen staining, a characteristic consistent with a Nocardia spp. Infected regions demonstrated positive In situ hybridization reactivity with a probe complementary to the 16S rRNA gene of Nocardia spp. There was no evidence of primary bacterial infection in the other organs examined.
C1 [Malarkey, D. E.] NIEHS, Natl Toxicol Program, Pathol Grp, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
[Reynolds, T. L.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Barnes, H. J.] N Carolina State Univ, Coll Vet Med, Dept Populat Hlth & Pathobiol, Raleigh, NC USA.
[Wolfe, B.] Hanes Vet Med Ctr, Asheboro, NC USA.
[Lu, L.] RFU, Sch Med, N Chicago, IL USA.
[Camp, D. M.] William Beaumont Hosp, Res Inst, Royal Oak, MI 48072 USA.
RP Malarkey, DE (reprint author), NIEHS, Natl Toxicol Program, Pathol Grp, Cellular & Mol Pathol Branch, 111 Alexander Dr,Maildrop B3-O6,POB 12233, Res Triangle Pk, NC 27709 USA.
EM malarkey@niehs.nih
FU Intramural NIH HHS [Z99 ES999999]
NR 16
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL VET PATHOLOGIST
PI LAWRENCE
PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 USA
SN 0300-9858
J9 VET PATHOL
JI Vet. Pathol.
PD JAN
PY 2009
VL 46
IS 1
BP 120
EP 123
PG 4
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA 392UD
UT WOS:000262326800018
PM 19112125
ER
PT B
AU Paul, AV
Belov, GA
Ehrenfeld, E
Wimmer, E
AF Paul, Aniko V.
Belov, George A.
Ehrenfeld, Ellie
Wimmer, Eckard
BE Cameron, CE
Gotte, M
Raney, KD
TI Model of Picornavirus RNA Replication
SO VIRAL GENOME REPLICATION
LA English
DT Article; Book Chapter
ID POLY(RC) BINDING-PROTEIN; HUMAN RHINOVIRUS TYPE-14; RIBOSOMAL ENTRY
SITE; MOUTH-DISEASE VIRUS; POLIOVIRUS RNA; VPG URIDYLYLATION;
NEGATIVE-STRAND; VIRAL REPLICATION; ELEMENT CRE; IN-VITRO
C1 [Paul, Aniko V.] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA.
[Belov, George A.; Ehrenfeld, Ellie] NIAID, Picornavirus Replicat Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Paul, AV (reprint author), SUNY Stony Brook, Dept Mol Genet & Microbiol, Nicolls Rd, Stony Brook, NY 11794 USA.
EM apaul@notes.cc.sunysb.edu; gbelov@niaid.nih.gov;
eehrenfeld@niaid.nih.gov; ewim-mer@ms.cc.sunysb.edu
RI Belov, George/B-4625-2008
OI Belov, George/0000-0002-0892-1731
NR 59
TC 4
Z9 4
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-0-387-89425-6
PY 2009
BP 3
EP 23
DI 10.1007/b135974_1
D2 10.1007/b135974
PG 21
WC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
SC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
GA BKY23
UT WOS:000269607500001
ER
PT B
AU McDonald, SM
Patton, JT
AF McDonald, Sarah M.
Patton, John T.
BE Cameron, CE
Gotte, M
Raney, KD
TI Core-Associated Genome Replication Mechanisms of dsRNA Viruses
SO VIRAL GENOME REPLICATION
LA English
DT Article; Book Chapter
ID DOUBLE-STRANDED-RNA; ROTAVIRUS MESSENGER-RNA; L-A-VIRUS; CYTOPLASMIC
POLYHEDROSIS-VIRUS; POL FUSION PROTEIN; RICE-DWARF-VIRUS; CRYOELECTRON
MICROSCOPY; ELECTRON CRYOMICROSCOPY; 3-DIMENSIONAL STRUCTURE; ASSEMBLY
PATHWAY
C1 [Patton, John T.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[McDonald, Sarah M.] NIAID, Dept Lab Infect Dis, NIH, Bethesda, MD 20892 USA.
RP McDonald, SM (reprint author), NIAID, Dept Lab Infect Dis, NIH, Bethesda, MD 20892 USA.
EM mcdonaldsa@niaid.nih.gov; jpatton@niaid.nih.gov
RI Patton, John/P-1390-2014
NR 83
TC 3
Z9 3
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-0-387-89425-6
PY 2009
BP 201
EP 224
DI 10.1007/b135974_11
D2 10.1007/b135974
PG 24
WC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
SC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
GA BKY23
UT WOS:000269607500011
ER
PT B
AU Wendeler, M
Miller, JT
Le Grice, SFJ
AF Wendeler, Michaela
Miller, Jennifer T.
Le Grice, Stuart F. J.
BE Cameron, CE
Gotte, M
Raney, KD
TI Human Immunodeficiency Virus Reverse Transcriptase
SO VIRAL GENOME REPLICATION
LA English
DT Article; Book Chapter
ID CENTRAL DNA FLAP; TYPE-1 POLYPURINE TRACT; RNASE-H CLEAVAGE; PRIMER
ACTIVATION SIGNAL; INFECTIOUS-ANEMIA VIRUS; NUCLEOSIDE ANALOG
INTERFERENCE; TRYPTOPHAN-REPEAT MOTIF; UNNATURAL AMINO-ACIDS;
DOUBLE-STRANDED DNA; PLUS-STRAND
C1 [Wendeler, Michaela; Miller, Jennifer T.; Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
RP Le Grice, SFJ (reprint author), NCI, HIV Drug Resistance Program, Bldg 535,Room 312,POB B, Frederick, MD 21702 USA.
EM mwendeler@ncifcrf.gov; jtmiller@ncifcrf.gov; slegrice@ncifcrf.gov
NR 195
TC 1
Z9 2
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
BN 978-0-387-89425-6
PY 2009
BP 403
EP 427
DI 10.1007/b135974_19
D2 10.1007/b135974
PG 25
WC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
SC Biotechnology & Applied Microbiology; Cell Biology; Immunology;
Microbiology; Virology
GA BKY23
UT WOS:000269607500019
ER
PT J
AU Cui, J
Wilke, M
Logothetis, NK
Leopold, DA
Liang, HL
AF Cui, Jie
Wilke, Melanie
Logothetis, Nikos K.
Leopold, David A.
Liang, Hualou
TI Visibility states modulate microsaccade rate and direction
SO VISION RESEARCH
LA English
DT Article
DE Microsaccade; Generalized flash suppression; Multistable perception;
Fixation; Visual attention
ID FIXATIONAL EYE-MOVEMENTS; PRIMARY VISUAL-CORTEX; COVERT ATTENTION;
BINOCULAR-RIVALRY; INHIBITION; SUPPRESSION; NEURONS; INDEX;
PROLONGATION; ORIENTATION
AB We investigated how the perceptual visibility of a target influences the pattern of microsaccadic eye movements expressed during generalized flash suppression. We found that the microsaccade rate was highly dependent on the reported visibility of the target. In the visible trials, the microsaccade rate promptly rebounded to the pre-onset level, whereas on the invisible trials the rate remained low, reaching pre-onset levels hundreds of milliseconds later. In addition, the directional distributions of microsaccades were biased to the target positions in the visible condition. The present findings indicate that the microsaccade behavior is highly correlated with the perceptual state of target visibility, and suggest that the measured microsaccade rate and direction are reliable indicators of the perception. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Cui, Jie; Liang, Hualou] Univ Texas Houston, Sch Hlth Informat Sci, Houston, TX 77030 USA.
[Wilke, Melanie; Leopold, David A.] NIMH, UCNI, Bethesda, MD 20892 USA.
[Logothetis, Nikos K.] Max Planck Inst Biol Cybernet, D-72076 Tubingen, Germany.
RP Liang, HL (reprint author), Univ Texas Houston, Sch Hlth Informat Sci, Houston, TX 77030 USA.
EM Hualou.Liang@uth.tmc.edu
OI Leopold, David/0000-0002-1345-6360
FU NIH [R01 MH072034]; Max Planck Society; NSERC postdoctoral fellowship
FX We thank Dr. Igor Kagan for helpful discussions. This work was supported
by NIH Grant R01 MH072034 (H.L.), Max Planck Society, and partially by a
NSERC postdoctoral fellowship (J.C.).
NR 48
TC 35
Z9 35
U1 1
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0042-6989
J9 VISION RES
JI Vision Res.
PD JAN
PY 2009
VL 49
IS 2
BP 228
EP 236
DI 10.1016/j.visres.2008.10.015
PG 9
WC Neurosciences; Ophthalmology
SC Neurosciences & Neurology; Ophthalmology
GA 396QK
UT WOS:000262606000007
PM 19007803
ER
PT S
AU Jian, B
Vemuri, BC
Ozarslan, E
AF Jian, Bing
Vemuri, Baba C.
Oezarslan, Evren
BE Laidlaw, D
Weickert, J
TI A Mixture of Wisharts (MOW) Model for Multifiber Reconstruction
SO VISUALIZATION AND PROCESSING OF TENSOR FIELDS: ADVANCES AND PERSPECTIVES
SE Mathematics and Visualization
LA English
DT Article; Book Chapter
ID DIFFUSION-WEIGHTED MRI; FIBER ORIENTATIONS; HUMAN BRAIN; RESOLUTION;
TENSOR; TRACKING; SIGNAL; DECONVOLUTION; ARCHITECTURE; COEFFICIENT
AB Diffusion-weighted magnetic resonance imaging (DW-MRI) is a noninvasive imaging technique that allows neural tissue architecture, to be probed at a microscopic scale in vivo. By producing quantitative data on the motion of water molecules that naturally occurs in brain tissues as part of the physical diffusion process; DW-MRI can be used to map the fiber paths in the brain white matter. Estimating the local complex architecture in the presence of intra-voxel heterogeneity caused by multiple fiber pathways is of great importance and requires sophisticated modeling techniques.
In this chapter, we present a review of our recently introduced novel mathematical model [27] and an accompanying unified computational Framework for spherical deconvolution to perform multi-fiber reconstruction [28]. In our model, the diffusion-weighted MR signal attenuation is characterized by the Laplace transform of a continuous mixture of diffusion tensors. When the mixing distribution is a Wishart distribution; the Laplace transform yields a, closed form expression. Additionally, we show that the traditional diffusion tensor model is a limiting case of this continuous mixture of tensors model. We then formulate the reconstruction problem in a unified deconvolution framework that facilitates investigation of several deconvolution schemes and achieves stable, sparse and accurate solutions. Finally, we present, results of testing this theoretical model and the accompanying unified computational framework, on synthetic data and real rat brain data. The comparisons with several competing methods empirically suggest that the proposed model yields efficient and accurate solutions in the presence of intra-voxel orientational heterogeneity.
C1 [Jian, Bing; Vemuri, Baba C.] Univ Florida, Dept Comp & Informat Sci & Engn, Gainesville, FL 32611 USA.
[Oezarslan, Evren] NICHD, Sect Tissue Biophys & Biomimet, LIMB, NIH, Bethesda, MD 20892 USA.
[Vemuri, Baba C.] E324 Univ Florida, Dept CISE, Ctr Vis Graph & Med Imaging, Gainesville, FL 32611 USA.
RP Jian, B (reprint author), Univ Florida, Dept Comp & Informat Sci & Engn, POB 116120,Room E331,CISE Bldg, Gainesville, FL 32611 USA.
EM bjian@cise.ufl.edu; vemuri@cise.ufl.edu; evren@helix.nih.gov
RI Ozarslan, Evren/B-4858-2013
OI Ozarslan, Evren/0000-0003-0859-1311
NR 45
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 1612-3786
BN 978-3-540-88377-7
J9 MATH VIS
PY 2009
BP 39
EP 56
DI 10.1007/978-3-540-88378-4_3
D2 10.1007/978-3-540-88378-4
PG 18
WC Computer Science, Artificial Intelligence; Mathematics, Applied; Imaging
Science & Photographic Technology
SC Computer Science; Mathematics; Imaging Science & Photographic Technology
GA BJU86
UT WOS:000267219100003
ER
PT S
AU Kehrl, JH
Hwang, IY
Park, C
AF Kehrl, John H.
Hwang, Il-Young
Park, Chung
BE McGavern, D
Dustin, M
TI Chemoattractant Receptor Signaling and Its Role in Lymphocyte Motility
and Trafficking
SO VISUALIZING IMMUNITY
SE Current Topics in Microbiology and Immunology
LA English
DT Review; Book Chapter
ID T-CELL MOTILITY; HETEROTRIMERIC G-PROTEINS; HIGH ENDOTHELIAL VENULES;
IN-VIVO; PHOSPHOINOSITIDE 3-KINASE; SPHINGOSINE 1-PHOSPHATE; LEUKOCYTE
MIGRATION; RGS PROTEINS; 2-PHOTON MICROSCOPY; IMMUNE FUNCTION
AB Intravital microscopy has provided extraordinary glimpses of lymphocytes crossing high endothelial venules, detailed the movements and interactions of lymphocytes within lymph organs, and recorded lymphocytes crossing the lymphatic endothelium into the efferent lymph. Helping to orchestrate these movements are signals generated by the engagement of chemoattractants with their cognate receptors. Chemokines present on high endothelial venules and within lymph organs, and the high levels of sphingosine I-phosphate in the lymph provide signposts to help guide lymphocytes and provide intracellular signals that affect lymphocyte polarity and motility. Within lymph nodes, T and B lymphocytes migrate along networks of fibroblastic reticular cells and follicular dendritic, respectively, which provide an adhesive platform and solid phased chemokines. Illustrating the importance of chemoattractant receptors in these processes, lymphocytes that lack CXCR4, CXCR5, CCR7, or S1PR1, or which lack crucial signaling molecules activated by these receptors, exhibit defects in lymph node entrance, positioning, polarity, motility, and/or lymph node egress. This review will focus on the contributions of in vivo imaging of lymphocytes from various mouse mutants to our understanding of the roles chemoattractants play in lymphocyte entrance into and exit from lymph nodes, and in coordinating and facilitating the movements of lymphocytes within lymph nodes.
C1 [Kehrl, John H.; Hwang, Il-Young; Park, Chung] NIAID, Cell Mol Immunol Sect B, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Kehrl, JH (reprint author), NIAID, Cell Mol Immunol Sect B, Immunoregulat Lab, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM jkehrl@niaid.nih.gov; jkehrl@niaid.nih.gov; jkehrl@niaid.nih.gov
OI Kehrl, John/0000-0002-6526-159X
FU Intramural NIH HHS
NR 82
TC 20
Z9 20
U1 0
U2 1
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0070-217X
BN 978-3-540-93862-0
J9 CURR TOP MICROBIOL
JI Curr.Top.Microbiol.Immunol.
PY 2009
VL 334
BP 107
EP 127
DI 10.1007/978-3-540-93864-4_5
D2 10.1007/978-3-540-93864-4
PG 21
WC Engineering, Biomedical; Immunology; Microbiology
SC Engineering; Immunology; Microbiology
GA BKM58
UT WOS:000268504000005
PM 19521683
ER
PT S
AU Kang, SS
McGavern, DB
AF Kang, Silvia S.
McGavern, Dorian B.
BE McGavern, D
Dustin, M
TI Inflammation on the Mind: Visualizing Immunity in the Central Nervous
System
SO VISUALIZING IMMUNITY
SE Current Topics in Microbiology and Immunology
LA English
DT Review; Book Chapter
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
LYMPHOCYTIC-CHORIOMENINGITIS-VIRUS; CYTOTOXIC T-LYMPHOCYTES; GREEN
FLUORESCENT PROTEIN; BLOOD-BRAIN-BARRIER; POSITRON-EMISSION-TOMOGRAPHY;
DEEP CERVICAL LYMPH; CLASS-I MOLECULES; EXPERIMENTAL ALLERGIC
ENCEPHALOMYELITIS; MYELIN OLIGODENDROCYTE GLYCOPROTEIN
AB The central nervous system (CNS) is a remarkably complex structure that utilizes electrochemical signaling to coordinate activities throughout the entire body. Because the nervous system contains nonreplicative cells, it is postulated that, through evolutionary pressures, this compartment has acquired specialized mechanisms to limit damage. One potential source of damage comes from our immune system, which has the capacity to survey the CNS and periphery for the presence of foreign material. The immune system is equipped with numerous effector mechanisms and can greatly alter the homeostasis and function of the CNS. Degeneration, autoimmunity, and pathogen infection can all result in acute, and sometimes chronic, inflammation within the CNS. Understanding the specialized functionality of innate and adaptive immune cells within the CNS is critical to the design of more efficacious treatments to mitigate CNS inflammatory conditions. Much of our knowledge of CNS-immune interactions stems from seminal studies that have used static and dynamic imaging approaches to visualize inflammatory cells responding to different CNS conditions. This review will focus on how imaging techniques have elevated our understanding of CNS inflammation as well as the exciting prospects that lie ahead as we begin to pursue investigation of the inflamed CNS in real time.
C1 [Kang, Silvia S.; McGavern, Dorian B.] NINDS, NIH, Bethesda, MD 20892 USA.
RP McGavern, DB (reprint author), NINDS, NIH, 10 Ctr Dr,Bldg 10,Rm 7C213, Bethesda, MD 20892 USA.
EM mcgavernd@mail.nih.gov
OI McGavern, Dorian/0000-0001-9568-545X
FU Intramural NIH HHS [ZIA NS003112-07]; NIAID NIH HHS [AI 070967-01, AI
075298-01, R01 AI070967, R01 AI075298, R56 AI075298]; NINDS NIH HHS [NS
061447-01, F32 NS061447]
NR 204
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0070-217X
BN 978-3-540-93862-0
J9 CURR TOP MICROBIOL
JI Curr.Top.Microbiol.Immunol.
PY 2009
VL 334
BP 227
EP 263
DI 10.1007/978-3-540-93864-4_10
D2 10.1007/978-3-540-93864-4
PG 37
WC Engineering, Biomedical; Immunology; Microbiology
SC Engineering; Immunology; Microbiology
GA BKM58
UT WOS:000268504000010
PM 19521688
ER
PT S
AU Zhang, L
Xiong, W
AF Zhang, Li
Xiong, Wei
BE Litwack, G
TI MODULATION OF THE CYS-LOOP LIGAND-GATED ION CHANNELS BY FATTY ACID AND
CANNABINOIDS
SO VITAMINS AND HORMONES: ANANDAMIDE AN ENDOGENOUS CANNABINOID
SE Vitamins and Hormones
LA English
DT Review; Book Chapter
ID NICOTINIC ACETYLCHOLINE-RECEPTORS; RAT SPINAL-CORD; 5-HT3 RECEPTORS;
GLYCINE RECEPTORS; ARACHIDONIC-ACID; XENOPUS OOCYTES;
SYNAPTIC-TRANSMISSION; MEDIATED RESPONSES; DOCOSAHEXAENOIC ACID;
CHLORIDE CHANNEL
AB The Cys-loop ligand-gated ion channel (LGIC) family comprises a group of membrane ion channel receptors that play a crucial rote in fast synaptic neurotransmission in the central and peripheral nervous system. The members of this superfamily include gamma-aminobutyric acid type A (GABA(A)), neuronal nicotinic acetylcholine (nACh), 5-HT(3), and glycine receptors. These receptors serve as therapeutic sites for general anesthetic, antipsychoactive, antinociceptive, and anxiolytic drugs in the brain. These receptors are also thought to be primary targets of alcohol and other drugs of abuses. A number of studies reported that fatty acids affected the function of GABA(A) receptors in the early nineties. Accumulating evidence has suggested that the derivatives of arachidonic acid (AA), such as anandamide (N-arachidonoylethanolamine, AEA) and arachidonoylglycerol (2-AG), can critically regulate the other members of the Cys-loop LGIC superfamily through a cannabinoid receptor-independent mechanism. This chapter focuses on the results of recent studies showing that the Cys-loop LGICs could be additional molecular targets for fatty acid and endocannabinoid action in the central and peripheral nervous system. Some of these targets may mediate behavioral effects for cannabinoids to alter neuronal function.
C1 [Zhang, Li; Xiong, Wei] NIAAA, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
RP Zhang, L (reprint author), NIAAA, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
RI Xiong, Wei/F-8251-2011
NR 80
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0083-6729
BN 978-0-12-374782-2
J9 VITAM HORM
JI Vitam. Horm.
PY 2009
VL 81
BP 315
EP 335
DI 10.1016/S0083-6729(09)81012-1
PG 21
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA BKU39
UT WOS:000269266800012
PM 19647117
ER
PT S
AU Toth, A
Blumberg, PM
Boczan, J
AF Toth, Attila
Blumberg, Peter M.
Boczan, Judit
BE Litwack, G
TI ANANDAMIDE AND THE VANILLOID RECEPTOR (TRPV1)
SO VITAMINS AND HORMONES: ANANDAMIDE AN ENDOGENOUS CANNABINOID
SE Vitamins and Hormones
LA English
DT Review; Book Chapter
ID PRIMARY SENSORY NEURONS; ROOT GANGLION NEURONS; PROTEIN-KINASE-C;
ENDOGENOUS CANNABINOID ANANDAMIDE; ACID AMIDE HYDROLASE; ENDOCANNABINOID
TRANSPORTER INHIBITORS; CENTRAL-NERVOUS-SYSTEM; DORSAL-HORN NEURONS;
CAPSAICIN RECEPTOR; IN-VITRO
AB Arachidonylethanolamide (anandamide) was identified some 15 years ago as a brain constituent that binds to the cannabinoid receptor. After this seminal discovery, multiple new receptors for anandamide have been identified, including the vanilloid receptor (TRPV1), and anandamide is now frequently referred as an "endovanilloid." Characterization of the action of anandamide on TRPV1 revealed that (1) the potency and efficacy of anandamide on TRPV1 very much depend on the species and tissue, (2) anandamide responsiveness in vivo is significantly controlled by its local metabolism, (3) anandamide activation of cannabinoid receptors regulates TRPV1 responsiveness, (4) TRPV1 activation regulates anandamide synthesis, (5) anandamide metabolites affect TRPV1 responses, (6) the often observed convergent physiological actions of anandamide and TRPV1 agonists in neither case necessarily represent direct effects on TRPV1, and (7) coactivation of the cannabinoid receptors and TRPV1 often complicates the distinction between these pathways. These issues are reviewed here together with the potential implications for the pathophysiological and pharmacological regulation of inflammatory, respiratory, and cardiovascular disorders, as well as of appetite and fat metabolism.
C1 [Toth, Attila] Univ Debrecen, Inst Cardiol, Div Clin Physiol, H-4012 Debrecen, Hungary.
[Blumberg, Peter M.] NCI, Mol Mech Tumor Promot Sect, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Boczan, Judit] Univ Debrecen, Dept Neurol, H-4012 Debrecen, Hungary.
RP Toth, A (reprint author), Univ Debrecen, Inst Cardiol, Div Clin Physiol, H-4012 Debrecen, Hungary.
RI Toth, Attila/F-4859-2010
OI Toth, Attila/0000-0001-6503-3653
NR 142
TC 40
Z9 40
U1 0
U2 6
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0083-6729
BN 978-0-12-374782-2
J9 VITAM HORM
JI Vitam. Horm.
PY 2009
VL 81
BP 389
EP 419
DI 10.1016/S0083-6729(09)81015-7
PG 31
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA BKU39
UT WOS:000269266800015
PM 19647120
ER
PT J
AU Siantar, CH
Taylor, TP
Coleman, CN
AF Siantar, Christine Hartmann
Taylor, Tammy P.
Coleman, C. Norman
BE Maurer, SM
TI Recovering from Nuclear and Radiological Attacks
SO WMD TERRORISM: SCIENCE AND POLICY CHOICES
LA English
DT Article; Book Chapter
C1 [Siantar, Christine Hartmann] Lawrence Livermore Natl Lab, Livermore, CA 94550 USA.
[Coleman, C. Norman] Natl Canc Inst, Radiat Oncol Sci Program, Bethesda, MD 20892 USA.
RP Siantar, CH (reprint author), Lawrence Livermore Natl Lab, Livermore, CA 94550 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU M I T PRESS
PI CAMBRIDGE
PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA
BN 978-0-262-01298-0
PY 2009
BP 329
EP 364
PG 36
WC Planning & Development; Public Administration
SC Public Administration
GA BPL40
UT WOS:000279133000013
ER
PT J
AU Vines, AI
Ta, M
Esserman, D
Baird, DD
AF Vines, Anissa I.
Ta, Myduc
Esserman, Denise
Baird, Donna D.
TI A Comparison of the Occurrence and Perceived Stress of Major Life Events
in Black and White Women
SO WOMEN & HEALTH
LA English
DT Article
DE stress; life events; race; women's health
ID AFRICAN-AMERICAN; SOCIOECONOMIC-STATUS; DEPRESSIVE SYMPTOMS; SOCIAL
SUPPORT; HEALTH; DISCRIMINATION; GENDER; RACE; EPIDEMIOLOGY;
INEQUALITIES
AB Purpose: To describe the occurrence and perceived stress of major life events, and to investigate whether adjusting for socioeconomic status reduced race/ethnicity differences.
Methods: Black (n = 639) and white (n = 419) women aged 35-49 years responded to 14 major life event questions within the domains of employment, health, relationship, finance, residential change, and crime.
Main Findings: The total number of life events did not differ by race/ethnicity, but black women reported significantly more events in the domains of relationship, financial, and residential change than white women. White women generally reported higher stress for a given event than black women, although for "residential change'' black women reported more severe stress than the white women.
Conclusions: Inclusion of both the occurrence and perceived stress of major life events can improve our understanding of how this stressor may affect health.
C1 [Vines, Anissa I.; Ta, Myduc] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Esserman, Denise] Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC 27599 USA.
[Baird, Donna D.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Vines, AI (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, 266 Rosenau Hall,CB 7435, Chapel Hill, NC 27599 USA.
EM avines@email.unc.edu
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU NICHD NIH HHS [R03 HD055029-02, R03 HD055029]
NR 29
TC 5
Z9 5
U1 1
U2 3
PU HAWORTH PRESS INC
PI BINGHAMTON
PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA
SN 0363-0242
J9 WOMEN HEALTH
JI Women Health
PY 2009
VL 49
IS 5
BP 368
EP 380
DI 10.1080/03630240903238743
PG 13
WC Public, Environmental & Occupational Health; Women's Studies
SC Public, Environmental & Occupational Health; Women's Studies
GA 517LR
UT WOS:000271616300002
PM 19851943
ER
PT J
AU Bustamante, ML
Villarroel, J
Francesetti, V
Rios, M
Arcos-Burgos, M
Jerez, S
Iturra, P
Solari, A
Silva, H
AF Bustamante, M. Leonor
Villarroel, Juana
Francesetti, Valeria
Rios, Matias
Arcos-Burgos, Mauricio
Jerez, Sonia
Iturra, Patricia
Solari, Aldo
Silva, Hernan
TI Planning in borderline personality disorder: Evidence for distinct
subpopulations
SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Borderline personality disorder; neuropsychological tests; impulsivity
ID EXECUTIVE FUNCTION DEFICITS; COGNITIVE FUNCTION; MEMORY;
PSYCHOPATHOLOGY; NEUROPSYCHOLOGY; IMPULSIVITY; SCALE; ADHD
AB Objective. Borderline personality disorder is a severe mental disorder, whereas previous studies suggest executive functions may be impaired. The aim of this study was to evaluate executive planning in a sample of 85 individuals. Methods. Planning was assessed by means of the Tower of London (Drexel University version) task. Latent class cluster analysis models were adjusted to the data. Results. We identified two different subpopulations of borderline personality disorder patients, one of them with significantly reduced performance. Conclusion. Neuropsychological mechanisms may be involved in borderline personality disorder, at least in a subgroup of patients.
C1 [Bustamante, M. Leonor; Villarroel, Juana; Jerez, Sonia; Silva, Hernan] Univ Chile, Clin Hosp, Dept Psychiat & Mental Hlth, Personal Disorders Unit, Santiago, Chile.
[Bustamante, M. Leonor; Iturra, Patricia; Solari, Aldo] Univ Chile, Fac Med, Inst Biomed Sci, Santiago 7, Chile.
[Francesetti, Valeria; Rios, Matias] Univ Chile, Fac Social Sci, Santiago 7, Chile.
[Arcos-Burgos, Mauricio] Univ Miami, Leonard M Miller Sch Med, Dept Psychiat & Behav Sci, Coral Gables, FL 33124 USA.
[Arcos-Burgos, Mauricio] NIH, Med Genet Branch, Bethesda, MD 20892 USA.
RP Bustamante, ML (reprint author), Univ Chile, Clin Hosp, Dept Psychiat, Personal Disorders Unit, Av La Paz 1003, Santiago, Chile.
EM mbustamante@med.uchile.cl
RI Bustamante, Maria Leonor/H-3728-2014
OI Bustamante, Maria Leonor/0000-0001-9071-2463
FU Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT)
[1071045]; Clinical Hospital of the University of Chile [193/06]
FX This work was financed by the Fondo Nacional de Desarrollo Cientifico y
Tecnologico (FONDECYT) Project 1071045 and by the Oficina de Apoyo a la
Investigacion Cientifica (OAIC) from the Clinical Hospital of the
University of Chile, Project 193/06.
NR 34
TC 3
Z9 3
U1 1
U2 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1562-2975
J9 WORLD J BIOL PSYCHIA
JI World J. Biol. Psychiatry
PY 2009
VL 10
IS 4
BP 512
EP 517
DI 10.3109/15622970903079481
PN 2
PG 6
WC Psychiatry
SC Psychiatry
GA 535WS
UT WOS:000273003200022
PM 19658046
ER
PT J
AU Liu, A
Chen, Y
Yang, Z
Feng, Y
Rui, W
Luo, W
Liu, Y
Gonzalez, FJ
Dai, R
AF Liu, A.
Chen, Y.
Yang, Z.
Feng, Y.
Rui, W.
Luo, W.
Liu, Y.
Gonzalez, F. J.
Dai, R.
TI New metabolites of fenofibrate in Sprague-Dawley rats by
UPLC-ESI-QTOF-MS-based metabolomics coupled with LC-MS/MS
SO XENOBIOTICA
LA English
DT Article
DE Metabolomics; metabolites; metabolism pathway; fenofibrate; rat
ID ACTIVATED RECEPTOR-ALPHA; PPAR-ALPHA; PEROXISOME PROLIFERATORS;
SPECIES-DIFFERENCES; HEPATIC PEROXISOME; CLOFIBRIC ACID;
HEPATOCARCINOGENESIS; DISPOSITION; METABONOMICS; MECHANISM
AB Fenofibrate has been widely used for the treatment of dyslipidaemia with a long history. Species differences of its metabolism were reported, but its metabolites in rodent have not been fully investigated. Urine and plasma samples were collected before and after oral dosages of fenofibrate in Sprague-Dawley rats. Urine samples were subjected to ultra-performance liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOF-MS) analysis, and projection to latent structures discriminant analysis was used for the identification of metabolites. New metabolites in urine and plasma were also studied by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The metabolism pathway was studied in rat hepatocytes. Synthesized and purchased authentic compounds were used for metabolite identification by LC-MS/MS. Five ever-reported metabolites were identified and another four new ones were found. Among these new metabolites, fenofibric acid taurine and reduced fenofibric acid taurine indicate new phase II conjugation pathway of fenofibrate.
C1 [Liu, A.; Chen, Y.; Yang, Z.; Luo, W.; Liu, Y.; Dai, R.] Chinese Acad Sci, Guangzhou Inst Biomed & Hlth, Guangzhou 510663, Guangdong, Peoples R China.
[Feng, Y.; Rui, W.] Guangdong Pharmaceut Univ, Guangzhou, Guangdong, Peoples R China.
[Gonzalez, F. J.] NCI, NIH, Bethesda, MD 20892 USA.
RP Dai, R (reprint author), Chinese Acad Sci, Guangzhou Inst Biomed & Hlth, Guangzhou 510663, Guangdong, Peoples R China.
EM dai_renke@gibh.ac.cn
FU Intramural NIH HHS [Z01 BC005562-21]
NR 28
TC 16
Z9 18
U1 3
U2 16
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 0049-8254
J9 XENOBIOTICA
JI Xenobiotica
PY 2009
VL 39
IS 4
BP 345
EP 354
AR PII 909819518
DI 10.1080/00498250802680827
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 434VU
UT WOS:000265303000007
PM 19350456
ER
PT S
AU Bandettini, PA
AF Bandettini, Peter A.
BE Miller, MB
Kingstone, A
TI What's New in Neuroimaging Methods?
SO YEAR IN COGNITIVE NEUROSCIENCE 2009
SE Annals of the New York Academy of Sciences
LA English
DT Article
DE functional MRI (fMRI); voxel-based morphometry (VBM); diffusion tensor
imaging (DTI); diffusion spectrum imaging (DSI); magnetoencephalography
(MEG); electroencephalography (EEG); optical imaging; diffuse optical
tomography (DOT); endogenous oscillations; default network; resting
state fluctuations; fMRI decoding; multivariate analysis; positron
emission tomography (PET); region of interest (ROI)
ID VOXEL-BASED MORPHOMETRY; GRAY-MATTER DENSITY; STATE FUNCTIONAL
CONNECTIVITY; APPARENT-DIFFUSION-COEFFICIENT; DEFAULT-MODE NETWORK;
CEREBRAL-BLOOD-FLOW; HUMAN VISUAL-CORTEX;
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ENDOGENOUS BRAIN OSCILLATIONS;
TASK-INDUCED DEACTIVATION
AB The rapid advancement of neuroimaging methodology and its growing availability has transformed neuroscience research. The answers to many questions that we ask about how the brain is organized depend on the quality of data that we are able to obtain about the locations, dynamics, fluctuations, magnitudes, and types of brain activity and structural changes. In this review an attempt is made to take a snapshot of the cutting edge of a small. component of the very rapidly evolving field of neuroimaging. For each area covered, a brief context is provided along with a summary of a few of the current developments and issues. Then, several outstanding papers, published in the past year or so, are described, providing an example of the directions in which each area is progressing. The areas covered include functional magnetic resonance imaging (fMRI), voxel-based morphometry (VBM), diffusion tensor imaging (DTI), electroencephalography (EEG), magnetoencephalography (MEG), optical imaging, and positron emission tomography (PET). More detail is included on fMRI; its subsections include fMRI interpretation, new fMRI contrasts, MRI technology, MRI paradigms and processing, and endogenous oscillations in fMRI.
C1 NIMH, Sect Funct Imaging Methods, Bethesda, MD 20894 USA.
RP Bandettini, PA (reprint author), NIMH, Sect Funct Imaging Methods, Bldg 10,Rm LD80,10 Ctr Dr, Bethesda, MD 20894 USA.
EM bandettini@nih.gov
FU Intramural NIH HHS [Z01 MH002783-06]
NR 211
TC 98
Z9 99
U1 4
U2 46
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA
SN 0077-8923
BN 978-1-57331-752-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2009
VL 1156
BP 260
EP 293
DI 10.1111/j.1749-6632.2009.04420.x
PG 34
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA BJH40
UT WOS:000265827700013
PM 19338512
ER
PT J
AU Kim, EJ
Ro, H
Huh, TL
Lee, CJ
Choi, J
Rhee, M
AF Kim, Eun-joong
Ro, Hyunju
Huh, Tae-Lin
Lee, Chang Joong
Choi, Jinhee
Rhee, Myungchull
TI A Novel Kinesin-like Protein, Surhe is Associated with Dorsalization in
the Zebrafish Embryos
SO ANIMAL CELLS AND SYSTEMS
LA English
DT Article
DE kinesin-like protein; Surhe; dorsal determinant; dorsalization
ID BETA-CATENIN; SUPERFAMILY PROTEIN; MEDIATED TRANSPORT; DORSOVENTRAL
AXIS; MOLECULAR MOTORS; XENOPUS EMBRYOS; LIGHT-CHAIN; YOLK CELL;
MESODERM; DOMAIN
AB We are reporting the expression patterns and possible biological functions of a novel Kinesin-like protein, Surhe, in the zebrafish. Homology studies of derived amino acid sequences suggest that Surhe has an amino-terminal kinesin motor domain that is similar to that of the emerging MKLP-1 subfamily [Kim and Endow, 2000] and two coiled-coil domains in a central region. Cellular localization studies in mammalian cells revealed that Surhe protein is located in cytoplasm, suggesting that Surhe may be involved in the intracellular transport. During the developmental process, surhe transcripts are highly expressed in early embryonic stages. Overexpression of the dominant negative form of Surhe significantly down-regulates the dorsalization markers, such as goosecoid, bozozok, and chordin. Taken together, we postulate that Surhe may be involved in dorsalization process as a motor molecule.
C1 [Rhee, Myungchull] Chungnam Natl Univ, Coll Biosyst Sci, Dept Biol, Taejon 305764, South Korea.
[Kim, Eun-joong] Seoul Natl Univ, Sch Pharm, Seoul 151741, South Korea.
[Ro, Hyunju] NICHD, NIH, LMG, Bethesda, MD 20892 USA.
[Huh, Tae-Lin] Kyungpook Natl Univ, Dept Genet Engn, Taegu 702701, South Korea.
[Lee, Chang Joong] Inha Univ, Coll Nat Sci, Dept Biol, Inchon 402751, South Korea.
[Choi, Jinhee] Univ Seoul, Coll Urban Sci, Fac Environm Engn, Seoul 130743, South Korea.
RP Rhee, M (reprint author), Chungnam Natl Univ, Coll Biosyst Sci, Dept Biol, Taejon 305764, South Korea.
EM mrhee@cnu.ac.kr
FU Korean Government [KRF-2005-070-C00118]; Korean Ministry of Environment
[091-081-077]
FX Grant sponsors for this work: the Korean Research Foundation Grant
funded by the Korean Government (MOE HRD); Grant number:
KRF-2005-070-C00118; the Korean Ministry of Environment as "The
Eco-technopia 21 Project" (Grant number: 091-081-077)
NR 44
TC 4
Z9 4
U1 0
U2 3
PU ZOOLOGICAL SOC KOREA
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER, ROOM 1002, 635-4 YEOKSAM-DONG,
KANGNAM-GU, SEOUL, 135-703, SOUTH KOREA
SN 1976-8354
J9 ANIM CELLS SYST
JI Anim. Cells Syst.
PD DEC 31
PY 2008
VL 12
IS 4
BP 219
EP 230
DI 10.1080/19768354.2008.9647176
PG 12
WC Cell Biology; Zoology
SC Cell Biology; Zoology
GA 398NY
UT WOS:000262740000005
ER
PT J
AU Ding, JX
Jiang, D
Kurczy, M
Nalepka, J
Dudley, B
Merkel, EI
Porter, FD
Ewing, AG
Winograd, N
Burgess, J
Molyneaux, K
AF Ding, Jiaxi
Jiang, DeChen
Kurczy, Michael
Nalepka, Jennifer
Dudley, Brian
Merkel, Erin I.
Porter, Forbes D.
Ewing, Andrew G.
Winograd, Nicholas
Burgess, James
Molyneaux, Kathleen
TI Inhibition of HMG CoA reductase reveals an unexpected role for
cholesterol during PGC migration in the mouse
SO BMC DEVELOPMENTAL BIOLOGY
LA English
DT Article
ID PRIMORDIAL GERM-CELLS; PLASMA-MEMBRANE CHOLESTEROL; LIPID RAFTS;
EMBRYONIC LETHALITY; MICE LACKING; HEDGEHOG; BIOSYNTHESIS; ISOPRENOIDS;
GONADS; PROLIFERATION
AB Background: Primordial germ cells (PGCs) are the embryonic precursors of the sperm and eggs. Environmental or genetic defects that alter PGC development can impair fertility or cause formation of germ cell tumors.
Results: We demonstrate a novel role for cholesterol during germ cell migration in mice. Cholesterol was measured in living tissue dissected from mouse embryos and was found to accumulate within the developing gonads as germ cells migrate to colonize these structures. Cholesterol synthesis was blocked in culture by inhibiting the activity of HMG CoA reductase (HMGCR) resulting in germ cell survival and migration defects. These defects were rescued by co-addition of isoprenoids and cholesterol, but neither compound alone was sufficient. In contrast, loss of the last or penultimate enzyme in cholesterol biosynthesis did not alter PGC numbers or position in vivo. However embryos that lack these enzymes do not exhibit cholesterol defects at the stage at which PGCs are migrating. This demonstrates that during gestation, the cholesterol required for PGC migration can be supplied maternally.
Conclusion: In the mouse, cholesterol is required for PGC survival and motility. It may act cell-autonomously by regulating clustering of growth factor receptors within PGCs or non cell-autonomously by controlling release of growth factors required for PGC guidance and survival.
C1 [Ding, Jiaxi; Nalepka, Jennifer; Dudley, Brian; Molyneaux, Kathleen] Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA.
[Jiang, DeChen; Burgess, James] Case Western Reserve Univ, Dept Chem, Cleveland, OH 44106 USA.
[Kurczy, Michael; Ewing, Andrew G.; Winograd, Nicholas] Penn State Univ, Dept Chem, University Pk, PA 16802 USA.
[Merkel, Erin I.; Porter, Forbes D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA.
[Ewing, Andrew G.] Gothenburg Univ, Dept Chem, SE-41296 Gothenburg, Sweden.
RP Molyneaux, K (reprint author), Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA.
EM jiaxi.ding@osumc.edu; dechen.jiang@case.edu; mek20@psu.edu;
jennifer.nalepka@case.edu; brian.dudley@case.edu; merkele@mail.nih.edu;
fdporter@mail.nih.gov; age@psu.edu; nxw@psu.edu; jdb22@case.edu;
kam53@case.edu
RI Ewing, Andrew/A-3650-2009;
OI Kurczy, Michael/0000-0001-6579-9691; Winograd,
Nicholas/0000-0002-2690-7714
FU NIH-NCRR [RR-017980-01]; Case Western; Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD)
FX We acknowledge Patty Conrad for microscopy assistance. Funding support
for the Leica AOBS confocal multi-user facility was supplied by a grant
from NIH-NCRR (RR-017980-01). We thank Joe Nadeau, Jenny Liang and Helen
Salz for critical reading of the manuscript. The MC-480/SSEA1 antibody
developed by David Solter was obtained for the Developmental Studies
Hybridoma Bank developed under the auspices of the NICHD and maintained
by the University of Iowa, Department of Biological Sciences, Iowa City,
IA 52242. Financial support for this project was supplied by Case
Western. This work was also funded in part by the intramural research of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD).
NR 44
TC 12
Z9 13
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-213X
J9 BMC DEV BIOL
JI BMC Dev. Biol.
PD DEC 31
PY 2008
VL 8
AR 120
DI 10.1186/1471-213X-8-120
PG 14
WC Developmental Biology
SC Developmental Biology
GA 402ZT
UT WOS:000263052300001
PM 19117526
ER
PT J
AU Esibizione, D
Cui, CY
Schlessinger, D
AF Esibizione, Diana
Cui, Chang-Yi
Schlessinger, David
TI Candidate EDA targets revealed by expression profiling of primary
keratinocytes from Tabby mutant mice
SO GENE
LA English
DT Article
DE Anhidrotic ectodermal dysplasia; Ectodysplasin; Edar; Tbx1; Bmp7; Jag1
ID ANHIDROTIC ECTODERMAL DYSPLASIA; HAIR FOLLICLE DEVELOPMENT; SKIN;
GROWTH; CELL; IMMUNODEFICIENCY; DIFFERENTIATION; INVOLVEMENT; INDUCTION;
PSORIASIS
AB EDA, the gene mutated in anhidrotic ectodermal dysplasia, encodes ectodysplasin, a TNF superfamily member that activates NF-kappa B mediated transcription. To identify EDA target genes, we have earlier used expression profiling to infer genes differentially expressed at various developmental time points in Tabby (Eda-deficient) compared to wild-type mouse skin. To increase the resolution to find genes whose expression may be restricted to epidermal cells, we have now extended studies to primary keratinocyte cultures established from E19 wild-type and Tabby skin. Using microarrays bearing 44,000 gene probes, we found 385 preliminary candidate genes whose expression was significantly affected by Eda loss. By comparing expression profiles to those from Eda-A1 transgenic skin, we restricted the list to 38 "candidate EDA targets", 14 of which were already known to be expressed in hair follicles or epidermis. We confirmed expression changes for 3 selected genes. Tbx1, Bmp7, and Jag1, both in keratinocytes and in whole skin, by Q-PCR and Western blotting analyses. Thus, by the analysis of keratinocytes, novel candidate pathways downstream of EDA were detected. 2008 Published by Elsevier B.V.
C1 [Esibizione, Diana; Cui, Chang-Yi; Schlessinger, David] NIA, Genet Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
[Esibizione, Diana] Univ Bologna, Dept Histol Embryol & Appl Biol, I-40126 Bologna, Italy.
RP Schlessinger, D (reprint author), NIA, Genet Lab, NIH, Biomed Res Ctr, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM SchlessingerD@grc.nia.nih.gov
FU IRP of the NIH, National Institute on Aging
FX We thank Drs. Kunisada M, Ko M, Piao Y and Nagaraja R for their helpful
discussions and technical assistances. This work was supported by the
IRP of the NIH, National Institute on Aging.
NR 35
TC 4
Z9 4
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD DEC 31
PY 2008
VL 427
IS 1-2
BP 42
EP 46
DI 10.1016/j.gene.2008.09.014
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 378VX
UT WOS:000261353800005
PM 18848976
ER
PT J
AU Kwong, KY
Baskar, S
Zhang, H
Mackall, CL
Rader, C
AF Kwong, Ka Yin
Baskar, Sivasubramanian
Zhang, Hua
Mackall, Crystal L.
Rader, Christoph
TI Generation, Affinity Maturation, and Characterization of a Human
Anti-Human NKG2D Monoclonal Antibody with Dual Antagonistic and
Agonistic Activity
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE NKG2D; NK cells; human monoclonal antibodies; phage display; antibody
engineering
ID ACTIVATING IMMUNORECEPTOR NKG2D; IN-VITRO; T-CELLS; CROSS-REACTIVITY;
PHAGE DISPLAY; IMMUNE-SYSTEM; NK CELLS; RECEPTOR; LIBRARIES; VIRUS
AB In humans, NKG2D is an activating receptor on natural killer (NK) cells and a costimulatory receptor on certain T cells and plays a central role in mediating immune responses in autoimmune diseases, infectious diseases, and cancer. Monoclonal antibodies that antagonize or agonize immune responses mediated by human NKG2D are considered to be of broad and potent therapeutic utility. Nonetheless, monoclonal antibodies to NKG2D that are suitable for clinical investigations have not been published yet. Here, we describe the generation, affinity maturation, and characterization of a fully human monoclonal antibody to human NKG2D. Using phage display technology based on a newly generated naive human Fab library in phage display vector pC3C followed by a tandem chain shuffling process designed for minimal deviation from natural human antibody sequences, we selected a human Fab, designated KYK-2.0, with high specificity and affinity to human NKG2D. KYK-2.0 Fab blocked the binding of the natural human NKG2D ligands MICA, MICB, and ULBP2 as potently as a commercially available mouse anti-human NKG2D monoclonal antibody in immunoglobulin G (IgG) format. Conversion of KYK-2.0 Fab to IgG1 resulted in subnanomolar avidity for human NKG2D. KYK-2.0 IgG1. Was found to selectively recognize defined subpopulations of human lymphocytes known to express NKG2D, that is, the majority of human CD8+, CD16+, and CD56+ cells as well as a small fraction of human CD4+ cells. In solution, KYK-2.0 IgG1 interfered with the cytolytic activity of ex vivo expanded human NK cells. By contrast, immobilized KYK-2.0 IgG1 was found to strongly induce human NK cell activation. The dual antagonistic and agonistic activity promises a wide range of therapeutic applications for KYK-2.0 IgG1 and its derivatives. Published by Elsevier Ltd.
C1 [Kwong, Ka Yin; Baskar, Sivasubramanian; Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zhang, Hua; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Rader, C (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM raderc@mail.nih.gov
FU Center for Cancer Research; National Cancer Iristitute; NIH
FX This research was supported by the Intramural Research Program of the
Center for Cancer Research, National Cancer Iristitute, NIH. We thank
Dr. Charles L. Sentman (Dartmouth Medical School, Lebanon, NH) for
full-length human NKG2D cDNA; Dr. David H. Margulies (National Institute
of Allergy and Infectious Diseases, NIH, Bethesda, MD) for providing
access to his BIAcore 2000 instrument; Johan Lindberg and Dr. Alexander
Kovacs (Attana AB, Stockholm, Sweden) for facilitating and carrying out
quartz crystal microbalance measurements, respectively; Veena Kapoor
(National Cancer Institute, NTH, Bethesda, MD) for sorting stable
transfectants by fluorescence-activated cell sorting; and Drs. Steven J.
Burgess and Francisco Borrego (National Institute of Allergy and
Infectious Diseases, NIH, Rockville, MD) for technical advice on the
degranulation assay.
NR 44
TC 15
Z9 19
U1 0
U2 6
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 DEC 31
PY 2008
VL 384
IS 5
BP 1143
EP 1156
DI 10.1016/j.jmb.2008.09.008
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 388JR
UT WOS:000262016600012
PM 18809410
ER
PT J
AU Peabody, NC
Diao, FQ
Luan, HJ
Wang, H
Dewey, EM
Honegger, HW
White, BH
AF Peabody, Nathan C.
Diao, Fengqiu
Luan, Haojiang
Wang, Howard
Dewey, Elizabeth M.
Honegger, Hans-Willi
White, Benjamin H.
TI Bursicon Functions within the Drosophila CNS to Modulate Wing Expansion
Behavior, Hormone Secretion, and Cell Death
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE ecdysis; eclosion; network; circuit; apoptosis; Drosophila
ID INSECT ECDYSIS; IMAGINAL ECDYSIS; MANDUCA-SEXTA; CONTAINING NEURONS;
TOBACCO HORNWORM; CASCADE CONTROLS; CUTICLE; MELANOGASTER; ECLOSION;
RECEPTOR
AB Hormones are often responsible for synchronizing somatic physiological changes with changes in behavior. Ecdysis (i.e., the shedding of the exoskeleton) in insects has served as a useful model for elucidating the molecular and cellular mechanisms of this synchronization, and has provided numerous insights into the hormonal coordination of body and behavior. An example in which the mechanisms have remained enigmatic is the neurohormone bursicon, which, after the final molt, coordinates the plasticization and tanning of the initially folded wings with behaviors that drive wing expansion. The somatic effects of the hormone are governed by bursicon that is released into the blood from neurons in the abdominal ganglion ( the B(AG)), which die after wing expansion. How bursicon induces the behavioral programs required for wing expansion, however, has remained unknown. Here we show by targeted suppression of excitability that a pair of bursicon-immunoreactive neurons distinct from the B(AG) and located within the subesophageal ganglion in Drosophila ( the B(SEG)) is involved in controlling wing expansion behaviors. Unlike the B(AG), the B(SEG) arborize widely in the nervous system, including within the abdominal neuromeres, suggesting that, in addition to governing behavior, they also may modulate the B(AG). Indeed, we show that animals lacking bursicon receptor function have deficits both in the humoral release of bursicon and in posteclosion apoptosis of the B(AG). Our results reveal novel neuromodulatory functions for bursicon and support the hypothesis that the B(SEG) are essential for orchestrating both the behavioral and somatic processes underlying wing expansion.
C1 [Peabody, Nathan C.; Diao, Fengqiu; Luan, Haojiang; Wang, Howard; White, Benjamin H.] NIMH, NIH, Mol Biol Lab, Bethesda, MD 20892 USA.
[Dewey, Elizabeth M.; Honegger, Hans-Willi] Vanderbilt Univ, Dept Biol Sci, Nashville, TN 37325 USA.
RP White, BH (reprint author), NIMH, NIH, Mol Biol Lab, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM benjaminwhite@mail.nih.gov
FU National Institute of Mental Health
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health. We thank Aaron Hsueh, John Ewer,
and John Carlson for reagents, the Bloomington Stock Center for fly
lines, and Howard Nash, Grace Gray, and anonymous reviewers for
constructive comments on this manuscript.
NR 33
TC 43
Z9 45
U1 3
U2 12
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD DEC 31
PY 2008
VL 28
IS 53
BP 14379
EP 14391
DI 10.1523/JNEUROSCI.2842-08.2008
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 390AX
UT WOS:000262137800007
PM 19118171
ER
PT J
AU Pavel, J
Tang, H
Brimijoin, S
Moughamian, A
Nishioku, T
Benicky, J
Saavedra, JM
AF Pavel, Jaroslau
Tang, Hui
Brimijoin, Stephen
Moughamian, Armen
Nishioku, Tsuyoshi
Benicky, Julius
Saavedra, Juan M.
TI Expression and transport of Angiotensin II AT(1) receptors in spinal
cord, dorsal root ganglia and sciatic nerve of the rat
SO BRAIN RESEARCH
LA English
DT Article
DE Renin angiotensin system; Dorsal root ganglia; Spinal cord; Angiotensin
II AT(1) and AT(2) receptor types; Sciatic nerve ligation; Dorsal
rhizotomy
ID SPONTANEOUSLY HYPERTENSIVE-RATS; SUBTYPE GENE-EXPRESSION; QUANTITATIVE
AUTORADIOGRAPHY; SENSORY NEURONS; PERIPHERAL AXOTOMY; PASTE STANDARDS;
MESSENGER-RNAS; UP-REGULATION; BRAIN PASTE; SYSTEM
AB To clarify the role of Angiotensin II in the regulation of peripheral sensory and motor systems, we initiated a study of the expression, localization and transport of Angiotensin II receptor types in the rat sciatic nerve pathway, including L-4-L-5 spinal cord segments, the corresponding dorsal root ganglia (DRGs) and the sciatic nerve. We used quantitative autoradiography for AT(1) and AT(2) receptors, and in situ hybridization to detect AT(1A), AT(1B) and AT(2) mRNAs. We found substantial expression and discrete localization of Angiotensin II AT(1) receptors, with much higher numbers in the grey than in the white matter. A very high AT(1) receptor expression was detected in the superficial dorsal horns and in neuronal clusters of the DRGs. Expression of AT(1A) mRNA was significantly higher than that of AT(1B). AT(1) receptor binding and AT(1A) and AT(1B) mRNAs were especially prominent in ventral horn motor neurons, and in the DRG neuronal cells. Unilateral dorsal rhizotomy significantly reduced AT(1) receptor binding in the ipsilateral side of the superficial dorsal horn, indicating that a substantial number of dorsal horn AT(1) receptors have their origin in the DRGs. After ligation of the sciatic nerve, there was a high accumulation of AT, receptors proximal to the ligature, a demonstration of anterograde receptor transport. We found inconsistent levels of AT(2) receptor binding and mRNA. Our results suggest multiple roles of Angiotensin II AT(1) receptors in the regulation of sensory and motor functions. Published by Elsevier B.V.
C1 [Pavel, Jaroslau; Moughamian, Armen; Nishioku, Tsuyoshi; Benicky, Julius; Saavedra, Juan M.] NIMH, Pharmacol Sect, Bethesda, MD 20892 USA.
[Tang, Hui; Brimijoin, Stephen] Mayo Fdn, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN 55905 USA.
RP Pavel, J (reprint author), 10 Ctr Dr,MSC 1514,Bldg 10,Rm 2D57, Bethesda, MD 20892 USA.
EM pavelj@mail.nih.gov
FU Division of Intramural Research Programs; National Institutes of Mental
Health; National Institutes of Health; Department of Health and Human
Services, USA
FX This study was supported by the Division of Intramural Research
Programs, National Institutes of Mental Health, National Institutes of
Health, Department of Health and Human Services, USA.
NR 46
TC 25
Z9 25
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD DEC 30
PY 2008
VL 1246
BP 111
EP 122
DI 10.1016/j.brainres.2008.09.099
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 396NE
UT WOS:000262597600013
PM 18976642
ER
PT J
AU Kim, PK
Hailey, DW
Mullen, RT
Lippincott-Schwartz, J
AF Kim, Peter Kijun
Hailey, Dale Warren
Mullen, Robert Thomas
Lippincott-Schwartz, Jennifer
TI Ubiquitin signals autophagic degradation of cytosolic proteins and
peroxisomes
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE autophagy; p62; pexophagy
ID HANSENULA-POLYMORPHA; MEMBRANE-PROTEIN; SELECTIVE DEGRADATION;
FLUORESCENT PROTEINS; CELLS; PATHWAY; MITOCHONDRIA; PROTEOLYSIS;
BIOGENESIS; PEXOPHAGY
AB Autophagy is responsible for nonspecific, bulk degradation of cytoplasmic components. Recent work has revealed also that there is specific, autophagic degradation of polyubiquitinated protein aggregates, whose buildup occurs during neurodegenerative disease. Here, we report that simple mono-ubiquitination of normally long-lived cytoplasmic substrates is sufficient to target these substrates for autophagic degradation in mammalian cells. That is, upon their ubiquitination, both small [i.e., red fluorescent protein (RFP)] and large ( i.e., peroxisomes) substrates are efficiently targeted to autophagosomes and then degraded within lysosomes upon autophagosome-lysosome fusion. This targeting requires the ubiquitin-binding protein, p62, and is blocked by the Class III phosphatidylinositol 3-kinase (PI3K) inhibitor, 3-methyladenine (3-MA), or by depletion of the autophagy-related-12 (Atg12) protein homolog. Mammalian cells thus use a common pathway involving ubiquitin and p62 for targeting diverse types of substrates for autophagy.
C1 [Kim, Peter Kijun; Hailey, Dale Warren; Lippincott-Schwartz, Jennifer] NICHHD, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
[Mullen, Robert Thomas] Univ Guelph, Dept Mol & Cellular Biol, Guelph, ON N1G 2W1, Canada.
RP Lippincott-Schwartz, J (reprint author), NICHHD, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
EM lippincj@mail.nih.gov
FU National Institutes of Health; Natural Sciences and Engineering Research
Council of Canada
FX We thank Dr. Satinder Gidda ( University of Guelph) for assistance with
the construction of PEX3-GFP-UBko and UBko-RFP. This work was supported
by grants from the National Institutes of Health ( to J.L.-S.) and the
Natural Sciences and Engineering Research Council of Canada ( to R. T.
M.).
NR 49
TC 262
Z9 267
U1 4
U2 23
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 30
PY 2008
VL 105
IS 52
BP 20567
EP 20574
DI 10.1073/pnas.0810611105
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 389LB
UT WOS:000262092800003
PM 19074260
ER
PT J
AU Lam, LT
Davis, RE
Ngo, VN
Lenz, G
Wright, G
Xu, WH
Zhao, H
Yu, X
Dang, LN
Staudt, LM
AF Lam, Lloyd T.
Davis, R. Eric
Ngo, Vu N.
Lenz, Georg
Wright, George
Xu, Weihong
Zhao, Hong
Yu, Xin
Dang, Lenny
Staudt, Louis M.
TI Compensatory IKK alpha activation of classical NF-kappa B signaling
during IKK beta inhibition identified by an RNA interference
sensitization screen
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Ikka; Ikkb; Nf-kB; RNAi
ID T-CELL-ACTIVATION; GENE-EXPRESSION; NF-KAPPA-B2 P100; KINASE-ACTIVITY;
DEFICIENT MICE; PHOSPHORYLATION; LYMPHOMA; CARMA1; PATHWAYS; COMPLEX
AB A subtype of diffuse large B- cell lymphoma (DLBCL), termed activated B- cell- like (ABC) DLBCL, depends on constitutive nuclear factor-kappa B (NF-kappa B) signaling for survival. Small molecule inhibitors of I kappa B kinase beta(IKK beta), a key regulator of the NF-kappa B pathway, kill ABC DLBCL cells and hold promise for the treatment of this lymphoma type. We conducted an RNA interference genetic screen to investigate potential mechanisms of resistance of ABC DLBCL cells to IKK beta inhibitors. We screened a library of small hairpin RNAs (shRNAs) targeting 500 protein kinases for shRNAs that would increase the killing of an ABC DLBCL cell line in the presence of a small molecule IKK beta inhibitor. Two independent shRNAs targeting IKK alpha synergized with the IKK beta inhibitor to kill three different ABC DLBCL cell lines but were not toxic by themselves. Surprisingly, IKK alpha shRNAs blocked the classical rather than the alternative NF-kappa B pathway in ABC DLBCL cells, as judged by inhibition of I kappa B alpha phosphorylation. IKK alpha shRNA toxicity was reversed by coexpression of wild-type but not kinase inactive forms of IKK alpha, suggesting that IKK alpha may directly phosphorylate I kappa B alpha under conditions of IKK beta inhibition. In models of physiologic NF-kappa B pathway activation by CARD11 or tumor necrosis factor-alpha, compensatory IKK alpha activity was also observed with IKK alpha inhibition. These results suggest that therapy for ABC DLBCL may be improved by targeting both IKK alpha and IKK alpha, possibly through CARD11 inhibition.
C1 [Lam, Lloyd T.; Davis, R. Eric; Ngo, Vu N.; Lenz, Georg; Xu, Weihong; Zhao, Hong; Yu, Xin; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Wright, George] NCI, Biometr Res Branch, Rockville, MD 20892 USA.
[Dang, Lenny] Millennium Pharmaceut Inc, Cambridge, MA 02139 USA.
RP Staudt, LM (reprint author), 9000 Rockville Pike,Bldg 10,Room 4N114, Bethesda, MD 20892 USA.
EM lstaudt@mail.nih.gov
RI Lenz, Georg/I-6844-2012
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research; German Research Foundation (DFG)
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research. G. L was also supported by a research grant from the
German Research Foundation (DFG). We thank members of the Staudt
laboratory for helpful discussions, and Kathleen Meyer for her
assistance with GEO submissions.
NR 41
TC 55
Z9 58
U1 2
U2 17
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 30
PY 2008
VL 105
IS 52
BP 20798
EP 20803
DI 10.1073/pnas.0806491106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 389LB
UT WOS:000262092800043
PM 19104039
ER
PT J
AU Piatigorsky, J
AF Piatigorsky, Joram
TI Evolution of mollusc lens crystallins: Glutathione
S-transferase/S-crystallins and aldehyde dehydrogenase/ohm-crystallins
SO AMERICAN MALACOLOGICAL BULLETIN
LA English
DT Article; Proceedings Paper
CT Symposium on Molluscan Models - Advancing our Understanding of the Eye
CY JUL 15-20, 2007
CL Antwerp, BELGIUM
SP Natl Sci Fdn, Amer Malacol Soc
DE cephalopods; scallops; enzymes; lens proteins; eye; gene expression
ID EYE LENS; OMEGA-CRYSTALLIN; DETOXIFICATION ENZYMES; CUBOMEDUSAN
JELLYFISH; CONVERGENT EVOLUTION; STRUCTURAL PROTEIN; GENE-EXPRESSION;
ETA-CRYSTALLIN; SCALLOP LENS; OCTOPUS LENS
AB Diverse crystallins (abundant water-soluble proteins) are responsible for the optical properties of transparent cellular eye lenses and are multifunctional proteins that have been recruited from stress proteins and enzymes by enhanced lens expression. The major (S-crystallins) and minor (ohm-crystallin) cephalopod crystallins were recruited from glutathione S-transferase (GST) and aldehyde dehydrogenase (ALDH), respectively, S-crystallins underwent multiple gene duplications while ohm-crystallin appears to be encoded in a single- copy gene. Except for one S-crystallin (considered a "molecular fossil"), S-crystallins lack enzyme activity due to mutation and insertion of a variable central peptide by exon shuffling. The ohm-crystallin is the sole crystallin in scallops. Scallop ohm-crystallin does not bind the co-factor NAD(+/)NADH, lacks enzyme activity, and is a tetramer but migrates as a dimer by gel filtration, suggesting structural adaptations for crystallin function. Similar transcription factors (Pax6 among others) appear to drive high lens expression of crystallin genes in molluscs and other species consistent with convergent recruitment of the non-homologous crystallin genes.
C1 NEI, NIH, Mol & Dev Biol Lab, Bethesda, MD 20892 USA.
RP Piatigorsky, J (reprint author), NEI, NIH, Mol & Dev Biol Lab, 7 Mem Dr,Bldg 7,Room 100, Bethesda, MD 20892 USA.
EM joramp@nei.nih.gov
NR 65
TC 3
Z9 3
U1 1
U2 14
PU AMER MALACOLOGICAL SOC, INC
PI WILMINGTON
PA DELAWARE MUSEUM NATURAL HISTORY, BOX 3937, WILMINGTON, DE 19807-0937 USA
SN 0740-2783
EI 2162-2698
J9 AM MALACOL BULL
JI Am. Malacol. Bull.
PD DEC 29
PY 2008
VL 26
IS 1-2
BP 73
EP 81
DI 10.4003/006.026.0208
PG 9
WC Marine & Freshwater Biology; Zoology
SC Marine & Freshwater Biology; Zoology
GA 387PC
UT WOS:000261963100008
ER
PT J
AU Ratnayaka, K
Faranesh, AZ
Guttman, MA
Kocaturk, O
Saikus, CE
Lederman, RJ
AF Ratnayaka, Kanishka
Faranesh, Anthony Z.
Guttman, Michael A.
Kocaturk, Ozgur
Saikus, Christina E.
Lederman, Robert J.
TI Interventional cardiovascular magnetic resonance: still tantalizing
SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
LA English
DT Review
ID RADIOFREQUENCY ABLATION LESIONS; GUIDED PERCUTANEOUS ANGIOPLASTY; ARTERY
STENT PLACEMENT; VENA-CAVA FILTER; PULMONARY VASCULAR-RESISTANCE;
RESOLUTION INTRAVASCULAR MRI; PASSIVE CATHETER TRACKING; CONGENITAL
HEART-DISEASE; ATRIAL SEPTAL-DEFECTS; REAL-TIME MRI
AB The often touted advantages of MR guidance remain largely unrealized for cardiovascular interventional procedures in patients. Many procedures have been simulated in animal models. We argue these opportunities for clinical interventional MR will be met in the near future. This paper reviews technical and clinical considerations and offers advice on how to implement a clinical-grade interventional cardiovascular MR (iCMR) laboratory. We caution that this reflects our personal view of the "state of the art."
C1 [Ratnayaka, Kanishka; Faranesh, Anthony Z.; Guttman, Michael A.; Kocaturk, Ozgur; Saikus, Christina E.; Lederman, Robert J.] NHLBI, Translat Med Branch, Div Intramural Res, NIH, Bethesda, MD USA.
[Ratnayaka, Kanishka] Childrens Natl Med Ctr, Div Cardiol, Washington, DC 20010 USA.
RP Lederman, RJ (reprint author), NHLBI, Translat Med Branch, Div Intramural Res, NIH, Bethesda, MD USA.
EM ratnayakak@nhlbi.nih.gov; faranesa@nhlbi.nih.gov;
guttmanm@nhlbi.nih.gov; Kocaturko@nhlbi.nih.gov; saikusc@nhlbi.nih.gov;
lederman@nih.gov
RI Kocaturk, Ozgur/A-1419-2016;
OI lederman, robert/0000-0003-1202-6673
FU Division of Intramural Research, National Heart Lung and Blood
Institute, National Institutes of Health, USA
FX Supported by the Division of Intramural Research, National Heart Lung
and Blood Institute, National Institutes of Health, USA.
NR 165
TC 33
Z9 33
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1097-6647
J9 J CARDIOVASC MAGN R
JI J. Cardiov. Magn. Reson.
PD DEC 29
PY 2008
VL 10
AR 62
DI 10.1186/1532-429X-10-62
PG 23
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 409WD
UT WOS:000263535600001
PM 19114017
ER
PT J
AU Houzet, L
Yeung, ML
de Lame, V
Desai, D
Smith, SM
Jeang, KT
AF Houzet, Laurent
Yeung, Man Lung
de Lame, Valery
Desai, Dhara
Smith, Stephen M.
Jeang, Kuan-Teh
TI MicroRNA profile changes in human immunodeficiency virus type 1 (HIV-1)
seropositive individuals
SO RETROVIROLOGY
LA English
DT Article
ID EXPRESSION PROFILES; CELLULAR MICRORNAS; GENE-EXPRESSION; INFECTION;
CELLS; REPLICATION; PATHOGENESIS; MODULATION; ACTIVATION; APOPTOSIS
AB MicroRNAs ( miRNAs) play diverse roles in regulating cellular and developmental functions. We have profiled the miRNA expression in peripheral blood mononuclear cells from 36 HIV-1 seropositive individuals and 12 normal controls. The HIV-1-positive individuals were categorized operationally into four classes based on their CD4+ T-cell counts and their viral loads. We report that specific miRNA signatures can be observed for each of the four classes.
C1 [Houzet, Laurent; Yeung, Man Lung; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[de Lame, Valery; Desai, Dhara; Smith, Stephen M.] St Michaels Hosp, Dept Infect Dis, Newark, NJ 07102 USA.
RP Jeang, KT (reprint author), NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
EM houzetl@niaid.nih.gov; yeungm@niaid.nih.gov; delame.lab@gmail.com;
desai.dhara@gmail.com; SSmith1824@aol.com; kjeang@niaid.nih.gov
RI Jeang, Kuan-Teh/A-2424-2008
FU NIH Bench-to-Bedside Program; Intramural AIDS Targeted Anti-viral
Program (IATAP); NIAID; NIH
FX This study was supported in part by the NIH Bench-to-Bedside Program,
the Intramural AIDS Targeted Anti-viral Program (IATAP), and intramural
funding from NIAID, NIH. We thank the NIAID microarray core facility for
advice and assistance.
NR 41
TC 119
Z9 122
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD DEC 29
PY 2008
VL 5
AR 118
DI 10.1186/1742-4690-5-118
PG 9
WC Virology
SC Virology
GA 412OB
UT WOS:000263733000001
PM 19114009
ER
PT J
AU Rajesh, M
Mukhopadhyay, P
Hasko, G
Pacher, P
AF Rajesh, Mohanraj
Mukhopadhyay, Partha
Hasko, Gyoergy
Pacher, Pal
TI Cannabinoid CB1 receptor inhibition decreases vascular smooth muscle
migration and proliferation
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Cannabinoid receptors; Vascular smooth muscle; Proliferation; Migration;
Atherosclerosis; Endocannabinoids; Rimonabant; Restenosis
ID GROWTH-FACTOR; ENDOCANNABINOID SYSTEM; PHARMACOLOGICAL INHIBITION;
CELL-PROLIFERATION; TNF-ALPHA; ATHEROSCLEROSIS; DISEASE; RIMONABANT;
MECHANISM; APOPTOSIS
AB Vascular smooth muscle proliferation and migration triggered by inflammatory stimuli and chemoattractants such as platelet-derived growth factor (PDGF) are key events in the development and progression of atherosclerosis and restenosis. Cannabinoids may modulate cell proliferation and migration in various cell types through cannabinoid receptors. Here we investigated the effects of CB1 receptor antagonist rimonabant (SR141716A), which has recently been shown to have anti-atherosclerotic effects both in mice and humans, on PDGF-induced proliferation, migration, and signal transduction of human coronary artery smooth Muscle cells (HCASMCs). PDGF induced Ras and ERK 1/2 activation, while increasing proliferation and migration of HCASMCs, which were dose dependently attenuated by CB1 antagonist, rimonabant. These findings suggest that in addition to improving plasma lipid alterations and decreasing inflammatory cell migration and inflammatory response, CB1 antagonists may exert beneficial effects in atherosclerosis and restenosis by decreasing Vascular smooth muscle proliferation and migration. Published by Elsevier Inc.
C1 [Rajesh, Mohanraj; Mukhopadhyay, Partha; Pacher, Pal] NIAAA, Lab Physiol Studies, NIH, Sect Oxidat Stress & Tissue Injury, Bethesda, MD 20892 USA.
[Hasko, Gyoergy] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
RP Pacher, P (reprint author), NIAAA, Lab Physiol Studies, NIH, Sect Oxidat Stress & Tissue Injury, 5625 Fishers Lane,MSC 9413, Bethesda, MD 20892 USA.
EM pacher@mail.nih.gov
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Pacher, Pal/B-6378-2008
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
Pal/0000-0001-7036-8108
FU NIH
FX This publication was supported by Intramural Research Program of NIH.
The authors declare no conflicting financial interests.
NR 24
TC 27
Z9 27
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD DEC 26
PY 2008
VL 377
IS 4
BP 1248
EP 1252
DI 10.1016/j.bbrc.2008.10.159
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 382UM
UT WOS:000261630900043
PM 18996082
ER
PT J
AU Thangudu, RR
Manoharan, M
Srinivasan, N
Cadet, F
Sowdhamini, R
Offmann, B
AF Thangudu, Ratna R.
Manoharan, Malini
Srinivasan, N.
Cadet, Frederic
Sowdhamini, R.
Offmann, Bernard
TI Analysis on conservation of disulphide bonds and their structural
features in homologous protein domain families
SO BMC STRUCTURAL BIOLOGY
LA English
DT Article
ID AMINO-ACID-COMPOSITION; X-RAY-STRUCTURE; CRYSTAL-STRUCTURE; CONNECTIVITY
PREDICTION; GLOBULAR-PROTEINS; ESCHERICHIA-COLI;
SUBCELLULAR-LOCALIZATION; EVOLUTIONARY INFORMATION; 3-DIMENSIONAL
STRUCTURE; ANGSTROM RESOLUTION
AB Background: Disulphide bridges are well known to play key roles in stability, folding and functions of proteins. Introduction or deletion of disulphides by site-directed mutagenesis have produced varying effects on stability and folding depending upon the protein and location of disulphide in the 3-D structure. Given the lack of complete understanding it is worthwhile to learn from an analysis of extent of conservation of disulphides in homologous proteins. We have also addressed the question of what structural interactions replaces a disulphide in a homologue in another homologue.
Results: Using a dataset involving 34,752 pairwise comparisons of homologous protein domains corresponding to 300 protein domain families of known 3-D structures, we provide a comprehensive analysis of extent of conservation of disulphide bridges and their structural features. We report that only 54% of all the disulphide bonds compared between the homologous pairs are conserved, even if, a small fraction of the non-conserved disulphides do include cytoplasmic proteins. Also, only about one fourth of the distinct disulphides are conserved in all the members in protein families. We note that while conservation of disulphide is common in many families, disulphide bond mutations are quite prevalent. Interestingly, we note that there is no clear relationship between sequence identity between two homologous proteins and disulphide bond conservation. Our analysis on structural features at the sites where cysteines forming disulphide in one homologue are replaced by non-Cys residues show that the elimination of a disulphide in a homologue need not always result in stabilizing interactions between equivalent residues.
Conclusion: We observe that in the homologous proteins, disulphide bonds are conserved only to a modest extent. Very interestingly, we note that extent of conservation of disulphide in homologous proteins is unrelated to the overall sequence identity between homologues. The non-conserved disulphides are often associated with variable structural features that were recruited to be associated with differentiation or specialisation of protein function.
C1 [Manoharan, Malini; Sowdhamini, R.] Natl Ctr Biol Sci, Bangalore, Karnataka, India.
[Thangudu, Ratna R.; Cadet, Frederic; Offmann, Bernard] Univ Reunion, Lab Biochim & Genet Mol, St Denis 97715 09, Reunion.
[Srinivasan, N.] Indian Inst Sci, Mol Biophys Unit, Bangalore 560012, Karnataka, India.
[Thangudu, Ratna R.] US Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RP Offmann, B (reprint author), Natl Ctr Biol Sci, GKVK Campus, Bangalore, Karnataka, India.
EM thangudr@ncbi.nlm.nih.gov; malinim@ncbs.res.in; ns@mbu.iisc.ernet.in;
frederic.cadet@univ-reunion.fr; mini@ncbs.res.in;
bernard.offmann@univ-reunion.fr
FU Conseil Regional de La Reunion
FX RRT was supported by a PhD grant from the Conseil Regional de La
Reunion. NS and RS thank the authorities of Universit de La Reunion for
their visiting professorships. We thank Dr. Alexandre G. de Brevern for
useful comments.
NR 100
TC 18
Z9 18
U1 1
U2 25
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2237
J9 BMC STRUCT BIOL
JI BMC Struct. Biol.
PD DEC 26
PY 2008
VL 8
AR 55
DI 10.1186/1472-6807-8-55
PG 22
WC Biophysics
SC Biophysics
GA 407BC
UT WOS:000263337600001
PM 19111067
ER
PT J
AU Chu, G
Yang, W
AF Chu, Gilbert
Yang, Wei
TI Here Comes the Sun: Recognition of UV-Damaged DNA
SO CELL
LA English
DT Editorial Material
ID UBIQUITIN LIGASE; REPAIR; PROTEIN; LESION
AB The first step in the repair of DNA damage is lesion detection. In this issue, Scrima et al. (2008) report the structure of the complex of DNA Damage-Binding Protein 1 (DDB1) and DDB2 bound to a DNA photodimer, providing critical insight into the repair of DNA damage caused by ultraviolet light.
C1 [Yang, Wei] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Chu, Gilbert] Stanford Univ, Med Ctr, Dept Med, Div Oncol, Stanford, CA 94305 USA.
[Chu, Gilbert] Stanford Univ, Med Ctr, Dept Biochem, Div Oncol, Stanford, CA 94305 USA.
RP Yang, W (reprint author), NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM wei.yang@nih.gov
RI Yang, Wei/D-4926-2011
OI Yang, Wei/0000-0002-3591-2195
NR 9
TC 7
Z9 7
U1 2
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD DEC 26
PY 2008
VL 135
IS 7
BP 1172
EP 1174
DI 10.1016/j.cell.2008.12.015
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 387ZJ
UT WOS:000261989800009
PM 19109889
ER
PT J
AU Bashkirov, PV
Akimov, SA
Evseev, AI
Schmid, SL
Zimmerberg, J
Frolov, VA
AF Bashkirov, Pavel V.
Akimov, Sergey A.
Evseev, Alexey I.
Schmid, Sandra L.
Zimmerberg, Joshua
Frolov, Vadim A.
TI GTPase Cycle of Dynamin Is Coupled to Membrane Squeeze and Release,
Leading to Spontaneous Fission
SO CELL
LA English
DT Article
ID DEPENDENT CONFORMATIONAL-CHANGES; BIOLOGICAL-MEMBRANES; NERVE-TERMINALS;
ENDOCYTOSIS; CURVATURE; VESICLES; TENSION; FUSION; DOMAIN; CELLS
AB The GTPase dynamin is critically involved in membrane fission during endocytosis. How does dynamin use the energy of GTP hydrolysis for membrane remodeling? By monitoring the ionic permeability through lipid nanotubes (NT), we found that dynamin was capable of squeezing NT to extremely small radii, depending on the NT lipid composition. However, long dynamin scaffolds did not produce fission: instead, fission followed GTPase-dependent cycles of assembly and disassembly of short dynamin scaffolds and involved a stochastic process dependent on the curvature stress imposed by dynamin. Fission happened spontaneously upon NT release from the scaffold, without leakage. Our calculations revealed that local narrowing of NT could induce cooperative lipid tilting, leading to self-merger of the inner monolayer of NT (hemifission), consistent with the absence of leakage. We propose that dynamin transmits GTP's energy to periodic assembling of a limited curvature scaffold that brings lipids to an unstable intermediate.
C1 [Bashkirov, Pavel V.; Akimov, Sergey A.; Zimmerberg, Joshua; Frolov, Vadim A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD 20892 USA.
[Bashkirov, Pavel V.; Akimov, Sergey A.; Evseev, Alexey I.] Russian Acad Sci, AN Frumkin Inst Phys Chem & Electrochem, Moscow 119991, Russia.
[Schmid, Sandra L.] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA.
RP Zimmerberg, J (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD 20892 USA.
EM joshz@mail.nih.gov
RI Bashkirov, Pavel/J-2385-2012; Akimov, Sergey/L-2001-2013; Akimov,
Sergey/I-6432-2015;
OI Frolov, Vadim/0000-0002-0653-5669
FU National Institutes of Health (NIH) [R01GM42455, R37MH61345]; RFBR
[08-04-00085]; CRDF GAP [RUB1-1297(5)-MO-05]; Russian Federal Agency for
Science and Innovations [02.512.11.0010]; Program of Molecular and
Cellular Biology RAS; Leading Scientific Schools of Russian Federation
[4181.2008.4]
FX This work was partially supported by the National Institutes of Health
(NIH) intramural program (NICHD), and grants NIH R01GM42455 and
R37MH61345, RFBR 08-04-00085, and CRDF GAP RUB1-1297(5)-MO-05, Russian
Federal Agency for Science and Innovations 02.512.11.0010, Program of
Molecular and Cellular Biology RAS, and the grant for State Support of
Leading Scientific Schools of Russian Federation 4181.2008.4. The
BODIPY-labeled dynamin was generously provided by Rajesh Ramachandran.
We are grateful to Vladimir Lizunov and Gennady Kushnir for their
technical help and Thomas Pucadyil, Anna Shnyrova, and Yuri Chizmadzhev
for a careful reading of the manuscript and fruitful discussions.
NR 42
TC 164
Z9 166
U1 1
U2 25
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD DEC 26
PY 2008
VL 135
IS 7
BP 1276
EP 1286
DI 10.1016/j.cell.2008.11.028
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 387ZJ
UT WOS:000261989800018
PM 19084269
ER
PT J
AU Franco, R
DeHaven, WI
Sifre, MI
Bortner, CD
Cidlowski, JA
AF Franco, Rodrigo
DeHaven, Wayne I.
Sifre, Maria I.
Bortner, Carl D.
Cidlowski, John A.
TI Glutathione Depletion and Disruption of Intracellular Ionic Homeostasis
Regulate Lymphoid Cell Apoptosis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MITOCHONDRIAL PERMEABILITY TRANSITION; PLASMA-MEMBRANE DEPOLARIZATION;
FAS-MEDIATED APOPTOSIS; CYTOCHROME-C RELEASE; REDUCED GLUTATHIONE;
OXIDATIVE STRESS; K+ CHANNELS; VOLUME DECREASE; T-LYMPHOCYTES; POTASSIUM
CHANNELS
AB Intracellular glutathione (GSH) depletion is an important hallmark of apoptosis. We have recently shown that GSH depletion by its extrusion regulates apoptosis independently of excessive reactive oxygen species accumulation. However, the mechanisms by which GSH depletion regulates apoptosis are still unclear. Because disruption of intracellular ionic homeostasis, associated with apoptotic volume decrease (AVD), is necessary for the progression of apoptotic cell death, we sought to evaluate the relationship between GSH transport and ionic homeostasis during Fas ligand (FasL)-induced apoptosis in Jurkat cells. GSH depletion in response to FasL was paralleled by distinct degrees of AVD identified by differences in cellular forward scatter and electronic impedance analysis. Inhibition of GSH efflux prevented AVD, K(+) loss, and the activation of two distinct ionic conductances, mediated by Kv1.3 and outward rectifying Cl(-) channels. Reciprocally, stimulation of GSH loss accelerated the loss of K(+), AVD, and consequently the progression of the execution phase of apoptosis. Although high extracellular K(+) inhibited FasL-induced apoptosis, GSH depletion was largely independent of K(+) loss. These results suggest that deregulation of GSH and ionic homeostasis converge in the regulation of apoptosis in lymphoid cells.
C1 [Franco, Rodrigo; DeHaven, Wayne I.; Sifre, Maria I.; Bortner, Carl D.; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), NIEHS, Lab Signal Transduct, NIH, POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM cidlows1@mail.nih.gov
RI Franco, Rodrigo/D-9470-2013
OI Franco, Rodrigo/0000-0003-3241-8615
FU National Institutes of Health grant
FX This work was supported, in whole or in part, by a National Institutes
of Health grant (intramural research program of the NIEHS). The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 97
TC 27
Z9 28
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 DEC 26
PY 2008
VL 283
IS 52
BP 36071
EP 36087
DI 10.1074/jbc.M807061200
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385VA
UT WOS:000261840500003
PM 18940791
ER
PT J
AU Dvir-Ginzberg, M
Gagarina, V
Lee, EJ
Hall, DJ
AF Dvir-Ginzberg, Mona
Gagarina, Viktoria
Lee, Eun-Jin
Hall, David J.
TI Regulation of Cartilage-specific Gene Expression in Human Chondrocytes
by SirT1 and Nicotinamide Phosphoribosyltransferase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA; HISTONE DEACETYLASE INHIBITORS;
II COLLAGEN GENE; CELL-SURVIVAL; SOX9; CHONDROGENESIS; PROTEIN;
CHROMATIN; COMPLEX; MUSCLE
AB SirT1 is an NAD-dependent histone deacetylase that regulates gene expression, differentiation, development, and organism life span. Here we investigate the function of SirT1 in human chondrocytes derived from osteoarthritic patients. Elevation of SirT1 protein levels or activity in these chondrocytes led to a dramatic increase in cartilage-specific gene expression, whereas a reduction in SirT1 levels or activity significantly lowered cartilage gene expression. SirT1 associated with the cartilage-specific transcription factor Sox9, enhancing transcription from the collagen 2(alpha 1) promoter in a Sox9-dependent fashion. Consistent with this association, SirT1 was targeted to the collagen 2(alpha 1) enhancer and promoter, which in turn recruited the coactivators GCN5, PGC1 alpha, and p300. This led to elevated marks of active chromatin within the promoter; that is, acetylated histone K9/K14 and histone H4K5 as well as trimethylated histone H3K4. Finally, alterations in the NAD salvage pathway enzyme nicotinamide phosphoribosyltransferase led to changes in NAD levels, SirT activity, and cartilage-specific gene expression in human chondrocytes. SirT1, nicotinamide phosphoribosyltransferase, and NAD may, therefore, provide a positive function in human cartilage by elevating expression of genes encoding cartilage extracellular matrix.
C1 [Dvir-Ginzberg, Mona; Gagarina, Viktoria; Lee, Eun-Jin; Hall, David J.] NIAMS, Cartilage Mol Genet Grp, Cartilage Biol & Orthopaed Branch, NIH, Bethesda, MD 20892 USA.
RP Hall, DJ (reprint author), 50 South Dr,Rm 1524, Bethesda, MD 20892 USA.
EM halld@mail.nih.gov
OI Dvir-Ginzberg, Mona/0000-0003-3089-6875
FU National Institutes of Health
FX This work was supported, in whole or in part, by the National Institutes
of Health (Intramural Research Program of the NIAMS). The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 47
TC 86
Z9 92
U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 26
PY 2008
VL 283
IS 52
BP 36300
EP 36310
DI 10.1074/jbc.M803196200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385VA
UT WOS:000261840500026
PM 18957417
ER
PT J
AU Hazelwood, LA
Free, RB
Cabrera, DM
Skinbjerg, M
Sibley, DR
AF Hazelwood, Lisa A.
Free, R. Benjamin
Cabrera, David M.
Skinbjerg, Mette
Sibley, David R.
TI Reciprocal Modulation of Function between the D-1 and D-2 Dopamine
Receptors and the Na+, K+-ATPase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-KINASE-C; PLASMA-MEMBRANE; NA+,K+-ATPASE ENDOCYTOSIS;
INTERACTING PROTEINS; D1; DESENSITIZATION; RECRUITMENT; PHOSPHORYLATION;
NA,K-ATPASE; INHIBITION
AB It is well documented that dopamine can increase or decrease the activity of the Na+, K+-ATPase (NKA, sodium pump) in an organ-specific fashion. This regulation can occur, at least partially, via receptor-mediated second messenger activation and can promote NKA insertion or removal from the plasma membrane. Using co-immunoprecipitation and mass spectrometry, we now show that, in both brain and HEK293T cells, D-1 and D-2 dopamine receptors (DARs) can exist in a complex with the sodium pump. To determine the impact of NKA on DAR function, biological assays were conducted with NKA and DARs co-expressed in HEK293T cells. In this system, expression of NKA dramatically decreased D-1 and D-2 DAR densities with a concomitant functional decrease in DAR-mediated regulation of cAMP levels. Interestingly, pharmacological inhibition of endogenous or overexpressed NKA enhanced DAR function without altering receptor number or localization. Similarly, DAR function was also augmented by small interfering RNA reduction of the endogenous NKA. These data suggest that, under basal conditions, NKA negatively regulates DAR function via protein-protein interactions. In reciprocal fashion, expression of DARs decreases endogenous NKA function in the absence of dopamine, implicating DAR proteins as regulators of NKA activity. Notably, dopamine stimulation or pertussis toxin inhibition of D-2 receptor signaling did not alter NKA activity, indicating that the D-2-mediated decrease in NKA function is dependent upon protein-protein interactions rather than signaling molecules. This evidence for reciprocal regulation between DARs and NKA provides a novel control mechanism for both DAR signaling and cellular ion balance.
C1 [Hazelwood, Lisa A.; Free, R. Benjamin; Cabrera, David M.; Skinbjerg, Mette; Sibley, David R.] NINDS, Mol Neuropharmacol Sect, NIH, Bethesda, MD 20892 USA.
RP Sibley, DR (reprint author), NINDS, Mol Neuropharmacol Sect, NIH, 5625 Fishers Ln,Rm 4S-04,MSC 9405, Bethesda, MD 20852 USA.
EM sibley@helix.nih.gov
RI Cabrera, David/I-1013-2014
FU National Institutes of Health
FX This work was supported, in whole or in part, by National Institutes of
Health grant (Intramural Research Program of NINDS). The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 36
TC 23
Z9 26
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 DEC 26
PY 2008
VL 283
IS 52
BP 36441
EP 36453
DI 10.1074/jbc.M805520200
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385VA
UT WOS:000261840500042
PM 18984584
ER
PT J
AU Tessmer, I
Yang, Y
Zhai, J
Du, CW
Hsieh, P
Hingorani, MM
Erie, DA
AF Tessmer, Ingrid
Yang, Yong
Zhai, Jie
Du, Chungwei
Hsieh, Peggy
Hingorani, Manju M.
Erie, Dorothy A.
TI Mechanism of MutS Searching for DNA Mismatches and Signaling Repair
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ESCHERICHIA-COLI MUTS; THERMUS-AQUATICUS; CRYSTAL-STRUCTURE; DAMAGE
RECOGNITION; ATPASE ACTIVITY; PROTEIN MUTS; MINOR-GROOVE; BINDING;
HYDROLYSIS; DOMAINS
AB DNA mismatch repair is initiated by the recognition of mismatches by MutS proteins. The mechanism by which MutS searches for and recognizes mismatches and subsequently signals repair remains poorly understood. We used single-molecule analyses of atomic force microscopy images of MutS-DNA complexes, coupled with biochemical assays, to determine the distributions of conformational states, the DNA binding affinities, and the ATPase activities of wild type and two mutants of MutS, with alanine substitutions in the conserved Phe-Xaa-Glu mismatch recognition motif. We find that on homoduplex DNA, the conserved Glu, but not the Phe, facilitates MutS-induced DNA bending, whereas at mismatches, both Phe and Glu promote the formation of an unbent conformation. The data reveal an unusual role for the Phe residue in that it promotes the unbending, not bending, of DNA at mismatch sites. In addition, formation of the specific unbent MutS-DNA conformation at mismatches appears to be required for the inhibition of ATP hydrolysis by MutS that signals initiation of repair. These results provide a structural explanation for the mechanism by which MutS searches for and recognizes mismatches and for the observed phenotypes of mutants with substitutions in the Phe-Xaa-Glu motif.
C1 [Tessmer, Ingrid; Yang, Yong; Erie, Dorothy A.] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Erie, Dorothy A.] Univ N Carolina, Curriculum Appl Sci & Engn, Chapel Hill, NC 27599 USA.
[Du, Chungwei; Hsieh, Peggy] NIDDK, NIH, Bethesda, MD 20892 USA.
[Zhai, Jie; Hingorani, Manju M.] Wesleyan Univ, Dept Biochem & Mol Biol, Middletown, CT 06459 USA.
RP Erie, DA (reprint author), Univ N Carolina, Dept Chem, CB 3290, Chapel Hill, NC 27599 USA.
EM derie@unc.edu
FU National Institutes of Health [GM079480]; American Cancer Society
[RSG03- 047-04-GMC]; National Science Foundation [0448379]; Intramural
Research Program of NIDDK
FX This work was supported, in whole or in part, by National Institutes of
Health Grant GM079480 (to D.A.E.). This work was also supported by Grant
RSG03- 047-04-GMC from the American Cancer Society (to D.A.E.), National
Science Foundation Grant MCB 0448379 (to M.M.H.), and the Intramural
Research Program of NIDDK (to P.H. and C.D.). The costs of publication
of this article were defrayed in part by the payment of page charges.
This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 48
TC 28
Z9 28
U1 1
U2 12
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 DEC 26
PY 2008
VL 283
IS 52
BP 36646
EP 36654
DI 10.1074/jbc.M805712200
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385VA
UT WOS:000261840500063
PM 18854319
ER
PT J
AU Willard, FS
Zheng, Z
Guo, J
Digby, GJ
Kimple, AJ
Conley, JM
Johnston, CA
Bosch, D
Willard, MD
Watts, VJ
Lambert, NA
Ikeda, SR
Du, QS
Siderovski, DP
AF Willard, Francis S.
Zheng, Zhen
Guo, Juan
Digby, Gregory J.
Kimple, Adam J.
Conley, Jason M.
Johnston, Christopher A.
Bosch, Dustin
Willard, Melinda D.
Watts, Val J.
Lambert, Nevin A.
Ikeda, Stephen R.
Du, Quansheng
Siderovski, David P.
TI A Point Mutation to G alpha(i) Selectively Blocks GoLoco Motif Binding
DIRECT EVIDENCE FOR G alpha.GoLoco COMPLEXES IN MITOTIC SPINDLE DYNAMICS
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ASYMMETRIC CELL-DIVISION; HETEROTRIMERIC G-PROTEIN; DISSOCIATION
INHIBITOR ACTIVITY; G-ALPHA-I; CAENORHABDITIS-ELEGANS EMBRYOS;
VOLTAGE-DEPENDENT MODULATION; GUANINE-NUCLEOTIDE EXCHANGE; RAT
SYMPATHETIC NEURONS; ENDOGENOUS RGS PROTEINS; BETA-GAMMA-SUBUNITS
AB Heterotrimeric G-protein G alpha subunits and GoLoco motif proteins are key members of a conserved set of regulatory proteins that influence invertebrate asymmetric cell division and vertebrate neuroepithelium and epithelial progenitor differentiation. GoLoco motif proteins bind selectively to the inhibitory subclass (G alpha(i)) of G alpha subunits, and thus it is assumed that a G alpha(i.)GoLoco motif protein complex plays a direct functional role in microtubule dynamics underlying spindle orientation and metaphase chromosomal segregation during cell division. To address this hypothesis directly, we rationally identified a point mutation to G alpha(i) subunits that renders a selective loss-of-function for GoLoco motif binding, namely an asparagine-to-isoleucine substitution in the alpha D-alpha E loop of the G alpha helical domain. This GoLoco-insensitivity ("GLi") mutation prevented G alpha(i1) association with all human GoLoco motif proteins and abrogated interaction between the Caenorhabditis elegans G alpha sub-unit GOA-1 and the GPR-1 GoLoco motif. In contrast, the GLi mutation did not perturb any other biochemical or signaling properties of G alpha(i) subunits, including nucleotide binding, intrinsic and RGS protein-accelerated GTP hydrolysis, and interactions with G beta gamma dimers, adenylyl cyclase, and seven transmembrane-domain receptors. GoLoco insensitivity rendered G alpha(i) subunits unable to recruit GoLoco motif proteins such as GPSM2/LGN and GPSM3 to the plasma membrane, and abrogated the exaggerated mitotic spindle rocking normally seen upon ectopic expression of wild type G alpha(i) subunits in kidney epithelial cells. This GLi mutation should prove valuable in establishing the physiological roles of G alpha(i).GoLoco motif protein complexes in microtubule dynamics and spindle function during cell division as well as to delineate potential roles for GoLoco motifs in receptor-mediated signal transduction.
C1 [Willard, Francis S.; Kimple, Adam J.; Johnston, Christopher A.; Bosch, Dustin; Willard, Melinda D.; Siderovski, David P.] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Siderovski, David P.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Siderovski, David P.] Univ N Carolina, Ctr Neurosci, Chapel Hill, NC 27599 USA.
[Zheng, Zhen; Du, Quansheng] Med Coll Georgia, Inst Mol Med & Genet, Dept Neurol, Augusta, GA 30912 USA.
[Digby, Gregory J.; Lambert, Nevin A.] Med Coll Georgia, Inst Mol Med & Genet, Dept Pharmacol & Toxicol, Augusta, GA 30912 USA.
[Guo, Juan; Ikeda, Stephen R.] NIAAA, Lab Mol Physiol, Bethesda, MD 20892 USA.
[Conley, Jason M.; Watts, Val J.] Purdue Univ, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47906 USA.
RP Willard, FS (reprint author), Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA.
EM willardfs@lilly.com
RI Watts, Val/A-4633-2012;
OI Ikeda, Stephen/0000-0002-4088-9508
FU National Institutes of Health [R01 GM074268, GM079506, GM078319,
MH060397, F32 GM07694, F30 MH074266]; NIAAA intramural program; American
Cancer Society [RSG0717601CSM]; National Science Foundation [0620024];
American Heart Association; PhRMA Foundation
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01 GM074268 (to D.P.S.), GM079506 (to Q.D.), GM078319 (to
N.A.L.), MH060397 (to V.J.W.), F32 GM07694 (to C.A.J.), and F30 MH074266
(to A.J.K.). This work was also supported by the NIAAA intramural
program (to S. R. I.), American Cancer Society Grant RSG0717601CSM (to
Q.D.), National Science Foundation Grant MCB 0620024 (to N.A.L.), and
fellowships from the American Heart Association (to G.J.D.) and the
PhRMA Foundation (to M.D.W.). The costs of publication of this article
were defrayed in part by the payment of page charges. This article must
therefore be hereby marked "advertisement" in accordance with 18 U. S.
C. Section 1734 solely to indicate this fact.
NR 80
TC 28
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 DEC 26
PY 2008
VL 283
IS 52
BP 36698
EP 36710
DI 10.1074/jbc.M804936200
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385VA
UT WOS:000261840500068
PM 18984596
ER
PT J
AU Weisberg, RA
AF Weisberg, Robert A.
TI Transcription by Moonlight: Structural Basis of an Extraribosomal
Activity of Ribosomal Protein S10
SO MOLECULAR CELL
LA English
DT Editorial Material
ID ANTITERMINATION COMPLEX; TERMINATION; LAMBDA; REGION
C1 NIH, Bethesda, MD 20892 USA.
RP Weisberg, RA (reprint author), NIH, Bldg 37,Room 5138, Bethesda, MD 20892 USA.
EM rweisberg@nih.gov
FU Intramural NIH HHS [Z01 HD000066-37]
NR 10
TC 16
Z9 16
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD DEC 26
PY 2008
VL 32
IS 6
BP 747
EP 748
DI 10.1016/j.molcel.2008.12.010
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 390SO
UT WOS:000262184200001
PM 19111651
ER
PT J
AU Luo, X
Hsiao, HH
Bubunenko, M
Weber, G
Court, DL
Gottesman, ME
Urlaub, H
Wahl, MC
AF Luo, Xiao
Hsiao, He-Hsuan
Bubunenko, Mikhail
Weber, Gert
Court, Donald L.
Gottesman, Max E.
Urlaub, Henning
Wahl, Markus C.
TI Structural and Functional Analysis of the E. coli NusB-S10 Transcription
Antitermination Complex
SO MOLECULAR CELL
LA English
DT Article
ID LAMBDA-N-PROTEIN; RIBOSOMAL-RNA TRANSCRIPTION; ESCHERICHIA-COLI;
MYCOBACTERIUM-TUBERCULOSIS; BACTERIOPHAGE-LAMBDA; ANGSTROM RESOLUTION;
CRYSTAL-STRUCTURE; PHAGE-LAMBDA; FACTOR-NUSA; BINDING
AB Protein S10 is a component of the 30S ribosomal subunit and participates together with NusB protein in processive transcription antitermination. The molecular mechanisms by which S10 can act as a translation or a transcription factor are not understood. We used complementation assays and recombineering to delineate regions of S10 dispensable for antitermination, and determined the crystal structure of a transcriptionally active NusB-S10 complex. In this complex, S10 adopts the same fold as in the 30S subunit and is blocked from simultaneous association with the ribosome. Mass spectrometric mapping of UV-induced crosslinks revealed that the NusB-S10 complex presents an intermolecular, composite, and contiguous binding surface for RNAs containing BoxA antitermination signals. Furthermore, S10 overproduction complemented a nusB null phenotype. These data demonstrate that S10 and NusB together form a BoxA-binding module, that NusB facilitates entry of S10 into the transcription machinery, and that S10 represents a central hub in processive antitermination.
C1 [Gottesman, Max E.] Columbia Univ, Med Ctr, Dept Microbiol & Biochem, New York, NY 10032 USA.
[Gottesman, Max E.] Columbia Univ, Med Ctr, Dept Mol Biophys, New York, NY 10032 USA.
[Luo, Xiao; Weber, Gert; Wahl, Markus C.] Max Planck Inst Biophys Chem, Res Grp Xray Crystallog, D-37077 Gottingen, Germany.
[Hsiao, He-Hsuan; Urlaub, Henning] Max Planck Inst Biophys Chem, Res Grp Bioanalyt Mass Spectrometry, D-37077 Gottingen, Germany.
[Bubunenko, Mikhail; Court, Donald L.] NCI, Gene Regulat & Chromosomal Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Bubunenko, Mikhail] NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Wahl, Markus C.] Univ Gottingen, Dept Med, D-37077 Gottingen, Germany.
RP Gottesman, ME (reprint author), Columbia Univ, Med Ctr, Dept Microbiol & Biochem, New York, NY 10032 USA.
EM meg8@columbia.edu; mwahl@gwdg.de
RI Weber, Gert/I-1800-2013; Wahl, Markus/D-6365-2017
OI Wahl, Markus/0000-0002-2811-5307
FU Deutsche Forschungsgemeinschaft [WA 1126/3-1]; National Institutes of
Health (NIH) [GM37219]
FX We thank Elke Penka and Monika Raabe (Max-Planck-institute for
Biophysical Chemistry, Gdttingen, Germany) for excellent technical
assistance, the staff at beamlines PXI/II (SLS, Villigen, Switzerland)
and BL14.2 (BESSY, Berlin, Germany) for support during diffraction data
collection, and Andrew Byrd and Amanda Altieri (NCI, Frederick, MID,
USA) for communication of results prior to publication. M.C.W. was
supported by grant WA 1126/3-1 from the Deutsche Forschungsgemeinschaft.
M.E.G. was supported by National Institutes of Health (NIH) grant
GM37219. H.U. was supported by a young invest!gatorgrant ofEURASNET.
Thisresearch wassupported in part by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research, and by a
Trans NIH/FDA Intramural Biodefense Program Grant from MAID to D.L.C.
This project was funded in part with federal funds from the National
Cancer Institute, National Institutes of Health, under contract
N01CO-12400. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. government. The authors
declare that they have no competing financial interests.
NR 51
TC 51
Z9 51
U1 0
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD DEC 26
PY 2008
VL 32
IS 6
BP 791
EP 802
DI 10.1016/j.molcel.2008.10.028
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 390SO
UT WOS:000262184200009
PM 19111659
ER
PT J
AU Pelkey, KA
Topolnik, L
Yuan, XQ
Lacaille, JC
McBain, CJ
AF Pelkey, Kenneth A.
Topolnik, Lisa
Yuan, Xiao-Qing
Lacaille, Jean-Claude
McBain, Chris J.
TI State-Dependent cAMP Sensitivity of Presynaptic Function Underlies
Metaplasticity in a Hippocampal Feedforward Inhibitory Circuit
SO NEURON
LA English
DT Article
ID LONG-TERM POTENTIATION; METABOTROPIC GLUTAMATE RECEPTORS; BIDIRECTIONAL
SYNAPTIC PLASTICITY; FIBER-INTERNEURON SYNAPSES; DIVERGENT RELEASE
SITES; VISUAL-CORTEX; RAT HIPPOCAMPUS; CYCLIC-AMP; IN-VIVO; LTP
AB At hippocampal mossy fiber (MF)-st. lucidum interneuron (SLIN) synapses, mGluR7 serves as a metaplastic switch controlling bidirectional plasticity. mGluR7 activation during high-frequency stimulation (HFS) triggers presynaptic LTD due to persistent P/Q-type Ca(2+) channel inhibition. However, following mGluR7 internalization HFS produces presynaptic LTP. Surprisingly, LTP is not a simple molecular reversal of Ca(2+) channel depression. Rather, mGluR7 activation/internalization controls plasticity polarity by gating cAMP sensitivity of release. While naive surface mGluR7 expressing MF-SLIN synapses are insensitive to cAMP elevation, synapses that have internalized mGluR7 robustly potentiate following cAMP increases. Moreover, MF-SLIN LTP requires adenylate cyclase (AC) and protein kinase A (PKA) activities. We also discovered an association between mGluR7 and RIM1 alpha, an active zone molecule required for AC/PKA-dependent presynaptic LTP. Importantly, the mGluR7-RIM1 alpha interaction is regulated by mGluR7 activation, and mice lacking RIM1 alpha are deficient in MF-SLIN LTP. We conclude that state-dependent cAMP sensitivity controlled by mGluR7-RIM1 alpha interactions underlies MF-SLIN metaplasticity.
C1 [Pelkey, Kenneth A.; Yuan, Xiao-Qing; McBain, Chris J.] NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA.
[Topolnik, Lisa; Lacaille, Jean-Claude] Univ Montreal, Dept Physiol, Grp Rech Syst Nerveux Cent, Montreal, PQ H3C 3J7, Canada.
RP Pelkey, KA (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bldg 35, Bethesda, MD 20892 USA.
EM pelkeyk2@mail.nih.gov; mcbainc@mail.nih.gov
FU NIH; Savoy Foundation
FX The authors thank Brian Jeffries for expert technical assistance and
Richard Robitaille for expertise and guidance with two-photon confocal
imaging. Myc-mGluR7a/b constructs were a generous gift from Drs. Laurent
Fagni and Frederica Bertaso. Affinity-purified mGluR7b antibody was
kindly provided by Drs. Katherine Roche and Young Ho Suh. We are very
grateful to Drs. Tom Sudhof and Pascal Kaeser for providing RIM1 alpha
mice. This work was supported by an NICHD intramural award to C.J.M.,
CIHR and FRSO awards to J.-C.L., and an HFSP award to both C.J.M. and
J.-C.L. J.-C.L. is the recipient of the Canada Research Chair in
Cellular and Molecular Neurophysiology. K.A.P. is an NIH Fellow. L.T.
was supported by the Savoy Foundation.
NR 43
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U1 1
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD DEC 26
PY 2008
VL 60
IS 6
BP 980
EP 987
DI 10.1016/j.neuron.2008.11.018
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 391BW
UT WOS:000262208900007
PM 19109906
ER
PT J
AU Kriegeskorte, N
Mur, M
Ruff, DA
Kiani, R
Bodurka, J
Esteky, H
Tanaka, K
Bandettini, PA
AF Kriegeskorte, Nikolaus
Mur, Marieke
Ruff, Douglas A.
Kiani, Roozbeh
Bodurka, Jerzy
Esteky, Hossein
Tanaka, Keiji
Bandettini, Peter A.
TI Matching Categorical Object Representations in Inferior Temporal Cortex
of Man and Monkey
SO NEURON
LA English
DT Article
ID INFEROTEMPORAL CORTEX; HUMAN BRAIN; CEREBRAL-CORTEX; VISUAL-CORTEX;
RESPONSE PATTERNS; SINGLE NEURONS; FMRI ACTIVITY; FACE AREA; PRIMATE;
RECOGNITION
AB Inferior temporal (IT) object representations have been intensively studied in monkeys and humans, but representations of the same particular objects have never been compared between the species. Moreover, IT's role in categorization is not well understood. Here, we presented monkeys and humans with the same images of real-world objects and measured the IT response pattern elicited by each image. In order to relate the representations between the species and to computational models, we compare response-pattern dissimilarity matrices. IT response patterns form category clusters, which match between man and monkey. The clusters correspond to animate and inanimate objects; within the animate objects, faces and bodies form subclusters. Within each category, IT distinguishes individual exemplars, and the within-category exemplar similarities also match between the species. Our findings suggest that primate IT across species may host a common code, which combines a categorical and a continuous representation of objects.
C1 [Kriegeskorte, Nikolaus; Mur, Marieke; Ruff, Douglas A.; Bodurka, Jerzy; Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
[Mur, Marieke] Maastricht Univ, Fac Psychol, Dept Cognit Neurosci, NL-6229 ER Maastricht, Netherlands.
[Kiani, Roozbeh] Univ Washington, Dept Neurobiol & Behav, Seattle, WA 98195 USA.
[Bodurka, Jerzy; Bandettini, Peter A.] NIMH, Funct Magnet Resonance Imaging Facil, NIH, Bethesda, MD 20892 USA.
[Esteky, Hossein] Shahid Beheshti Univ, Sch Med, Res Grp Brain & Cognit Sci, Tehran, Iran.
[Esteky, Hossein] Inst Studies Theoret Phys & Math, Sch Cognit Sci, Tehran, Iran.
[Tanaka, Keiji] RIKEN Brain Sci Inst, Cognit Brain Mapping Lab, Wako, Saitama 3510198, Japan.
RP Kriegeskorte, N (reprint author), NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
EM kriegeskorten@mail.nih.gov
RI Tanaka, Keiji/N-5917-2015;
OI Kriegeskorte, Nikolaus/0000-0001-7433-9005; Ruff,
Douglas/0000-0001-7228-8822
FU Intramural Program of the National Institute of Mental Health
FX We thank Chris Baker, James Haxby, Alex Martin, Nancy Kanwisher, Dwight
Kravitz, Leslie Ungerleider. and Vina Vo for helpful discussions. This
research was supported in part by the Intramural Program of the National
Institute of Mental Health.
NR 70
TC 353
Z9 358
U1 9
U2 51
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD DEC 26
PY 2008
VL 60
IS 6
BP 1126
EP 1141
DI 10.1016/j.neuron.2008.10.043
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 391BW
UT WOS:000262208900017
PM 19109916
ER
PT J
AU Barinka, C
Byun, Y
Dusich, CL
Banerjee, SR
Chen, Y
Castanares, M
Kozikowski, AP
Mease, RC
Pomper, MG
Lubkowski, J
AF Barinka, Cyril
Byun, Youngjoo
Dusich, Crystal L.
Banerjee, Sangeeta R.
Chen, Ying
Castanares, Mark
Kozikowski, Alan P.
Mease, Ronnie C.
Pomper, Martin G.
Lubkowski, Jacek
TI Interactions between Human Glutamate Carboxypeptidase II and Urea-Based
Inhibitors: Structural Characterization
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID NAAG PEPTIDASE INHIBITORS; MEMBRANE ANTIGEN; PROSTATE-CANCER;
N-ACETYLASPARTYLGLUTAMATE; SUBSTRATE-SPECIFICITY; ACTIVE-SITE;
NAALADASE; THERAPY; DESIGN; EXPRESSION
AB Urea-based, low molecular weight ligands of glutamate carboxypeptidase II (GCPII) have demonstrated efficacy in various models of neurological disorders and call serve as imaging agents for prostate cancer. To enhance further development of such compounds, we determined X-ray structures Of four complexes between human GCPII and urea-based inhibitors at high resolution. All ligands demonstrate in invariant glutarate moiety within the S1' pocket of the enzyme. The Ureido linkage between P1 and P1' inhibitor sites interacts with the active-site Zn(1)(2+) ion and the side chains of Tyr552 and His553. Interactions within the S I pocket are defined primarily by a network of hydrogen bonds between the P1 carboxylate group of the inhibitors and the side chains of Arg534, Arg536, and Asn519. Importantly, we have identified a hydrophobic pocket accessory to the S1 site that call be exploited for structure-based design of novel GCPII inhibitors with increased lipophilicity.
C1 [Barinka, Cyril; Lubkowski, Jacek] NCI, Ctr Canc Res, Frederick, MD 21702 USA.
[Castanares, Mark; Pomper, Martin G.] Johns Hopkins Med Inst, Dept Pharmacol & Mol Sci, Baltimore, MD 21231 USA.
[Kozikowski, Alan P.] Univ Illinois, Dept Med Chem & Pharmacognosy, Chicago, IL 60612 USA.
[Byun, Youngjoo; Dusich, Crystal L.; Banerjee, Sangeeta R.; Chen, Ying; Mease, Ronnie C.; Pomper, Martin G.] Johns Hopkins Med Inst, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD 21231 USA.
RP Pomper, MG (reprint author), NCI, Macromol Crystallog Lab, 539 Boyles St, Frederick, MD 21702 USA.
EM mpomper@jhmi.edu; jacek@ncifcrf.gov
RI Barinka, Cyril/G-9803-2014
FU Intramural NIH HHS; NCI NIH HHS [CA1114111, CA111982, CA92871]; NIBIB
NIH HHS [EB005423]; NIMH NIH HHS [MH080580]
NR 41
TC 56
Z9 58
U1 0
U2 19
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 DEC 25
PY 2008
VL 51
IS 24
BP 7737
EP 7743
DI 10.1021/jm800765e
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 386IH
UT WOS:000261876400011
PM 19053759
ER
PT J
AU Kurimura, M
Liu, H
Sulima, A
Hashimoto, A
Przybyl, AK
Ohshima, E
Kodato, S
Deschamps, JR
Dersch, CM
Rothman, RB
Lee, YS
Jacobson, AE
Rice, KC
AF Kurimura, Muneaki
Liu, Hehua
Sulima, Agnieszka
Hashimoto, Akihiro
Przybyl, Anna K.
Ohshima, Etsuo
Kodato, Shinichi
Deschamps, Jeffrey R.
Dersch, Christina M.
Rothman, Richard B.
Lee, Yong Sok
Jacobson, Arthur E.
Rice, Kenner C.
TI Probes for Narcotic Receptor Mediated Phenomena. 37.(1) Synthesis and
Opioid Binding Affinity of the Final Pair of Oxide-Bridged
Phenylmorphans, the Ortho- and Para-b-Isomers and Their N-Phenethyl
Analogues, and the Synthesis of the N-Phenethyl Analogues of the Ortho-
and Para-d-Isomers
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; AGONIST DELTA-ANTAGONIST; FORCED-SWIM TEST;
5-(META-HYDROXYPHENYL)MORPHAN
AB In the isomeric series of 12 racemic topologically rigid N-methyl analogues of oxide-bridged phenylmorphans, all but two of the racemates, the ortho- and para-b-oxide-bridged phenylmorphans 20 and 12, have remained to be synthesized. The b-isomers were very difficult to synthesize because of the highly strained 5,6-transfused ring junction that had to be formed. Our successful strategy required functionalization of the position para (or ortho) to a fluorine atom on the aromatic ring using an electron-withdrawing nitro group to activate that fluorine. The racemic N-phenethyl analogues 24 and 16 were moderately potent K-receptor antagonists in the [S-35]GTP gamma S assay. We synthesized the N-phenethyl-substituted oxide-bridged phenylmorphans in the ortho- and para-d-oxide-bridged phenylmorphan series (51 and 52) which had not been previously evaluated using contemporary receptor binding assays to see whether they also have higher affinity for opioid receptors than their N-methyl relatives 46 and 47.
C1 [Kurimura, Muneaki; Liu, Hehua; Sulima, Agnieszka; Hashimoto, Akihiro; Przybyl, Anna K.; Ohshima, Etsuo; Kodato, Shinichi; Jacobson, Arthur E.; Rice, Kenner C.] NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Kurimura, Muneaki; Liu, Hehua; Sulima, Agnieszka; Hashimoto, Akihiro; Przybyl, Anna K.; Ohshima, Etsuo; Kodato, Shinichi; Jacobson, Arthur E.; Rice, Kenner C.] NIAAA, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Dersch, Christina M.; Rothman, Richard B.] NIDA, Clin Psychopharmacol Sect, Chem Biol Res Branch, Addict Res Ctr,Natl Inst Hlth,Dept Hlth & Human S, Baltimore, MD 21224 USA.
[Lee, Yong Sok] NIH, Ctr Mol Modeling, Div Computat Biosci, CIT,DHHS, Bethesda, MD 20892 USA.
[Deschamps, Jeffrey R.] USN, Res Lab, Struct Matter Lab, Washington, DC 20375 USA.
RP Rice, KC (reprint author), NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, 5625 Fishers Lane,Room 4N03, Bethesda, MD 20892 USA.
EM kr21f@nih.gov
FU Intramural NIH HHS [Z99 DA999999]; NIDA NIH HHS [Y01 DA006002]
NR 21
TC 15
Z9 15
U1 0
U2 6
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 DEC 25
PY 2008
VL 51
IS 24
BP 7866
EP 7881
DI 10.1021/jm800913d
PG 16
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 386IH
UT WOS:000261876400024
PM 19053757
ER
PT J
AU Andrei, D
Maciag, AE
Chakrapani, H
Citro, ML
Keefer, LK
Saavedra, JE
AF Andrei, Daniela
Maciag, Anna E.
Chakrapani, Harinath
Citro, Michael L.
Keefer, Larry K.
Saavedra, Joseph E.
TI Aryl Bis(diazeniumdiolates): Potent Inducers of S-Glutathionylation of
Cellular Proteins and Their in Vitro Antiproliferative Activities
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID NITRIC-OXIDE PRODRUGS; JS-K; ANTICANCER LEAD; LEUKEMIA-CELLS;
ANTILEUKEMIC ACTIVITY; SIGNALING MOLECULE; SECONDARY-AMINES; REDOX
REGULATION; RELAXING FACTOR; DONOR
AB A number of bis(diazeniumdiolates) that we designed to release up to 4 mol of nitric oxide (NO) and that are structural analogues of the NO prodrug and anticancer lead compound O(2)-{2,4-dinitro-5-[4-(N-methylamino)benzoyloxy]phenyl} 1-(N,N-dimethylamino)diazen-1-ium-1,2-diolate (PABA/NO) were synthesized and studied. A majority of these compounds yielded higher levels of NO, were better inhibitors of proliferation of a number of cancer cell lines, and more rapidly induced substantially increased levels of S-glutathionylation of cellular proteins in comparison with PABA/NO. In most cases, the antiproliferative activity and extents of S-glutathionylation correlated well with levels of intracellular NO release. We report bis(diazeniumdiolates) to be a class of S-glutathionylating agents with potent antiproliferative and S-glutathionylating activity.
C1 [Maciag, Anna E.; Citro, Michael L.; Saavedra, Joseph E.] Natl Canc Inst Frederick, SAIC Frederick, Basic Res Program, Ft Detrick, MD 21702 USA.
[Andrei, Daniela; Chakrapani, Harinath; Keefer, Larry K.] Natl Canc Inst Frederick, Chem Sect, Comparat Carcinogenesis Lab, Ft Detrick, MD 21702 USA.
RP Andrei, D (reprint author), Dominican Univ, Dept Chem, 7900 W Div St, River Forest, IL 60305 USA.
EM dandrei@dorn.edu; keefer@ncifcrf.gov
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU NIH; Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research; National Cancer Institute [N01-CO-12400]
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research, as well as
by National Cancer Institute Contract N01-CO-12400 to SAIC-Frederick.
NR 45
TC 17
Z9 18
U1 1
U2 6
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 DEC 25
PY 2008
VL 51
IS 24
BP 7944
EP 7952
DI 10.1021/jm800831y
PG 9
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 386IH
UT WOS:000261876400031
PM 19053760
ER
PT J
AU Jiang, JK
Ghoreschi, K
Deflorian, F
Chen, Z
Perreira, M
Pesu, M
Smith, J
Nguyen, DT
Liu, EH
Leister, W
Costanzi, S
O'Shea, JJ
Thomas, CJ
AF Jiang, Jian-Kang
Ghoreschi, Kamran
Deflorian, Francesca
Chen, Zhi
Perreira, Melissa
Pesu, Marko
Smith, Jeremy
Nguyen, Dac-Trung
Liu, Eric H.
Leister, William
Costanzi, Stefano
O'Shea, John J.
Thomas, Craig J.
TI Examining the Chirality, Conformation and Selective Kinase Inhibition of
3-((3R,4R)-4-methyl-3-(methyl(7H-pyrrolo[2,3-d]pyrimidin-4-yl)amino)pipe
ridin-1-yl)-3-oxopropanenitrile (CP-690,550)
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID TYROSINE PHOSPHORYLATION; JANUS KINASE-3; JAK3; ACTIVATION
AB Here, we examine the significance that stereochemistry plays within the clinically relevant Janus kinase 3 (Jak3) inhibitor 1 (CP-690,550). A synthesis of all four enantiopure stereoisomers of the drug was carried out and an examination of each compound revealed that only the enantiopure 3R,4R isomer was capable of blocking Stat5 phosphorylation (Jak3 dependent). Each compound was profiled across a panel of over 350 kinases, which revealed a high level of selectivity for the Jak family kinases for these related compounds. Each stereoisomer retained a degree of binding to Jak3 and Jak2 and the 3R,4S and 3S,4R stereoisomers were further revealed to have binding affinity for selected members of the STE7 and STE20 subfamily of kinases. finally, an appraisal of the minimum energy conformation of each stereoisomer and molecular docking at Jak3 was performed in an effort to better understand each compounds selectivity and potency profiles.
C1 [Jiang, Jian-Kang; Perreira, Melissa; Nguyen, Dac-Trung; Leister, William; Thomas, Craig J.] NHGRI, NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
[Ghoreschi, Kamran; Chen, Zhi; Pesu, Marko; O'Shea, John J.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Rockville, MD 20850 USA.
[Deflorian, Francesca; Costanzi, Stefano] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
[Liu, Eric H.] NIDDK, Transplantat & Autoimmun Branch, NIH, Bethesda, MD 20892 USA.
[Smith, Jeremy] Kelly Serv, Rockville, MD 20852 USA.
RP Thomas, CJ (reprint author), NHGRI, NIH, Chem Genom Ctr, 9800 Med Ctr Dr,Bldg B,Room 3005,Mail Stop Code 3, Bethesda, MD 20892 USA.
EM craigt@nhgri.nih.gov
RI Costanzi, Stefano/G-8990-2013; Pesu, marko/L-6344-2013;
OI Nguyen, Dac-Trung/0000-0003-2591-9948; Costanzi,
Stefano/0000-0003-3183-7332
FU Molecular Libraries Initiative of the National Institutes of Health
Roadmap for Medical Research; Intramural Research Program of the
National Human Genome Research Institute; National Institute of
Arthritis and Musculoskeletal and Skin Diseases; National Institute of
Diabetes and Digestive and Kidney Diseases; National Institutes of
Health
FX We thank Dr. David Maloney and Dr. Douglas Auld for advice and help
during the preparation of this manuscript. We thank Allison Peck for
critical reading of this manuscript. This research was supported by the
Molecular Libraries Initiative of the National Institutes of Health
Roadmap for Medical Research, the Intramural Research Program of the
National Human Genome Research Institute, the National Institute of
Arthritis and Musculoskeletal and Skin Diseases, and the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health.
NR 35
TC 62
Z9 65
U1 0
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD DEC 25
PY 2008
VL 51
IS 24
BP 8012
EP 8018
DI 10.1021/jm801142b
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 386IH
UT WOS:000261876400037
PM 19053756
ER
PT J
AU Walkup, JT
Albano, AM
Piacentini, J
Birmaher, B
Compton, SN
Sherrill, JT
Ginsburg, GS
Rynn, MA
McCracken, J
Waslick, B
Iyengar, S
March, JS
Kendall, PC
AF Walkup, John T.
Albano, Anne Marie
Piacentini, John
Birmaher, Boris
Compton, Scott N.
Sherrill, Joel T.
Ginsburg, Golda S.
Rynn, Moira A.
McCracken, James
Waslick, Bruce
Iyengar, Satish
March, John S.
Kendall, Philip C.
TI Cognitive Behavioral Therapy, Sertraline, or a Combination in Childhood
Anxiety
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID RANDOMIZED CLINICAL-TRIAL; PLACEBO-CONTROLLED TRIAL; DISORDERS;
CHILDREN; ADOLESCENTS; YOUTH; FLUOXETINE; ADULTHOOD; SAMPLE; RISK
AB Background: Anxiety disorders are common psychiatric conditions affecting children and adolescents. Although cognitive behavioral therapy and selective serotonin-reuptake inhibitors have shown efficacy in treating these disorders, little is known about their relative or combined efficacy.
Methods: In this randomized, controlled trial, we assigned 488 children between the ages of 7 and 17 years who had a primary diagnosis of separation anxiety disorder, generalized anxiety disorder, or social phobia to receive 14 sessions of cognitive behavioral therapy, sertraline (at a dose of up to 200 mg per day), a combination of sertraline and cognitive behavioral therapy, or a placebo drug for 12 weeks in a 2:2:2:1 ratio. We administered categorical and dimensional ratings of anxiety severity and impairment at baseline and at weeks 4, 8, and 12.
Results: The percentages of children who were rated as very much or much improved on the Clinician Global Impression-Improvement scale were 80.7% for combination therapy (P<0.001), 59.7% for cognitive behavioral therapy (P<0.001), and 54.9% for sertraline (P<0.001); all therapies were superior to placebo (23.7%). Combination therapy was superior to both monotherapies (P<0.001). Results on the Pediatric Anxiety Rating Scale documented a similar magnitude and pattern of response; combination therapy had a greater response than cognitive behavioral therapy, which was equivalent to sertraline, and all therapies were superior to placebo. Adverse events, including suicidal and homicidal ideation, were no more frequent in the sertraline group than in the placebo group. No child attempted suicide. There was less insomnia, fatigue, sedation, and restlessness associated with cognitive behavioral therapy than with sertraline.
Conclusions: Both cognitive behavioral therapy and sertraline reduced the severity of anxiety in children with anxiety disorders; a combination of the two therapies had a superior response rate. (ClinicalTrials.gov number, NCT00052078.).
C1 [Walkup, John T.; Ginsburg, Golda S.] Johns Hopkins Med Inst, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Baltimore, MD 21287 USA.
[Albano, Anne Marie; Rynn, Moira A.] Columbia Univ, Med Ctr, New York State Psychiat Inst, New York, NY USA.
[Piacentini, John; McCracken, James] Univ Calif Los Angeles, Los Angeles, CA USA.
[Birmaher, Boris; Iyengar, Satish] Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Compton, Scott N.; March, John S.] Duke Univ, Med Ctr, Durham, NC USA.
[Sherrill, Joel T.] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[Waslick, Bruce] Baystate Med Ctr, Springfield, MA USA.
[Kendall, Philip C.] Temple Univ, Philadelphia, PA 19122 USA.
RP Walkup, JT (reprint author), Johns Hopkins Med Inst, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, 600 N Wolfe St, Baltimore, MD 21287 USA.
RI Piacentini, John/C-4645-2011
FU NIMH NIH HHS [U01 MH064088, K23 MH075843, L40 MH072315, L40 MH072315-02,
U01 MH063747, U01 MH064003, U01 MH064089, U01 MH064092, U01 MH064107,
U01 MH63747, U01 MH64003, U01 MH64088, U01 MH64092, U01 MH64107]
NR 32
TC 432
Z9 435
U1 12
U2 59
PU MASSACHUSETTS MEDICAL SOC
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 DEC 25
PY 2008
VL 359
IS 26
BP 2753
EP 2766
DI 10.1056/NEJMoa0804633
PG 14
WC Medicine, General & Internal
SC General & Internal Medicine
GA 387KJ
UT WOS:000261950800003
PM 18974308
ER
PT J
AU Powell, SL
Goedecke, T
Nikolic, D
Chen, SN
Ahn, S
Dietz, B
Farnsworth, NR
van Breemen, RB
Lankin, DC
Pauli, GF
Bolton, JL
AF Powell, Sharla L.
Goedecke, Tanja
Nikolic, Dejan
Chen, Shao-Nong
Ahn, Soyoun
Dietz, Birgit
Farnsworth, Norman R.
van Breemen, Richard B.
Lankin, David C.
Pauli, Guido F.
Bolton, Judy L.
TI In Vitro Serotonergic Activity of Black Cohosh and Identification of
N-omega-Methylserotonin as a Potential Active Constituent
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE Black cohosh; N-methylserotonin; Cimicifuga; menopause; serotonin
ID PERFORMANCE LIQUID-CHROMATOGRAPHY; MIXED COMPETITIVE LIGAND;
MORPHINE-DEPENDENT RATS; DORSAL RAPHE NUCLEUS; CIMICIFUGA-RACEMOSA;
POSTMENOPAUSAL WOMEN; MENOPAUSAL SYMPTOMS; LIGHT-SCATTERING;
ACTAEA-RACEMOSA; PARTIAL AGONIST
AB Cimicifuga racemosa (L.) Nutt. (syn. Actaea racemosa L., black cohosh) is used to relieve menopausal hot flashes, although clinical studies have provided conflicting data, and the active constituent(s) and mechanism(s) of action remain unknown. Because serotonergic receptors and transporters are involved with thermoregulation, black cohosh and its phytoconstituents were evaluated for serotonergic activity using 5-HT7 receptor binding, cAMP induction, and serotonin selective re-uptake inhibitor (SSRI) assays. Crude extracts displayed 5-HT7 receptor binding activity and induced cAMP production. Fractionation of the methanol extract led to isolation of phenolic acids and identification of N-omega-methylserotonin by LC-MS/MS. Cimicifuga triterpenoids and phenolic acids bound weakly to the 5-HT7 receptor with no cAMP or SSRI activity. In contrast, N-omega-methylserotonin showed 5-HT7 receptor binding (IC50 = 23 pM), induced cAMP (EC50 = 22 nM), and blocked serotonin re-uptake (IC50 = 490 nM). These data suggest N-omega-methylserotonin may be responsible for the serotonergic activity of black cohosh.
C1 [Bolton, Judy L.] Univ Illinois, Dept Med Chem & Pharmacognosy, Coll Pharm, Ctr Bot Dietary Supplements Res, Chicago, IL 60612 USA.
Univ Illinois, NIH, Coll Pharm, Ctr Bot Dietary Supplements Res, Chicago, IL 60612 USA.
RP Bolton, JL (reprint author), Univ Illinois, Dept Med Chem & Pharmacognosy, Coll Pharm, Ctr Bot Dietary Supplements Res, 833 S Wood St,MC 781, Chicago, IL 60612 USA.
EM Judy.Bolton@uic.edu
RI Godecke, Tanja/G-7384-2011;
OI Godecke, Tanja/0000-0001-9188-1613
FU Office of Dietary Supplements (ODS) [P50 AT00155]; National Center for
Complementary and Alternative Medicine (NCCAM); Office for Research on
Women's Health (ORWH); National Institute of General Medicine (NIGMS) of
the National Institutes of Health (NIH); NCCAM [F31 AT 003995]
FX This work was supported by Grant P50 AT00155 provided jointly by the
Office of Dietary Supplements (ODS), the National Center for
Complementary and Alternative Medicine (NCCAM), the Office for Research
on Women's Health (ORWH), and the National Institute of General Medicine
NIGMS) of the National Institutes of Health (NIH). S.L.P. is grateful
for a Ruth L. Kirschstein NCCAM predoctoral fellowship, F31 AT 003995.
The contents of this paper are solely the responsibility of the authors
and do not necessarily represent the official views of the NIH.
NR 47
TC 35
Z9 43
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD DEC 24
PY 2008
VL 56
IS 24
BP 11718
EP 11726
DI 10.1021/jf803298z
PG 9
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
Technology
SC Agriculture; Chemistry; Food Science & Technology
GA 385GJ
UT WOS:000261802400024
PM 19049296
ER
PT J
AU Butterfield, LH
Disis, ML
Fox, BA
Lee, PP
Khleif, SN
Thurin, M
Trinchieri, G
Wang, E
Wigginton, J
Chaussabel, D
Coukos, G
Dhodapkar, M
Hakansson, L
Janetzki, S
Kleen, TO
Kirkwood, JM
Maccalli, C
Maecker, H
Maio, M
Malyguine, A
Masucci, G
Palucka, AK
Potter, DM
Ribas, A
Rivoltini, L
Schendel, D
Seliger, B
Selvan, S
Slingluff, CL
Stroncek, DF
Streicher, H
Wu, XF
Zeskind, B
Zhao, YD
Zocca, MB
Zwierzina, H
Marincola, FM
AF Butterfield, Lisa H.
Disis, Mary L.
Fox, Bernard A.
Lee, Peter P.
Khleif, Samir N.
Thurin, Magdalena
Trinchieri, Giorgio
Wang, Ena
Wigginton, Jon
Chaussabel, Damien
Coukos, George
Dhodapkar, Madhav
Hakansson, Leif
Janetzki, Sylvia
Kleen, Thomas O.
Kirkwood, John M.
Maccalli, Cristina
Maecker, Holden
Maio, Michele
Malyguine, Anatoli
Masucci, Giuseppe
Palucka, A. Karolina
Potter, Douglas M.
Ribas, Antoni
Rivoltini, Licia
Schendel, Dolores
Seliger, Barbara
Selvan, Senthamil
Slingluff, Craig L., Jr.
Stroncek, David F.
Streicher, Howard
Wu, Xifeng
Zeskind, Benjamin
Zhao, Yingdong
Zocca, Mai-Britt
Zwierzina, Heinz
Marincola, Francesco M.
TI A systematic approach to biomarker discovery; Preamble to "the iSBTc-FDA
taskforce on immunotherapy biomarkers"
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID CYTOKINE FLOW-CYTOMETRY; EXPRESSION ANALYSIS; CANCER; CELLS;
INTERLEUKIN-2; TETRAMER; ELISPOT; CRYOPRESERVATION; MELANOMA; THERAPY
AB The International Society for the Biological Therapy of Cancer (iSBTc) has initiated in collaboration with the United States Food and Drug Administration (FDA) a programmatic look at innovative avenues for the identification of relevant parameters to assist clinical and basic scientists who study the natural course of host/tumor interactions or their response to immune manipulation. The task force has two primary goals: 1) identify best practices of standardized and validated immune monitoring procedures and assays to promote inter-trial comparisons and 2) develop strategies for the identification of novel biomarkers that may enhance our understating of principles governing human cancer immune biology and, consequently, implement their clinical application. Two working groups were created that will report the developed best practices at an NCI/FDA/iSBTc sponsored workshop tied to the annual meeting of the iSBTc to be held in Washington DC in the Fall of 2009. This foreword provides an overview of the task force and invites feedback from readers that might be incorporated in the discussions and in the final document.
C1 [Butterfield, Lisa H.; Kirkwood, John M.] Univ Pittsburgh, Dept Med, Div Hematol Oncol, Inst Canc, Pittsburgh, PA 15213 USA.
[Disis, Mary L.] Univ Washington, Tumor Vaccine Grp, Ctr Translat Med Womens Hlth, Seattle, WA 98195 USA.
[Fox, Bernard A.] Providence Portland Med Ctr, Earle A Chiles Res Inst, Portland, OR 97213 USA.
[Fox, Bernard A.] Oregon Hlth & Sci Univ, Dept Mol Biol, Inst Canc, Portland, OR 97213 USA.
[Lee, Peter P.] Stanford Univ, Dept Med, Div Hematol, Stanford, CA 94305 USA.
[Khleif, Samir N.] NCI, Canc Vaccine Sect, NIH, Bethesda, MD 20892 USA.
[Thurin, Magdalena] NCI, Canc Diag Program, Rockville, MD 20852 USA.
[Trinchieri, Giorgio] NCI, Canc & Inflammat Program, NIH, Frederick, MD 21702 USA.
[Wang, Ena; Marincola, Francesco M.] NIH, IDIS, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Wang, Ena; Marincola, Francesco M.] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Wigginton, Jon] Bristol Myers Squibb Co, Princeton, NJ 08540 USA.
[Chaussabel, Damien; Palucka, A. Karolina] Baylor Inst Immunol Res, Dallas, TX 75204 USA.
[Chaussabel, Damien; Palucka, A. Karolina] Baylor Res Inst, Dallas, TX 75204 USA.
[Coukos, George] Univ Penn, Ctr Res Early Detect & Cure Ovarian Canc, Philadelphia, PA 19104 USA.
[Dhodapkar, Madhav] Yale Univ, Dept Hematol, New Haven, CT 06510 USA.
[Hakansson, Leif] Lund Univ, Div Clin Tumor Immunol, S-58185 Linkoping, Sweden.
[Janetzki, Sylvia] ZellNet Consulting Inc, Ft Lee, NJ 07024 USA.
[Kleen, Thomas O.] Cellular Technol Ltd, Shaker Hts, OH 44122 USA.
[Maccalli, Cristina] Ist Sci San Raffaele, DIBIT, Unit Immunobiotherapy Solid Tumors, Dept Mol Oncol, I-20132 Milan, Italy.
[Maecker, Holden] Baylor Inst Immunol Res, Dallas, TX 75204 USA.
[Maio, Michele] Univ Hosp Siena, Ist Toscano Tumori, Dept Oncol, Siena, Italy.
[Maio, Michele] IRCCS, Ctr Riferimento Oncol, Dept Med Oncol, Canc Bioimmunotherapy Unit, I-53100 Aviano, Italy.
[Malyguine, Anatoli] NCI, SAIC Frederick Inc, Lab Cell Mediated Immun, Frederick, MD 21702 USA.
[Masucci, Giuseppe] Karolinska Inst, Dept Oncol Pathol, S-17176 Stockholm, Sweden.
[Potter, Douglas M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15213 USA.
[Ribas, Antoni] Univ Calif Los Angeles, Dept Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Rivoltini, Licia] Ist Nazl Tumori, IRCCS Fdn, Unit Immunotherapy Human Tumors, I-20100 Milan, Italy.
[Schendel, Dolores] German Res Ctr Environm Hlth, Inst Mol Immunol, D-81377 Munich, Germany.
[Schendel, Dolores] German Res Ctr Environm Hlth, Clin Cooperat Grp Immune Monitoring, Helmholtz Zentrum Munchen, D-81377 Munich, Germany.
[Seliger, Barbara] Univ Halle Wittenberg, Inst Med Immunol, D-06112 Halle, Saale, Germany.
[Selvan, Senthamil] Hoag Canc Ctr, Newport Beach, CA 92663 USA.
[Slingluff, Craig L., Jr.] Univ Virginia, Sch Med, Div Surg Oncol, Dept Surg, Charlottesville, VA 22908 USA.
[Stroncek, David F.] NIH, Cell Therapy Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Streicher, Howard] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20852 USA.
[Wu, Xifeng] Univ Texas Houston, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Zeskind, Benjamin] Immuneering Corp, Boston, MA 02215 USA.
[Zhao, Yingdong] NCI, Biometr Res Branch, Bethesda, MD 20852 USA.
[Zocca, Mai-Britt] DanDritt Biotech AS, DK-2100 Copenhagen, Denmark.
[Zwierzina, Heinz] Innsbruck Med Univ, Dept Internal Med, A-6020 Innsbruck, Austria.
RP Butterfield, LH (reprint author), Univ Pittsburgh, Dept Med, Div Hematol Oncol, Inst Canc, Pittsburgh, PA 15213 USA.
EM butterfieldl@upmc.edu; ndisis@u.washington.edu; foxb@foxlab.org;
ppl@stanford.edu; khleif@nih.gov; thurinm@mail.nih.gov;
trinchig@mail.nih.gov; ewang@mail.cc.nih.gov; jon.wigginton@bms.com;
damienc@baylorhealth.edu; gcks@med.upenn.edu; dhodapk@rockefeller.edu;
Leif.Hakansson@lio.se; sylvia@zellnet.com; thomas.kleen@immunospot.com;
kirkwoodjm@upmc.edu; Maccalli.cristina@hsr.it; hmaecker@yahoo.com;
mmaio@cro.it; malyguinea@mail.nih.gov; giuseppe.masucci@ki.se;
karolinp@BaylorHealth.edu; potter@upci.pitt.edu; ARibas@mednet.ucla.edu;
licia.rivoltini@istitutotumori.mi.it; schendel@helmholtz-muenchen.de;
Barbara.seliger@meditiu.uni-halle.de; sselvan@hoaghospital.org;
CLS8H@virginia.edu; dstroncek@mail.cc.nih.gov; streicherh@mail.nih.gov;
xwu@mdanderson.org; bzeskind@immuneering.com; zhaoy@helix.nih.gov;
mbz@dandrit.com; Heinz.zwierzina@i-med.ac.at; fmarincola@mail.cc.nih.gov
OI Masucci, Giuseppe/0000-0002-9583-2306; coral,
sandra/0000-0002-1308-3082; Rivoltini, Licia/0000-0002-2409-6225;
Chaussabel, Damien/0000-0002-6131-7242
NR 44
TC 36
Z9 36
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD DEC 23
PY 2008
VL 6
AR 81
DI 10.1186/1479-5876-6-81
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 409WT
UT WOS:000263537200001
PM 19105846
ER
PT J
AU Mittal, J
Hummer, G
AF Mittal, Jeetain
Hummer, Gerhard
TI Static and dynamic correlations in water at hydrophobic interfaces
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE capillary waves; drying transition; hydrophobic effect; surface tension
ID SCALED-PARTICLE THEORY; DEWETTING TRANSITION; PERTURBATION-THEORY;
MOLECULAR-DYNAMICS; AQUEOUS-SOLUTIONS; LENGTH SCALES; HYDRATION;
COLLAPSE; SOLUTES; LIQUID
AB We study the static and dynamic properties of the water-density fluctuations in the interface of large nonpolar solutes. With the help of extensive molecular dynamics simulations of TIP4P water near smooth spherical solutes, we show that for large solutes, the interfacial density profile is broadened by capillary waves. For purely repulsive solutes, the squared width of the interface increases linearly with the logarithm of the solute size, as predicted by capillary-wave theory. The apparent interfacial tension extracted from the slope agrees with that of a free liquid-vapor interface. The characteristic length of local density fluctuations is approximate to 0.5 nm, measured along the arc, again consistent with that of a free liquid-vapor interface. Probed locally, the interfacial density fluctuations exhibit large variances that exceed those expected for an ideal gas. Qualitatively consistent with theories of the free liquid-vapor interface, we find that the water interface near large and strongly nonpolar solutes is flickering, broadened by capillary-wave fluctuations. These fluctuations result in transitions between locally wet and dry regions that are slow on a molecular time scale.
C1 [Mittal, Jeetain; Hummer, Gerhard] NIDDK, Chem Phys Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Hummer, G (reprint author), NIDDK, Chem Phys Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM gerhard.hummer@nih.gov
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU National Institutes of Health (NIH); National Institute of Diabetes and
Digestive and Kidney Diseases
FX J.M. thanks Dr. Artur Adib for several helpful discussions and
supporting a postdoctoral fellowship during this work. We also thank Dr.
Attila Szabo (National Institutes of Health), Dr. Robert Best
(University of Cambridge, Cambridge, U. K.), and Sapna Sarupria
(Rensselaer Polytechnic Institute, Troy, NY) for pertinent suggestions.
This work was supported by the Intramural Research Program of the
National Institutes of Health (NIH), National Institute of Diabetes and
Digestive and Kidney Diseases. This study used the high-performance
computational capabilities of the Biowulf PC/Linux cluster at the NIH
(http://biowulf.nih.gov).
NR 66
TC 84
Z9 84
U1 1
U2 44
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 23
PY 2008
VL 105
IS 51
BP 20130
EP 20135
DI 10.1073/pnas.0809029105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 388BP
UT WOS:000261995600025
PM 19074279
ER
PT J
AU Mittal, J
Best, RB
AF Mittal, Jeetain
Best, Robert B.
TI Thermodynamics and kinetics of protein folding under confinement
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE macromolecular crowding; course-grained simulation; energy landscape;
diffusion
ID MOLECULAR CONFINEMENT; ENERGY LANDSCAPE; STABILITY; SIMULATIONS;
DYNAMICS; MODEL; SPACES; RATES; ENHANCEMENT; ENVIRONMENT
AB Understanding the effects of confinement on protein stability and folding kinetics is important for describing protein folding in the cellular environment. We have investigated the effects of confinement on two structurally distinct proteins as a function of the dimension d(c) and characteristic size R of the confining boundary. We find that the stabilization of the folded state relative to bulk conditions is quantitatively described by R-gamma c, where the exponent gamma(c) is approximate to 5/3 independent of the dimension of confinement d(c) (cylindrical, planar, or spherical). Moreover, we find that the logarithm of the folding rates also scale as R-gamma c, with deviations only being seen for very small confining geometries, where folding is downhill; for both stability and kinetics, the dominant effect is the change in the free energy of the unfolded state. A secondary effect on the kinetics is a slight destabilization of the transition state by confinement, although the contacts present in the confined transition state are essentially identical to the bulk case. We investigate the effect of confinement on the position-dependent diffusion coefficients D(Q) for dynamics along the reaction coordinate Q (fraction of native contacts). The diffusion coefficients only change in the unfolded state basin, where they are increased because of compaction.
C1 [Best, Robert B.] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
[Mittal, Jeetain] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Best, RB (reprint author), Univ Cambridge, Dept Chem, Lensfield Rd, Cambridge CB2 1EW, England.
EM rbb24@cam.ac.uk
RI Best, Robert/H-7588-2016
OI Best, Robert/0000-0002-7893-3543
FU Royal Society University Research Fellowship
FX We thank Dr. Attila Szabo for constant encouragement and several helpful
discussions and Dr. Hoi Sung and Dr. David Minh for pertinent
suggestions. This work was supported by the National Institute of
Diabetes and Digestive and Kidney Diseases Intramural Research Program.
This study used the high-performance computational capabilities of the
Biowulf PC/Linux cluster at the National Institutes of Health. J. M.
thanks Dr. Artur Adib for supporting a postdoctoral fellowship. R. B.
was supported by a Royal Society University Research Fellowship.
NR 57
TC 88
Z9 88
U1 4
U2 32
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 23
PY 2008
VL 105
IS 51
BP 20233
EP 20238
DI 10.1073/pnas.0807742105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 388BP
UT WOS:000261995600041
PM 19073911
ER
PT J
AU Abdelmohsen, K
Srikantan, S
Kuwano, Y
Gorospe, M
AF Abdelmohsen, Kotb
Srikantan, Subramanya
Kuwano, Yuki
Gorospe, Myriam
TI miR-519 reduces cell proliferation by lowering RNA-binding protein HuR
levels
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE elav; microRNA; post-transcriptional gene regulation; ribonucleoprotein
complex; translational control
ID MESSENGER-RNA; TRANSLATION; PHOSPHORYLATION; EXPRESSION; MICRORNAS;
ELEMENT; SENESCENCE; STABILITY; CYTOPLASM; ALPHA
AB Gene expression is potently regulated through the action of RNA-binding proteins (RBPs) and microRNAs (miRNAs). Here, we present evidence of a miRNA regulating an RBP. The RBP HuR can stabilize and modulate the translation of numerous target mRNAs involved in cell proliferation, but little is known about the mechanisms that regulate HuR abundance. We identified two putative sites of miR-519 interaction on the HuR mRNA, one in its coding region (CR), one in its 3'-untranslated region (UTR). In several human carcinoma cell lines tested, HeLa (cervical), HCT116 and RKO (colon), and A2780 (ovarian), overexpression of a miR-519 precursor [(Pre) miR-519] reduced HuR abundance, while inhibiting miR-519 by using an antisense RNA [(AS) miR-519] elevated HuR levels. The influence of miR-519 was recapitulated using heterologous reporter constructs that revealed a greater repressive effect on the HuR CR than the HuR 3'-UTR target sequences. miR-519 did not alter HuR mRNA abundance, but reduced HuR biosynthesis, as determined by measuring nascent HuR translation and HuR mRNA association with polysomes. Modulation of miR-519 leading to altered HuR levels in turn affected the levels of proteins encoded by HuR target mRNAs. In keeping with HuR's proliferative influence, (AS) miR-519 significantly increased cell number and [H-3]-thymidine incorporation, while (Pre) miR-519 reduced these parameters. Importantly, the growth-promoting effects of (AS) miR-519 required the presence of HuR, because downregulation of HuR by RNAi dramatically suppressed its proliferative action. In sum, miR-519 represses HuR translation, in turn reducing HuR-regulated gene expression and cell division.
C1 [Abdelmohsen, Kotb; Srikantan, Subramanya; Kuwano, Yuki; Gorospe, Myriam] NIA, Cellular & Mol Biol Lab, IRP, NIH, Baltimore, MD 21224 USA.
RP Abdelmohsen, K (reprint author), NIA, Cellular & Mol Biol Lab, IRP, NIH, Baltimore, MD 21224 USA.
EM abdelmohsenk@grc.nia.nih.gov; myriam-gorospe@nih.gov
OI srikantan, subramanya/0000-0003-1810-6519; abdelmohsen,
Kotb/0000-0001-6240-5810
FU Intramural Research Program (IRP) of the NIA, National Institutes of
Health
FX We are grateful to P. J. Morin (National Institute on Aging, NIA) for
providing cell lines and to R. Wersto and his team for assistance with
flow cytometry. This research was supported entirely by the Intramural
Research Program (IRP) of the NIA, National Institutes of Health.
NR 33
TC 124
Z9 127
U1 1
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 23
PY 2008
VL 105
IS 51
BP 20297
EP 20302
DI 10.1073/pnas.0809376106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 388BP
UT WOS:000261995600052
PM 19088191
ER
PT J
AU Hou, CH
Zhao, H
Tanimoto, K
Dean, A
AF Hou, Chunhui
Zhao, Hui
Tanimoto, Keiji
Dean, Ann
TI CTCF-dependent enhancer-blocking by alternative chromatin loop formation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE beta-globin genes; insulator; locus control region; epigenetics;
transcription regulation
ID BETA-GLOBIN LOCUS; TRANSCRIPTION FACTOR GATA-1; CONTROL REGION;
GENE-EXPRESSION; ERYTHROID-CELLS; HISTONE MODIFICATION; DOMAIN
ACTIVATION; PROTEIN CTCF; HUMAN GENOME; FACTOR EKLF
AB The mechanism underlying enhancer-blocking by insulators is unclear. We explored the activity of human beta-globin HS5, the orthologue of the CTCF-dependent chicken HS4 insulator. An extra copy of HS5 placed between the beta-globin locus control region (LCR) and downstream genes on a transgene fulfills the classic predictions for an enhancer-blocker. Ectopic HS5 does not perturb the LCR but blocks gene activation by interfering with RNA pol II, activator and coactivator recruitment, and epigenetic modification at the downstream beta-globin gene. Underlying these effects, ectopic HS5 disrupts chromatin loop formation between beta-globin and the LCR, and instead forms a new loop with endogenous HS5 that topologically isolates the LCR. Both enhancer-blocking and insulator-loop formation depend on an intact CTCF site in ectopic HS5 and are sensitive to knock-down of the CTCF protein by siRNA. Thus, intrinsic looping activity of CTCF sites can nullify LCR function.
C1 [Hou, Chunhui; Zhao, Hui; Dean, Ann] NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Tanimoto, Keiji] Univ Tsukuba, Grad Sch Life & Environm Sci, Tsukuba, Ibaraki 3058577, Japan.
RP Dean, A (reprint author), NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
EM anndean@helix.nih.gov
RI Hou, Chunhui/A-6596-2009; Tanimoto, Keiji/B-2600-2014
FU Intramural Program of the National Institute of Diabetes and Digestive
and Kidney Diseases; National Institutes of Health
FX We thank Drs. Elissa Lei, Vasily Studitsky, and Rohinton Kamakaka for
critical comments on the manuscript. This research was supported by the
Intramural Program of the National Institute of Diabetes and Digestive
and Kidney Diseases, National Institutes of Health.
NR 43
TC 80
Z9 83
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 23
PY 2008
VL 105
IS 51
BP 20398
EP 20403
DI 10.1073/pnas.0808506106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 388BP
UT WOS:000261995600069
PM 19074263
ER
PT J
AU Heller, NM
Qi, XL
Junttila, IS
Shirey, KA
Vogel, SN
Paul, WE
Keegan, AD
AF Heller, Nicola M.
Qi, Xiulan
Junttila, Ilkka S.
Shirey, Kari Ann
Vogel, Stefanie N.
Paul, William E.
Keegan, Achsah D.
TI Type I IL-4Rs Selectively Activate IRS-2 to Induce Target Gene
Expression in Macrophages
SO SCIENCE SIGNALING
LA English
DT Article
AB Although interleukin-4 (IL-4) and IL-13 participate in allergic inflammation and share a receptor subunit (IL-4R alpha), they have different functions. We compared cells expressing type I and II IL-4Rs with cells expressing only type II receptors for their responsiveness to these cytokines. IL-4 induced highly efficient, gamma C-dependent tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2), whereas IL-13 was less effective, even when phosphorylation of signal transducer and activator of transcription 6 (STAT6) was maximal. Only type I receptor, gamma C-dependent signaling induced efficient association of IRS-2 with the p85 subunit of phosphoinositide 3-kinase or the adaptor protein growth factor receptor-bound protein 2. In addition, IL-4 signaling through type I IL-4Rs induced more robust expression of a subset of genes associated with alternatively activated macrophages than did IL-13. Thus, IL-4 activates signaling pathways through type I IL-4Rs qualitatively differently from IL-13, which cooperate to induce optimal gene expression.
C1 [Heller, Nicola M.; Qi, Xiulan; Keegan, Achsah D.] Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Heller, Nicola M.; Qi, Xiulan; Shirey, Kari Ann; Vogel, Stefanie N.; Keegan, Achsah D.] Univ Maryland, Sch Med, Dept Microbiol & Immunol, Baltimore, MD 21201 USA.
[Junttila, Ilkka S.; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Keegan, AD (reprint author), Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
EM akeegan@som.umaryland.edu
FU NHLBI NIH HHS [T32 HL 007698, T32 HL007698, T32 HL007698-13, T32
HL007698-14, T32 HL007698-15, T32 HL007698-16]; NIAID NIH HHS [R01
AI038985, AI 018797, AI 038985, AI 059775, R01 AI038985-12A1, R01
AI038985-13, R01 AI038985-14, R01 AI059775, R01 AI059775-01A2, R01
AI059775-02, R01 AI059775-03, R01 AI059775-04, R01 AI059775-05, R37
AI018797, R37 AI018797-25, R37 AI018797-26, R37 AI018797-27]
NR 91
TC 62
Z9 62
U1 0
U2 3
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD DEC 23
PY 2008
VL 1
IS 51
AR ra17
DI 10.1126/scisignal.1164795
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA V10XY
UT WOS:000207497900004
PM 19109239
ER
PT J
AU Tai, LH
Goulet, ML
Belanger, S
Toyama-Sorimachi, N
Fodil-Cornu, N
Vidal, SM
Troke, AD
McVicar, DW
Makrigiannis, AP
AF Tai, Lee-Hwa
Goulet, Marie-Line
Belanger, Simon
Toyama-Sorimachi, Noriko
Fodil-Cornu, Nassima
Vidal, Silvia M.
Troke, Angela D.
McVicar, Daniel W.
Makrigiannis, Andrew P.
TI Positive regulation of plasmacytoid dendritic cell function via Ly49Q
recognition of class I MHC
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID INTERFERON-PRODUCING CELLS; NATURAL-KILLER-CELLS; INHIBITORY NK
RECEPTOR; IIFN-PRODUCING CELLS; CYTOMEGALOVIRUS-INFECTION;
MOUSE-CYTOMEGALOVIRUS; MONOCLONAL-ANTIBODY; VIRAL-INFECTION; C57BL/6
MICE; CLUSTER
AB Plasmacytoid dendritic cells (pDCs) are an important source of type I interferon (IFN) during initial immune responses to viral infections. In mice, pDCs are uniquely characterized by high-level expression of Ly49Q, a C-type lectin-like receptor specific for class I major histocompatibility complex (MHC) molecules. Despite having a cytoplasmic immunoreceptor tyrosine-based inhibitory motif, Ly49Q was found to enhance pDC function in vitro, as pDC cytokine production in response to the Toll-like receptor (TLR) 9 agonist CpG-oligonucleotide (ODN) could be blocked using soluble monoclonal antibody (mAb) to Ly49Q or H-2K(b). Conversely, CpG-ODN-dependent IFN-alpha production by pDCs was greatly augmented upon receptor cross-linking using immobilized anti-Ly49Q mAb or recombinant H-2K(b) ligand. Accordingly, Ly49Q-deficient pDCs displayed a severely reduced capacity to produce cytokines in response to TLR7 and TLR9 stimulation both in vitro and in vivo. Finally, TLR9-dependent antiviral responses were compromised in Ly49Q-null mice infected with mouse cytomegalovirus. Thus, class I MHC recognition by Ly49Q on pDCs is necessary for optimal activation of innate immune responses in vivo.
C1 [Tai, Lee-Hwa; Goulet, Marie-Line; Belanger, Simon; Troke, Angela D.; Makrigiannis, Andrew P.] Clin Res Inst Montreal, Lab Mol Immunol, Montreal, PQ H2W 1R7, Canada.
[Tai, Lee-Hwa; Goulet, Marie-Line; Belanger, Simon; Vidal, Silvia M.; Troke, Angela D.; Makrigiannis, Andrew P.] McGill Univ, Dept Microbiol & Immunol, Montreal, PQ H3G 1Y6, Canada.
[Toyama-Sorimachi, Noriko] Int Med Ctr Japan, Res Inst, Dept Gastroenterol, Shinjuku Ku, Tokyo 1628655, Japan.
[Fodil-Cornu, Nassima; Vidal, Silvia M.] McGill Univ, Dept Human Genet, Montreal, PQ H3A 2B4, Canada.
[Fodil-Cornu, Nassima; Vidal, Silvia M.] McGill Univ, McGill Ctr Study Host Resistance, Montreal, PQ H3A 2B4, Canada.
[McVicar, Daniel W.] NCI, Canc & Inflammat Program, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Makrigiannis, AP (reprint author), Clin Res Inst Montreal, Lab Mol Immunol, 110 Pine Ave W, Montreal, PQ H2W 1R7, Canada.
EM makriga@ircm.qc.ca
RI McVicar, Daniel/G-1970-2015
FU Canadian Institutes of Health Research (CIHR) [MOP 62841]
FX This work was supported by an operating grant ( MOP 62841) from the
Canadian Institutes of Health Research (CIHR). L-H. Tai is supported by
a CIHR Cancer Training Program scholarship. S. Belanger is supported by
a Fonds de la recherche en sante Quebec scholarship. A. P. Makrigiannis
is supported by a New Investigator Award from the CIHR.
NR 39
TC 38
Z9 38
U1 0
U2 0
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD DEC 22
PY 2008
VL 205
IS 13
BP 3187
EP 3199
DI 10.1084/jem.20080718
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 450VH
UT WOS:000266428700022
PM 19075287
ER
PT J
AU Anton, O
Batista, A
Millan, J
Andres-Delgado, L
Puertollano, R
Correas, I
Alonso, MA
AF Anton, Olga
Batista, Alicia
Millan, Jaime
Andres-Delgado, Laura
Puertollano, Rosa
Correas, Isabel
Alonso, Miguel A.
TI An essential role for the MAL protein in targeting Lck to the plasma
membrane of human T lymphocytes
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID DARBY CANINE KIDNEY; RAFT-ASSOCIATED PROTEIN; INFLUENZA-VIRUS
HEMAGGLUTININ; NORMAL APICAL TRANSPORT; CELL ANTIGEN RECEPTOR; LIPID
RAFTS; IMMUNOLOGICAL SYNAPSE; ANCHORED PROTEINS; TYROSINE KINASES;
ACTIVATION
AB The MAL protein is an essential component of the specialized machinery for apical targeting in epithelial cells. The src family kinase Lck plays a pivotal role in T cell signaling. We show that MAL is required in T cells for efficient expression of Lck at the plasma membrane and activation of IL-2 transcription. To investigate the mechanism by which MAL regulates Lck targeting, we analyzed the dynamics of Lck and found that it travels to the plasma membrane in specific transport carriers containing MAL. Coimmunoprecipitation experiments indicated an association of MAL with Lck. Both carrier formation and partitioning of Lck into detergent-insoluble membranes were ablated in the absence of MAL. Polarization of T cell receptor for antigen (TCR) and microtubule-organizing center to immunological synapse ( IS) were also defective. Although partial correction of the latter defects was possible by forced expression of Lck at the plasma membrane, their complete correction, formation of transport vesicles, partitioning of Lck, and restoration of signaling pathways, which are required for IL-2 transcription up-regulation, were achieved by exogenous expression of MAL. We concluded that MAL is required for recruitment of Lck to specialized membranes and formation of specific transport carriers for Lck targeting. This novel transport pathway is crucial for TCR-mediated signaling and IS assembly.
C1 [Anton, Olga; Batista, Alicia; Millan, Jaime; Andres-Delgado, Laura; Correas, Isabel; Alonso, Miguel A.] Univ Autonoma Madrid, CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain.
[Puertollano, Rosa] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Alonso, MA (reprint author), Univ Autonoma Madrid, CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain.
EM maalonso@cbm.uam.es
RI Andres-Delgado, Laura/L-8249-2014; Alonso, Miguel/J-3945-2016
OI Andres-Delgado, Laura/0000-0002-8223-4841; Alonso,
Miguel/0000-0002-7001-8826
FU Ministerio de Educacion y Ciencia, Spain [BFU2006-01925]; Intramural
Research Program of the National Institutes of Health, National Heart,
Lung, and Blood Institute (NHLBI); Fundacion Ramon Areces to Centro de
Biolog a Molecular
FX This work was supported by grants from the Ministerio de Educacion y
Ciencia, Spain (BFU2006-01925 to M. A. Alonso) and from the Intramural
Research Program of the National Institutes of Health, National Heart,
Lung, and Blood Institute (NHLBI; to R. Puertollano). An institutional
grant from the Fundacion Ramon Areces to Centro de Biolog a Molecular
"Severo Ochoa" is also acknowledged.
NR 48
TC 30
Z9 30
U1 0
U2 4
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD DEC 22
PY 2008
VL 205
IS 13
BP 3201
EP 3213
DI 10.1084/jem.20080552
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 450VH
UT WOS:000266428700023
PM 19064697
ER
PT J
AU Peppercorn, J
Burstein, H
Miller, FG
Winer, E
Joffe, S
AF Peppercorn, Jeffrey
Burstein, Harold
Miller, Franklin G.
Winer, Eric
Joffe, Steve
TI Self-Reported Practices and Attitudes of US Oncologists Regarding
Off-Protocol Therapy
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID HIGH-DOSE CHEMOTHERAPY; BREAST-CANCER; CLINICAL-TRIALS; AMERICAN
ONCOLOGISTS; PARTICIPATION; INTERFERON; DECISION; SOCIETY; DRUGS; VIEWS
AB Purpose Investigational cancer therapies being tested in clinical trials may be available outside of trials, or off-protocol (OPRx). We evaluated the practices and attitudes among US oncologists with regard to this controversial practice.
Methods We mailed an anonymous survey to a random sample of US medical oncologists evaluating frequency and prevalence of OPRx and evaluated the correlation between demographic factors, attitudes, and practice.
Results One hundred forty-six (31%) of 471 oncologists responded. Ninety-three percent reported ever discussing and 81% ever prescribing OPRx. Academic oncologists were more likely than community oncologists to have ever provided OPRx (89% v 75%; P = .06), to discuss OPRx at least once/month (41% v 19%; P = .0004), and to deny requests for OPRx at least once/month (16% v 2%; P = .004). While 61% of oncologists believed that patients should be discouraged from OPRx, only 31% felt it should not be available. With regard to trial recruitment, 53% felt that informed consent requires discussion of OPRx, 34% disagree, and 26% feel that patients should be provided OPRx on request, while 56% disagree. There was lack of consensus on access to OPRx in scenarios based on open trials at the time of the survey, such as adjuvant trastuzumab, which 41% would provide, 59% would not.
Conclusion US oncologists report common discussion and use of OPRx, but attitudes and practices may vary substantially. There is need for greater debate regarding OPRx in oncology, further definition of the ethical and clinical issues at stake, and development of guidelines in this area.
C1 [Peppercorn, Jeffrey] Duke Univ, Med Ctr, Div Med Oncol, Durham, NC 27710 USA.
Duke Univ, Med Ctr, Duke Comprehens Canc Ctr, Durham, NC 27710 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NIH, Bethesda, MD 20892 USA.
RP Peppercorn, J (reprint author), Duke Univ, Med Ctr, Div Med Oncol, Box 3446, Durham, NC 27710 USA.
EM jeffrey.peppercorn@duke.edu
OI Joffe, Steven/0000-0002-0667-7384
FU American Society of Clinical Oncology Foundation; Breast Cancer Research
Foundation; Greenwall Foundation
FX Supported by the American Society of Clinical Oncology Foundation
(J.P.), Breast Cancer Research Foundation (J.P.), and by the Greenwall
Foundation Faculty Scholars Program in Bioethics (J.P.)
NR 24
TC 12
Z9 12
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 20
PY 2008
VL 26
IS 36
BP 5994
EP 6000
DI 10.1200/JCO.2008.18.1420
PG 7
WC Oncology
SC Oncology
GA 385WF
UT WOS:000261843600026
PM 19029413
ER
PT J
AU Muse, M
Kane, JAC
Carr, DJJ
Farber, JM
Lane, TE
AF Muse, Michael
Kane, Joy A. C.
Carr, Daniel J. J.
Farber, Joshua M.
Lane, Thomas E.
TI Insertion of the CXC chemokine ligand 9 (CXCL9) into the mouse hepatitis
virus genome results in protection from viral-induced encephalitis and
hepatitis
SO VIROLOGY
LA English
DT Article
DE Chemokines; Virus; Central nervous system; Host defense
ID CENTRAL-NERVOUS-SYSTEM; INTERFERON-INDUCIBLE CHEMOKINES; TARGETED RNA
RECOMBINATION; ACTIVITY IN-VIVO; HOST-DEFENSE; IFN-GAMMA; CORONAVIRUS
INFECTION; T-CELLS; NEUROTROPIC CORONAVIRUS; MULTIPLE-SCLEROSIS
AB The role of the CXC chemokine ligand 9 (CXCL9) in host defense following infection with mouse hepatitis virus (MHV) was determined. Inoculation of the central nervous system (CNS) of CXCL9-/- mice with MHV resulted in accelerated and increased mortality compared to wild type mice supporting an important role for CXCL9 in anti-viral defense. In addition, infection of RAG1-/- or CXCL9-/- mice with a recombinant MHV expressing CXCL9 (MHV-CXCL9) resulted in protection from disease that correlated with reduced viral titers within the brain and NK cell-mediated protection in the liver. Survival in MHV-CXCL9-infected CXCL9-/- Mice was associated with reduced viral burden within the brain that coincided with increased T cell infiltration. Similarly, viral clearance from the livers of MHV-CXCL9-infected mice was accelerated but independent of increased T cell or INK cell infiltration. These observations indicate that CXCL9 promotes protection from coronavirus-induced neurololgical and liver disease. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Muse, Michael; Kane, Joy A. C.; Lane, Thomas E.] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92619 USA.
[Carr, Daniel J. J.] Univ Oklahoma, Hlth Sci Ctr, Dept Ophthalmol, Oklahoma City, OK 73104 USA.
[Farber, Joshua M.] NIH, Lab Mol Immunol, Inflammat Biol Sect, Bethesda, MD 20892 USA.
[Lane, Thomas E.] Univ Calif Irvine, Ctr Immunol, Irvine, CA 92619 USA.
RP Lane, TE (reprint author), Univ Calif Irvine, Dept Mol Biol & Biochem, 3205 McGaugh Hall, Irvine, CA 92619 USA.
EM tlane@uci.edu
FU National Institutes of Health [NS41249, A1067309]; National Multiple
Sclerosis Society [3278-A-3]
FX This work was supported by National Institutes of Health grants NS41249
(T.E.L.) A1067309 (D.J.J.C.) and National Multiple Sclerosis Society
Grant 3278-A-3 to T.E.L.
NR 40
TC 11
Z9 11
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC 20
PY 2008
VL 382
IS 2
BP 132
EP 144
DI 10.1016/j.virol.2008.09.032
PG 13
WC Virology
SC Virology
GA 380NM
UT WOS:000261472400002
PM 18973912
ER
PT J
AU Bogers, WMJM
Davis, D
Baak, I
Kan, E
Hofman, S
Sun, Y
Mortier, D
Lian, Y
Oostermeijer, H
Fagrouch, Z
Dubbes, R
van der Maas, M
Mooij, P
Koopman, G
Verschoor, E
Langedijk, JPM
Zhao, J
Brocca-Cofano, E
Robert-Guroff, M
Srivastava, I
Barnett, S
Heeney, JL
AF Bogers, Willy M. J. M.
Davis, David
Baak, Ilona
Kan, Elaine
Hofman, Sam
Sun, Yide
Mortier, Daniella
Lian, Ying
Oostermeijer, Herman
Fagrouch, Zahra
Dubbes, Rob
van der Maas, Martin
Mooij, Petra
Koopman, Gerrit
Verschoor, Ernst
Langedijk, Johannes P. M.
Zhao, Jun
Brocca-Cofano, Egidio
Robert-Guroff, Marjorie
Srivastava, Indresh
Barnett, Susan
Heeney, Jonathan L.
TI Systemic neutralizing antibodies induced by long interval mucosally
primed systemically boosted immunization correlate with protection from
mucosal SHIV challenge
SO VIROLOGY
LA English
DT Article
DE HIV vaccine; Animal model; Mucosal challenge; Nabs; ADCC
ID HUMAN-IMMUNODEFICIENCY-VIRUS; VENEZUELAN EQUINE ENCEPHALITIS; RHESUS
MACAQUES; IMMUNE-RESPONSES; VACCINE VECTOR; ENVELOPE IMMUNOGENS;
SIVMAC251 CHALLENGE; REPLICON PARTICLES; CELLULAR-IMMUNITY; VAGINAL
CHALLENGE
AB Immune correlates of vaccine protection from HIV-1 infection would provide important milestones to guide HIV-1 vaccine development. In a proof of concept study using mucosal priming and systemic boosting, the titer of neutralizing antibodies in sera was found to correlate with protection of mucosally exposed rhesus macaques from SHIV infection. Mucosal priming consisted of two sequential immunizations at 12-week intervals with replicating host range mutants of adenovirus type 5 (Ad5hr) expressing the HIV-1(89.6p) env gene. Following boosting with either heterologous recombinant protein or alphavirus replicons at 12-week intervals animals were intrarectally exposed to infections doses of the CCR5 tropic SHIV(SF162p4). Heterologous mucosal prime systemic boost immunization elicited neutralizing antibodies (Nabs), antibody-dependent cytotoxicity (ADCC), and specific patterns of antibody binding to envelope peptides. Vaccine induced protection did not correlate with the type of boost nor-F-cell responses, but rather with the Nab titer prior to exposure. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Bogers, Willy M. J. M.; Davis, David; Baak, Ilona; Hofman, Sam; Mortier, Daniella; Oostermeijer, Herman; Fagrouch, Zahra; Dubbes, Rob; van der Maas, Martin; Mooij, Petra; Koopman, Gerrit; Verschoor, Ernst; Heeney, Jonathan L.] BPRC, Dept Virol, NL-2280 GH Rijswijk, Netherlands.
[Kan, Elaine; Sun, Yide; Lian, Ying; Srivastava, Indresh; Barnett, Susan] Novartis, Emeryville, CA 94608 USA.
[Langedijk, Johannes P. M.] Pepscan therapeut BV, Lelystad, Netherlands.
[Zhao, Jun; Brocca-Cofano, Egidio; Robert-Guroff, Marjorie] NCI, Vaccine Branch, Bethesda, MD 20892 USA.
[Heeney, Jonathan L.] Univ Cambridge, Cambridge CB3 0ES, England.
RP Bogers, WMJM (reprint author), BPRC, Dept Virol, POB 3306, NL-2280 GH Rijswijk, Netherlands.
EM bogers@bprc.nl
OI Heeney, Jonathan/0000-0003-2702-1621
FU National Institutes of Health, National Cancer Institute; National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, Department of Health and Human Services [1 P01 A148225-01A2, 5
PO1 A1066287-02]
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Cancer Institute, and by
Federal funds from the National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Department of Health and Human
Services, under Contract No. 1 P01 A148225-01A2 and No. 5 PO1
A1066287-02.
NR 49
TC 47
Z9 49
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC 20
PY 2008
VL 382
IS 2
BP 217
EP 225
DI 10.1016/j.virol.2008.09.016
PG 9
WC Virology
SC Virology
GA 380NM
UT WOS:000261472400010
PM 18947849
ER
PT J
AU Wang, L
Wildt, KF
Castro, E
Xiong, Y
Feigenbaum, L
Tessarollo, L
Bosselut, R
AF Wang, Lie
Wildt, Kathryn F.
Castro, Ehydel
Xiong, Yumei
Feigenbaum, Lionel
Tessarollo, Lino
Bosselut, Remy
TI The Zinc Finger Transcription Factor Zbtb7b Represses CD8-Lineage Gene
Expression in Peripheral CD4(+) T Cells
SO IMMUNITY
LA English
DT Article
ID CD4-CD8 LINEAGE DIFFERENTIATION; IFN-GAMMA PRODUCTION; HELPER TYPE-1
CELLS; IN-VIVO; THYMOCYTE DIFFERENTIATION; LYMPHOCYTE DEVELOPMENT;
POSITIVE SELECTION; RUNX PROTEINS; REGULATES CD4; FACTOR GATA-3
AB How CD4-CD8 differentiation is maintained in mature T cells is largely unknown. The present study has examined the role in this process of the zinc finger protein Zbtb7b, a critical factor for the commitment of MHC II-restricted thymocytes to the CD4(+) lineage. We showed that Zbtb7b acted in peripheral CD4(+) T cells to suppress CD8-lineage gene expression, including that of CD8 and cytotoxic effector genes perforin and Granzyme B, and was important for the proper repression of interferon-gamma (IFN-gamma) during effector differentiation. The inappropriate expression of IFN-gamma by Zbtb7b-deficient CD4(+) T cells required the activities of Eomesodermin and Runx transcription factors. Runx activity was needed for Granzyme B expression, indicating that Runx proteins control expression of the cytotoxic program. We conclude that a key function of Zbtb7b in the mature CD4(+) T cell compartment is to repress CD8-lineage gene expression.
C1 [Wang, Lie; Wildt, Kathryn F.; Castro, Ehydel; Xiong, Yumei; Bosselut, Remy] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI SAIC, Frederick, MD 21702 USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, CCR, Frederick, MD 21702 USA.
RP Bosselut, R (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM remy@helix.nih.gov
FU Intramural Research Program of the National Cancer Institute; Center for
Cancer Research, NIH
FX We thank E. Southon for ES cell recombination; G. Sanchez for mouse
technical assistance; B. Taylor and S. Banerjee for expert cell sorting;
S. Reiner, B. Paul, and J. Zhu for reagents; S.R. Jenkinson and J. Zhu
for helpful discussions and T cell activation protocols; and J. Ashwell,
Y. Belkaid, and S. Reiner for reading the manuscript. This work was
supported by the Intramural Research Program of the National Cancer
Institute, Center for Cancer Research, NIH.
NR 54
TC 60
Z9 62
U1 2
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD DEC 19
PY 2008
VL 29
IS 6
BP 876
EP 887
DI 10.1016/j.immuni.2008.09.019
PG 12
WC Immunology
SC Immunology
GA 388IB
UT WOS:000262012400008
PM 19062319
ER
PT J
AU Migueles, SA
Osborne, CM
Royce, C
Compton, AA
Joshi, RP
Weeks, KA
Rood, JE
Berkley, AM
Sacha, JB
Cogliano-Shutta, NA
Lloyd, M
Roby, G
Kwan, R
McLaughlin, M
Stallings, S
Rehm, C
O'Shea, MA
Mican, J
Packard, BZ
Komoriya, A
Palmer, S
Wiegand, AP
Maldarelli, F
Coffin, JM
Mellors, JW
Hallahan, CW
Follman, DA
Connors, M
AF Migueles, Stephen A.
Osborne, Christine M.
Royce, Cassandra
Compton, Alex A.
Joshi, Rohan P.
Weeks, Kristin A.
Rood, Julia E.
Berkley, Amy M.
Sacha, Jonah B.
Cogliano-Shutta, Nancy A.
Lloyd, Margaret
Roby, Gregg
Kwan, Richard
McLaughlin, Mary
Stallings, Sara
Rehm, Catherine
O'Shea, Marie A.
Mican, JoAnn
Packard, Beverly Z.
Komoriya, Akira
Palmer, Sarah
Wiegand, Ann P.
Maldarelli, Frank
Coffin, John M.
Mellors, John W.
Hallahan, Claire W.
Follman, Dean A.
Connors, Mark
TI Lytic Granule Loading of CD8(+) T Cells Is Required for HIV-Infected
Cell Elimination Associated with Immune Control
SO IMMUNITY
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; IMMUNODEFICIENCY-VIRUS REPLICATION;
LONG-TERM NONPROGRESSORS; VIRAL SUPPRESSION; ELITE SUPPRESSORS; ANTIGEN
LOAD; MEMORY; EXPRESSION; INDIVIDUALS; EFFECTOR
AB Virus-specific CD8(+) T cells probably mediate control over HIV replication in rare individuals, termed long-term nonprogressors; (LTNPs) or elite controllers. Despite extensive investigation, the mechanisms responsible for this control remain incompletely understood. We observed that HIV-specific CD8(+) T cells of LTNPs persisted at higher frequencies than those of treated progressors with equally low amounts of HIV. Measured on a per-cell basis, HIV-specific CDB+ T cells of LTNPs efficiently eliminated primary autologous HIV-infected CD4(+) T cells. This function required lytic granule loading of effectors and delivery of granzyme B to target cells. Defective cytotoxicity of progressor effectors could be restored after treatment with phorbol ester and calcium ionophore. These results establish an effector function and mechanism that clearly segregate with immunologic control of HIV. They also demonstrate that lytic granule contents of memory cells are a critical determinant of cytotoxicity that must be induced for maximal per-cell killing capacity.
C1 [Migueles, Stephen A.; Osborne, Christine M.; Royce, Cassandra; Compton, Alex A.; Joshi, Rohan P.; Weeks, Kristin A.; Rood, Julia E.; Berkley, Amy M.; Cogliano-Shutta, Nancy A.; Lloyd, Margaret; Roby, Gregg; Kwan, Richard; McLaughlin, Mary; Stallings, Sara; Rehm, Catherine; O'Shea, Marie A.; Mican, JoAnn; Hallahan, Claire W.; Follman, Dean A.; Connors, Mark] NIAID, NIH, Bethesda, MD 20892 USA.
[Sacha, Jonah B.] Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI 53719 USA.
[Packard, Beverly Z.; Komoriya, Akira] Oncolmmunin, Gaithersburg, MD 20877 USA.
[Palmer, Sarah; Wiegand, Ann P.; Maldarelli, Frank; Coffin, John M.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Mellors, John W.] Univ Pittsburgh, Med Ctr, Div Infect Dis, Pittsburgh, PA 15261 USA.
RP Connors, M (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM mconnors@nih.gov
OI Compton, Alex/0000-0002-7508-4953
FU Intramural NIH HHS [Z01 AI000855-09]
NR 45
TC 299
Z9 303
U1 1
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD DEC 19
PY 2008
VL 29
IS 6
BP 1009
EP 1021
DI 10.1016/j.immuni.2008.10.010
PG 13
WC Immunology
SC Immunology
GA 388IB
UT WOS:000262012400019
PM 19062316
ER
PT J
AU Zhang, J
Gao, ZG
Yin, J
Quon, MJ
Ye, JP
AF Zhang, Jin
Gao, Zhanguo
Yin, Jun
Quon, Michael J.
Ye, Jianping
TI S6K Directly Phosphorylates IRS-1 on Ser-270 to Promote Insulin
Resistance in Response to TNF-alpha Signaling through IKK2
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SUBSTRATE-1 TYROSINE PHOSPHORYLATION; NECROSIS-FACTOR INHIBITION;
MULTIPLE SERINE KINASES; RECEPTOR SUBSTRATE-1; PROTEIN-KINASE;
SKELETAL-MUSCLE; KAPPA-B; MAMMALIAN TARGET; 3T3-L1 ADIPOCYTES;
FATTY-ACID
AB S6K1 (p70S6K) is a serine kinase downstream from Akt in the insulin signaling pathway that is involved in negative feedback regulation of insulin action. S6K1 is also activated by TNF-alpha, a pro- inflammatory cytokine. However, its role remains to be characterized. In the current study, we elucidated a mechanism for S6K1 to mediate TNF-alpha-induced insulin resistance in adipocytes and hepatocytes. S6K1 was phosphorylated at Thr-389 in response to TNF-alpha. This led to phosphorylation of IRS-1 by S6K1 at multiple serine residues including Ser-270, Ser-307, Ser-636, and Ser-1101 in human IRS-1 (Ser-265, Ser-302, Ser-632, and Ser- 1097, in rodent IRS-1). Direct phosphorylation of these sites by S6K1 was observed in an in vitro kinase assay using purified IRS-1 and S6K1. Phosphorylation of all these serines was increased in the adipose tissue of obese mice. RNAi knockdown demonstrated an important role for S6K1 in mediating TNF-alpha-induced IRS-1 inhibition that led to impaired insulin-stimulated glucose uptake in adipocytes. A point mutant of IRS-1 (S270A) impaired association of IRS-1 with S6K1 resulting in diminished phosphorylation of IRS-1 at three other S6K1 phosphorylation sites (Ser- 307, Ser- 636, and Ser- 1101). Expression of a dominant negative S6K1 mutant prevented TNF-induced Ser- 270 phosphorylation and IRS-1 protein degradation. Moreover, in IKK2 (but not IKK1)-null cells, TNF-alpha treatment did not result in Thr-389 phosphorylation of S6K1. We present a new mechanism for TNF-alpha to induce insulin resistance that involves activation of S6K by an IKK2-dependent pathway. S6K directly phosphorylates IRS-1 on multiple serine residues to inhibit insulin signaling.
C1 [Zhang, Jin; Gao, Zhanguo; Yin, Jun; Ye, Jianping] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
[Quon, Michael J.] Natl Ctr Complementary & Alternat Med, Diabet Unit, NIH, Bethesda, MD 20892 USA.
RP Ye, JP (reprint author), Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
EM yej@pbrc.edu
OI Quon, Michael/0000-0002-9601-9915
FU National Institutes of Health Intramural Research Program (NCCAM) [1P30
DK072476]; NIH Grant [DK68036]; ADA Research Award [7-07-RA-189]
FX This work was supported, in whole or in part, by National Institutes of
Health Intramural Research Program (NCCAM) ( to M. J. Q.), NIDDK CNRU
Grant 1P30 DK072476 ( Genomic Core), and the NIH Grant DK68036 and ADA
Research Award 7-07-RA-189 ( to J. Y.). The costs of publication of this
article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 50
TC 114
Z9 126
U1 1
U2 9
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 DEC 19
PY 2008
VL 283
IS 51
BP 35375
EP 35382
DI 10.1074/jbc.M806480200
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 383QH
UT WOS:000261687900008
PM 18952604
ER
PT J
AU Chi, YH
Haller, K
Ward, MD
Semmes, OJ
Li, Y
Jeang, KT
AF Chi, Ya-Hui
Haller, Kerstin
Ward, Michael D.
Semmes, O. John
Li, Yan
Jeang, Kuan-Teh
TI Requirements for Protein Phosphorylation and the Kinase Activity of
Polo-like Kinase 1 (Plk1) for the Kinetochore Function of Mitotic Arrest
Deficiency Protein 1 (Mad1)
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SPINDLE-ASSEMBLY CHECKPOINT; ANAPHASE-PROMOTING COMPLEX/CYCLOSOME; YEAST
SACCHAROMYCES-CEREVISIAE; SMALL-MOLECULE INHIBITOR; BUDDING YEAST; BOX
DOMAIN; CELLULAR-TRANSFORMATION; MPS1 KINASE; HUMAN LUNG; IN-VITRO
AB Mitotic arrest deficiency protein 1 (Mad1) is associated with microtubule-unattached kinetochores in mitotic cells and is a component of the spindle assembly checkpoint (SAC). Here, we have studied the phosphorylation of Mad1 and mapped using liquid chromatography-tandem mass spectrometry several phosphorylated amino acids in this protein. One phosphorylated residue, Thr(680), was characterized to be important for the kinetochore localization of Mad1 and its SAC function. We also found that in mitotic cells Mad1 co-immunoprecipitated with Plk1. Depletion of cellular Plk1 using small interfering RNAs and inhibition of the kinase activity of Plk1 using a kinase-dead mutant or a small molecule inhibitor attenuated Mad1 phosphorylation and its association with kinetochores. Collectively, these findings indicate mechanistic roles contributed by protein phosphorylation and Plk1 to the SAC activity of Mad1.
C1 [Chi, Ya-Hui; Haller, Kerstin; Li, Yan; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Ward, Michael D.; Semmes, O. John] Eastern Virginia Med Sch, Dept Microbiol & Mol Cell Biol, Ctr Biomed Proteom, Norfolk, VA 23501 USA.
RP Jeang, KT (reprint author), Bldg 4,Rm 306,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kj7e@nih.gov
RI Chi, Ya-Hui/B-1080-2010; Jeang, Kuan-Teh/A-2424-2008
FU National Institutes of Health; NIAID
FX Supported through intramural funding from the NIAID, National Institutes
of Health. To whom correspondence should be addressed: Bldg. 4, Rm. 306,
9000 Rockville Pike, Bethesda, MD 20892-0460. Tel.: 301-496-6680; Fax:
301-480-3686; E- mail: kj7e@ nih. gov.
NR 74
TC 14
Z9 16
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 DEC 19
PY 2008
VL 283
IS 51
BP 35834
EP 35844
DI 10.1074/jbc.M804967200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 383QH
UT WOS:000261687900058
PM 18922800
ER
PT J
AU Elias, EV
Quiroga, R
Gottig, N
Nakanishi, H
Nash, TE
Neiman, A
Lujan, HD
AF Elias, Eliana V.
Quiroga, Rodrigo
Gottig, Natalia
Nakanishi, Hideki
Nash, Theodore E.
Neiman, Aaron
Lujan, Hugo D.
TI Characterization of SNAREs Determines the Absence of a Typical Golgi
Apparatus in the Ancient Eukaryote Giardia lamblia
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CYST WALL PROTEINS; PRIMITIVE EUKARYOTE; ENDOPLASMIC-RETICULUM;
STRUCTURE PREDICTION; PERIPHERAL VACUOLES; ENDOMEMBRANE SYSTEM;
SECRETORY PATHWAY; SURFACE-PROTEINS; SYNTAXIN GENES; BREFELDIN-A
AB Giardia is a eukaryotic protozoal parasite with unusual characteristics, such as the absence of a morphologically evident Golgi apparatus. Although both constitutive and regulated pathways for protein secretion are evident in Giardia, little is known about the mechanisms involved in vesicular docking and fusion. In higher eukaryotes, soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) of the vesicle-associated membrane protein and syntaxin families play essential roles in these processes. In this work we identified and characterized genes for 17 SNAREs in Giardia to define the minimal set of subcellular organelles present during growth and encystation, in particular the presence or not of a Golgi apparatus. Expression and localization of all Giardia SNAREs demonstrate their presence in distinct subcellular compartments, which may represent the extent of the endomembrane system in eukaryotes. Remarkably, Giardia SNAREs, homologous to Golgi SNAREs from other organisms, do not allow the detection of a typical Golgi apparatus in either proliferating or differentiating trophozoites. However, some features of the Golgi, such as the packaging and sorting function, seem to be performed by the endoplasmic reticulum and/or the nuclear envelope. Moreover, depletion of individual genes demonstrated that several SNAREs are essential for viability, whereas others are dispensable. Thus, Giardia requires a smaller number of SNAREs compared with other eukaryotes to accomplish all of the vesicle trafficking events that are critical for the growth and differentiation of this important human pathogen.
C1 [Elias, Eliana V.; Quiroga, Rodrigo; Gottig, Natalia; Lujan, Hugo D.] Catholic Univ Cordoba, Sch Med, Natl Council Sci & Technol, Biochem & Mol Biol Lab, Cordoba, Argentina.
[Nakanishi, Hideki; Neiman, Aaron] SUNY Stony Brook, Dept Biochem & Cell Biol, Stony Brook, NY 11794 USA.
[Nash, Theodore E.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Lujan, HD (reprint author), Univ Catolica Cordoba, Fac Med, Lab Bioquim & Biol Mol, Jacinto Rios 571,CP X5004ASK, Cordoba, Argentina.
EM hlujan@ucc.edu.ar
OI Quiroga, Rodrigo/0000-0001-5015-0531
FU National Institutes of Health NIAID Intramural Research Program; Agencia
Nacional para la Promocion de la Ciencia y la Tecnologia (FONCYT);
Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET);
Howard Hughes Medical Institute (HHMI); Universidad Catolica de Cordoba
FX This work was supported, in whole or in part, by the National Institutes
of Health NIAID Intramural Research Program. This work was also
supported by the Agencia Nacional para la Promocion de la Ciencia y la
Tecnologia (FONCYT), the Consejo Nacional de Investigaciones Cientificas
y Tecnicas (CONICET), the Howard Hughes Medical Institute (HHMI), and
the Universidad Catolica de Cordoba. The costs of publication of this
article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 77
TC 19
Z9 19
U1 1
U2 4
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 DEC 19
PY 2008
VL 283
IS 51
BP 35996
EP 36010
DI 10.1074/jbc.M806545200
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 383QH
UT WOS:000261687900074
PM 18930915
ER
PT J
AU Simpanya, MF
Wistow, G
Gao, J
David, LL
Giblin, FJ
Mitton, KP
AF Simpanya, Mukoma F.
Wistow, Graeme
Gao, James
David, Larry L.
Giblin, Frank J.
Mitton, Kenneth P.
TI Expressed sequence tag analysis of guinea pig (Cavia porcellus) eye
tissues for NEIBank
SO MOLECULAR VISION
LA English
DT Article
ID OXYGEN IN-VIVO; HYPERBARIC-OXYGEN; GENE-EXPRESSION; TRABECULAR MESHWORK;
LENS CRYSTALLINS; NUCLEAR CATARACT; ZETA-CRYSTALLIN; MACULAR
DEGENERATION; CORNEAL EPITHELIUM; LIGHT-SCATTERING
AB Purpose: To characterize gene expression patterns in guinea pig ocular tissues and identify orthologs of human genes from NEIBank expressed sequence tags.
Methods: RNA was extracted from dissected eye tissues of 2.5-month-old guinea pigs to make three unamplified and unnormalized cDNA libraries in the pCMVSport-6 vector for the lens, retina, and eye minus lens and retina. Over 4,000 clones were sequenced from each library and were analyzed using GRIST for clustering and gene identification. Lens crystallin EST data were validated using two-dimensional electrophoresis (2-DE), matrix assisted laser desorption (MALDI), and electrospray ionization mass spectrometry (ESIMS).
Results: Combined data from the three libraries generated a total of 6,694 distinctive gene clusters, with each library having between 1,000 and 3,000 clusters. Approximately 60% of the total gene clusters were novel cDNA sequences and had significant homologies to other mammalian sequences in GenBank. Complete cDNA sequences were obtained for many guinea pig lens proteins, including alpha A/alpha Ainsert-, beta N-, and gamma S-crystallins, lengsin and GRIFIN. The ratio of alpha A- to alpha B-crystallin on 2-DE gels was 8: 1 in the lens nucleus and 6.5: 1 in the cortex. Analysis of ESTs, genome sequence, and proteins (by MALDI), did not reveal any evidence for the presence of gamma D-, gamma E-, and gamma F-crystallin in the guinea pig. Predicted masses of many guinea pig lens crystallins were confirmed by ESIMS analysis. For the retina, orthologs of human phototransduction genes were found, such as Rhodopsin, S-antigen (Sag, Arrestin), and Transducin. The guinea-pig ortholog of NRL, a key rod photoreceptor-specific transcription factor, was also represented in EST data. In the 'rest-of-eye' library, the most abundant transcripts included decorin and keratin 12, representative of the cornea.
Conclusions: Genomic analysis of guinea pig eye tissues provides sequence-verified clones for future studies. Guinea pig orthologs of many human eye specific genes were identified. Guinea pig gene structures were similar to their human and rodent gene counterparts. Surprisingly, no orthologs of gamma D-, gamma E-, and gamma F-crystallin were found in EST, proteomic, or the current guinea pig genome data.
C1 [Simpanya, Mukoma F.; Giblin, Frank J.; Mitton, Kenneth P.] Oakland Univ, Eye Res Inst, Rochester, MI 48309 USA.
[Wistow, Graeme; Gao, James] NEI, Sect Mol Struct & Funct Genom, NIH, Bethesda, MD 20892 USA.
[David, Larry L.] Oregon Hlth & Sci Univ, Sch Med, Dept Biochem & Mol Biol, Portland, OR 97201 USA.
RP Mitton, KP (reprint author), Oakland Univ, Eye Res Inst, 2200 N Squirrel Rd, Rochester, MI 48309 USA.
EM mitton@oakland.edu
FU NIH [EY02027, EY014803, EY014626, EY07755, EY10572]; NEI intramural
FX This work was supported in part by NIH grants EY02027 (F.J.G.), EY014803
(F.J.G.) EY014626 ( K. P. M.), EY07755 ( L. L. D.) and EY10572 ( L. L.
D.). G. W. and J.G. are supported by the NEI intramural program. We
thank Victor Leverenz for isolation of guinea pig eye tissues and
helping in the preparation of the figures, Megan Stewart for
photography, Lucinda Robertson for assistance with 2- DE gels, Phillip
Wilmarth for assistance in analysis of MS/ MS data, and Paula Pierce
(Excalibur Pathology) for eye tissue staining. Sidney Schechet, Lisa
Block, Ed Guzman and Patee Buchoff provided additional technical
assistance.
NR 80
TC 11
Z9 11
U1 0
U2 4
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD DEC 19
PY 2008
VL 14
IS 275-80
BP 2413
EP 2427
PG 15
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 413WH
UT WOS:000263822800004
PM 19104676
ER
PT J
AU Michelson, AM
AF Michelson, Alan M.
TI DEVELOPMENTAL BIOLOGY From Genetic Association to Genetic Switch
SO SCIENCE
LA English
DT Editorial Material
ID SICKLE-CELL-DISEASE; FETAL-HEMOGLOBIN; COMMON; BCL11A
C1 [Michelson, Alan M.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Michelson, AM (reprint author), NHLBI, NIH, 31 Ctr Dr, Bethesda, MD 20892 USA.
EM michelsonam@mail.nih.gov
NR 11
TC 4
Z9 6
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 DEC 19
PY 2008
VL 322
IS 5909
BP 1803
EP 1804
DI 10.1126/science.1169216
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 385FF
UT WOS:000261799400043
PM 19095932
ER
PT J
AU Johnson, C
Drgon, T
Liu, QR
Zhang, PW
Walther, D
Li, CY
Anthony, JC
Ding, YL
Eaton, WW
Uhl, GR
AF Johnson, Catherine
Drgon, Tomas
Liu, Qing-Rong
Zhang, Ping-Wu
Walther, Donna
Li, Chuan-Yun
Anthony, James C.
Ding, Yulan
Eaton, William W.
Uhl, George R.
TI Genome wide association for substance dependence: convergent results
from epidemiologic and research volunteer samples
SO BMC MEDICAL GENETICS
LA English
DT Article
ID FAGERSTROM TOLERANCE QUESTIONNAIRE; DIAGNOSTIC-INTERVIEW-SCHEDULE;
ADDICTION MOLECULAR-GENETICS; NICOTINE DEPENDENCE; INFORMED CONSENT;
POLYSUBSTANCE ABUSERS; VULNERABILITY LOCI; SIZE CALCULATIONS; RESPONSE
BIAS; RISK RATIOS
AB Background: Dependences on addictive substances are substantially-heritable complex disorders whose molecular genetic bases have been partially elucidated by studies that have largely focused on research volunteers, including those recruited in Baltimore. Maryland. Subjects recruited from the Baltimore site of the Epidemiological Catchment Area (ECA) study provide a potentially-useful comparison group for possible confounding features that might arise from selecting research volunteer samples of substance dependent and control individuals. We now report novel SNP (single nucleotide polymorphism) genome wide association (GWA) results for vulnerability to substance dependence in ECA participants, who were initially ascertained as members of a probability sample from Baltimore, and compare the results to those from ethnically-matched Baltimore research volunteers.
Results: We identify substantial overlap between the home address zip codes reported by members of these two samples. We find overlapping clusters of SNPs whose allele frequencies differ with nominal significance between substance dependent vs control individuals in both samples. These overlapping clusters of nominally-positive SNPs identify 172 genes in ways that are never found by chance in Monte Carlo simulation studies. Comparison with data from human expressed sequence tags suggests that these genes are expressed in brain, especially in hippocampus and amygdala, to extents that are greater than chance.
Conclusion: The convergent results from these probability sample and research volunteer sample datasets support prior genome wide association results. They fail to support the idea that large portions of the molecular genetic results for vulnerability to substance dependence derive from factors that are limited to research volunteers.
C1 [Johnson, Catherine; Drgon, Tomas; Liu, Qing-Rong; Zhang, Ping-Wu; Walther, Donna; Li, Chuan-Yun; Uhl, George R.] NIH IRP NIDA, Mol Neurobiol Branch, Baltimore, MD 21224 USA.
[Li, Chuan-Yun] Peking Univ, Coll Life Sci, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Beijing 100871, Peoples R China.
[Anthony, James C.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Ding, Yulan; Eaton, William W.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mental Hlth & Hyg, Baltimore, MD 21221 USA.
RP Uhl, GR (reprint author), NIH IRP NIDA, Mol Neurobiol Branch, Suite 3510,333 Cassell Dr Baltimore, Baltimore, MD 21224 USA.
EM johnsoncat@intra.nida.nih.gov; tdrgon@intra.nida.nih.gov;
qrliu@intra.nida.nih.gov; pwzhang@intra.nida.nih.gov;
dwalther@intra.nida.nih.gov; lichua@nida.nih.gov; janthony@msu.edu;
yding@jhsph.edu; weaton@jhsph.edu; guhl@intra.nida.nih.gov
RI Liu, Qing-Rong/A-3059-2012
OI Liu, Qing-Rong/0000-0001-8477-6452
FU NIH; NIDA; DHSS; National Institute of Mental Health [R01-47447,
T32-14592]; Johns Hopkins site [UO1 MH 33870]
FX We are grateful for thoughtful advice and discussion from Drs N Ialongo,
C Storer and P Zandi. This research was supported financially by the NIH
Intramural Research Program, NIDA, DHSS and National Institute of Mental
Health grants R01-47447 and T32-14592, and Johns Hopkins Bloomberg
School of Public Health IRB H. 33.01.03.26.A2 (WE). We are also grateful
to the Epidemiologic Catchment Area Program's principal collaborators (D
Regier, B Locke, WE and J Burke) and to Drs M Kramer, E Gruenberg, and S
Shapiro from the Johns Hopkins site, supported by UO1 MH 33870.
NR 39
TC 28
Z9 30
U1 1
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2350
J9 BMC MED GENET
JI BMC Med. Genet.
PD DEC 18
PY 2008
VL 9
AR 113
DI 10.1186/1471-2350-9-113
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 404BB
UT WOS:000263124600001
PM 19094236
ER
PT J
AU Chen, J
Bryngelson, JD
Thirumalai, D
AF Chen, Jie
Bryngelson, J. D.
Thirumalai, D.
TI Estimations of the Size of Nucleation Regions in Globular Proteins
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID FOLDING ENERGY LANDSCAPES; TRANSITION-STATE; CONDENSATION MECHANISM;
COLLAPSE MECHANISM; LATTICE MODELS; TIME SCALES; KINETICS; NUCLEUS;
SEQUENCES; FUNNELS
AB Folding of many single-domain proteins has been described using the nucleation-collapse (NC) mechanism. According to NC, folding (formation of secondary structures and tertiary interactions) and chain collapse occur synchronously upon formation of native-like structures involving a critical number of residues. Using simple nucleation theory together with structure-based thermodynamic data, the average size of the most probable nucleus N(R)* for single-domain proteins, is estimated to be between 15 and 30 residues. We argue that finite-sized fluctuations in this estimate can be large so that nearly half of the residues of a 100 residue protein can be part of the folding nucleus. Inclusion of surface area changes in the folded and unfolded states are important in the determination of N(R)*.
C1 [Chen, Jie; Thirumalai, D.] Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
[Thirumalai, D.] Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA.
[Bryngelson, J. D.] NIH, Div Comp Res & Technol, Phys Sci Lab, Bethesda, MD 20892 USA.
RP Thirumalai, D (reprint author), Univ Maryland, Inst Phys Sci & Technol, Biophys Program, College Pk, MD 20742 USA.
EM thirum@glue.umd.edu
FU NSF [CHE 05-14056]; Air Force Office of Scientific Research
[FA9550-07-1-0098]
FX We thank Peter Wolynes for several constructive suggestions. Most of the
analysis was performed while J. D. Bryngelson was part of the scientific
staff at NIH. This work was supported by grants from NSF (CHE 05-14056)
and the Air Force Office of Scientific Research (FA9550-07-1-0098).
NR 38
TC 11
Z9 11
U1 0
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD DEC 18
PY 2008
VL 112
IS 50
BP 16115
EP 16120
DI 10.1021/jp806161k
PG 6
WC Chemistry, Physical
SC Chemistry
GA 383CY
UT WOS:000261652900020
PM 19367923
ER
PT J
AU Sarin, H
Kanevsky, AS
Wu, HT
Brimacombe, KR
Fung, SH
Sousa, AA
Auh, S
Wilson, CM
Sharma, K
Aronova, MA
Leapman, RD
Griffiths, GL
Hall, MD
AF Sarin, Hemant
Kanevsky, Ariel S.
Wu, Haitao
Brimacombe, Kyle R.
Fung, Steve H.
Sousa, Alioscka A.
Auh, Sungyoung
Wilson, Colin M.
Sharma, Kamal
Aronova, Maria A.
Leapman, Richard D.
Griffiths, Gary L.
Hall, Matthew D.
TI Effective transvascular delivery of nanoparticles across the blood-brain
tumor barrier into malignant glioma cells
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID IRON-OXIDE NANOPARTICLES; IMAGING CONTRAST AGENTS; DRUG-DELIVERY;
CHEMICAL-PROPERTIES; RECURRENT GLIOMAS; MOLECULAR-SIZE; CHEMOTHERAPY;
MODEL; PERMEABILITY; DENDRIMERS
AB Background: Effective transvascular delivery of nanoparticle-based chemotherapeutics across the blood-brain tumor barrier of malignant gliomas remains a challenge. This is due to our limited understanding of nanoparticle properties in relation to the physiologic size of pores within the blood-brain tumor barrier. Polyamidoamine dendrimers are particularly small multigenerational nanoparticles with uniform sizes within each generation. Dendrimer sizes increase by only 1 to 2 nm with each successive generation. Using functionalized polyamidoamine dendrimer generations 1 through 8, we investigated how nanoparticle size influences particle accumulation within malignant glioma cells.
Methods: Magnetic resonance and fluorescence imaging probes were conjugated to the dendrimer terminal amines. Functionalized dendrimers were administered intravenously to rodents with orthotopically grown malignant gliomas. Transvascular transport and accumulation of the nanoparticles in brain tumor tissue was measured in vivo with dynamic contrast-enhanced magnetic resonance imaging. Localization of the nanoparticles within glioma cells was confirmed ex vivo with fluorescence imaging.
Results: We found that the intravenously administered functionalized dendrimers less than approximately 11.7 to 11.9 nm in diameter were able to traverse pores of the blood-brain tumor barrier of RG-2 malignant gliomas, while larger ones could not. Of the permeable functionalized dendrimer generations, those that possessed long blood half-lives could accumulate within glioma cells.
Conclusion: The therapeutically relevant upper limit of blood-brain tumor barrier pore size is approximately 11.7 to 11.9 nm. Therefore, effective transvascular drug delivery into malignant glioma cells can be accomplished by using nanoparticles that are smaller than 11.7 to 11.9 nm in diameter and possess long blood half-lives.
C1 [Sarin, Hemant; Sousa, Alioscka A.; Aronova, Maria A.; Leapman, Richard D.] Natl Inst Biomed Imaging & Bioengn, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Sarin, Hemant; Kanevsky, Ariel S.] Natl Inst Hlth, Ctr Clin, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
[Wu, Haitao; Wilson, Colin M.; Griffiths, Gary L.] NHLBI, Imaging Probe Dev Ctr, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Brimacombe, Kyle R.; Hall, Matthew D.] NCI, Cell Biol Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Fung, Steve H.] Massachusetts Gen Hosp, Dept Neuroradiol, Boston, MA 02114 USA.
[Auh, Sungyoung] Natl Inst Neurol Disorders & Stroke, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Sharma, Kamal] Natl Canc Inst, Metab Branch, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Sharma, Kamal] US FDA, Div Biol Drug Prod, Off Oncol Prod, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
RP Sarin, H (reprint author), Natl Inst Biomed Imaging & Bioengn, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM sarinh@mail.nih.gov; kanevskya@mail.nih.gov; wuh3@mail.nih.gov;
brimacombek@mail.nih.gov; sfung@partners.org; sousaali@mail.nih.gov;
auhs@mail.nih.gov; wilsoncm@mail.nih.gov; kamal.sharma@fda.hhs.gov;
aronovaa@mail.nih.gov; leapmanr@mail.nih.gov; griffithsgl@mail.nih.gov;
hallma@mail.nih.gov
RI Hall, Matthew/B-2132-2010;
OI Fung, Steve/0000-0002-1177-682X
FU National Institute of Biomedical Imaging Bioengineering (NIBIB);
National Cancer Institute (NCI); Radiology and Imaging Sciences Program
(CC)
FX This study was funded by the National Institute of Biomedical Imaging
Bioengineering (NIBIB), National Cancer Institute (NCI), and the
Radiology and Imaging Sciences Program (CC). We thank Guofeng Zhang of
the Laboratory of Bioengineering and Physical Science (NIBIB) and Yide
Mi of the Radiology and Imaging Sciences Program (CC) for technical
assistance. We thank Daniel Glen and Rick Reynolds of the Scientific and
Statistical Computing Core (National Institute of Mental Health [ NIMH])
for their assistance during our use of the Analysis of Functional
NeuroImages (AFNI) software suite for data analyses.
NR 71
TC 116
Z9 118
U1 2
U2 38
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD DEC 18
PY 2008
VL 6
AR 80
DI 10.1186/1479-5876-6-80
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 409WS
UT WOS:000263537100001
PM 19094226
ER
PT J
AU Swartz, KJ
AF Swartz, Kenton J.
TI Sensing voltage across lipid membranes
SO NATURE
LA English
DT Review
ID SHAKER K+ CHANNEL; GATED POTASSIUM CHANNELS; FOCUSED ELECTRIC-FIELD;
DEPENDENT K+; SODIUM-CHANNELS; GATING-CHARGE; S4 SEGMENT; SENSOR
MOVEMENT; PROTON CHANNEL; TRANSMEMBRANE MOVEMENT
AB The detection of electrical potentials across lipid bilayers by specialized membrane proteins is required for many fundamental cellular processes such as the generation and propagation of nerve impulses. These membrane proteins possess modular voltage- sensing domains, a notable example being the S1- S4 domains of voltage- activated ion channels. Ground- breaking structural studies on these domains explain how voltage sensors are designed and reveal important interactions with the surrounding lipid membrane. Although further structures are needed to understand the conformational changes that occur during voltage sensing, the available data help to frame several key concepts that are fundamental to the mechanism of voltage sensing.
C1 [Swartz, Kenton J.] NINDS, Porter Neurosci Res Ctr, Mol Physiol & Biophys Sect, NIH, Bethesda, MD 20892 USA.
RP Swartz, KJ (reprint author), NINDS, Porter Neurosci Res Ctr, Mol Physiol & Biophys Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM swartzk@ninds.nih.gov
FU Intramural Research Program of the NINDS; NIH
FX I thank J. Diamond, J. Mindell, S. Silberberg and the members of the
Swartz laboratory for discussions. I thank R. MacKinnon for providing
coordinates for the paddle- chimera and those for the superimposed
structures shown in Fig. 3. This work was supported by the Intramural
Research Program of the NINDS, NIH.
NR 87
TC 165
Z9 166
U1 5
U2 43
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD DEC 18
PY 2008
VL 456
IS 7224
BP 891
EP 897
DI 10.1038/nature07620
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 384TY
UT WOS:000261768300033
PM 19092925
ER
PT J
AU Lu, JH
Marnell, LL
Marjon, KD
Mold, C
Du Clos, TW
Sun, PD
AF Lu, Jinghua
Marnell, Lorraine L.
Marjon, Kristopher D.
Mold, Carolyn
Du Clos, Terry W.
Sun, Peter D.
TI Structural recognition and functional activation of Fc gamma R by innate
pentraxins
SO NATURE
LA English
DT Article
ID C-REACTIVE PROTEIN; AMYLOID-P-COMPONENT; HUMAN MONOCYTES;
CRYSTAL-STRUCTURE; RECEPTOR-II; SERUM; CELLS; RIIA; PHAGOCYTOSIS;
EXPRESSION
AB Pentraxins are a family of ancient innate immune mediators conserved throughout evolution. The classical pentraxins include serum amyloid P component ( SAP) and C- reactive protein, which are two of the acute- phase proteins synthesized in response to infection(1,2). Both recognize microbial pathogens and activate the classical complement pathway through C1q ( refs 3 and 4). More recently, members of the pentraxin family were found to interact with cell- surface Fc gamma receptors (Fc gamma R) and activate leukocyte-mediated phagocytosis(5-8). Here we describe the structural mechanism for pentraxin's binding to Fc gamma R and its functional activation of Fc gamma R- mediated phagocytosis and cytokine secretion. The complex structure between human SAP and Fc gamma RIIa reveals a diagonally bound receptor on each SAP pentamer with both D1 and D2 domains of the receptor contacting the ridge helices from two SAP subunits. The 1: 1 stoichiometry between SAP and Fc gamma RIIa infers the requirement for multivalent pathogen binding for receptor aggregation. Mutational and binding studies show that pentraxins are diverse in their binding specificity for Fc gamma R isoforms but conserved in their recognition structure. The shared binding site for SAP and IgG results in competition for Fc gamma R binding and the inhibition of immune- complex- mediated phagocytosis by soluble pentraxins. These results establish antibody- like functions for pentraxins in the Fc gamma R pathway, suggest an evolutionary overlap between the innate and adaptive immune systems, and have new therapeutic implications for autoimmune diseases.
C1 [Lu, Jinghua; Sun, Peter D.] NIAID, Struct Immunol Sect, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Marnell, Lorraine L.; Marjon, Kristopher D.; Mold, Carolyn; Du Clos, Terry W.] Univ New Mexico, Dept Internal Med, Albuquerque, NM 87131 USA.
[Marnell, Lorraine L.; Marjon, Kristopher D.; Mold, Carolyn; Du Clos, Terry W.] Univ New Mexico, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA.
[Du Clos, Terry W.] Vet Adm Med Ctr, Albuquerque, NM 87108 USA.
RP Sun, PD (reprint author), NIAID, Struct Immunol Sect, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
EM psun@nih.gov
RI lu, jinghua/G-5872-2012
FU US Department of Energy; Basic Energy Sciences; Office of Science
[W-31-109-Eng-83]; National Institute of Allergy and Infectious
Diseases; National Institutes of Health; Department of Veterans Affairs;
[RO1 AI28358]
FX We thank D. Klinman, G. Cheng, P. W. Dempsey and S. Bolland for
providing the bone marrow from the Myd88 2/2, RIP2 2/2 and wild- type
C57BL/6 mice, respectively; M. Pancera and B. Dey for technical support
in the isothermal titration calorimetry experiments; V. Deretic and S.
Master for assistance with confocal microscopy; and B. Bottazzi for
providing PTX-3. The X-ray SER-CAT beamlines
(www.ser-cat.org/members.html) at the Advanced Photon Source is
supported by the US Department of Energy, Basic Energy Sciences, Office
of Science, under contract no. W-31-109-Eng-83. This work was supported
by intramural research funding from the National Institute of Allergy
and Infectious Diseases, National Institutes of Health, and by RO1
AI28358 and by the Department of Veterans Affairs.
NR 41
TC 142
Z9 147
U1 1
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD DEC 18
PY 2008
VL 456
IS 7224
BP 989
EP U86
DI 10.1038/nature07468
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 384TY
UT WOS:000261768300054
PM 19011614
ER
PT J
AU Nickel, JC
Krieger, JN
McNaughton-Collins, M
Anderson, RU
Pontari, M
Shoskes, DA
Litwin, MS
Alexander, RB
White, PC
Berger, R
Nadler, R
O'Leary, M
Liong, ML
Zeitlin, S
Chuai, S
Landis, JR
Kusek, JW
Nyberg, LM
Schaeffer, AJ
AF Nickel, J. Curtis
Krieger, John N.
McNaughton-Collins, Mary
Anderson, Rodney U.
Pontari, Michel
Shoskes, Daniel A.
Litwin, Mark S.
Alexander, Richard B.
White, Paige C.
Berger, Richard
Nadler, Robert
O'Leary, Michael
Liong, Men Long
Zeitlin, Scott
Chuai, Shannon
Landis, J. Richard
Kusek, John W.
Nyberg, Leroy M.
Schaeffer, Anthony J.
CA Chronic Prostatitis Collaborative
TI Alfuzosin and Symptoms of Chronic Prostatitis-Chronic Pelvic Pain
Syndrome
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID CHRONIC NONBACTERIAL PROSTATITIS; DOUBLE-BLIND TRIAL; QUALITY-OF-LIFE;
ALPHA-BLOCKERS; MEN; MULTICENTER; THERAPY; SCALE; INDEX; QUESTIONNAIRE
AB Background: In men with chronic prostatitis-chronic pelvic pain syndrome, treatment with alpha-adrenergic receptor blockers early in the course of the disorder has been reported to be effective in some, but not all, relatively small randomized trials.
Methods: We conducted a multicenter, randomized, double-blind, placebo-controlled trial to evaluate the efficacy of alfuzosin, an alpha-adrenergic receptor blocker, in reducing symptoms in men with chronic prostatitis-chronic pelvic pain syndrome. Participation in the study required diagnosis of the condition within the preceding 2 years and no previous treatment with an alpha-adrenergic receptor blocker. Men were randomly assigned to treatment for 12 weeks with either 10 mg of alfuzosin per day or placebo. The primary outcome was a reduction of at least 4 points (from baseline to 12 weeks) in the score on the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) (range, 0 to 43; higher scores indicate more severe symptoms). A 4-point decrease is the minimal clinically significant difference in the score.
Results: A total of 272 eligible participants underwent randomization, and in both study groups, 49.3% of participants had a decrease of at least 4 points in their total NIH-CPSI score (rate difference associated with alfuzosin, 0.1%; 95% confidence interval, -11.2 to 11.0; P=0.99). In addition, a global response assessment showed similar response rates at 12 weeks: 33.6% in the placebo group and 34.8% in the alfuzosin group (P=0.90). The rates of adverse events in the two groups were also similar.
Conclusions: Our findings do not support the use of alfuzosin to reduce the symptoms of chronic prostatitis-chronic pelvic pain syndrome in men who have not received prior treatment with an alpha-blocker. (ClinicalTrials.gov number, NCT00103402.).
C1 [Nickel, J. Curtis] Queens Univ, Kingston Gen Hosp, Dept Urol, Kingston, ON K7L 2V7, Canada.
[Nickel, J. Curtis] Queens Univ, Dept Urol, Kingston, ON, Canada.
[Krieger, John N.; Berger, Richard] Univ Washington, Dept Urol, Seattle, WA USA.
[McNaughton-Collins, Mary] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Anderson, Rodney U.] Stanford Univ, Med Ctr, Dept Urol, Stanford, CA 94305 USA.
[Pontari, Michel] Temple Univ, Dept Urol, Philadelphia, PA 19122 USA.
[Shoskes, Daniel A.] Cleveland Clin, Glickman Urol Inst, Cleveland, OH 44106 USA.
[Litwin, Mark S.; Chuai, Shannon] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
[Litwin, Mark S.; Chuai, Shannon] Univ Calif Los Angeles, David Geffen Sch Med, Dept Hlth Serv, Los Angeles, CA 90095 USA.
[Litwin, Mark S.; Chuai, Shannon] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90095 USA.
[Alexander, Richard B.] Univ Maryland, Dept Urol, Baltimore, MD 21201 USA.
[White, Paige C.] Univ Mississippi, Dept Surg, Jackson, MS 39216 USA.
[Nadler, Robert; Schaeffer, Anthony J.] Northwestern Univ, Dept Urol, Chicago, IL 60611 USA.
[O'Leary, Michael] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Liong, Men Long] Univ Sci Malaysia, George Town, Malaysia.
[Zeitlin, Scott; Landis, J. Richard] Univ Penn, Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Kusek, John W.; Nyberg, Leroy M.] NIDDKD, Bethesda, MD 20892 USA.
RP Nickel, JC (reprint author), Queens Univ, Kingston Gen Hosp, Dept Urol, Kingston, ON K7L 2V7, Canada.
EM jcn@queensu.ca
RI Landis, J. Richard/A-9330-2010
FU NIDDK NIH HHS [U01 DK065209-04S1, U01 DK065174, U01 DK065174-05, U01
DK065186, U01 DK065186-05, U01 DK065187, U01 DK065187-05, U01 DK065189,
U01 DK065189-06, U01 DK065209, U01 DK065209-01, U01 DK065209-02, U01
DK065209-02S1, U01 DK065209-03, U01 DK065209-03S1, U01 DK065209-03S2,
U01 DK065209-04, U01 DK065209-04S2, U01 DK065209-05, U01 DK065209-05S1,
U01 DK065209-06, U01 DK065257, U01 DK065257-05, U01 DK065266, U01
DK065266-05, U01 DK065268, U01 DK065268-05, U01 DK065277, U01
DK065277-05, U01 DK065287, U01 DK065287-03, U01 DK065297, U01
DK065297-05, U01 DK65174, U01 DK65186, U01 DK65187, U01 DK65189, U01
DK65209, U01 DK65257, U01 DK65266, U01 DK65268, U01 DK65277, U01
DK65287, U01 DK65297]
NR 36
TC 67
Z9 76
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
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 DEC 18
PY 2008
VL 359
IS 25
BP 2663
EP 2673
DI 10.1056/NEJMoa0803240
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 384PS
UT WOS:000261757300006
PM 19092152
ER
PT J
AU Dotson, CD
Zhang, L
Xu, H
Shin, YK
Vigues, S
Ott, SH
Elson, AET
Choi, HJ
Shaw, H
Egan, JM
Mitchell, BD
Li, XD
Steinle, NI
Munger, SD
AF Dotson, Cedrick D.
Zhang, Lan
Xu, Hong
Shin, Yu-Kyong
Vigues, Stephan
Ott, Sandra H.
Elson, Amanda E. T.
Choi, Hyun Jin
Shaw, Hillary
Egan, Josephine M.
Mitchell, Braxton D.
Li, Xiaodong
Steinle, Nanette I.
Munger, Steven D.
TI Bitter Taste Receptors Influence Glucose Homeostasis
SO PLOS ONE
LA English
DT Article
AB TAS1R- and TAS2R-type taste receptors are expressed in the gustatory system, where they detect sweet- and bitter-tasting stimuli, respectively. These receptors are also expressed in subsets of cells within the mammalian gastrointestinal tract, where they mediate nutrient assimilation and endocrine responses. For example, sweeteners stimulate taste receptors on the surface of gut enteroendocrine L cells to elicit an increase in intracellular Ca(2+) and secretion of the incretin hormone glucagon-like peptide-1 (GLP-1), an important modulator of insulin biosynthesis and secretion. Because of the importance of taste receptors in the regulation of food intake and the alimentary responses to chemostimuli, we hypothesized that differences in taste receptor efficacy may impact glucose homeostasis. To address this issue, we initiated a candidate gene study within the Amish Family Diabetes Study and assessed the association of taste receptor variants with indicators of glucose dysregulation, including a diagnosis of type 2 diabetes mellitus and high levels of blood glucose and insulin during an oral glucose tolerance test. We report that a TAS2R haplotype is associated with altered glucose and insulin homeostasis. We also found that one SNP within this haplotype disrupts normal responses of a single receptor, TAS2R9, to its cognate ligands ofloxacin, procainamide and pirenzapine. Together, these findings suggest that a functionally compromised TAS2R receptor negatively impacts glucose homeostasis, providing an important link between alimentary chemosensation and metabolic disease.
C1 [Dotson, Cedrick D.; Vigues, Stephan; Elson, Amanda E. T.; Choi, Hyun Jin; Munger, Steven D.] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
[Zhang, Lan; Xu, Hong; Li, Xiaodong] Senomyx Inc, San Diego, CA USA.
[Shin, Yu-Kyong; Egan, Josephine M.] NIA, NIH, Baltimore, MD USA.
[Ott, Sandra H.; Shaw, Hillary; Mitchell, Braxton D.; Steinle, Nanette I.] Univ Maryland, Sch Med, Dept Med, Div Endocrinol, Baltimore, MD USA.
RP Dotson, CD (reprint author), Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
EM smung001@umaryland.edu
OI Elson, Amanda/0000-0002-5744-5954; Mitchell, Braxton/0000-0003-4920-4744
FU NIDCD [DC005786, DC007317]; NHLBI [HL076768]; University of Maryland
School of Medicine, the Clinical Nutrition Research Unit of Maryland
[DK072488]; Intramural Research Program of the NIH/National Institute on
Aging; NIDCR
FX This work was supported by grants from the NIDCD (DC005786 to S.D.M.;
DC007317 to S.V.), NHLBI (HL076768 to N.I.S.), the University of
Maryland School of Medicine, the Clinical Nutrition Research Unit of
Maryland (DK072488), and the Intramural Research Program of the
NIH/National Institute on Aging (Y.-K.S. and J.M.E.). C.D.D. was
supported by NIDCD and NIDCR training grants. L.Z., H.X. and X.L. are
employees of Senomyx, Inc. The funders had no role in decision to
publish or preparation of the manuscript. With the exception of studies
performed at, and funded by, Senomyx, Inc., the funders had no role in
the study design, data collection or analysis. For experiments performed
at and funded by Senomyx, Inc. (these are restricted to the receptor
deorphaning experiments reported in Figure 2), study design, data
collection and analysis was performed according to good scientific
practices. Analysis and interpretation of these (Figure 2) experiments
were also performed by authors CDD and SDM (University of Maryland
School of Medicine).
NR 63
TC 86
Z9 89
U1 3
U2 27
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 18
PY 2008
VL 3
IS 12
AR e3974
DI 10.1371/journal.pone.0003974
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 437AT
UT WOS:000265458600009
PM 19092995
ER
PT J
AU Luke, BT
Collins, JR
AF Luke, Brian T.
Collins, Jack R.
TI Examining the significance of fingerprint-based classifiers
SO BMC BIOINFORMATICS
LA English
DT Article
ID SELDI-TOF-MS; SERUM BIOMARKERS; PROSTATE-CANCER; PROTEOMIC ANALYSIS;
PANCREATIC-CANCER; BREAST-CANCER; PATTERN; IDENTIFICATION; DIAGNOSIS;
DISCOVERY
AB Background: Experimental examinations of biofluids to measure concentrations of proteins or their fragments or metabolites are being explored as a means of early disease detection, distinguishing diseases with similar symptoms, and drug treatment efficacy. Many studies have produced classifiers with a high sensitivity and specificity, and it has been argued that accurate results necessarily imply some underlying biology-based features in the classifier. The simplest test of this conjecture is to examine datasets designed to contain no information with classifiers used in many published studies.
Results: The classification accuracy of two fingerprint-based classifiers, a decision tree (DT) algorithm and a medoid classification algorithm (MCA), are examined. These methods are used to examine 30 artificial datasets that contain random concentration levels for 300 biomolecules. Each dataset contains between 30 and 300 Cases and Controls, and since the 300 observed concentrations are randomly generated, these datasets are constructed to contain no biological information. A modest search of decision trees containing at most seven decision nodes finds a large number of unique decision trees with an average sensitivity and specificity above 85% for datasets containing 60 Cases and 60 Controls or less, and for datasets with 90 Cases and 90 Controls many DTs have an average sensitivity and specificity above 80%. For even the largest dataset (300 Cases and 300 Controls) the MCA procedure finds several unique classifiers that have an average sensitivity and specificity above 88% using only six or seven features.
Conclusion: While it has been argued that accurate classification results must imply some biological basis for the separation of Cases from Controls, our results show that this is not necessarily true. The DT and MCA classifiers are sufficiently flexible and can produce good results from datasets that are specifically constructed to contain no information. This means that a chance fitting to the data is possible. All datasets used in this investigation are available on the web.
C1 [Luke, Brian T.; Collins, Jack R.] NCI, SAIC Frederick Inc, Adv Technol Program, Adv Biomed Comp Ctr, Frederick, MD 21702 USA.
RP Luke, BT (reprint author), NCI, SAIC Frederick Inc, Adv Technol Program, Adv Biomed Comp Ctr, Frederick, MD 21702 USA.
EM lukeb@ncifcrf.gov; collinsj@ncifcrf.gov
FU National Cancer Institute; National Institutes of Health [NO1-CO-12400]
FX The authors would like to thank the reviewers for their helpful
questions and comments. This project has been funded in whole or in part
with federal funds from the National Cancer Institute, National
Institutes of Health, under Contract NO1-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the
United States Government.
NR 38
TC 2
Z9 2
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD DEC 17
PY 2008
VL 9
AR 545
DI 10.1186/1471-2105-9-545
PG 9
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA 402FL
UT WOS:000262999500002
PM 19091087
ER
PT J
AU Kostera-Pruszczyk, A
Pruszczyk, P
Kaminska, A
Lee, HS
Goldfarb, LG
AF Kostera-Pruszczyk, Anna
Pruszczyk, Piotr
Kaminska, Anna
Lee, Hee-Suk
Goldfarb, Lev G.
TI Diversity of cardiomyopathy phenotypes caused by mutations in desmin
SO INTERNATIONAL JOURNAL OF CARDIOLOGY
LA English
DT Letter
ID RESTRICTIVE CARDIOMYOPATHY; DILATED CARDIOMYOPATHY; MYOPATHY
C1 [Pruszczyk, Piotr] Med Univ Warsaw, Dept Internal Med & Cardiol, Warsaw, Poland.
[Kostera-Pruszczyk, Anna; Kaminska, Anna] Med Univ Warsaw, Dept Neurol, Warsaw, Poland.
[Kaminska, Anna] Polish Acad Sci, Med Res Ctr, Neuromuscular Unit, Warsaw, Poland.
[Lee, Hee-Suk; Goldfarb, Lev G.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Pruszczyk, P (reprint author), Med Univ Warsaw, Dept Internal Med & Cardiol, Warsaw, Poland.
EM pprusz@amwaw.edu.pl
NR 11
TC 9
Z9 12
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-5273
J9 INT J CARDIOL
JI Int. J. Cardiol.
PD DEC 17
PY 2008
VL 131
IS 1
BP 146
EP 147
DI 10.1016/j.ijcard.2007.08.095
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 377KX
UT WOS:000261251200030
ER
PT J
AU Rudebeck, PH
Behrens, TE
Kennerley, SW
Baxter, MG
Buckley, MJ
Walton, ME
Rushworth, MFS
AF Rudebeck, Peter H.
Behrens, Timothy E.
Kennerley, Steven W.
Baxter, Mark G.
Buckley, Mark J.
Walton, Mark E.
Rushworth, Matthew F. S.
TI Frontal Cortex Subregions Play Distinct Roles in Choices between Actions
and Stimuli
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE reward; prefrontal cortex; learning; macaque; decision; cingulate
ID ANTERIOR CINGULATE CORTEX; ORBITAL PREFRONTAL CORTEX; ORBITOFRONTAL
CORTEX; DECISION-MAKING; MACAQUE MONKEYS; RHESUS-MONKEYS; REWARD
PREFERENCE; MOTOR CORTEX; SELECTION; AMYGDALA
AB The orbitofrontal cortex (OFC) has been implicated in reinforcement-guided decision making, error monitoring, and the reversal of behavior in response to changing circumstances. The anterior cingulate cortex sulcus (ACC(S)), however, has also been implicated in similar aspects of behavior. Dissociating the unique functions of these areas would improve our understanding of the decision-making process. The effect of selective OFC lesions on how monkeys used the history of reinforcement to guide choices of either particular actions or particular stimuli was studied and compared with the effects of ACC(S) lesions. Both lesions disrupted decision making, but their effects were differentially modulated by the dependence on action-or stimulus-value contingencies. OFClesions caused a deficit in stimulus but not action selection, whereas ACC(S) lesions had the opposite effect, disrupting action but not stimulus selection. Furthermore, OFClesions that have previously been found to impair decision making when deterministic stimulus-reward contingencies are switched were found to cause a more general learning impairment in more naturalistic situations in which reward was stochastic. Both OFC and ACC(S) are essential for reinforcement-guided decision making rather than just error monitoring or behavioral reversal. The OFC and ACC(S) are both, however, more concerned with learning and making decisions, but their roles in selecting between stimulus and action values are distinct.
C1 [Rudebeck, Peter H.; Behrens, Timothy E.; Baxter, Mark G.; Buckley, Mark J.; Walton, Mark E.; Rushworth, Matthew F. S.] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England.
[Kennerley, Steven W.] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA.
RP Rudebeck, PH (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Suite 1B80,49 Convent Dr, Bethesda, MD 20892 USA.
EM rudebeckp@mail.nih.gov
RI Rudebeck, Peter/G-7931-2012;
OI Rudebeck, Peter/0000-0002-1411-7555
FU Medical Research Council United Kingdom; The Wellcome Trust
FX This work was supported by the Medical Research Council United Kingdom
(P.H.R., T.E.B., M.J.B., M.F.S.R.) and The Wellcome Trust (M.E.W.,
M.G.B.). We thank Dr. D. Gaffan for his advice and encouragement as well
as Greg Daubeny for assistance with histology.
NR 45
TC 154
Z9 154
U1 0
U2 12
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD DEC 17
PY 2008
VL 28
IS 51
BP 13775
EP 13785
DI 10.1523/JNEUROSCI.3541-08.2008
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 384YM
UT WOS:000261780100008
PM 19091968
ER
PT J
AU Lathia, JD
Okun, E
Tang, SC
Griffioen, K
Cheng, AW
Mughal, MR
Laryea, G
Selvaraj, PK
Ffrench-Constant, C
Magnus, T
Arumugam, TV
Mattson, MP
AF Lathia, Justin D.
Okun, Eitan
Tang, Sung-Chun
Griffioen, Kathleen
Cheng, Aiwu
Mughal, Mohamed R.
Laryea, Gloria
Selvaraj, Pradeep K.
Ffrench-Constant, Charles
Magnus, Tim
Arumugam, Thiruma V.
Mattson, Mark P.
TI Toll-Like Receptor 3 Is a Negative Regulator of Embryonic Neural
Progenitor Cell Proliferation
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE stem cells; embryo; immunity; cortex; neurogenesis; ventricle
ID CENTRAL-NERVOUS-SYSTEM; DOUBLE-STRANDED-RNA; DENDRITIC CELLS;
BRAIN-INJURY; ACTIVATION; NEUROGENESIS; PATHWAYS; LIGANDS; INNATE; CNS
AB Toll-like receptors (TLRs) play important roles in innate immunity. Several TLR family members have recently been shown to be expressed by neurons and glial cells in the adult brain, and may mediate responses of these cells to injury and infection. To address the possibility that TLRs play a functional role in development of the nervous system, we analyzed the expression of TLRs during different stages of mouse brain development and assessed the role of TLRs in cell proliferation. TLR3 protein is present in brain cells in early embryonic stages of development, and in cultured neural stem/progenitor cells (NPC). NPC from TLR3-deficient embryos formed greater numbers of neurospheres compared with neurospheres from wild-type embryos. Numbers of proliferating cells, as assessed by phospho histone H3 and proliferating cell nuclear antigen labeling, were also increased in the developing cortex of TLR3-deficient mice compared with wild-type mice in vivo. Treatment of cultured embryonic cortical neurospheres with a TLR3 ligand (polyIC) significantly reduced proliferating (BrdU-labeled) cells and neurosphere formation in wild type but not TLR3(-/-)-derived NPCs. Our findings reveal a novel role for TLR3 in the negative regulation of NPC proliferation in the developing brain.
C1 [Lathia, Justin D.; Okun, Eitan; Tang, Sung-Chun; Griffioen, Kathleen; Cheng, Aiwu; Mughal, Mohamed R.; Laryea, Gloria; Magnus, Tim; Arumugam, Thiruma V.; Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Lathia, Justin D.; Ffrench-Constant, Charles] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England.
[Lathia, Justin D.; Ffrench-Constant, Charles] Univ Cambridge, Ctr Brain Repair, Cambridge CB2 1QP, England.
[Tang, Sung-Chun] Natl Taiwan Univ Hosp, Dept Neurol, Yun Lin Branch, Yunlin 640, Taiwan.
[Selvaraj, Pradeep K.; Arumugam, Thiruma V.] Texas Tech Univ, Hlth Sci Ctr, Dept Pharmaceut Sci, Amarillo, TX 79106 USA.
[Ffrench-Constant, Charles] Univ Edinburgh, Queens Med Res Inst, Multiple Sclerosis Soc Translat Res Ctr, Edinburgh EH16 4TJ, Midlothian, Scotland.
[Ffrench-Constant, Charles] MRC, Ctr Regenerat Med, Edinburgh EH16 4TJ, Midlothian, Scotland.
[Magnus, Tim] Univ Hamburg, Neurol Univ Klin, D-20246 Hamburg, Germany.
[Mattson, Mark P.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Arumugam, Thiruma/C-7969-2009; Arumugam, Thiruma/B-4898-2011; Mattson,
Mark/F-6038-2012; Messier, Claude/A-2322-2008;
OI Messier, Claude/0000-0002-4791-1763; Tang, Sung-Chun/0000-0003-3731-5973
FU National Institute on Aging; National Institutes of Health; Wellcome
Trust
FX This work was supported by the National Institute on Aging Intramural
Research Program. J. D. L. is supported by the National Institutes of
Health-Cambridge Graduate Partnership Program. C.ff.-C. is supported by
the Wellcome Trust.
NR 24
TC 81
Z9 82
U1 3
U2 8
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD DEC 17
PY 2008
VL 28
IS 51
BP 13978
EP 13984
DI 10.1523/JNEUROSCI.2140-08.2008
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 384YM
UT WOS:000261780100026
PM 19091986
ER
PT J
AU Melis, M
Pillolla, G
Luchicchi, A
Muntoni, AL
Yasar, S
Goldberg, SR
Pistis, M
AF Melis, Miriam
Pillolla, Giuliano
Luchicchi, Antonio
Muntoni, Anna Lisa
Yasar, Sevil
Goldberg, Steven R.
Pistis, Marco
TI Endogenous Fatty Acid Ethanolamides Suppress Nicotine-Induced Activation
of Mesolimbic Dopamine Neurons through Nuclear Receptors
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE dopamine neurons; nicotine; electrophysiology; endocannabinoids; fatty
acid amide hydrolase; patch clamp; peroxisome proliferator-activated
receptor
ID VENTRAL TEGMENTAL AREA; MOUSE THALAMIC SYNAPTOSOMES; AMIDE HYDROLASE;
ACETYLCHOLINE-RECEPTORS; ANANDAMIDE HYDROLYSIS; PPAR-ALPHA; INFLAMMATORY
PAIN; CORTICAL-NEURONS; CB1 RECEPTORS; ESTER URB597
AB Nicotine stimulates the activity of mesolimbic dopamine neurons, which is believed to mediate the rewarding and addictive properties of tobacco use. Accumulating evidence suggests that the endocannabinoid system might play a major role in neuronal mechanisms underlying the rewarding properties of drugs of abuse, including nicotine. Here, we investigated the modulation of nicotine effects by the endocannabinoid system on dopamine neurons in the ventral tegmental area with electrophysiological techniques in vivo and in vitro. We discovered that pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme that catabolizes fatty acid ethanolamides, among which the endocannabinoid anandamide (AEA) is the best known, suppressed nicotine-induced excitation of dopamine cells. Importantly, this effect was mimicked by the administration of the FAAH substrates oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), but not methanandamide, the hydrolysis resistant analog of AEA. OEA and PEA are naturally occurring lipid signaling molecules structurally related to AEA, but devoid of affinity for cannabinoid receptors. They blocked the effects of nicotine by activation of the peroxisome proliferator-activated receptor-alpha (PPAR-alpha), a nuclear receptor transcription factor involved in several aspects of lipid metabolism and energy balance. Activation of PPAR-alpha triggered a nongenomic stimulation of tyrosine kinases, which might lead to phosphorylation and negative regulation of neuronal nicotinic acetylcholine receptors. These data indicate for the first time that the anorexic lipids OEA and PEA possess neuromodulatory properties as endogenous ligands of PPAR-alpha in the brain and provide a potential new target for the treatment of nicotine addiction.
C1 [Melis, Miriam; Pillolla, Giuliano; Luchicchi, Antonio; Pistis, Marco] Univ Cagliari, Bb Brodie Dept Neurosci, I-09042 Monserrato, Italy.
[Muntoni, Anna Lisa] Univ Cagliari, CNR, Inst Neurosci, I-09042 Monserrato, Italy.
[Yasar, Sevil] Johns Hopkins Univ, Sch Med, Dept Med, Div Geriatr Med & Gerontol, Baltimore, MD 21224 USA.
[Goldberg, Steven R.] NIDA, Preclin Pharmacol Sect, Behav Neurosci Res Branch,NIH, Intramural Res Program,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Pistis, M (reprint author), Univ Cagliari, Bb Brodie Dept Neurosci, I-09042 Monserrato, Italy.
EM mpistis@unica.it
RI Pistis, Marco/A-3773-2013;
OI Pistis, Marco/0000-0002-4622-3205; Luchicchi,
Antonio/0000-0002-0189-4347; Pillolla, Giuliano/0000-0002-6797-4905
FU Italian Ministry of University (PRIN 2005); Philip Morris USA; Philip
Morris International; National Institute on Drug Abuse; National
Institutes of Health; Department of Health and Human Services
FX This work was supported by a grant from the Italian Ministry of
University (PRIN 2005), Philip Morris USA and Philip Morris
International, and by the Intramural Research Program of National
Institute on Drug Abuse, National Institutes of Health, and Department
of Health and Human Services.
NR 57
TC 80
Z9 82
U1 0
U2 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD DEC 17
PY 2008
VL 28
IS 51
BP 13985
EP 13994
DI 10.1523/JNEUROSCI.3221-08.2008
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 384YM
UT WOS:000261780100027
PM 19091987
ER
PT J
AU Yabroff, KR
Bradley, CJ
Mariotto, AB
Brown, ML
Feuer, EJ
AF Yabroff, K. Robin
Bradley, Cathy J.
Mariotto, Angela B.
Brown, Martin L.
Feuer, Eric J.
TI Estimates and Projections of Value of Life Lost From Cancer Deaths in
the United States
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID SERVICES TASK-FORCE; COLORECTAL-CANCER; ECONOMIC BURDEN; BREAST-CANCER;
CALIFORNIA
AB Value-of-life methods are increasingly used in policy analyses of the economic burden of disease. The purpose of this study was to estimate and project the value of life lost from cancer deaths in the United States.
We estimated and projected US age-specific mortality rates for all cancers and for 16 types of cancer in men and 18 cancers in women in the years 2000-2020 and applied them to US population projections to estimate the number of deaths in each year. Cohort life tables were used to calculate the remaining life expectancy in the absence of cancer deaths-025EFthe person-years of life lost (PYLL). We used a willingness-to-pay approach in which the value of life lost due to cancer death was calculated by multiplying PYLL by an estimate of the value of 1 year of life ($150 000). We performed sensitivity analyses for female breast, colorectal, lung, and prostate cancers using varying assumptions about future cancer mortality rates through the year 2020.
The value of life lost from all cancer deaths in the year 2000 was $960.6 billion; lung cancer alone represented more than 25% of this value. Projections for the year 2020 with current cancer mortality rates showed a 53% increase in the total value of life lost ($1472.5 billion). Projected annual decreases of cancer mortality rates of 2% reduced the expected value of life lost in the year 2020 from $121.0 billion to $80.7 billion for breast cancer, $140.1 billion to $93.5 billion for colorectal cancer, from $433.4 billion to $289.4 billion for lung cancer, and from $58.4 billion to $39.0 billion for prostate cancer.
Estimated value of life lost due to cancer deaths in the United States is substantial and expected to increase dramatically, even if mortality rates remain constant, because of expected population changes. These estimates and projections may help target investments in cancer control strategies to tumor sites that are likely to result in the greatest burden of disease and to interventions that are the most cost-effective.
C1 [Yabroff, K. Robin] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Bradley, Cathy J.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
RP Yabroff, KR (reprint author), NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Execut Plaza N,Rm 4005,6130 Execut Blvd,MSC 7344, Bethesda, MD 20892 USA.
EM yabroffr@mail.nih.gov
OI Yabroff, K. Robin/0000-0003-0644-5572
NR 25
TC 51
Z9 51
U1 0
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 17
PY 2008
VL 100
IS 24
BP 1755
EP 1762
DI 10.1093/jnci/djn383
PG 8
WC Oncology
SC Oncology
GA 386SE
UT WOS:000261902100010
PM 19066267
ER
PT J
AU Bradley, CJ
Yabroff, KR
Dahman, B
Feuer, EJ
Mariotto, A
Brown, ML
AF Bradley, Cathy J.
Yabroff, K. Robin
Dahman, Bassam
Feuer, Eric J.
Mariotto, Angela
Brown, Martin L.
TI Productivity Costs of Cancer Mortality in the United States: 2000-2020
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID US
AB A model that predicts the economic benefit of reduced cancer mortality provides critical information for allocating scarce resources to the interventions with the greatest benefits.
We developed models using the human capital approach, which relies on earnings as a measure of productivity, to estimate the value of productivity lost as a result of cancer mortality. The base model aggregated age- and sex-specific data from four primary sources: 1) the US Bureau of the Census, 2) US death certificate data for 1999-2003, 3) cohort life tables from the Berkeley Mortality Database for 1900-2000, and 4) the Bureau of Labor Statistics Current Population Survey. In a model that included costs of caregiving and household work, data from the National Human Activity Pattern Survey and the Caregiving in the U.S. study were used. Sensitivity analyses were performed using six types of cancer assuming a 1% decline in cancer mortality rates. The values of forgone earnings for employed individuals and imputed forgone earnings for informal caregiving were then estimated for the years 2000-2020.
The annual productivity cost from cancer mortality in the base model was approximately $115.8 billion in 2000; the projected value was $147.6 billion for 2020. Death from lung cancer accounted for more than 27% of productivity costs. A 1% annual reduction in lung, colorectal, breast, leukemia, pancreatic, and brain cancer mortality lowered productivity costs by $814 million per year. Including imputed earnings lost due to caregiving and household activity increased the base model total productivity cost to $232.4 billion in 2000 and to $308 billion in 2020.
Investments in programs that target the cancers with high incidence and/or cancers that occur in younger, working-age individuals are likely to yield the greatest reductions in productivity losses to society.
C1 [Bradley, Cathy J.] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Hlth Adm, Richmond, VA 23298 USA.
[Dahman, Bassam] Virginia Commonwealth Univ, Div Qual Hlth Care, Dept Internal Med, Richmond, VA 23298 USA.
[Yabroff, K. Robin; Brown, Martin L.] NCI, Hlth Serv & Econ Branch, Appl Res Program, Bethesda, MD 20892 USA.
[Feuer, Eric J.; Mariotto, Angela] NCI, Stat Res & Applicat Branch, Surveillance Res Program, Bethesda, MD 20892 USA.
RP Bradley, CJ (reprint author), Virginia Commonwealth Univ, Massey Canc Ctr, Dept Hlth Adm, 1008 E Clay St,POB 980203, Richmond, VA 23298 USA.
EM cjbradley@vcu.edu
OI Yabroff, K. Robin/0000-0003-0644-5572
FU National Cancer Institute
FX This research was supported by National Cancer Institute contract with
C. J. Bradley, PhD.
NR 27
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Z9 83
U1 0
U2 11
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 17
PY 2008
VL 100
IS 24
BP 1763
EP 1770
DI 10.1093/jnci/djn384
PG 8
WC Oncology
SC Oncology
GA 386SE
UT WOS:000261902100011
PM 19066273
ER
PT J
AU Anderson, WF
Rosenberg, PS
Menashe, I
Mitani, A
Pfeiffer, RM
AF Anderson, William F.
Rosenberg, Philip S.
Menashe, Idan
Mitani, Aya
Pfeiffer, Ruth M.
TI Age-Related Crossover in Breast Cancer Incidence Rates Between Black and
White Ethnic Groups
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID BIRTH COHORT PATTERNS; CHRONIC DISEASE RATES; UNITED-STATES;
RISK-FACTORS; TEMPORAL VARIATION; RECEPTOR STATUS; RECENT TRENDS;
PERIOD; WOMEN; MODELS
AB Although breast cancer incidence is higher in black women than in white women among women younger than 40 years, the reverse is true among those aged 40 years or older. This crossover in incidence rates between black and white ethnic groups has been well described, has not been completely understood, and has been viewed as an artifact.
To quantify this incidence rate crossover, we examined data for 440 653 women with invasive breast cancer from the National Cancer Institute's Surveillance, Epidemiology, and End Results database from January 1, 1975, through December 31, 2004. Data on invasive female breast cancers were stratified by race, age at diagnosis, year of diagnosis, and tumor characteristics. Standard descriptive analyses were supplemented with Poisson regression models, age-period-cohort models, and two-component mixture models. All statistical tests were two-sided.
We observed qualitative (ie, crossing or reversing) interactions between age and race. That is, age-specific incidence rates overall (expressed as number of breast cancers per 100 000 woman-years) were higher among black women (15.5) than among white women (13.1) younger than 40 years (difference = 2.4, 95% confidence interval [CI] = 2.4 to 2.4), and then, age-specific rates crossed with rates higher among white women (281.3) than among black women (239.5) aged 40 years or older (difference = 41.8, 95% CI = 41.7 to 41.9). The black-to-white incidence rate crossover was observed for all tumor characteristics assessed, although the crossover occurred at earlier ages of diagnosis for low-risk tumor characteristics than for high-risk tumor characteristics. The incidence rate crossover between ethnic groups was robust (ie, reliable and reproducible) to adjustment for calendar period and birth cohort effects in age-period-cohort models (P < .001 for difference by race).
Although this ecologic study cannot determine the individual-level factors responsible for the racial crossover in vital rates, it confirms that the age-related crossover in breast cancer incidence rates between black and white ethnic groups is a robust age-specific effect that is independent of period and cohort effects.
C1 [Anderson, William F.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,US Dept HHS,EPS, Bethesda, MD 20892 USA.
[Mitani, Aya] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
RP Anderson, WF (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH,US Dept HHS,EPS, Rm 8036,6120 Execut Blvd, Bethesda, MD 20892 USA.
EM wanderso@mail.nih.gov
RI Pfeiffer, Ruth /F-4748-2011
FU National Institutes of Health; National Cancer Institute
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute.
NR 56
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Z9 67
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 17
PY 2008
VL 100
IS 24
BP 1804
EP 1814
DI 10.1093/jnci/djn411
PG 11
WC Oncology
SC Oncology
GA 386SE
UT WOS:000261902100015
PM 19066264
ER
PT J
AU Gustafson-Vickers, SL
Lu, VB
Lai, AY
Todd, KG
Ballanyi, K
Smith, PA
AF Gustafson-Vickers, Sabrina L.
Lu, Van B.
Lai, Aaron Y.
Todd, Kathryn G.
Ballanyi, Klaus
Smith, Peter A.
TI Long-term actions of interleukin-1 beta on delay and tonic firing
neurons in rat superficial dorsal horn and their relevance to central
sensitization
SO MOLECULAR PAIN
LA English
DT Article
ID SUBSTANTIA-GELATINOSA NEURONS; PRO-INFLAMMATORY CYTOKINES; PATHOLOGICAL
PAIN STATES; PERIPHERAL-NERVE INJURY; NEUROPATHIC PAIN; SPINAL-CORD;
PYRAMIDAL NEURONS; LAMINAE-I; MICE; SENSITIVITY
AB Background: Cytokines such as interleukin 1 beta (IL-1 beta) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1 beta for 6-8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and Ca(2+) imaging techniques.
Results: Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1 beta increased the change in intracellular Ca2+ produced by exposure to 35-50 mM K(+). This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1 beta did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1 beta were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1 beta included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons.
Conclusion: Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1 beta at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1 beta may contribute to the central sensitization associated with chronic neuropathic pain.
C1 [Ballanyi, Klaus; Smith, Peter A.] Univ Alberta, Ctr Neurosci, Edmonton, AB, Canada.
[Ballanyi, Klaus; Smith, Peter A.] Univ Alberta, Dept Pharmacol, Edmonton, AB, Canada.
[Ballanyi, Klaus; Smith, Peter A.] Univ Alberta, Dept Physiol, Edmonton, AB, Canada.
[Lai, Aaron Y.; Todd, Kathryn G.] Univ Alberta, Dept Psychiat, Edmonton, AB, Canada.
[Gustafson-Vickers, Sabrina L.] Univ British Columbia, Fac Med Class 2011, Vancouver, BC V6T 1Z3, Canada.
[Lu, Van B.] NIAAA, Sect Transmitter Signaling, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
RP Smith, PA (reprint author), Univ Alberta, Ctr Neurosci, Edmonton, AB, Canada.
EM sgv@interchange.ubc.ca; luvb@mail.nih.gov; aylai@ualberta.ca;
kgtodd@ualberta.ca; klaus.ballanyi@ualberta.ca;
peter.a.smith@ualberta.ca
OI Lu, Van/0000-0002-4880-6455
FU Canadian Institutes of Health Research (CIHR)
FX Supported by the Canadian Institutes of Health Research (CIHR). We thank
Drs. W. F. Colmers and Q. Pittman for useful discussions.
NR 43
TC 21
Z9 25
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1744-8069
J9 MOL PAIN
JI Mol. Pain
PD DEC 17
PY 2008
VL 4
AR 63
DI 10.1186/1744-8069-4-63
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 393WA
UT WOS:000262406000001
PM 19091115
ER
PT J
AU Akashi, YJ
Goldstein, DS
Barbaro, G
Ueyama, T
AF Akashi, Yoshihiro J.
Goldstein, David S.
Barbaro, Giuseppe
Ueyama, Takashi
TI Takotsubo Cardiomyopathy A New Form of Acute, Reversible Heart Failure
SO CIRCULATION
LA English
DT Article
DE catecholamines; heart failure; nervous system, autonomic; stress; apical
ballooning
ID TAKO-TSUBO CARDIOMYOPATHY; LEFT-VENTRICULAR DYSFUNCTION; ACUTE
MYOCARDIAL-INFARCTION; APICAL BALLOONING SYNDROME; EMOTIONAL-STRESS;
OVARIECTOMIZED RATS; NERVOUS-SYSTEM; PLASMA-LEVELS; ANIMAL-MODEL;
ESTROGEN
C1 [Akashi, Yoshihiro J.] St Marianna Univ, Sch Med, Dept Internal Med, Div Cardiol,Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan.
[Goldstein, David S.] Natl Inst Neurol Disorders & Stroke, Clin Neurosci Program, Div Intramural Res, NIH, Bethesda, MD USA.
[Barbaro, Giuseppe] Univ Roma La Sapienza, Dept Med Pathophysiol, Cardiol Unit, Rome, Italy.
[Ueyama, Takashi] Wakayama Med Univ, Sch Med, Dept Anat & Cell Biol, Wakayama, Japan.
RP Akashi, YJ (reprint author), St Marianna Univ, Sch Med, Dept Internal Med, Div Cardiol,Miyamae Ku, 2-16-1 Sugao, Kawasaki, Kanagawa 2168511, Japan.
EM Johnny@marianna-u.ac.jp
RI Akashi, Yoshihiro/E-5227-2011
OI Akashi, Yoshihiro/0000-0001-7670-7326
FU Intramural NIH HHS [Z01 NS003033-02]
NR 51
TC 298
Z9 316
U1 6
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD DEC 16
PY 2008
VL 118
IS 25
BP 2754
EP 2762
DI 10.1161/CIRCULATIONAHA.108.767012
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 387JO
UT WOS:000261948700013
PM 19106400
ER
PT J
AU Bluemke, DA
Kronmal, RA
Lima, JAC
Liu, K
Olson, J
Burke, GL
Folsom, AR
AF Bluemke, David A.
Kronmal, Richard A.
Lima, Joao A. C.
Liu, Kiang
Olson, Jean
Burke, Gregory L.
Folsom, Aaron R.
TI The Relationship of Left Ventricular Mass and Geometry to Incident
Cardiovascular Events
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE heart failure; stroke; coronary heart disease; epidemiology; magnetic
resonance imaging; left ventricular hypertrophy
ID CONGESTIVE-HEART-FAILURE; CORONARY-ARTERY-DISEASE; END-POINT REDUCTION;
MAGNETIC-RESONANCE; 2-DIMENSIONAL ECHOCARDIOGRAPHY;
PROGNOSTIC-SIGNIFICANCE; LOSARTAN INTERVENTION; SYSTEMIC HYPERTENSION;
ELDERLY COHORT; BLOOD-PRESSURE
AB Objective The purpose of this study was to evaluate the relationship of left ventricular (LV) mass and geometry measured with cardiac magnetic resonance imaging (MRI) to incident cardiovascular events in the MESA (Multi-Ethnic Study of Atherosclerosis) study.
Background MRI is highly accurate for evaluation of heart size and structure and has not previously been used in a large epidemiologic study to predict cardiovascular events.
Methods A total of 5,098 participants in the MESA study underwent cardiac MRI at the baseline examination and were followed up for a median of 4 years. Cox proportional hazard models were constructed to predict the end points of coronary heart disease (CHD), stroke, and heart failure (HF) after adjustment for cardiovascular risk factors.
Results A total of 216 incident events were observed during the follow-up period. In adjusted models, the end points of incident CHD and stroke were positively associated with increased LV mass-to-volume ratio (CHD, hazard ratio [HR]: 2.1 per g/ml, p = 0.02; stroke, HR: 4.2 per g/ml, p = 0.005). In contrast, LV mass showed the strongest association with incident HF events (HR: 1.4 per 10% increment, p < 0.0001). The HF events occurred primarily in participants with LV hypertrophy, that is, >= 95th percentile of LV mass (HR: 8.6, 95% confidence interval: 3.7 to 19.9, reference group <50th percentile of LV mass).
Conclusions The LV size was related to incident HF, stroke, and CHD in this multiethnic cohort. Whereas body size-adjusted LV mass alone predicted incident HF, concentric ventricular remodeling predicted incident stroke and CHD. (J Am Coll Cardiol 2008; 52: 2148-55) (C) 2008 by the American College of Cardiology Foundation
C1 [Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Radiol, Div Cardiol, Baltimore, MD 21205 USA.
[Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Radiol Sci, Div Cardiol, Baltimore, MD USA.
[Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
[Kronmal, Richard A.] Univ Washington, Sch Publ Hlth & Community Med, Dept Biostat, Seattle, WA 98195 USA.
[Liu, Kiang] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Olson, Jean] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Burke, Gregory L.] Wake Forest Univ, Bowman Gray Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27103 USA.
[Folsom, Aaron R.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
RP Bluemke, DA (reprint author), NIH, Ctr Clin, Room 10-1C355, Bethesda, MD 20892 USA.
EM bluemked@nih.gov
OI Bluemke, David/0000-0002-8323-8086
FU MESA
FX The authors thank the other investigators, the staff, and the
participants of the MESA study for their valuable contributions. A full
list of participating MESA study investigators and institutions can be
found at http://www.mesa-nhlbi.org.
NR 46
TC 222
Z9 226
U1 0
U2 5
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 DEC 16
PY 2008
VL 52
IS 25
BP 2148
EP 2155
DI 10.1016/j.jacc.2008.09.014
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 384PR
UT WOS:000261757200005
PM 19095132
ER
PT J
AU Fleg, JL
Mete, M
Howard, BV
Umans, JG
Roman, MJ
Ratner, RE
Silverman, A
Galloway, JM
Henderson, JA
Weir, MR
Wilson, C
Stylianou, M
Howard, WJ
AF Fleg, Jerome L.
Mete, Mihriye
Howard, Barabara V.
Umans, Jason G.
Roman, Mary J.
Ratner, Robert E.
Silverman, Angela
Galloway, James M.
Henderson, Jeffrey A.
Weir, Matthew R.
Wilson, Charlton
Stylianou, Mario
Howard, Wm. James
TI Effect of Statins Alone Versus Statins Plus Ezetimibe on Carotid
Atherosclerosis in Type 2 Diabetes
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE ezetimibe; carotid artery intima-media thickness; atherosclerosis
ID LDL CHOLESTEROL; BLOOD-PRESSURE; LOWER TARGETS; SIMVASTATIN; THERAPY;
DISEASE; NIACIN; SANDS
AB Objectives This secondary analysis from the SANDS (Stop Atherosclerosis in Native Diabetics Study) trial examines the effects of lowering low-density lipoprotein cholesterol (LDL-C) with statins alone versus statins plus ezetimibe on common carotid artery intima-media thickness (CIMT) in patients with type 2 diabetes and no prior cardiovascular event.
Background It is unknown whether the addition of ezetimibe to statin therapy affects subclinical atherosclerosis.
Methods Within an aggressive group (target LDL-C <= 70 mg/dl; non-high-density lipoprotein cholesterol <= 100 mg/dl; systolic blood pressure <= 115 mm Hg), change in CIMT over 36 months was compared in diabetic individuals >40 years of age receiving statins plus ezetimibe versus statins alone. The CIMT changes in both aggressive subgroups were compared with changes in the standard subgroups (target LDL-C <= 100 mg/dl; non-high-density lipoprotein cholesterol <= 130 mg/dl; systolic blood pressure <= 130 mm Hg).
Results Mean (95% confidence intervals) LDL-C was reduced by 31 (23 to 37) mg/dl and 32 (27 to 38) mg/dl in the aggressive group receiving statins plus ezetimibe and statins alone, respectively, compared with changes of 1 (-3 to 6) mg/dl in the standard group (p < 0.0001) versus both aggressive subgroups. Within the aggressive group, mean CIMT at 36 months regressed from baseline similarly in the ezetimibe (-0.025 [-0.05 to 0.003] mm) and nonezetimibe subgroups (-0.012 [-0.03 to 0.008] mm) but progressed in the standard treatment arm (0.039 [0.02 to 0.06] mm), intergroup p < 0.0001.
Conclusions Reducing LDL-C to aggressive targets resulted in similar regression of CIMT in patients who attained equivalent LDL-C reductions from a statin alone or statin plus ezetimibe. Common carotid artery IMT increased in those achieving standard targets. (Stop Atherosclerosis in Native Diabetics Study [SANDS]; NCT00047424) (J Am Coll Cardiol 2008; 52: 2198-205) (C) 2008 by the American College of Cardiology Foundation
C1 [Fleg, Jerome L.; Stylianou, Mario] NHLBI, Bethesda, MD 20892 USA.
[Fleg, Jerome L.; Mete, Mihriye; Howard, Barabara V.; Umans, Jason G.; Ratner, Robert E.; Silverman, Angela] MedStar Res Inst, Hyattsville, MD 20783 USA.
[Roman, Mary J.] Weill Cornell Med Coll, New York, NY USA.
[Galloway, James M.] Univ Arizona, Hlth Sci Ctr, Tucson, AZ USA.
[Henderson, Jeffrey A.] Black Hills Ctr Amer Indian Hlth, Rapid City, SD USA.
[Weir, Matthew R.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Wilson, Charlton] Phoenix Indian Med Ctr, Phoenix, AZ USA.
[Howard, Wm. James] Washington Hosp Ctr, Washington, DC 20010 USA.
RP Fleg, JL (reprint author), MedStar Res Inst, 6495 New Hampshire Ave, Hyattsville, MD 20783 USA.
EM wm.james.howard@medstar.net
FU NHLBI NIH HHS [U01 HL067031, U01 HL067031-01A1, 1U01 HL67031-01A1]
NR 17
TC 149
Z9 162
U1 6
U2 10
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 DEC 16
PY 2008
VL 52
IS 25
BP 2198
EP 2205
DI 10.1016/j.jacc.2008.10.031
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 384PR
UT WOS:000261757200012
PM 19095139
ER
PT J
AU Wei, Q
Jiang, H
Matthews, CP
Colburn, NH
AF Wei, Qiou
Jiang, Hong
Matthews, Connie P.
Colburn, Nancy H.
TI Sulfiredoxin is an AP-1 target gene that is required for transformation
and shows elevated expression in human skin malignancies
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE skin tumor; tumor promotion; peroxiredoxin
ID CYSTEINE-SULFINIC ACID; MOUSE EPIDERMAL-CELLS; C-JUN; 2-CYS
PEROXIREDOXIN; OXIDATIVE STRESS; JB6 CELLS; MAMMALIAN SULFIREDOXIN;
TUMOR PROMOTION; REDUCTION; PRODUCT
AB Previous studies have shown that a dominant negative form of c-Jun (TAM67) suppresses mouse skin carcinogenesis both in vitro and in vivo. The current study identifies Sulfiredoxin (Srx) as a unique target of activator protein-1 (AP-1) activation and TAM67 inhibition. Manipulation of Srx levels by ShRNA or over-expression demonstrates that Srx is critical for redox homeostasis through reducing hyperoxidized peroxiredoxins. In JB6 cells, knockdown of Srx abolishes tumor promoter-induced transformation and enhances cell sensitivity to oxidative stress. Knockdown of Srx also impairs c-Jun phosphorylation, implicating a role for Srx in the feedback regulation of AP-1 activity. Screening of patient tissues by tissue microarray reveals elevated Srx expression in several types of human skin cancers. Our study indicates that Srx is a functionally significant target of AP-1 blockade that may have value in cancer prevention or treatment.
C1 [Wei, Qiou; Jiang, Hong; Matthews, Connie P.; Colburn, Nancy H.] Natl Canc Inst, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21701 USA.
RP Colburn, NH (reprint author), Natl Canc Inst, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21701 USA.
EM colburn@ncifcrf.gov
FU National Cancer Institute
FX We thank Dr. Kenneth Tew for kindly providing reagents. We also thank
Dr. Matthew Young and Ms. AlysonBakerfor helpwiththe mouse epidermis and
JB6 models, and all other members of the Colburn laboratory for
thoughtful discussions and suggestions. Q.W. is a recipient of the
Cancer Research Training Award from the National Cancer Institute. This
work was supported in part by the Intramural Research Program of the
National Cancer Institute
NR 42
TC 44
Z9 48
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 16
PY 2008
VL 105
IS 50
BP 19738
EP 19743
DI 10.1073/pnas.0810676105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 385GI
UT WOS:000261802300032
PM 19057013
ER
PT J
AU Catalfamo, M
Di Mascio, M
Hu, Z
Srinivasula, S
Thaker, V
Adelsberger, J
Rupert, A
Baseler, M
Tagaya, Y
Roby, G
Rehm, C
Follmann, D
Lane, HC
AF Catalfamo, Marta
Di Mascio, Michele
Hu, Zonghui
Srinivasula, Sharat
Thaker, Vishakha
Adelsberger, Joseph
Rupert, Adam
Baseler, Michael
Tagaya, Yutaka
Roby, Gregg
Rehm, Catherine
Follmann, Dean
Lane, H. Clifford
TI HIV infection-associated immune activation occurs by two distinct
pathways that differentially affect CD4 and CD8 T cells
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE CD4 T cell homeostasis; IL-7; STAT-5
ID VIRUS TYPE-1 INFECTION; IMMUNODEFICIENCY-VIRUS; POTENTIAL ROLE; CENTRAL
MEMORY; HLA-DR; LYMPHOCYTES; EXPRESSION; TURNOVER; HOMEOSTASIS; IL-7
AB HIV infection is characterized by a brisk immune activation that plays an important role in the CD4 depletion and immune dysfunction of patients with AIDS. The mechanism underlying this activation is poorly understood. In the current study, we tested the hypothesis that this activation is the net product of two distinct pathways: the inflammatory response to HIV infection and the homeostatic response to CD4 T cell depletion. Using ex vivo BrdU incorporation of PBMCs from 284 patients with different stages of HIV infection, we found that CD4 proliferation was better predicted by the combination of CD4 depletion and HIV viral load (R(2) = 0.375, P < 0.001) than by either parameter alone (CD4 T cell counts, R(2) = 0.202, P < 0.001; HIV viremia, R(2) = 0.302, P < 0.001). Interestingly, CD8 T cell proliferation could be predicted by HIV RNA levels alone (R(2) = 0.334, P < 0.001) and this predictive value increased only slightly (R(2) = 0.346, P < 0.001) when CD4 T cell depletion was taken into account. Consistent with the hypothesis that CD4 T cell proliferation is driven by IL-7 as a homeostatic response to CD4 T cell depletion, levels of phosphorylated STAT-5 were found to be elevated in naive subsets of CD4 and CD8 T cells from patients with HIV infection and in the central memory subset of CD4 T cells. Taken together these data demonstrate that at least two different pathways lead to immune activation of T cells in patients with HIV infection and these pathways differentially influence CD4 and CD8 T cell subsets.
C1 [Catalfamo, Marta; Thaker, Vishakha; Roby, Gregg; Rehm, Catherine; Lane, H. Clifford] NIAID, Clin & Mol Retrovirol Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Di Mascio, Michele; Hu, Zonghui; Follmann, Dean] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
[Adelsberger, Joseph; Rupert, Adam; Baseler, Michael] Sci Applicat Int Corp, AIDS Monitoring Labs, Frederick, MD 21702 USA.
[Srinivasula, Sharat] Sci Applicat Int Corp, Biostat Res Branch, Frederick, MD 21702 USA.
[Tagaya, Yutaka] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Catalfamo, M (reprint author), NIAID, Clin & Mol Retrovirol Sect, Immunoregulat Lab, NIH, Bldg 10,Room 7N246,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM catalfam@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases; National Institutes of Health; National Cancer
Institute [N01-CO-12400]
FX We thank the patients of the National Institute of Allergy and
Infectious Diseases HIV-Clinic for their participation in this study,
the normal volunteers of the National Institutes of Health Blood Bank,
and Dr. Anthony Fauci for his guidance and support. This work was
supported by the Intramural Research Program of the National Institute
of Allergy and Infectious Diseases, National Institutes of Health;
National Cancer Institute, National Institutes of Health Contract
N01-CO-12400 (to Science Applications International).
NR 39
TC 82
Z9 84
U1 0
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 16
PY 2008
VL 105
IS 50
BP 19851
EP 19856
DI 10.1073/pnas.0810032105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 385GI
UT WOS:000261802300051
PM 19060209
ER
PT J
AU Peddada, SD
Laughlin, SK
Miner, K
Guyon, JP
Haneke, K
Vahdat, HL
Semelka, RC
Kowalik, A
Armao, D
Davis, B
Baird, DD
AF Peddada, Shyamal D.
Laughlin, Shannon K.
Miner, Kelly
Guyon, Jean-Philippe
Haneke, Karen
Vahdat, Heather L.
Semelka, Richard C.
Kowalik, Ania
Armao, Diane
Davis, Barbara
Baird, Donna Day
TI Growth of uterine leiomyomata among premenopausal black and white women
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE ethnic; fibroid; MRI; tumor growth; longitudinal data
ID NATURAL-HISTORY; UNITED-STATES; TUMOR SIZE; FIBROIDS; EXPRESSION; GENE;
AGE; INACTIVATION; HYSTERECTOMY; DIAGNOSIS
AB Uterine leiomyomata (fibroids) are the leading cause of hysterectomy in the United States. Black women have a greater fibroid burden than whites, yet no study has systematically evaluated the growth of fibroids in blacks and whites. We prospectively tracked growth for 262 fibroids (size range: 1-13 cm in diameter) from 72 premenopausal participants (38 blacks and 34 whites). Fibroid volume was measured by computerized analysis of up to four MRI scans over 12 months. We used mixed effects models to identify factors that are associated with growth, and results were converted to percent change per 6 months for clinical relevance. The median growth rate was 9% (range: -89% to +138%). Seven percent of fibroids regressed (> 20% shrinkage). Tumors from the same woman grew at different rates (within-woman component of variation was twice the component among women; both were significant, P < 0.001). Black and white women less than 35 years of age had similar fibroid growth rates. However, growth rates declined with age for whites but not for blacks (P = 0.05). The odds of a tumor growing more than 20% in 6 months also decreased with age for whites but not for blacks (P < 0.01). Growth rates were not influenced by tumor size, location, body mass index, or parity. We conclude that (i) spontaneous regression of fibroids occurs; (ii) fibroids from the same woman grow at different rates, despite a uniform hormonal milieu; (iii) fibroid size does not predict growth rate; and (iv) age-related differences in fibroid growth between blacks and whites may contribute to the higher symptom burden for black women.
C1 [Laughlin, Shannon K.; Baird, Donna Day] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Peddada, Shyamal D.; Miner, Kelly] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Guyon, Jean-Philippe; Haneke, Karen; Vahdat, Heather L.] Integrated Syst Lab, Durham, NC 27713 USA.
[Semelka, Richard C.; Armao, Diane] Univ N Carolina, Dept Radiol, Chapel Hill, NC 27599 USA.
[Kowalik, Ania] Univ N Carolina, Dept Obstet Gynecol, Chapel Hill, NC 27599 USA.
[Davis, Barbara] NIEHS, Lab Womens Hlth, Res Triangle Pk, NC 27709 USA.
RP Baird, DD (reprint author), NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
EM baird@niehs.nih.gov
RI Peddada, Shyamal/D-1278-2012; Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU Intramural Research Program of the NIEHS; National Institutes of Health
[Z01ES 101663-05]; National Center on Minority Health and Health
Disparities [MO1RR00046]; NIEHS [N01-ES-95446, 27301-C-0157]
FX The authors thank study participants; Ms. Edelstein (National Institute
on Environmental and Health Sciences [NIEHS]) for graphics; Ms. Greasby
(Graduate Student, Department of Biostatistics, University of
California, Davis) for initial data quality control checks; Ms. Firat
(Radiology Technician, University of North Carolina, Chapel Hill); Mss.
Daniel, Davis, and Pope for managing radiology films and digital images
(all at Integrated Laboratory Systems); and Ms. Ragan and Drs. Kissling,
Korach, Weinberg, and Wilcox (NIEHS) and Dr. Leppert (Duke University)
for reviewing an earlier version of the manuscript. Research was
supported by the Intramural Research Program of the NIEHS, National
Institutes of Health (Grant Z01ES 101663-05), with partial funding from
the National Center on Minority Health and Health Disparities Grant
MO1RR00046 and NIEHS Contracts N01-ES-95446 and 27301-C-0157.
NR 32
TC 110
Z9 114
U1 0
U2 4
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 16
PY 2008
VL 105
IS 50
BP 19887
EP 19892
DI 10.1073/pnas.0808188105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 385GI
UT WOS:000261802300057
PM 19047643
ER
PT J
AU Nofsinger, RR
Li, P
Hong, SH
Jonker, JW
Barish, GD
Ying, H
Cheng, SY
LeBlanc, M
Xu, W
Pei, LM
Kang, YJ
Nelson, M
Downes, M
Yu, RT
Olefsky, JM
Lee, CH
Evans, RM
AF Nofsinger, Russell R.
Li, Pingping
Hong, Suk-Hyun
Jonker, Johan W.
Barish, Grant D.
Ying, Hao
Cheng, Sheue-Yann
LeBlanc, Mathias
Xu, Wei
Pei, Liming
Kang, Yeon-Joo
Nelson, Michael
Downes, Michael
Yu, Ruth T.
Olefsky, Jerrold M.
Lee, Chih-Hao
Evans, Ronald M.
TI SMRT repression of nuclear receptors controls the adipogenic set point
and metabolic homeostasis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE adipogenesis; corepressor; PPAR; TR; glucose regulation
ID TRANSCRIPTIONAL COREPRESSOR RIP140; PPAR-GAMMA; ADAPTIVE THERMOGENESIS;
OXIDATIVE-METABOLISM; HORMONE-RECEPTORS; ENERGY-BALANCE; ADIPOCYTES;
COACTIVATOR; COMPLEXES; COFACTOR
AB The nuclear receptor corepressor, silencing mediator of retinoid and thyroid hormone receptors (SMRT), is recruited by a plethora of transcription factors to mediate lineage and signal-dependent transcriptional repression. We generated a knockin mutation in the receptor interaction domain (RID) of SMRT (SMRT(mRID)) that solely disrupts its interaction with nuclear hormone receptors (NHRs). SMRTmRID mice are viable and exhibit no gross developmental abnormalities, demonstrating that the reported lethality of SMRT knockouts is determined by non-NHR transcription factors. However, SMRTmRID mice exhibit widespread metabolic defects including reduced respiration, altered insulin sensitivity, and 70% increased adiposity. The latter phenotype is illustrated by the observation that SMRT(mRID)-derived MEFs display a dramatically increased adipogenic capacity and accelerated differentiation rate. Collectively, our results demonstrate that SMRT-RID-dependent repression is a key determinant of the adipogenic set point as well as an integrator of glucose metabolism and whole-body metabolic homeostasis.
C1 [Nofsinger, Russell R.; Hong, Suk-Hyun; Jonker, Johan W.; Barish, Grant D.; LeBlanc, Mathias; Pei, Liming; Nelson, Michael; Downes, Michael; Yu, Ruth T.; Evans, Ronald M.] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
[Li, Pingping; Olefsky, Jerrold M.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Ying, Hao; Cheng, Sheue-Yann] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Xu, Wei] Univ Wisconsin, McArdle Lab Canc Res, Madison, WI 53706 USA.
[Kang, Yeon-Joo] Burnham Inst Med REs, Ctr Neurosci Aging & Stem Cell Res, La Jolla, CA 92037 USA.
[Lee, Chih-Hao] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA.
[Evans, Ronald M.] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA.
RP Evans, RM (reprint author), Salk Inst Biol Studies, Gene Express Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM evans@salk.edu
OI Jonker, Johan/0000-0002-3919-5437
FU Molecular Cardiology Training Grant [T32 HL07770-14]; Human Frontier
Science Program; American Heart Association and American Diabetes
Association; National Institutes of Health [R01DK075046]; Howard Hughes
Medical Institute and National Institutes of Health [5R37DK057978,
5R01HD027183]
FX We thank E. Banayo, H. Juguilon, J. Alvarez, and Y. Zou for technical
assistance; J. Wong for anti-SMRT antibody; and E. Ong and S. Ganley for
administrative assistance. R.R.N. was supported by Molecular Cardiology
Training Grant T32 HL07770-14. J. W. J. is supported by a Human Frontier
Science Program fellowship. C-H. L. is supported by the American Heart
Association and American Diabetes Association and National Institutes of
Health Grant R01DK075046. R. M. E. is an investigator of the Howard
Hughes Medical Institute at the Salk Institute for Biological Studies
and March of Dimes Chair in Molecular and Developmental Biology. This
work was supported by the Howard Hughes Medical Institute and National
Institutes of Health Grants 5R37DK057978 and 5R01HD027183.
NR 27
TC 57
Z9 59
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 16
PY 2008
VL 105
IS 50
BP 20021
EP 20026
DI 10.1073/pnas.0811012105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 385GI
UT WOS:000261802300080
PM 19066220
ER
PT J
AU Logroscino, G
Gao, X
Chen, HL
Wing, A
Ascherio, A
AF Logroscino, Giancarlo
Gao, Xiang
Chen, Honglei
Wing, Al
Ascherio, Alberto
TI Dietary Iron Intake and Risk of Parkinson's Disease
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE ascorbic acid; diet; heme; iron; Parkinson disease; prospective studies
ID FOOD FREQUENCY QUESTIONNAIRE; SUBSTANTIA-NIGRA; HUMAN BRAIN; VITAMIN-C;
MEN; WOMEN; ACCUMULATION; CAROTENOIDS; MANGANESE; FERRITIN
AB Dietary iron is the most important source of iron stores. Several case-control studies have described the association of high dietary iron and Parkinson's disease, but prospective data are lacking. The authors prospectively followed 47,406 men and 76,947 women from the United States who provided information through a mailed questionnaire on their diet, medical history, and lifestyle practices between 1984 and 2000. The authors documented 422 new cases of Parkinson's disease. Total iron intake was not associated with an increased risk of Parkinson's disease (relative risk (RR) = 1.10, 95% confidence interval (CI): 0.74, 1.65; P(trend) = 0.84), but dietary nonheme iron intake from food was associated with a 30% increased risk of Parkinson's disease (RR = 1.27, 95% CI: 0.92, 1.76; P(trend) = 0.02). A secondary analysis revealed that Parkinson's disease risk was significantly increased among individuals with high nonheme iron and low vitamin C intakes (RR = 1.92, 95% CI: 1.14, 3.32; P(trend) = 0.002). Supplemental iron intake was associated with a borderline increase in Parkinson's disease risk among men. Although the authors' prospective data did not support an association between total iron intake (dietary and supplemental) and risk of Parkinson's disease, a 30% increased risk was associated with a diet rich in nonheme iron. This increase in risk was present in those who had low vitamin C intake.
C1 [Logroscino, Giancarlo] Univ Bari, Sch Med, Dept Neurol & Psychiat, Bari, Italy.
[Ascherio, Alberto] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Gao, Xiang; Wing, Al; Ascherio, Alberto] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Logroscino, Giancarlo] Harvard Univ, Sch Med, Div Aging, Boston, MA 02115 USA.
[Ascherio, Alberto] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
RP Logroscino, G (reprint author), Univ Bari, Sch Med, Dept Neurol & Psychiat, Bari, Italy.
EM giancarlo.logroscino@neurol.uniba.it
RI LOGROSCINO, GIANCARLO/K-5148-2016;
OI LOGROSCINO, GIANCARLO/0000-0003-0423-3242; Chen,
Honglei/0000-0003-3446-7779
FU Michael J. Fox Foundation; Kinetics Foundation; National Institutes of
Health; National Institute of Environmental Health Sciences
FX The work presented in this manuscript was supported in part by grants
from the Michael J. Fox Foundation and the Kinetics Foundation. Dr. Chen
is supported by the Intramural Research Program of the National
Institutes of Health and the National Institute of Environmental Health
Sciences.
NR 44
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Z9 33
U1 1
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 15
PY 2008
VL 168
IS 12
BP 1381
EP 1388
DI 10.1093/aje/kwn273
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 383OO
UT WOS:000261683100006
PM 18945687
ER
PT J
AU Namiki, T
Valencia, JC
Hall, MD
Hearing, VJ
AF Namiki, Takeshi
Valencia, Julio C.
Hall, Matthew D.
Hearing, Vincent J.
TI A novel approach to enhance antibody sensitivity and specificity by
peptide cross-linking
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Western blot; Antibody; Sensitivity; Specificity; Biuret reaction
ID PROTEIN; MELANOCYTES; TYROSINASE; TRANSPORT
AB Most current techniques employed to improve antigen-antibody signals in Western blotting and in immunohistochemistry rely on sample processing prior to staining (e.g., microwaving) or using a more robust reporter (e.g., a secondary antibody with biotin-streptavidin). We have developed and optimized a new approach intended to stabilize the complexes formed between antigens and their respective primary antibodies by cupric ions at high pH. This technique improves the affinity and lowers cross-reactivity with nonspecific bands of approximately 20% of antibodies tested (5/25). Here we report that this method can enhance antigen-antibody specificity and can improve the utility of some poorly reactive primary antibodies. Published by Elsevier Inc.
C1 [Namiki, Takeshi; Valencia, Julio C.; Hall, Matthew D.; Hearing, Vincent J.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20814 USA.
RP Hearing, VJ (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37,Room 3132, Bethesda, MD 20814 USA.
EM hearingv@nih.gov
RI Hall, Matthew/B-2132-2010
FU National Cancer Institute at the National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Cancer Institute at the National Institutes of Health. We thank
Michael M. Gottesman (Bethesda, MD, USA), Steve Wilson (Bedfordshire,
UK), and Nancy Mangini (Gary, IN, USA) for the gifts of antibodies to
ABCB5, NCKX5, and SLC24A5, respectively.
NR 17
TC 2
Z9 2
U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD DEC 15
PY 2008
VL 383
IS 2
BP 265
EP 269
DI 10.1016/j.ab.2008.08.024
PG 5
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 372KQ
UT WOS:000260900900018
PM 18801330
ER
PT J
AU Ward, MM
AF Ward, Michael M.
TI Interpreting Studies of Cardiovascular Mortality in Rheumatoid
Arthritis: The Importance of Timing
SO ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH
LA English
DT Editorial Material
ID INFLAMMATORY POLYARTHRITIS; MYOCARDIAL-INFARCTION; DISEASE ONSET;
COHORT; REGISTER; PREDICTS
C1 [Ward, Michael M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Ward, MM (reprint author), Bldg 10,Room 9S205,10 Ctr Dr,MSC 1828, Bethesda, MD 20892 USA.
EM wardm1@mail.nih.gov
FU Intramural NIH HHS [Z01 AR041153-04]
NR 21
TC 8
Z9 8
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0004-3591
J9 ARTHRIT RHEUM-ARTHR
JI Arthritis Rheum-Arthritis Care Res.
PD DEC 15
PY 2008
VL 59
IS 12
BP 1687
EP 1689
DI 10.1002/art.24170
PG 3
WC Rheumatology
SC Rheumatology
GA 382DW
UT WOS:000261586300001
PM 19035434
ER
PT J
AU Angers, M
Uldry, M
Kong, D
Gimble, JM
Jetten, AM
AF Angers, Martin
Uldry, Marc
Kong, Dong
Gimble, Jeffrey M.
Jetten, Anton M.
TI Mfsd2a encodes a novel major facilitator superfamily domain-containing
protein highly induced in brown adipose tissue during fasting and
adaptive thermogenesis
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE beta-adrenergic receptor (beta AR); brown adipose tissue (BAT);
permease; symporter; thermogenesis
ID DIET-INDUCED THERMOGENESIS; BETA-ADRENERGIC-RECEPTORS; ESCHERICHIA-COLI;
MELIBIOSE PERMEASE; ENERGY-EXPENDITURE; MEMBRANE TOPOLOGY; TRANSPORTERS;
FAMILY; ALPHA; COACTIVATORS
AB This study describes the identification of Mfsd2a (major facilitator superfamily domain-containing protein 2a), a novel mammalian major facilitator superfamily domain-containing protein, and ail additional closely related protein, Mfsd2b. Most intron/exon junctions are conserved between the two genes, suggesting that they are derived from a common ancestor. Mfsd2a and Mfsd2b share a 12 transmembrane alpha-helical domain structure that bears greatest similarity to that of the bacterial Na(+)/melibiose symporters. Confocal microscopy demonstrated that Mfsd2a localizes to the endoplasmic reticulum. Mfsd2a is expressed in many tissues and is highly induced in liver and BAT (brown adipose tissue) during fasting. Mfsd2a displays an oscillatory expression profile in BAT and liver, consistent with a circadian rhythm. Although the basal level of Mfsd2a expression is relatively low in mouse BAT, it is greatly induced during cold-induced thermogenesis and after treatment with beta AR (beta-adrenergic receptor) agonists. This induction is totally abolished in beta-less (beta AR-deficient) mice. These findings indicate that Mfsd2a is greatly up-regulated in BAT during thermogenesis and that its induction is controlled by the beta AR signalling pathway. The observed induction of Mfsd2a expression in cultured BAT cells by dibutyryl-cAMP is in agreement with this conclusion. The present study suggests that Mfsd2a plays a role in adaptive thermogenesis.
C1 [Angers, Martin; Jetten, Anton M.] NIEHS, Cell Biol Sect, LRB, Div Intramural Res,NIH, Res Triangle Pk, NC 27709 USA.
[Uldry, Marc] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kong, Dong] Beth Israel Deaconess Med Ctr, Dept Med, Div Endocrinol, Boston, MA 02115 USA.
[Gimble, Jeffrey M.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Stem Cell Lab, Baton Rouge, LA 70808 USA.
RP Jetten, AM (reprint author), NIEHS, Cell Biol Sect, LRB, Div Intramural Res,NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM jetten@niehs.nih.gov
OI Jetten, Anton/0000-0003-0954-4445
FU NIEHS (National Institute of Environmental Health Sciences); NIH
(National Institutes of Health) [Z01-ES-101586]; CNRU (Clinical
Nutrition Research Unit) Center [1P30 DK072476]; NIDDK (National
Institute of Diabetes and Digestive and Kidney Disease)
FX We thank Or John Pritchard and Or Jennifer Perry for their valuable
comments on the manuscript, Laura Miller for her assistance with the
mice and Or Xiying Wu for his assistance with the circadian rhythm
analysis. This research was supported by the Intramural Research Program
of the NIEHS (National Institute of Environmental Health Sciences), NIH
(National Institutes of Health) (Z01-ES-101586 awarded to A. M.J.) and
by a CNRU (Clinical Nutrition Research Unit) Center Grant 1P30 DK072476
entitled 'Nutritional Programming: Environmental and Molecular
Interactions' sponsored by the NIDDK (National Institute of Diabetes and
Digestive and Kidney Disease) (awarded to J.M.G.).
NR 34
TC 21
Z9 25
U1 0
U2 5
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD DEC 15
PY 2008
VL 416
BP 347
EP 355
DI 10.1042/BJ20080165
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 384ZA
UT WOS:000261781500004
PM 18694395
ER
PT J
AU Wang, LL
Li, Y
Hu, P
Teng, CT
AF Wang, Liangli
Li, Yin
Hu, Peng
Teng, Christina T.
TI PGC-1 alpha induces dynamic protein interactions on the ERR alpha gene
multi-hormone response element nucleosome in kidney cells
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE chromatin immunoprecipitation (ChIP); co-regulator; human kidney HK2
cell; oestrogen-related receptor (ERR) alpha and gamma; nucleosome;
peroxisome proliferator-activated receptor-gamma coactivator-1 alpha
(PGC-1 alpha)
ID ESTROGEN-RELATED RECEPTOR; TRANSCRIPTIONAL COACTIVATOR PGC-1; ORPHAN
NUCLEAR RECEPTORS; HUMAN LACTOFERRIN GENE; CHAIN ACYL-COENZYME; HISTONE
ACETYLATION; ANDROGEN RECEPTOR; SKELETAL-MUSCLE; EXPRESSION; GAMMA
AB ERR (oestrogen-related receptor)-alpha modulates the oestrogen signalling pathway and regulates genes participating in the physiological energy balance programme. Oestrogen and PGC-1 alpha (peroxisome proliferator-activated receptor-gamma coactivator-1 alpha), the master regulator of the energy homoeostasis programme, both regulate the expression of ERR alpha through the MHRE (multi-hormone response element) of the ERR alpha gene. Although the molecular mechanism of oestrogen action on ERR alpha regulation is well characterized, the mechanism of PGC-1 alpha induction is unclear. In this study, we examine chromatin Structural changes and protein interactions at the MHRE nucleosome in response to PGC-1 alpha expression in HK2 human kidney cells. We mapped the nucleosome positions of the ERR alpha gene promoter and examined the changes of historic acetylation in response to PGC-1 alpha expression. The interactions of DNA-binding proteins, ERR alpha and ERR gamma. co-activators {CBP [CREB (cAMP-response-element-binding protein)-binding protein], p300, PCAF (p300/CBP-associated factor)}, co-repressor [RIP140 (receptor-interacting protein of 140kDa)] and RNA polymerase II at the MHRE nucleosome region were investigated over time before and after PGC-1 alpha expression in the HK2 cells. We found a dynamic cyclic interaction of these proteins shortly after PGC-1 alpha expression and a slower cycling interaction, with fewer proteins involved, 20 h later. By Using the siRNA (small interfering RNA) knockdown approach, we discovered that ERR gamma was involved in the initial phase, but not in the later phase, of PGC-1 alpha-induced ERR alpha expression.
C1 [Wang, Liangli; Li, Yin; Hu, Peng; Teng, Christina T.] NIEHS, Gene Regulat Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Teng, CT (reprint author), NIEHS, Gene Regulat Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM teng1@niehs.nih.gov
FU NIH (National Institutes of Health); NIEHS (National Institute of
Environmental Health Sciences)
FX This research was supported by the Intramural Research Program of NIH
(National Institutes of Health), the NIEHS (National Institute of
Environmental Health Sciences). We acknowledge Dr P. Hebbar and Dr M.
Fatemi [LMC (Laboratory of Molecular Carcinogenesis), NIEHS] for helpful
discussions throughout this study. We thank Dr Leping Li (Biostatistics,
NIEHS) for performing the comparative sequence analysis. We also thank
Dr A. Kralli (Scripps Laboratory, CA, U.S.A.) for providing the PGC-1
alpha adeno-virus construct. We appreciate the critical reading of the
manuscript and valuable comments by Dr P. A. Wade and Dr K. Adelman
(LMC, NIEHS). This paper was edited by Dr Peggy Kaminski.
NR 41
TC 7
Z9 7
U1 0
U2 1
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0264-6021
EI 1470-8728
J9 BIOCHEM J
JI Biochem. J.
PD DEC 15
PY 2008
VL 416
BP 407
EP 419
DI 10.1042/BJ20081085
PN 3
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 384ZA
UT WOS:000261781500010
PM 18673300
ER
PT J
AU Johnson, AD
Handsaker, RE
Pulit, SL
Nizzari, MM
O'Donnell, CJ
de Bakker, PIW
AF Johnson, Andrew D.
Handsaker, Robert E.
Pulit, Sara L.
Nizzari, Marcia M.
O'Donnell, Christopher J.
de Bakker, Paul I. W.
TI SNAP: a web-based tool for identification and annotation of proxy SNPs
using HapMap
SO BIOINFORMATICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; LOCI
AB The interpretation of genome-wide association results is confounded by linkage disequilibrium between nearby alleles. We have developed a flexible bioinformatics query tool for single-nucleotide polymorphisms (SNPs) to identify and to annotate nearby SNPs in linkage disequilibrium (proxies) based on HapMap. By offering functionality to generate graphical plots for these data, the SNAP server will facilitate interpretation and comparison of genome-wide association study results, and the design of fine-mapping experiments (by delineating genomic regions harboring associated variants and their proxies).
C1 [Handsaker, Robert E.; Nizzari, Marcia M.; de Bakker, Paul I. W.] MIT, Broad Inst, Cambridge, MA 02142 USA.
[Handsaker, Robert E.; Nizzari, Marcia M.; de Bakker, Paul I. W.] Harvard Univ, Cambridge, MA 02142 USA.
[Johnson, Andrew D.; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, NIH, Framingham, MA 01702 USA.
[Johnson, Andrew D.; O'Donnell, Christopher J.] Boston Univ, Sch Med, Framingham, MA 01702 USA.
[Pulit, Sara L.; de Bakker, Paul I. W.] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02215 USA.
[Pulit, Sara L.; de Bakker, Paul I. W.] Harvard Univ, Sch Med, Partners HealthCare Ctr Genet & Genom, Boston, MA 02215 USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP de Bakker, PIW (reprint author), MIT, Broad Inst, Cambridge, MA 02142 USA.
EM debakker@broad.mit.edu
RI Johnson, Andrew/G-6520-2013; de Bakker, Paul/B-8730-2009
OI de Bakker, Paul/0000-0001-7735-7858
FU NHLBI's Framingham Heart Study [N01-HC-25195]; NHLBI CARe (Candidate
Gene Association Resource) [N01-HC-65226]; Intramural training program
of the NHLBI
FX Funding: NHLBI's Framingham Heart Study (N01-HC-25195 to A. D. J.);
Intramural training program of the NHLBI (to A. D. J.); NHLBI CARe
(Candidate Gene Association Resource) grant (N01-HC-65226 to R. E. H.).
NR 9
TC 677
Z9 683
U1 1
U2 16
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD DEC 15
PY 2008
VL 24
IS 24
BP 2938
EP 2939
DI 10.1093/bioinformatics/btn564
PG 2
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 380HL
UT WOS:000261456700026
PM 18974171
ER
PT J
AU Naoz, M
Manor, U
Sakaguchi, H
Kachar, B
Gov, NS
AF Naoz, Moshe
Manor, Uri
Sakaguchi, Hirofumi
Kachar, Bechara
Gov, Nir S.
TI Protein Localization by Actin Treadmilling and Molecular Motors
Regulates Stereocilia Shape and Treadmilling Rate
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID HAIR-CELL STEREOCILIA; ENA/VASP PROTEINS; FILOPODIA FORMATION; ARP2/3
COMPLEX; MYOSIN-VI; MOTILITY; FILAMENTS; DYNAMICS; GROWTH; ORGANIZATION
AB We present a physical model that describes the active localization of actin-regulating proteins inside stereocilia during steady-state conditions. The mechanism of localization is through the interplay of free diffusion and directed motion, which is driven by coupling to the treadmilling actin. laments and to myosin motors that move along the actin. laments. The resulting localization of both the molecular motors and their cargo is calculated, and is found to have an exponential (or steeper) profile. This localization can be at the base (driven by actin retrograde flow and minus-end myosin motors), or at the stereocilia tip (driven by plus-end myosin motors). The localization of proteins that influence the actin depolymerization and polymerization rates allow us to describe the narrow shape of the stereocilia base, and the observed increase of the actin polymerization rate with the stereocilia height.
C1 [Naoz, Moshe; Gov, Nir S.] Weizmann Inst Sci, Dept Chem Phys, IL-76100 Rehovot, Israel.
[Manor, Uri; Kachar, Bechara] Natl Inst Deafness & Other Commun Disorders, NIH, Lab Cellular Biol, Bethesda, MD USA.
[Sakaguchi, Hirofumi] Kyoto Prefectural Univ Med, Dept Otolaryngol Head & Neck Surg, Kyoto, Japan.
RP Gov, NS (reprint author), Weizmann Inst Sci, Dept Chem Phys, IL-76100 Rehovot, Israel.
EM nir.gov@weizmann.ac.il
FU Alvin and Gertrude Levine Career Development Chair; Israel Science
Foundation [337/05]; National Institute on Deafness and Other
Communication Disorders intramural funding
FX N.S.G. thanks the Alvin and Gertrude Levine Career Development Chair,
for their support. This research was supported by the Israel Science
Foundation (grant No. 337/05) and by National Institute on Deafness and
Other Communication Disorders intramural funding. This research is made
possible in part by the historic generosity of the Harold Perlman
Family.
NR 47
TC 21
Z9 21
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD DEC 15
PY 2008
VL 95
IS 12
BP 5706
EP 5718
DI 10.1529/biophysj.108.143453
PG 13
WC Biophysics
SC Biophysics
GA 381TR
UT WOS:000261559300017
PM 18936243
ER
PT J
AU Kennedy, AD
Deleo, FR
AF Kennedy, Adam D.
Deleo, Frank R.
TI PI3K and NADPH oxidase: a class act
SO BLOOD
LA English
DT Editorial Material
ID P40(PHOX); BINDING; PHAGOCYTOSIS; ACTIVATION; PHAGOSOME; DOMAIN
C1 [Kennedy, Adam D.; Deleo, Frank R.] NIAID, Bethesda, MD 20892 USA.
RP Kennedy, AD (reprint author), NIAID, Bethesda, MD 20892 USA.
OI DeLeo, Frank/0000-0003-3150-2516
FU Intramural NIH HHS
NR 8
TC 5
Z9 5
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD DEC 15
PY 2008
VL 112
IS 13
BP 4788
EP 4789
DI 10.1182/blood-2008-09-179135
PG 4
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400006
PM 19064736
ER
PT J
AU Johnson, DC
Corthals, S
Ramos, C
Hoering, A
Cocks, K
Dickens, NJ
Haessler, J
Goldschmidt, H
Child, JA
Bell, SE
Jackson, G
Baris, D
Rajkumar, SV
Davies, FE
Durie, BGM
Crowley, J
Sonneveld, P
Van Ness, B
Morgan, GJ
AF Johnson, David C.
Corthals, Sophie
Ramos, Christine
Hoering, Antje
Cocks, Kim
Dickens, Nicholas J.
Haessler, Jeff
Goldschmidt, Harmut
Child, J. Anthony
Bell, Sue E.
Jackson, Graham
Baris, Dalsu
Rajkumar, S. Vincent
Davies, Faith E.
Durie, Brian G. M.
Crowley, John
Sonneveld, Pieter
Van Ness, Brian
Morgan, Gareth J.
TI Genetic associations with thalidomide mediated venous thrombotic events
in myeloma identified using targeted genotyping
SO BLOOD
LA English
DT Article
ID HUMAN MULTIPLE-MYELOMA; PROTHROMBOTIC COAGULATION ABNORMALITIES;
DOXORUBICIN-INDUCED APOPTOSIS; PROTECTS ENDOTHELIAL-CELLS; PHASE-II
TRIAL; COMBINATION THERAPY; GROWTH-FACTOR; ANGIOGENIC CYTOKINES; TISSUE
FACTOR; TNF-ALPHA
AB A venous thromboembolism (VTE) with the subsequent risk of pulmonary embolism is a major concern in the treatment of patients with multiple myeloma with thalidomide. The susceptibility to developing a VTE in response to thalidomide therapy is likely to be influenced by both genetic and environmental factors. To test genetic variation associated with treatment related VTE in patient peripheral blood DNA, we used a custom-built molecular inversion probe (MIP)-based single nucleotide polymorphism (SNP) chip containing 3404 SNPs. SNPs on the chip were selected in "functional regions" within 964 genes spanning 67 molecular pathways thought to be involved in the pathogenesis, treatment response, and side effects associated with myeloma therapy. Patients and controls were taken from 3 large clinical trials: Medical Research Council (MRC) Myeloma IX, Hovon-50, and Eastern Cooperative Oncology Group (ECOG) EA100, which compared conventional treatments with thalidomide in patients with myeloma. Our analysis showed that the set of SNPs associated with thalidomide-related VTE were enriched in genes and pathways important in drug transport/metabolism, DNA repair, and cytokine balance. The effects of the SNPs associated with thalidomide-related VTE may be functional at the level of the tumor cell, the tumor-related microenvironment, and the endothelium. The clinical trials described in this paper have been registered as follows: MRC Myeloma IX: ISRCTN68454111; Hovon-50: NCT00028886; and ECOG EA100: NCT00033332. (Blood. 2008;112:4924-4934)
C1 [Johnson, David C.; Dickens, Nicholas J.; Davies, Faith E.; Morgan, Gareth J.] Inst Canc Res, Sect Haematooncol, London SW3 6JB, England.
[Corthals, Sophie; Sonneveld, Pieter] Erasmus MC, Dept Hematol, Rotterdam, Netherlands.
[Ramos, Christine; Van Ness, Brian] Univ Minnesota, Dept Genet Cell Biol & Dev, Minneapolis, MN USA.
[Hoering, Antje; Haessler, Jeff; Crowley, John] Canc Res & Biostat CRAB, Seattle, WA USA.
[Cocks, Kim; Child, J. Anthony; Bell, Sue E.] Univ Leeds, Clin Trials Res Unit, Leeds, W Yorkshire, England.
[Goldschmidt, Harmut] Heidelberg Univ, Dept Internal Med, Amyloidosis Clin, Div Hematol Oncol, D-6900 Heidelberg, Germany.
[Jackson, Graham] Newcastle Univ, Sch Lab & Clin Sci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Baris, Dalsu] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Rajkumar, S. Vincent] Mayo Clin, Dept Internal Med, Div Hematol, Rochester, MN USA.
[Durie, Brian G. M.] Int Myeloma Fdn, Los Angeles, CA USA.
[Durie, Brian G. M.] Cedars Sinai Comprehens Canc Ctr, Los Angeles, CA USA.
RP Morgan, GJ (reprint author), Inst Canc Res, Sect Haematooncol, Sutton SM2 5NG, Surrey, England.
EM gareth.morgan@icr.ac.uk
RI Johnson, David/A-3907-2011;
OI Johnson, David/0000-0003-0887-3343; Rajkumar, S.
Vincent/0000-0002-5862-1833; Dickens, Nicholas/0000-0003-0492-5855;
Cocks, Kim/0000-0003-2595-708X
FU International Myeloma Foundation (IMF)
FX We would like to thank the staff at the Haematological Malignancy
Diagnostic Service, Leeds, and members of the MRC Myeloma IX Trial
Management Group, as well as consultants and patients entered in the MRC
Myeloma IX, ECOG, and Hovon-50 trials.; This study was supported by the
International Myeloma Foundation (IMF) as part of the Bank on a Cure
(BOAC) Consortium. We are also grateful for support received from
Myeloma UK.
NR 93
TC 43
Z9 46
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD DEC 15
PY 2008
VL 112
IS 13
BP 4924
EP 4934
DI 10.1182/blood-2008-02-140434
PG 11
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400023
PM 18805967
ER
PT J
AU Castermans, K
Tabruyn, SP
Zeng, R
van Beijnum, JR
Eppolito, C
Leonard, WJ
Shrikant, PA
Griffioen, AW
AF Castermans, Karolien
Tabruyn, Sebastien P.
Zeng, Rong
van Beijnum, Judy R.
Eppolito, Cheryl
Leonard, Warren J.
Shrikant, Protul A.
Griffioen, Arjan W.
TI Angiostatic activity of the antitumor cytokine interleukin-21
SO BLOOD
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; NATURAL-KILLER-CELLS; COMMON GAMMA-CHAIN;
TUMOR ANGIOGENESIS; IL-21 RECEPTOR; IN-VIVO; INHIBITS ANGIOGENESIS;
TYROSINE KINASE; GENE-EXPRESSION; NITRIC-OXIDE
AB Interleukin-21 (IL-21) is a recently described immunoregulatory cytokine. It has been identified as a very potent immunotherapeutic agent in several cancer types in animal models, and clinical studies are ongoing. IL-21 belongs to the type I cytokine family of which other members, ie, IL-2, IL-15, and IL-4, have been shown to exert activities on vascular endothelial cells (ECs). We hypothesized that IL-21, in addition to inducing the antitumor immune response, also inhibits tumor angiogenesis. In vitro experiments showed a decrease of proliferation and sprouting of activated ECs after IL-21 treatment. We found that the IL-21 receptor is expressed on vascular ECs. Furthermore, in vivo studies in the chorioallantoic membrane of the chick embryo and in mouse tumors demonstrated that IL-21 treatment disturbs vessel architecture and negatively affects vessel outgrowth. Our results also confirm the earlier suggested angiostatic potential of IL-2 in vitro and in vivo. The angiostatic effect of IL-21 is confirmed by the decrease in expression of angiogenesis-related genes. Interestingly, IL-21 treatment of ECs leads to a decrease of Stat3 phosphorylation. Our research shows that IL-21 is a very powerful antitumor compound that combines the induction of an effective antitumor immune response with inhibition of tumor angiogenesis. (Blood. 2008;112: 4940-4947)
C1 [Griffioen, Arjan W.] Univ Hosp Maastricht, Dept Pathol, Angiogenesis Lab, NL-6202 AZ Maastricht, Netherlands.
[Castermans, Karolien; Tabruyn, Sebastien P.; van Beijnum, Judy R.; Griffioen, Arjan W.] Maastricht Univ, Sch Oncol & Dev Biol, Dept Pathol, Angiogenesis Lab, Maastricht, Netherlands.
[Castermans, Karolien; Tabruyn, Sebastien P.; van Beijnum, Judy R.; Griffioen, Arjan W.] Maastricht Univ, Sch Oncol & Dev Biol, Dept Internal Med, Angiogenesis Lab, Maastricht, Netherlands.
[Zeng, Rong; Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Eppolito, Cheryl; Shrikant, Protul A.] Roswell Pk Canc Inst, Dept Immunol, Buffalo, NY 14263 USA.
RP Griffioen, AW (reprint author), Univ Hosp Maastricht, Dept Pathol, Angiogenesis Lab, POB 5800, NL-6202 AZ Maastricht, Netherlands.
EM aw.griffioen@path.unimaas.nl
NR 50
TC 30
Z9 31
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD DEC 15
PY 2008
VL 112
IS 13
BP 4940
EP 4947
DI 10.1182/blood-2007-09-113878
PG 8
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400025
PM 18515660
ER
PT J
AU Ahmadzadeh, M
Felipe-Silva, A
Heemskerk, B
Powell, DJ
Wunderlich, JR
Merino, MJ
Rosenberg, SA
AF Ahmadzadeh, Mojgan
Felipe-Silva, Aloisio
Heemskerk, Bianca
Powell, Daniel J., Jr.
Wunderlich, John R.
Merino, Maria J.
Rosenberg, Steven A.
TI FOXP3 expression accurately defines the population of intratumoral
regulatory T cells that selectively accumulate in metastatic melanoma
lesions
SO BLOOD
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXP3; HUMAN PERIPHERAL-BLOOD; CANCER-PATIENTS;
TGF-BETA; CUTTING EDGE; IN-VIVO; TUMOR; CD4(+); IL-2; LYMPHOCYTES
AB Regulatory T(T(reg)) cells are often found in human tumors; however, their functional characteristics have been difficult to evaluate due to low cell numbers and the inability to adequately distinguish between activated and T(reg) cell populations. Using a novel approach, we examined the intracellular cytokine production capacity of tumor-infiltrating T cells in the single-cell suspensions of enzymatically digested tumors to differentiate T(reg) cells from effector T cells. Similar to T(reg) cells in the peripheral blood of healthy individuals, tumor-infiltrating FOXP3 + CD4 T cells, unlike FOXP3 + T cells, were unable to produce IL-2 and IFN-gamma upon ex vivo stimulation, indicating that FOXP3 expression is a valid biological marker for human T(reg) cells even in the tumor microenvironment. Accordingly, we enumerated FOXP3 + CD4 T(reg) cells in intratumoral and peritumoral sections of metastatic melanoma tumors and found a significant increase in proportion of FOXP3 + CD4 T(reg) cells in the intratumoral compared with peritumoral areas. Moreover, their frequencies were 3-to 5-fold higher in tumors than in peripheral blood from the same patients or healthy donors, respectively. These findings demonstrate that the tumor-infiltrating CD4 T(reg) cell population is accurately depicted by FOXP3 expression, they selectively accumulate in tumors, and their frequency in peripheral blood does not properly reflect tumor microenvironment. (Blood. 2008; 112: 4953-4960)
C1 [Ahmadzadeh, Mojgan; Heemskerk, Bianca; Powell, Daniel J., Jr.; Wunderlich, John R.; Rosenberg, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Felipe-Silva, Aloisio; Merino, Maria J.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Rosenberg, SA (reprint author), NCI, Surg Branch, NIH, CRC Bldg,Room 3W-3940,10 Ctr Dr, Bethesda, MD 20892 USA.
EM mojgan_ahmadzadeh@nih.gov; sar@nih.gov
RI Heemskerk, Bianca/C-4635-2012; FELIPE-SILVA, ALOISIO/J-9295-2012
OI FELIPE-SILVA, ALOISIO/0000-0001-6668-7907
NR 45
TC 82
Z9 87
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD DEC 15
PY 2008
VL 112
IS 13
BP 4953
EP 4960
DI 10.1182/blood-2008-06-163048
PG 8
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400027
PM 18820132
ER
PT J
AU Chu, CC
Catera, R
Hatzi, K
Yan, XJ
Zhang, L
Wang, XB
Fales, HM
Allen, SL
Kolitz, JE
Rai, KR
Chiorazzi, N
AF Chu, Charles C.
Catera, Rosa
Hatzi, Katerina
Yan, Xiao-Jie
Zhang, Lu
Wang, Xiao Bo
Fales, Henry M.
Allen, Steven L.
Kolitz, Jonathan E.
Rai, Kanti R.
Chiorazzi, Nicholas
TI Chronic lymphocytic leukemia antibodies with a common stereotypic
rearrangement recognize nonmuscle myosin heavy chain IIA
SO BLOOD
LA English
DT Article
ID IMMUNOGLOBULIN MUTATION GENOTYPE; MEMORY B-CELLS; ANTIGEN RECEPTORS;
APOPTOTIC CELLS; SOMATIC HYPERMUTATION; CARDIAC MYOSIN; T-CELLS;
SELECTION; EXPRESS; AUTOANTIBODIES
AB Leukemic B lymphocytes of a large group of unrelated chronic lymphocytic leukemia (CLL) patients express an unmutated heavy chain immunoglobulin variable (V) region encoded by IGHV1-69, IGHD3-16, and IGHJ3 with nearly identical heavy and light chain complementarity-determining region 3 sequences. The likelihood that these patients developed CLL clones with identical antibody V regions randomly is highly improbable and suggests selection by a common antigen. Monoclonal antibodies (mAbs) from this stereotypic subset strongly bind cytoplasmic structures in HEp-2 cells. Therefore, HEp-2 cell extracts were immunoprecipitated with recombinant stereotypic subset-specific CLL mAbs, revealing a major protein band at approximately 225 kDa that was identified by mass spectrometry as nonmuscle myosin heavy chain IIA (MYHIIA). Reactivity of the stereotypic mAbs with MYHIIA was confirmed by Western blot and immunofluorescence colocalization with anti-MYHIIA antibody. Treatments that alter MYHIIA amounts and cytoplasmic localization resulted in a corresponding change in binding to these mAbs. The appearance of MYHIIA on the surface of cells undergoing stress or apoptosis suggests that CLL mAb may generally bind molecules exposed as a consequence of these events. Binding of CLL mAb to MYHIIA could promote the development, survival, and expansion of these leukemic cells. (Blood. 2008; 112: 5122-5129)
C1 [Chu, Charles C.; Catera, Rosa; Hatzi, Katerina; Yan, Xiao-Jie; Zhang, Lu; Wang, Xiao Bo; Allen, Steven L.; Kolitz, Jonathan E.; Rai, Kanti R.; Chiorazzi, Nicholas] N Shore LIJ Hlth Syst, Feinstein Inst Med Res, Manhasset, NY 11030 USA.
[Chu, Charles C.; Allen, Steven L.; Kolitz, Jonathan E.; Rai, Kanti R.; Chiorazzi, Nicholas] N Shore Univ Hosp, Dept Med, Manhasset, NY USA.
[Chu, Charles C.; Allen, Steven L.; Kolitz, Jonathan E.; Rai, Kanti R.; Chiorazzi, Nicholas] N Shore Univ Hosp, Dept Med, New Hyde Pk, NY USA.
[Chu, Charles C.; Allen, Steven L.; Kolitz, Jonathan E.; Rai, Kanti R.; Chiorazzi, Nicholas] N Shore LIJ Hlth Syst, LIJ Med Ctr, Manhasset, NY USA.
[Chu, Charles C.; Allen, Steven L.; Kolitz, Jonathan E.; Rai, Kanti R.; Chiorazzi, Nicholas] N Shore LIJ Hlth Syst, LIJ Med Ctr, New Hyde Pk, NY USA.
[Chu, Charles C.; Kolitz, Jonathan E.] NYU, Dept Med, Sch Med, New York, NY 10003 USA.
[Fales, Henry M.] NHLBI, Lab Appl Mass Spectrometry, NIH, Bethesda, MD 20892 USA.
[Allen, Steven L.; Rai, Kanti R.; Chiorazzi, Nicholas] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
[Chiorazzi, Nicholas] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10467 USA.
RP Chu, CC (reprint author), N Shore LIJ Hlth Syst, Feinstein Inst Med Res, 350 Community Dr, Manhasset, NY 11030 USA.
EM cchu@nshs.edu
OI Allen, Steven/0000-0002-3482-3182
FU NIH [CA81554, CA87956, RR018535]; Karches Foundation; Peter Jay Sharp
Foundation; Prince Family Foundation; Marks Foundation; Jean Walton Fund
for Leukemia and Lymphoma Research; Joseph Eletto Leukemia Research Fund
FX This work was supported in part by R01 grants from NIH (CA81554 and
CA87956; N. C.), an M01 General Clinical Research Center grant from the
NIH (RR018535; N. C.), the Intramural Research Program of NIH (H. M.
F.), the Karches Foundation, the Peter Jay Sharp Foundation, the Prince
Family Foundation, the Marks Foundation, the Jean Walton Fund for
Leukemia and Lymphoma Research, and the Joseph Eletto Leukemia Research
Fund.
NR 51
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Z9 100
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 DEC 15
PY 2008
VL 112
IS 13
BP 5122
EP 5129
DI 10.1182/blood-2008-06-162024
PG 8
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400045
PM 18812466
ER
PT J
AU Morton, LM
Wang, SS
Cozen, W
Linet, MS
Chatterjee, N
Davis, S
Severson, RK
Colt, JS
Vasef, MA
Rothman, N
Blair, A
Bernstein, L
Cross, AJ
De Roos, AJ
Engels, EA
Hein, DW
Hill, DA
Kelemen, LE
Lim, UH
Lynch, CF
Schenk, M
Wacholder, S
Ward, MH
Zahm, SH
Chanock, SJ
Cerhan, JR
Hartge, P
AF Morton, Lindsay M.
Wang, Sophia S.
Cozen, Wendy
Linet, Martha S.
Chatterjee, Nilanjan
Davis, Scott
Severson, Richard K.
Colt, Joanne S.
Vasef, Mohammad A.
Rothman, Nathaniel
Blair, Aaron
Bernstein, Leslie
Cross, Amanda J.
De Roos, Anneclaire J.
Engels, Eric A.
Hein, David W.
Hill, Deirdre A.
Kelemen, Linda E.
Lim, Unhee
Lynch, Charles F.
Schenk, Maryjean
Wacholder, Sholom
Ward, Mary H.
Zahm, Shelia Hoar
Chanock, Stephen J.
Cerhan, James R.
Hartge, Patricia
TI Etiologic heterogeneity among non-Hodgkin lymphoma subtypes
SO BLOOD
LA English
DT Article
ID EPIDEMIOLOGY CONSORTIUM INTERLYMPH; ONE-CARBON METABOLISM; POOLED
ANALYSIS; UNITED-STATES; RISK-FACTORS; GENETIC-VARIATION;
T(14/18)-DEFINED SUBTYPES; ULTRAVIOLET-RADIATION; MALIGNANT-LYMPHOMAS;
CIGARETTE-SMOKING
AB Understanding patterns of etiologic commonality and heterogeneity for non-Hodgkin lymphomas may illuminate lymphomagenesis. We present the first systematic comparison of risks by lymphoma subtype for a broad range of putative risk factors in a population-based case-control study, including diffuse large B-cell (DLBCL; N = 416), follicular (N = 318), and marginal zone lymphomas (N = 106), and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; N = 133). We required at least 2 of 3 analyses to support differences in risk: (1) polytomous logistic regression, (2) homogeneity tests, or (3) dichotomous logistic regression, analyzing all 7 possible pairwise comparisons among the subtypes, corresponding to various groupings by clinical behavior, genetic features, and differentiation. Late birth order and high body mass index (>= 35) kg/m(2)) increased risk for DLBCL alone. Autoimmune conditions increased risk for marginal zone lymphoma alone. The tumor necrosis factor G-308A polymorphism (rs1800629) increased risks for both DLBCL and marginal zone lymphoma. Exposure to certain dietary heterocyclic amines from meat consumption increased risk for CLL/SLL alone. We observed no significant risk factors for follicular lymphoma alone. These data clearly support both etiologic commonality and heterogeneity for lymphoma subtypes, suggesting that immune dysfunction is of greater etiologic importance for DLBCL and marginal zone lymphoma than for CLL/SLL and follicular lymphoma. (Blood. 2008; 112: 5150-5160)
C1 [Morton, Lindsay M.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
[Cozen, Wendy] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Davis, Scott; De Roos, Anneclaire J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Davis, Scott; De Roos, Anneclaire J.] Univ Washington, Seattle, WA 98195 USA.
[Severson, Richard K.; Schenk, Maryjean] Wayne State Univ, Dept Family Med, Detroit, MI USA.
[Severson, Richard K.; Schenk, Maryjean] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Vasef, Mohammad A.] Univ New Mexico, Dept Pathol, Albuquerque, NM 87131 USA.
[Bernstein, Leslie] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Duarte, CA 91010 USA.
[Hein, David W.] Univ Louisville, Sch Med, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA.
[Hein, David W.] Univ Louisville, Sch Med, James Graham Brown Canc Ctr, Louisville, KY 40292 USA.
[Hill, Deirdre A.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Hill, Deirdre A.] Univ New Mexico, Dept Internal Med, Albuquerque, NM 87131 USA.
[Kelemen, Linda E.; Cerhan, James R.] Mayo Clin, Coll Med, Rochester, MN USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Chanock, Stephen J.] NCI, Core Genotyping Facil, Adv Technol Ctr, NIH, Gaithersburg, MD USA.
RP Morton, LM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS 7040,MSC 7238, Rockville, MD 20852 USA.
EM mortonli@mail.nih.gov
RI Hein, David/A-9707-2008; Morton, Lindsay/B-5234-2015;
OI Morton, Lindsay/0000-0001-9767-2310; Cerhan, James/0000-0002-7482-178X
FU National Cancer Institute; National Institutes of Health; Public Health
Service [N01-PC-65064, N01-PC-67008, N01-PC-67009, N01-PC-67010,
N02-PC-71105]
FX This research was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health, and Public
Health Service (contracts N01-PC-65064, N01-PC-67008, N01-PC-67009,
N01-PC-67010, N02-PC-71105).
NR 66
TC 101
Z9 104
U1 1
U2 14
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 DEC 15
PY 2008
VL 112
IS 13
BP 5150
EP 5160
DI 10.1182/blood-2008-01-133587
PG 11
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400048
PM 18796628
ER
PT J
AU Tamary, H
Shalev, H
Perez-Avraham, G
Zoldan, M
Levi, I
Swinkels, DW
Tanno, T
Miller, JL
AF Tamary, Hannah
Shalev, Hanna
Perez-Avraham, Galit
Zoldan, Meira
Levi, Itai
Swinkels, Dorine W.
Tanno, Toshihiko
Miller, Jeffery L.
TI Elevated growth differentiation factor 15 expression in patients with
congenital dyserythropoietic anemia type I
SO BLOOD
LA English
DT Article
ID HEPCIDIN; ERYTHROPOIESIS; THALASSEMIA; CODANIN-1
AB Congenital dyserythropoietic anemia (CDA) is a rare group of red blood cell disorders characterized by ineffective erythropoiesis and increased iron absorption. To determine whether growth differentation factor 15 (GDF15) hyper-expression is associated with the ineffective erythropoiesis and iron-loading complications of CDA type I ( CDA I), GDF15 levels and other markers of erythropoiesis and iron overload were studied in blood from 17 CDA I patients. Significantly higher levels of GDF15 were detected among the CDA I patients (10 239 +/- 3049 pg/mL) compared with healthy volunteers (269 +/- 238 pg/mL). In addition, GDF15 correlated significantly with several erythropoietic and iron parameters including Hepcidin-25, Ferritin, and Hepcidin-25/Ferritin ratios. These novel results suggest that CDA I patients express very high levels of serum GDF15, and that GDF15 contributes to the inappropriate suppression of hepcidin with subsequent secondary hemochromatosis. (Blood. 2008; 112: 5241-5244)
C1 [Tamary, Hannah; Zoldan, Meira] Tel Aviv Univ, Sackler Fac Med, Schneider Childrens Med Ctr Israel Petah Tikva, Hematol Oncol Ctr, IL-69978 Tel Aviv, Israel.
[Shalev, Hanna; Perez-Avraham, Galit; Levi, Itai] Ben Gurion Univ Negev, Hematol Soroka Med Ctr, Fac Med, IL-84105 Beer Sheva, Israel.
[Swinkels, Dorine W.] Radboud Univ Nijmegen, Dept Clin Chem, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Tanno, Toshihiko; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
RP Tamary, H (reprint author), Schneider Childrens Med Ctr Israel, Dept Pediat Hematol Oncol, IL-49202 Petah Tiqwa, Israel.
EM htamary@post.tau.ac.il
RI Swinkels, D.W./H-8098-2014
FU NIH; NIDDK
FX This research was supported ( in part) by the Intramural Research
Program of the NIH, NIDDK.
NR 16
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U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD DEC 15
PY 2008
VL 112
IS 13
BP 5241
EP 5244
DI 10.1182/blood-2008-06-165738
PG 4
WC Hematology
SC Hematology
GA 381CR
UT WOS:000261513400059
PM 18824595
ER
PT J
AU Dores, GM
Curtis, RE
Toro, JR
Devesa, SS
Fraumeni, JF
AF Dores, Graca M.
Curtis, Rochelle E.
Toro, Jorge R.
Devesa, Susan S.
Fraumeni, Joseph F., Jr.
TI Incidence of Cutaneous Sebaceous Carcinoma and Risk of Associated
Neoplasms Insight Into Muir-Torre Syndrome
SO CANCER
LA English
DT Article
DE sebaceous carcinoma; Muir-Torre syndrome; multiple primary cancers; skin
cancer
ID MALIGNANT EYELID TUMORS; MICROSATELLITE INSTABILITY; GLAND CARCINOMA;
TRANSPLANT RECIPIENTS; LYNCH-SYNDROME; CANCERS; KERATOACANTHOMAS;
POPULATION; FREQUENCY; PATIENT
AB BACKGROUND. Sebaceous tumors of the skin occurring in association with ail internal malignancy characterize Muir-Torre syndrome (MTS), a variant of hereditary nonpolyposis colon cancer (Lynch syndrome). To the authors' knowledge, only limited information exists regarding incidence patterns of sebaceous carcinoma (SC), and no prior study has quantified risks of associated cancers.
METHODS. The authors calculated cutaneous SC incidence rates (IRs) and IR ratios in 9 US Surveillance, Epidemiology, and End Results program registries (1973-2003). Indirectly standardized incidence ratios and 95% confidence intervals (95% Cls) were calculated for subsequent cancers among 2-month survivors of SC and for subsequent SC after other primary cancers.
RESULTS. Among 664 cases Of cutaneous SC, nearly 90% were diagnosed among whites (IR, 0.11 per 100,000 person-years), with significantly lower IR noted among blacks (IR, 0.04). Whereas eyelid SC IRs demonstrated no sex differences and stabilized in recent years, IRs of noneyelid SC predominated in men and rose steadily over time. Survivors of SC had a 43% (95% CI, 15%-76%) increased risk of subsequent cancer, and risk of SC was elevated by 52% (95% CI, 24%-84%) among survivors of other cancers. Whether before or after SC, the significant excesses of other primary cancers were limited to noneyelid SC. Patterns suggestive of genetic predisposition included >20-fold risks for early-onset (diagnosed in patients aged <50 years) S(. associated with colon, pancreatic, ovarian, or uterine corpus cancers, whereas late-onset SC (diagnosed in patients aged >= 50 years) predisposed to Ureter cancer.
CONCLUSIONS. This population-based study Of cutaneous SC revealed ail association with a spectrum of early-onset cancers consistent with NITS. Etiologic heterogeneity Was suggested by differences between eyelid and noneyelid SC in incidence patterns and associated cancer risks. Cancer 2008;113:3372-81. Published 2008 by the American Cancer Society.
C1 [Dores, Graca M.] Dept Vet Affairs Med Ctr, Med Serv, Oklahoma City, OK 73104 USA.
[Dores, Graca M.; Curtis, Rochelle E.; Toro, Jorge R.; Devesa, Susan S.; Fraumeni, Joseph F., Jr.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Dores, GM (reprint author), Dept Vet Affairs Med Ctr, Med Serv 111, 921 NE 13th St, Oklahoma City, OK 73104 USA.
EM doresg@mail.nih.gov
FU National Cancer Institute/National Institutes of Health; Department of
Veterans Affairs
FX Supported by the Intramural Research Program of the National Cancer
Institute/National Institutes of Health and the Department of Veterans
Affairs.
NR 50
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Z9 39
U1 2
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD DEC 15
PY 2008
VL 113
IS 12
BP 3372
EP 3381
DI 10.1002/cncr.23963
PG 10
WC Oncology
SC Oncology
GA 383HQ
UT WOS:000261665100013
PM 18932259
ER
PT J
AU Bellizzi, KM
Mustian, KM
Bowen, DJ
Resnick, B
Miller, SM
AF Bellizzi, Keith M.
Mustian, Karen M.
Bowen, Deborah J.
Resnick, Barbara
Miller, Suzanne M.
TI Aging in the Context of Cancer Prevention and Control Prespectives From
Behavioral Medicine
SO CANCER
LA English
DT Editorial Material
ID DECISION-MAKING; AGE; PREVALENCE; SURVIVORS; FUTURE; HEALTH
C1 [Bellizzi, Keith M.] Univ Connecticut, Storrs, CT 06269 USA.
[Bellizzi, Keith M.] Natl Canc Inst, Off Canc Survivorship, Bethesda, MD USA.
[Mustian, Karen M.] Univ Rochester, James P Wilmot Canc Ctr, Behav Med Unit, Rochester, NY USA.
[Bowen, Deborah J.] Boston Univ, Dept Social & Behav Sci, Boston, MA 02215 USA.
[Resnick, Barbara] Univ Maryland, Sch Nursing, Baltimore, MD 21201 USA.
[Miller, Suzanne M.] Fox Chase Canc Ctr, Behav Med Program, Philadelphia, PA 19111 USA.
RP Bellizzi, KM (reprint author), Univ Connecticut, 348 Mansfield Rd,Unit 2058, Storrs, CT 06269 USA.
EM keith.m.bellizzi@uconn.edu
FU NCI NIH HHS [R25 CA102618, R25 CA102618-05, R01 CA104979, R01
CA104979-01A1, U10 CA037420, P30 CA006927-47S59046]
NR 40
TC 3
Z9 3
U1 1
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 DEC 15
PY 2008
VL 113
IS 12
BP 3479
EP 3483
DI 10.1002/cncr.23937
PG 5
WC Oncology
SC Oncology
GA 384KQ
UT WOS:000261744100001
PM 19058144
ER
PT J
AU Bellizzi, KM
Mustian, KM
Palesh, OG
Diefenbach, M
AF Bellizzi, Keith M.
Mustian, Karen M.
Palesh, Oxana G.
Diefenbach, Michael
TI Cancer Survivorship and Aging Moving the Science Forward
SO CANCER
LA English
DT Article; Proceedings Paper
CT Society-of-Behavioral-Medicine Preconference on Cancer and Aging -
Challenges and Opportunities across the Cancer Control Continuum
CY MAR 21, 2007
CL Washington, DC
SP Soc Behav Med
DE cancer survivorship; aging; elderly; quality of life; well being
ID QUALITY-OF-LIFE; BREAST-CANCER; OLDER WOMEN; PHYSICAL FUNCTION;
PROSTATE-CANCER; UNITED-STATES; GERIATRIC ONCOLOGY; HEALTH; AGE; CARE
AB Given the high incidence and prevalence of cancer in older adults and the anticipated growth of this population over the next few decades, oncologists, geriatricians, and primary care providers will be challenged to provide timely and appropriate post-treatment care to a diverse Population of older cancer survivors. To the authors' knowledge to date, few post-treatment epidemiologic or clinical trial Studies have investigated the mental, social, and physical health issues among older cancer survivors. For this article, the authors reviewed the behavioral oncology, gerontology, geriatric, and psychology literature on cancer survivorship and aging. This report highlights several methodologic challenges that investigators face when conducting epidemiologic and cancer clinical trial research with older cancer Survivors after treatment. These challenges must be considered and overcome to develop an informative body of scientific knowledge to address the post-treatment healthcare needs of this growing population. Future research directions, new models of care, and the need for transdisciplinary approaches are discussed. Cancer 2008;113(12 suppl):3530-39. Published 2008 by the American Cancer Society.
C1 [Bellizzi, Keith M.] Univ Connecticut, Storrs, CT 06269 USA.
[Bellizzi, Keith M.] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Mustian, Karen M.; Palesh, Oxana G.] Univ Rochester, James P Wilmot Canc Ctr, Behav Med Unit, Rochester, NY USA.
[Diefenbach, Michael] Mt Sinai Sch Med, Oncol Serv, New York, NY USA.
RP Bellizzi, KM (reprint author), Univ Connecticut, 348 Mansfield Rd,Unit 2058, Storrs, CT 06269 USA.
EM Keith.M.Bellizzi@uconn.edu
FU NCI NIH HHS [R25 CA102618, R25 CA102618-05, U10 CA037420]
NR 89
TC 24
Z9 24
U1 7
U2 10
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD DEC 15
PY 2008
VL 113
IS 12
BP 3530
EP 3539
DI 10.1002/cncr.23942
PG 10
WC Oncology
SC Oncology
GA 384KQ
UT WOS:000261744100007
PM 19058147
ER
PT J
AU Harper, DP
Aplan, PD
AF Harper, David P.
Aplan, Peter D.
TI Chromosomal Rearrangements Leading to MLL Gene Fusions: Clinical and
Biological Aspects
SO CANCER RESEARCH
LA English
DT Review
ID ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; HOMOLOGOUS
RECOMBINATION; TOPOISOMERASE-II; INFANT-LEUKEMIA; TRANSLOCATIONS;
TRANSFORMATION; PROGENITORS; CHILDREN; THERAPY
AB Rearrangements of the MLL gene located at 11q23 are common chromosomal abnormalities associated with acute leukemia, especially infant and therapy-related leukemias. A variety of chimeric oncoproteins resulting from these rearrangements has been described; all of these include the NH(2)-terminal region of MLL implicated in protein-protein interactions and transcriptional repression. Although the molecular basis for the oncogenic activity of MLL chimeric proteins is incompletely understood, it seems to be derived, at least in part, through activation of clustered homeobox (HOX) genes. Here, we survey MLL gene rearrangements that are associated with acute leukemia and discuss molecular pathways leading to these rearrangements. [Cancer Res 2008;68(24):10024-7]
C1 [Aplan, Peter D.] NCI, Genet Branch, NIH, Natl Naval Med Ctr,Ctr Canc Res, Bethesda, MD 20889 USA.
[Harper, David P.] Uniformed Serv Univ Hlth Sci, Dept Pediat, Bethesda, MD 20814 USA.
RP Aplan, PD (reprint author), NCI, Genet Branch, NIH, Natl Naval Med Ctr,Ctr Canc Res, Bldg 8,Room 5101,8901 Rockville Pike, Bethesda, MD 20889 USA.
EM aplanp@mail.nih.gov
RI Aplan, Peter/K-9064-2016
FU Intramural Research Program of the INK National Cancer Institute
FX We apologize in advance to authors whose work we have not cited due to
space limitations. We thank Michael Kuehl, Ilan Mrsch, Rolf Marschalek.
Shai lzraeli, Jay Hess, Matthew Strout, Michael Caligiuri. Clara
Bloomfield, Martin StanuUa. Carolyn Felix, Terrance Babbitts, Janet
Rowley, Nancy Zeleznik-Le. and Michael Thirman for many thotightftil and
stimulating discussions regarding MLL translocations.
NR 20
TC 40
Z9 42
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10024
EP 10027
DI 10.1158/0008-5472.CAN-08-2208
PG 4
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800003
PM 19074864
ER
PT J
AU Thomas, DC
Baurley, JW
Brown, EE
Figueiredo, JC
Goldstein, A
Hazra, A
Wilson, RT
Rothman, N
AF Thomas, Duncan C.
Baurley, James W.
Brown, Elizabeth E.
Figueiredo, Jane C.
Goldstein, Alisa
Hazra, Aditi
Wilson, Robin T.
Rothman, Nathaniel
TI Approaches to Complex Pathways in Molecular Epidemiology: Summary of a
Special Conference of the American Association for Cancer Research
SO CANCER RESEARCH
LA English
DT Article
C1 [Thomas, Duncan C.] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90089 USA.
[Brown, Elizabeth E.] Univ Alabama, Dept Epidemiol, Birmingham, AL USA.
[Brown, Elizabeth E.] Univ Alabama, Dept Med & Microbiol, Birmingham, AL USA.
[Goldstein, Alisa] NCI, Genet Epidemiol Branch, NIH, Rockville, MD USA.
[Rothman, Nathaniel] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Hazra, Aditi] Program Mol & Genet Epidemiol, Boston, MA USA.
[Hazra, Aditi] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Wilson, Robin T.] Penn State Univ, Coll Med, Hershey, PA USA.
RP Thomas, DC (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, 1540 Alcazar St,CHP-222, Los Angeles, CA 90089 USA.
EM dthomas@usc.edu; rothmann@mail.nih.gov
NR 0
TC 7
Z9 8
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10028
EP 10030
DI 10.1158/0008-5472.CAN-08-1690
PG 3
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800004
PM 19074865
ER
PT J
AU Hillion, J
Dhara, S
Sumter, TF
Mukherjee, M
Di Cello, F
Belton, A
Turkson, J
Jaganathan, S
Cheng, LZ
Ye, ZH
Jove, R
Aplan, P
Lin, YW
Wertzler, K
Reeves, R
Elbahlouh, O
Kowalski, J
Bhattacharya, R
Resar, LMS
AF Hillion, Joelle
Dhara, Surajit
Sumter, Takita Felder
Mukherjee, Mita
Di Cello, Francescopaolo
Belton, Amy
Turkson, James
Jaganathan, Souyma
Cheng, Linzhao
Ye, Zhaohui
Jove, Richard
Aplan, Peter
Lin, Ying-Wei
Wertzler, Kelsey
Reeves, Ray
Elbahlouh, Ossama
Kowalski, Jeanne
Bhattacharya, Raka
Resar, Linda M. S.
TI The High-Mobility Group A1a/Signal Transducer and Activator of
Transcription-3 Axis: An Achilles Heel for Hematopoietic Malignancies?
SO CANCER RESEARCH
LA English
DT Article
ID TRANSGENIC MICE; CANCER CELLS; UTERINE TUMORIGENESIS; HMGA PROTEINS;
GENE; EXPRESSION; ONCOGENE; PROMOTER; BREAST; GROWTH
AB 6 Although HMGA1 (high-mobility group A1; formerly HMG-I/Y) is an oncogene that is widely overexpressed in aggressive cancers, the molecular mechanisms underlying transformation by HMGA-1 are only beginning to emerge. HMGA1 encodes the HMGA1a and HMGA1b protein isoforms, which function in regulating gene expression. To determine how HMGA1 leads to neoplastic transformation, we looked for genes regulated by HMGA1 using gene expression profile analysis. Here, we show that the SIAT3 gene, which encodes the signaling molecule signal transducer and activator of transcription 3 (STAT3), is a critical downstream target of RMGA1a. SIAT3 mRNA and protein are up-regulated in fibroblasts overexpressing HMGA1a and activated STAT3 recapitulates the transforming activity of HMGA1a in fibroblasts. HMGA1a also binds directly to a conserved region of the STAT3 promoter in vivo in human leukemia cells by chromatin inummoprecipitation and activates transcription of the STAT3 promoter in transfection experiments. To determine if this pathway contributes to HMGA1-mediated transformation, we investigated STAT3 expression in our HMGA1a transgenic mice, all of which developed aggressive lymphoid malignancy. STAT3 expression was increased in the leukemia cells from our transgenics but not in control cells. Blocking STAT3 function induced apoptosis in the transgenic leukemia cells but not in controls. In primary human leukemia samples, there was a positive correlation between HMGA1a and STAT3 mRNA. Moreover, blocking STAT3 function in human leukemia or lymphoma cells led to decreased cellular motility and foci formation. Our results show that the HMGA1a-STAT3 axis is a potential Achilles heel that could be exploited therapeutically in hematopoietic and other malignancies overexpressing HMGA1a. [Cancer Res 2008:68(24):101.21-7]
C1 [Hillion, Joelle; Dhara, Surajit; Sumter, Takita Felder; Mukherjee, Mita; Di Cello, Francescopaolo; Elbahlouh, Ossama; Bhattacharya, Raka; Resar, Linda M. S.] Johns Hopkins Univ, Sch Med, Div Hematol, Baltimore, MD 21205 USA.
[Hillion, Joelle; Dhara, Surajit; Sumter, Takita Felder; Mukherjee, Mita; Di Cello, Francescopaolo; Belton, Amy; Elbahlouh, Ossama; Bhattacharya, Raka; Resar, Linda M. S.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Dhara, Surajit; Sumter, Takita Felder; Mukherjee, Mita; Elbahlouh, Ossama; Bhattacharya, Raka; Resar, Linda M. S.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA.
[Dhara, Surajit; Cheng, Linzhao; Ye, Zhaohui; Resar, Linda M. S.] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
[Kowalski, Jeanne] Johns Hopkins Univ, Sch Med, Dept Biostat, Baltimore, MD 21205 USA.
[Turkson, James; Jaganathan, Souyma] Univ Cent Florida, BioMol Sci Ctr, Orlando, FL 32816 USA.
[Turkson, James; Jaganathan, Souyma] Univ Cent Florida, Dept Mol Biol & Microbiol, Orlando, FL 32816 USA.
[Jove, Richard] City Hope Comprehens Canc Ctr, Expt Therapeut Program, Duarte, CA USA.
[Jove, Richard] City Hope Natl Med Ctr, Beckman Res Inst, Div Mol Med, Duarte, CA 91010 USA.
[Aplan, Peter; Lin, Ying-Wei] NCI, Ctr Canc Res, Genet Branch, Bethesda, MD 20892 USA.
[Wertzler, Kelsey; Reeves, Ray] Washington State Univ, Pullman, WA 99164 USA.
RP Resar, LMS (reprint author), Johns Hopkins Univ, Sch Med, Div Hematol, Ross Res Bldg,Room 1025,720 Rutland Ave, Baltimore, MD 21205 USA.
EM lresar@jhmi.edu
RI Aplan, Peter/K-9064-2016;
OI Ye, Zhaohui/0000-0001-5272-9168
FU Intramural NIH HHS; NCI NIH HHS [R01 CA128865, P50 CA096888, P50
CA96888, R01 CA092339, R01 CA106439, R01 CA106439-04, R01 CA128865-01A1,
T32 CA060441, T32 CA60441]
NR 21
TC 46
Z9 46
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10121
EP 10127
DI 10.1158/0008-5472.CAN-08-2121
PG 7
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800016
PM 19074878
ER
PT J
AU Dissanayake, SK
Olkhanud, PB
O'Connell, MP
Carter, A
French, AD
Camilli, TC
Emeche, CD
Hewitt, KJ
Rosenthal, DT
Leotlela, PD
Wade, MS
Yang, SW
Brant, L
Nickoloff, BJ
Messina, JL
Biragyn, A
Hoek, KS
Taub, DD
Longo, DL
Sondak, VK
Hewitt, SM
Weeraratna, AT
AF Dissanayake, Samudra K.
Olkhanud, Purevdorj B.
O'Connell, Michael P.
Carter, Arnell
French, Amanda D.
Camilli, Tura C.
Emeche, Chineye D.
Hewitt, Kyle J.
Rosenthal, Devin T.
Leotlela, Poloko D.
Wade, Michael S.
Yang, Sherry W.
Brant, Larry
Nickoloff, Brian J.
Messina, Jane L.
Biragyn, Arya
Hoek, Keith S.
Taub, Dennis D.
Longo, Dan L.
Sondak, Vernon K.
Hewitt, Stephen M.
Weeraratna, Ashani T.
TI Wnt5A Regulates Expression of Tumor-Associated Antigens in Melanoma via
Changes in Signal Transducers and Activators of Transcription 3
Phosphorylation
SO CANCER RESEARCH
LA English
DT Article
ID PROTEIN-KINASE-C; FRIZZLED HOMOLOGS; STAT3 ACTIVATION; T-LYMPHOCYTES;
CELL MOTILITY; BETA-CATENIN; CANCER; PATHWAY; METASTASIS; TRANSITION
AB There are currently no effective therapies for metastatic melanoma and targeted immunotherapy results in the remission of only a very small percentage of tumors. In this study, we show that the noncanonical Wnt ligand, Wnt5A, can increase melanoma metastasis in vivo while down-regulating the expression of tumor-associated antigens important in eliciting CTL responses (e.g., MART-1, GP100, and tyrosinase). Melanosomal antigen expression is governed by MITF, PAX3, and SOX10 and is inhibited upon signal transducers and activators of transcription 3 (STAT3) activation, via decreases in PAX3 and subsequently MITF expression. Increasing Wnt5A in Wnt5A-low cells activated STAT3, and STAT3 was decreased upon Wnt5A knockdown. Downstream targets such as PAX3, MITF, and MART-1 were also affected by Wnt5A treatment or knockdown. Staining of a melanoma tissue array also highlighted the inverse relationship between MART-I and Wnt5A expression. PKC activation by phorbol ester mimicked Wnt5A effects, and Wnt5A treatment in the presence of STAT3 or PKC inhibitors did not lower MART-1 levels. CTL activation studies showed that increases in Wnt5A correspond to decreased CTL activation and vice versa, suggesting that targeting Wnt5A before immunotherapy may lead to the enhancement of current targeted immunotherapy for patients with metastatic melanoma. [Cancer Res 2008;68(24):10205-14]
C1 [Dissanayake, Samudra K.; Olkhanud, Purevdorj B.; O'Connell, Michael P.; Carter, Arnell; French, Amanda D.; Camilli, Tura C.; Emeche, Chineye D.; Hewitt, Kyle J.; Rosenthal, Devin T.; Leotlela, Poloko D.; Wade, Michael S.; Yang, Sherry W.; Biragyn, Arya; Taub, Dennis D.; Longo, Dan L.; Weeraratna, Ashani T.] NIA, Immunol Lab, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Brant, Larry] NIA, Res Resources Branch, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Nickoloff, Brian J.] Loyola Univ, Med Ctr, Dept Pathol, Maywood, IL 60153 USA.
[Messina, Jane L.; Sondak, Vernon K.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Hoek, Keith S.] Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland.
[Hewitt, Stephen M.] NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Weeraratna, AT (reprint author), NIA, Immunol Lab, NIH, Gerontol Res Ctr, 5600 Nathan Shock Dr,Box 21, Baltimore, MD 21224 USA.
EM weerarat@grc.nia.nih.gov
OI Hewitt, Stephen/0000-0001-8283-1788
FU National Institute on Aging
FX Intramural Research program of the National Institute on Aging.
NR 38
TC 55
Z9 58
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10205
EP 10214
DI 10.1158/0008-5472.CAN-08-2149
PG 10
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800026
PM 19074888
ER
PT J
AU Solomon, DA
Kim, JS
Cronin, JC
Sibenaller, Z
Ryken, T
Rosenberg, SA
Ressom, H
Jean, W
Bigner, D
Yan, H
Samuels, Y
Waldman, T
AF Solomon, David A.
Kim, Jung-Sik
Cronin, Julia C.
Sibenaller, Zita
Ryken, Timothy
Rosenberg, Steven A.
Ressom, Habtom
Jean, Walter
Bigner, Darell
Yan, Hai
Samuels, Yardena
Waldman, Todd
TI Mutational Inactivation of PTPRD in Glioblastoma Multiforme and
Malignant Melanoma
SO CANCER RESEARCH
LA English
DT Article
ID PROTEIN-TYROSINE-PHOSPHATASE; TUMOR-SUPPRESSOR LOCI; COLORECTAL CANCERS;
CHROMOSOME 9P; CELL-ADHESION; LUNG-CANCER; HOMOZYGOUS DELETIONS; HUMAN
BREAST; SHORT ARM; GENE
AB An additional tumor suppressor gene on chromosome 9p telomeric to the CDKN2A/B locus has long been postulated to exist. Using Affymetrix 250K single nucleotide polymorphism arrays to screen for copy number changes in glioblastoma multiforme (GBM), we detected a high frequency of deletions of the PTPRD gene, which encodes a receptor protein tyrosme phosphatase at chromosome 9p23-24.1. Missense and nonsense mutations of PTPRD were identified in a subset of the samples lacking deletions, including an inherited mutation with somatic loss of the wild-type allele. We then sequenced the gene in melanoma and identified 10 somatic mutations in 7 of 57 tumors (12%). Reconstitution of PTPRD expression in GBM and melanoma cells harboring deletions or mutations led to growth suppression and apoptosis that was alleviated by both the somatic and constitutional mutations. These data implicate PTPRD in the pathogenesis of tumors of neuroectodermal origin and, when taken together with other recent reports of PTPRD mutations in adenocarcinoma of the colon and lung, suggest that PTPRD may be one of a select group of tumor suppressor genes that are inactivated in a wide range of common human tumor types. (Cancer Res 2008; 68(24):10300-6]
C1 [Solomon, David A.; Kim, Jung-Sik; Ressom, Habtom; Waldman, Todd] Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA.
[Jean, Walter] Georgetown Univ, Sch Med, Dept Neurosurg, Washington, DC 20057 USA.
[Cronin, Julia C.; Samuels, Yardena] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Rosenberg, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Sibenaller, Zita; Ryken, Timothy] Univ Iowa, Coll Med, Dept Neurosurg, Iowa City, IA USA.
[Bigner, Darell; Yan, Hai] Duke Univ, Sch Med, Dept Pathol, Preston Robert Tisch Brain Tumor Ctr, Durham, NC 27706 USA.
RP Waldman, T (reprint author), Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Dept Oncol, New Res Bldg E304,3970 Reservoir Rd NW, Washington, DC 20057 USA.
EM waldmant@georgetown.edu
FU National Cancer Institute; American Cancer Society; National Human
Genuine Research Institute; The Harry J. Lloyd Charitable Trust
FX T. Waldman is funded by the National Cancer Institute and the American
Cancer Society. Y. Samuels is funded by the National Human Genuine
Research Institute and The Harry J. Lloyd Charitable Trust.
NR 29
TC 67
Z9 68
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10300
EP 10306
DI 10.1158/0008-5472.CAN-08-3272
PG 7
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800036
PM 19074898
ER
PT J
AU Tuomisto, A
Sund, M
Tahkola, J
Latvanlehto, A
Savolainen, ER
Autio-Harmainen, H
Liakka, A
Sormunen, R
Vuoristo, J
West, A
Lahesmaa, R
Morse, HC
Pihlajaniemi, T
AF Tuomisto, Anne
Sund, Malin
Tahkola, Jenni
Latvanlehto, Anne
Savolainen, Eeva-Riitta
Autio-Harmainen, Helena
Liakka, Annikki
Sormunen, Raija
Vuoristo, Jussi
West, Anne
Lahesmaa, Riitta
Morse, Herbert C., III
Pihlajaniemi, Taina
TI A Mutant Collagen XIII Alters Intestinal Expression of Immune Response
Genes and Predisposes Transgenic Mice to Develop B-Cell Lymphomas
SO CANCER RESEARCH
LA English
DT Article
ID T-CELLS; CHROMOSOMAL TRANSLOCATIONS; INHIBITORY RECEPTORS;
MOLECULAR-FEATURES; CANCER; LAIR-1; DIFFERENTIATION; INFLAMMATION;
LEUKEMIA; PATHOGENESIS
AB Epithelial cells of mucosal surfaces are critical for maintaining immune homeostasis by aiding in the discrimination of pathogenic and commensal microorganisms and modulating the activities of antigen-presenting cells and lymphocytes. Functional breakdowns resulting in chronic infection and inflammation are associated with the development of hematologic and solid neoplasms for which detailed pathogenetic mechanisms are poorly understood. Mice heterozygous or a transgene Col13a1(del) expressing a mutant collagen XIII developed clonal mature B-cell lineage lymphomas originating in mesenteric lymph nodes (MLN). The tumors were associated with T cells and macrophages. The incidence of disease was reduced 2-fold in transgenic mice raised under specific pathogen-free conditions, suggesting a role for infectious agents. The lymphomas did not express the mutant collagen XIII, indicating that its influence on tumorigenesis was B-cell extrinsic and likely to be associated with collagen XIII-positive tissues drained by the MLN. Studies of the small intestines of transgenic mice showed that the subepithelial basement membranes (BM) were highly abnormal and that they exhibited heightened expression of genes involved in immune responses. These results define collagen XIII-dependent maintenance of the intestinal BM as a previously unappreciated component of immune responses and a critical determinant of cancer susceptibility. [Cancer Res 2008;68(24):10324-32]
C1 [Tuomisto, Anne; Sund, Malin; Tahkola, Jenni; Latvanlehto, Anne; Pihlajaniemi, Taina] Univ Oulu, Bioctr, Oulu Ctr Cell Matrix Res, Dept Med Biochem & Mol Biol,Inst Biomed, FIN-90014 Oulu, Finland.
[Savolainen, Eeva-Riitta] Univ Oulu, Dept Clin Chem, FIN-90014 Oulu, Finland.
[Autio-Harmainen, Helena; Liakka, Annikki; Sormunen, Raija] Univ Oulu, Dept Pathol, FIN-90014 Oulu, Finland.
[West, Anne; Lahesmaa, Riitta] Univ Turku, Turku Ctr Biotechnol, Turku, Finland.
[West, Anne; Lahesmaa, Riitta] Abo Akad Univ, Turku, Finland.
[Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA.
RP Pihlajaniemi, T (reprint author), Univ Oulu, Bioctr, Oulu Ctr Cell Matrix Res, Dept Med Biochem & Mol Biol,Inst Biomed, FIN-90014 Oulu, Finland.
EM hm16c@nih.gov; taina.pihlajaniemi@oulu.fi
OI Sund, Malin/0000-0002-7516-9543; Morse, Herbert/0000-0002-9331-3705
FU Health Sciences Council of the Academy of Finland [115237, 53377];
Finnish Cancer Foundation; Sigrid Juselius Foundation; sixth EU
Framework Programme [504743]; NIH; National Institute of Allergy and
Infectious Diseases
FX Health Sciences Council of the Academy of Finland (115237 and 53377),
Finnish Cancer Foundation and Sigrid Juselius Foundation, sixth EU
Framework Programme (Integrated project "Angiotargeting"; contract no.
504743) in the area of "Life sciences, genomics and biotechnology for
health,'' and Intramural Research Program of the NIH, National Institute
of Allergy and Infectious Diseases.
NR 42
TC 7
Z9 7
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 2008
VL 68
IS 24
BP 10324
EP 10332
DI 10.1158/0008-5472.CAN-08-2582
PG 9
WC Oncology
SC Oncology
GA 386FD
UT WOS:000261866800039
PM 19074901
ER
PT J
AU Zhang, YJ
Pastan, I
AF Zhang, Yujan
Pastan, Ira
TI High Shed Antigen Levels within Tumors: An Additional Barrier to
Immunoconjugate Therapy
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; ACUTE MYELOID-LEUKEMIA; NON-HODGKINS-LYMPHOMA;
SOLID TUMORS; CONVERTING-ENZYME; MONOCLONAL-ANTIBODIES; ADAM
METALLOPROTEASES; SELECTIVE-INHIBITION; CHEMOTHERAPY PLUS; CIRCULATING
CD20
AB Shedding of cell surface antigens is an important biological process that is used by cells to modulate responses to signals in the extracellular environment. Because antibody-based therapies of cancer target cell surface antigens, it is important to understand more about the shedding process and how it affects tumor responses to this type of therapy. Up to now most attention has been focused on measuring the concentration of shed antigens in the blood and using these to determine the presence of a tumor and as a measure of response. The recent finding that the concentration of the tumor antigen mesothelin is extremely high within the interstitial space of tumors, where it can block antibody action, and that the concentration of shed mesothelin within the tumor is lowered by chemotherapy has important implications for the successful treatment of solid tumors by immunoconjugates and whole antibodies.
C1 [Zhang, Yujan; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pastan, I (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA.
EM pastani@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX Grant support: Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 52
TC 31
Z9 31
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 15
PY 2008
VL 14
IS 24
BP 7981
EP 7986
DI 10.1158/1078-0432.CCR-08-0324
PG 6
WC Oncology
SC Oncology
GA 384ZL
UT WOS:000261782600004
PM 19088013
ER
PT J
AU Garcia-Closas, M
Chanock, S
AF Garcia-Closas, Montserrat
Chanock, Stephen
TI Genetic Susceptibility Loci for Breast Cancer by Estrogen Receptor
Status
SO CLINICAL CANCER RESEARCH
LA English
DT Review
ID GENOME-WIDE ASSOCIATION; KERATINOCYTE GROWTH-FACTOR; SINGLE-NUCLEOTIDE
POLYMORPHISMS; DEL PROMOTER POLYMORPHISM; LOW-PENETRANCE BREAST;
PROSTATE-CANCER; BRCA2 MUTATIONS; COMMON VARIANTS; CONFER
SUSCEPTIBILITY; PROGESTERONE-RECEPTOR
AB Breast cancer is a heterogeneous disease, and risk factors could be differentially associated with the development of distinct tumor subtypes that manifest different biological behavior and progression. In support of this view, there is growing evidence that known breast cancer risk factors vary by hormone receptor status and perhaps other pathologic characteristics of disease. Recent work from large consortial studies has led to the discovery of novel breast cancer susceptibility loci in genic (CASP8, FGFRZ TNRC9, MAP3K1, LSP1) and nongenic regions (8q24, 2q35, 5p12) of the genome, and to the finding of substantial heterogeneity by tumor characteristics. In particular, susceptibility loci in FGFR2, TNRC9, 8q24, 2q35, and 5p12 have stronger associations for estrogen receptor - positive (ER+) disease than estrogen receptor - negative (ER) disease. These findings suggest that common genetic variants can influence the pathologic subtype of breast cancer, and provide further support for the hypothesis that ER+ and ER- disease result from different etiologic pathways. Current studies had limited power to detect susceptibility loci for less common tumor subtypes, such as ER- disease including triple-negative and basal-like tumors. Ongoing work targeting uncommon subtypes is likely to identify additional tumor-specific susceptibility loci in the near future. Characterization of etiologic heterogeneity of breast cancer may lead to improvements in the understanding of the biological mechanisms for breast cancer, and ultimately result in improvements in prevention, early detection, and treatment.
C1 [Garcia-Closas, Montserrat; Chanock, Stephen] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
RP Garcia-Closas, M (reprint author), NCI, Div Canc Epidemiol & Genet, Room 5014,6120 Execut Blvd, Rockville, MD 20852 USA.
EM montse@nih.gov
RI Garcia-Closas, Montserrat /F-3871-2015
OI Garcia-Closas, Montserrat /0000-0003-1033-2650
FU Intramural NIH HHS [Z99 CA999999, Z01 CP010126-12]
NR 108
TC 84
Z9 85
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 15
PY 2008
VL 14
IS 24
BP 8000
EP 8009
DI 10.1158/1078-0432.CCR-08-0975
PG 10
WC Oncology
SC Oncology
GA 384ZL
UT WOS:000261782600006
PM 19088016
ER
PT J
AU Amornphimoltham, P
Leelahavanichkul, K
Molinolo, A
Patel, V
Gutkind, JS
AF Amornphimoltham, Panomwat
Leelahavanichkul, Kantima
Molinolo, Alfredo
Patel, Vyomesh
Gutkind, J. Silvio
TI Inhibition of Mammalian Target of Rapamycin by Rapamycin Causes the
Regression of Carcinogen-induced Skin Tumor Lesions
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMAS; MOUSE SKIN; DEPENDENT PHOSPHORYLATION;
PERSISTENT ACTIVATION; NECK-CANCER; HEAD; MTOR; MODELS; RAS;
IDENTIFICATION
AB Purpose: The activation of Akt/mammalian target of rapamycin (mTOR) pathway represents a frequent event in squamous cell carcinoma (SCC) progression, thus raising the possibility of using specific mTOR inhibitors for the treatment of SCC patients. In this regard, blockade of mTOR with rapamycin prevents the growth of human head and neck SCC cells when xenotransplanted into immunodeficient mice. However, therapeutic responses in xenograft tumors are not always predictive of clinical anticancer activity.
Experimental Design: As genetically defined and chemically induced animal cancer models often reflect better the complexity of the clinical setting, we used here a two-step chemical carcinogenesis model to explore the effectiveness of rapamycin for the treatment of skin SCC.
Results: Rapamycin exerted a remarkable anticancer activity in this chemically induced cancer model, decreasing the tumor burden of mice harboring early and advanced tumor lesions, and even recurrent skin SCCs. Immunohistochemical studies on tumor biopsies and clustering analysis revealed that rapamycin causes the rapid decrease in the phosphorylation status of mTOR targets followed by the apoptotic death of cancer cells and the reduction in the growth and metabolic activity of the surviving ones, concomitant with a decrease in the population of cancer cells expressing mutant p53. This approach enabled investigating the relationship among molecular changes caused by mTOR inhibition, thus helping identify relevant biomarkers for monitoring the effectiveness of mTOR inhibition in the clinical setting.
Conclusions: Together, these findings provide a strong rationale for the early evaluation of mTOR inhibitors as a molecular targeted approach to treat SCC.
C1 [Amornphimoltham, Panomwat; Leelahavanichkul, Kantima; Molinolo, Alfredo; Patel, Vyomesh; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Res, NIH, 30 Convent Dr,Bldg 30,Room 212, Bethesda, MD 20892 USA.
EM sg39v@nih.gov
RI Gutkind, J. Silvio/A-1053-2009
FU Intramural NIH HHS [ZIA DE000558-19]
NR 29
TC 39
Z9 40
U1 0
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 15
PY 2008
VL 14
IS 24
BP 8094
EP 8101
DI 10.1158/1078-0432.CCR-08-0703
PG 8
WC Oncology
SC Oncology
GA 384ZL
UT WOS:000261782600016
PM 19073969
ER
PT J
AU Balleine, RL
Webster, LR
Davis, S
Salisbury, EL
Palazzo, JP
Schwartz, GF
Cornfield, DB
Walker, RL
Byth, K
Clarke, CL
Meltzer, PS
AF Balleine, Rosemary L.
Webster, Lucy R.
Davis, Sean
Salisbury, Elizabeth L.
Palazzo, Juan P.
Schwartz, Gordon F.
Cornfield, Dennis B.
Walker, Robert L.
Byth, Karen
Clarke, Christine L.
Meltzer, Paul S.
TI Molecular Grading of Ductal Carcinoma In situ of the Breast
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PATHOLOGICAL PROGNOSTIC-FACTORS; GENE-EXPRESSION PROFILES; SURGICAL
ADJUVANT BREAST; TERM-FOLLOW-UP; ARCHITECTURAL HETEROGENEITY;
INTRADUCTAL-CARCINOMA; HISTOLOGIC GRADE; BIOLOGIC MARKERS; CANCER;
CLASSIFICATION
AB Purpose: Increased incidence of ductal carcinoma in situ (DCIS) associated with mammographic screening for breast cancer has emphasized the challenges of managing this condition. The aim of this study was to identify informative clinical indicators of DCIS biology by molecular profiling.
Experimental Design: Areas of in situ carcinoma, atypical ductal hyperplasia, and benign epithelium were microdissected from 46 invasive breast cancers. Oligonucleotide probes showing differential expression between DCIS associated with grade 1 and 3 invasive cancer were identified by microarray-based gene expression profiling. Expression at these probes was used to define a "molecular grade" subcategorization of all samples. The genomic basis of molecular grade was examined by array-based comparative genomic hybridization. Clinical course was examined in a cohort of 134 patients with DCIS treated by surgery alone.
Results: DCIS samples were designated as low or high molecular grade based on expression at 173 probes. The low molecular grade subgroup included low (n = 10) and intermediate (n = 11) nuclear grade DCIS as well as all samples of atypical ductal hyperplasia (n = 4) and benign epithelium (n = 7). The high molecular grade subgroup included DCIS of intermediate (n = 7) and high (n = 19) nuclear grade. The character and degree of genomic aberration were distinct between molecular grade subgroups. A classification tree model including nuclear grade and Ki67 score accurately predicted molecular grade for 95.7% of samples. In an independent cohort, this showed a pattern of rapid disease recurrence for high molecular grade DCIS.
Conclusions: Molecular profiling indicates a binary grading scheme for DCIS. This practical approach has potential to improve clinical evaluation of DCIS.
C1 [Davis, Sean; Walker, Robert L.; Meltzer, Paul S.] NCI, Genet Branch, Bethesda, MD 20892 USA.
[Balleine, Rosemary L.; Webster, Lucy R.; Clarke, Christine L.] Translat Oncol Sydney W Area Hlth Serv, Sydney, NSW, Australia.
[Balleine, Rosemary L.; Webster, Lucy R.; Clarke, Christine L.] Westmead Inst Canc Res, Westmead, NSW, Australia.
[Balleine, Rosemary L.; Webster, Lucy R.; Byth, Karen; Clarke, Christine L.] Westmead Millennium Inst, Westmead, NSW, Australia.
[Balleine, Rosemary L.; Webster, Lucy R.; Clarke, Christine L.] Univ Sydney, Sydney, NSW 2006, Australia.
[Salisbury, Elizabeth L.] Inst Clin Pathol & Med Res, Westmead, NSW, Australia.
[Palazzo, Juan P.] Thomas Jefferson Univ Hosp, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA.
[Schwartz, Gordon F.] Thomas Jefferson Univ Hosp, Dept Surg, Philadelphia, PA 19107 USA.
[Cornfield, Dennis B.] Lehigh Valley Hosp, Hlth Network Labs, Dept Pathol, Allentown, PA USA.
RP Meltzer, PS (reprint author), NCI, Genet Branch, 37 Convent Dr,MSC 4265,Room 6138, Bethesda, MD 20892 USA.
EM pmeltzer@mail.nih.gov
OI Davis, Sean/0000-0002-8991-6458
FU Cure Cancer Australia Foundation; National Health and Medical Research
Council [306700]; National Breast Cancer Foundation Scholarship; Estee
Lauder group of companies; The University of Sydney; The Australian
Federation of University Women-South Australia Inc; Cancer Institute New
South Wales Research; National Health and Medical Research Council
FX Project grant support from the Cure Cancer Australia Foundation and
National Health and Medical Research Council project grant 306700 (R.L.
Balleine, L.R.Webster, and C.L. Clarke). L.R.Webster was recipient of a
National Breast Cancer Foundation Scholarship (supported by the Estee
Lauder group of companies) and travel grants from The University of
Sydney (Grants-in-Aid) and The Australian Federation of University
Women-South Australia Inc. Trust Fund (Jean Gilmore Bursary). She was a
Cancer Institute New South Wales Research Scholar. R.L. Balleine is a
Cancer Institute New South Wales Fellow, and C.L. Clarke a Principal
Research Fellow of the National Health and Medical Research Council.
NR 39
TC 27
Z9 30
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 15
PY 2008
VL 14
IS 24
BP 8244
EP 8252
DI 10.1158/1078-0432.CCR-08-0939
PG 9
WC Oncology
SC Oncology
GA 384ZL
UT WOS:000261782600034
PM 19088042
ER
PT J
AU Chumakov, K
Ehrenfeld, E
AF Chumakov, Konstantin
Ehrenfeld, Ellie
TI New Generation of Inactivated Poliovirus Vaccines for Universal
Immunization after Eradication of Poliomyelitis
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID SYNONYMOUS CODON USAGE; ATTENUATED POLIOVIRUS; PROTECTIVE PROPERTIES;
SABIN STRAINS; UNITED-STATES; VIRUS; IMMUNOGENICITY; VACCINATION; CELLS;
DEOPTIMIZATION
AB Twenty years of global polio eradication efforts may soon eliminate the transmission of wild-type poliovirus. However, new information that has been learned about poliovirus, as well as the political realities of a modern world, demand that universal immunity against poliomyelitis be maintained, even after wild-type poliovirus is eradicated. Although 2 excellent vaccines have proven to be highly effective in the past, neither the live-attenuated vaccine nor the currently used inactivated vaccine are optimal for use in the posteradication era. Therefore, concerted efforts are urgently needed to develop a new generation of vaccine that is risk-free and affordable and can be produced on a global scale. Here, we discuss the desired properties of a vaccine and methods to create a new polio vaccine.
C1 [Chumakov, Konstantin] US FDA, Off Vaccine Res & Review, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA.
[Ehrenfeld, Ellie] NIAID, NIH, Bethesda, MD 20892 USA.
RP Chumakov, K (reprint author), US FDA, Off Vaccine Res & Review, Ctr Biol Evaluat & Res, 1401 Rockville Pike HFM-470, Rockville, MD 20852 USA.
EM konstantin.chumakov@fda.hhs.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health; US Food and Drug Administration; US Department of
Health and Human Services
FX National Institute of Allergy and Infectious Diseases, National
Institutes of Health; US Food and Drug Administration; and US Department
of Health and Human Services.
NR 57
TC 29
Z9 32
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD DEC 15
PY 2008
VL 47
IS 12
BP 1587
EP 1592
DI 10.1086/593310
PG 6
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 376DO
UT WOS:000261163600020
PM 18990066
ER
PT J
AU Ramanathan, R
Pau, AK
Busse, KH
Zemskova, M
Nieman, L
Kwan, R
Hammer, JH
Mican, JM
Maldarelli, F
AF Ramanathan, Roshan
Pau, Alice K.
Busse, Kristin H.
Zemskova, Marina
Nieman, Lynnette
Kwan, Richard
Hammer, Jean H.
Mican, JoAnn M.
Maldarelli, Frank
TI Iatrogenic Cushing Syndrome after Epidural Triamcinolone Injections in
an HIV Type 1-Infected Patient Receiving Therapy with
Ritonavir-Lopinavir
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID MECHANISM-BASED INHIBITION; IN-VITRO; PHARMACOKINETICS; PREDNISONE; 3A4
AB We report the first case of a human immunodeficiency virus type 1 (HIV-1)-infected individual receiving combination antiretroviral therapy, which included ritonavir, who developed Cushing syndrome with profound complications after epidural triamcinolone injections. This case highlights the potential of ritonavir interactions even with local injections of a corticosteroid.
C1 [Ramanathan, Roshan] NIAID, Helminth Immunol Sect, Parasit Dis Lab, Bethesda, MD 20892 USA.
[Ramanathan, Roshan] NIAID, Clin Parasitol Unit, Bethesda, MD 20892 USA.
[Pau, Alice K.; Kwan, Richard; Hammer, Jean H.; Mican, JoAnn M.] NIAID, Div Clin Res, Bethesda, MD 20892 USA.
[Busse, Kristin H.] Clin Pharmacokinet Res Lab, Warren G Magnuson Clin Ctr, Dept Pharm, Bethesda, MD USA.
[Zemskova, Marina; Nieman, Lynnette] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program Reprod & Adult Endocrinol, Bethesda, MD USA.
[Maldarelli, Frank] NCI, HIV Drug Resistance Program, NIH, Bethesda, MD 20892 USA.
RP Ramanathan, R (reprint author), NIAID, Helminth Immunol Sect, Parasit Dis Lab, 4 Ctr Dr,Bldg 4,Rm B1-05, Bethesda, MD 20892 USA.
EM ramanathanr@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National Cancer
Institute; National Institute of Child Health and Human Development,
National Institutes of Health
FX National Institute of Allergy and Infectious Diseases, National Cancer
Institute, and National Institute of Child Health and Human Development,
National Institutes of Health.
NR 12
TC 16
Z9 16
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD DEC 15
PY 2008
VL 47
IS 12
BP E97
EP E99
DI 10.1086/593314
PG 3
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 376DO
UT WOS:000261163600036
PM 18991509
ER
PT J
AU Trzeciak, AR
Barnes, J
Ejiogu, N
Foster, K
Brant, LJ
Zonderman, AB
Evans, MK
AF Trzeciak, Andrzej R.
Barnes, Janice
Ejiogu, Ngozi
Foster, Kamala
Brant, Larry J.
Zonderman, Alan B.
Evans, Michele K.
TI Age, sex, and race influence single-strand break repair capacity in a
human population
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE SSB repair capacity; SSB repair kinetics; DNA repair; Comet assay;
gamma-irradiation; Cryopreserved lymphocytes; Oxidative DNA damage;
Reference standards; Biomonitoring study; Dispersion coefficient H;
Coefficient of variation
ID INDUCED DNA-DAMAGE; ALKALINE COMET ASSAY; IONIZING-RADIATION;
CANCER-PATIENTS; LUNG-CANCER; MOLECULAR EPIDEMIOLOGY;
HEALTHY-INDIVIDUALS; HUMAN-LYMPHOCYTES; CELLS; SENSITIVITY
AB Recently, we developed an improved comet assay protocol for evaluating single-strand break repair capacity (SSB-RC) in Unstimulated cryopreserved human peripheral blood mononuclear cells (PBMCs). This methodology facilitates control of interexperimental variability [A.R. Trzeciak, J. Barnes, M.K. Evans, A modified alkaline comet assay for measuring DNA repair capacity in human populations. Radiat. Res. 169 (2008) 110-121]. The fast component of SSB repair (F-SSB-RC) was assessed using a novel parameter, the initial rate of DNA repair, and the widely used half-time of DNA repair. The slow component of SSB repair (S-SSB-RC) was estimated using the residual DNA damage after 60 min. We have examined repair of gamma-radiation-induced DNA damage in PBMCs from four age-matched groups of male and female whites and African-Americans between ages 30 and 64. There is an increase in F-SSB-RC with age in white females (P<0.01) and nonsignificant decrease in F-SSB-RC in African-American females (P=0.061). F-SSB-RC is lower in white females than in white males (P<0.01). There is a decrease in F-SSB-RC with age in African-American females as compared to white females (P<0.002) and African-American males (nonsignificant, P=0.059). Age, sex, and race had a similar effect on intercellular variability of DNA damage in gamma-irradiated and repairing PBMCs. Our findings suggest that age, sex, and race influence SSB-RC as measured by the alkaline comet assay. SSB-RC may be a useful clinical biomarker. Published by Elsevier Inc.
C1 [Trzeciak, Andrzej R.; Barnes, Janice; Evans, Michele K.] NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
[Ejiogu, Ngozi; Foster, Kamala; Evans, Michele K.] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Brant, Larry J.; Zonderman, Alan B.] NIA, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
RP Evans, MK (reprint author), NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
EM evansmi@grc.nia.nih.gov
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural Research Program of the NIH; National Institute on Aging
FX We thank Drs. Michael J. Pazin and Patrice J. Morin for valuable
discussions. We thank to Althaf Lohani for technical assistance. We also
thank nurses Catherine Sackett, Mary Sam-Nwoha, and Patricia
Julien-Williams who work in the HANDLS study for their careful
assessment of the participants and the acquisition of clinical samples.
This research was Supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 42
TC 14
Z9 17
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC 15
PY 2008
VL 45
IS 12
BP 1631
EP 1641
DI 10.1016/j.freeradbiomed.2008.08.031
PG 11
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 384CL
UT WOS:000261721800004
PM 18845243
ER
PT J
AU Knight, MA
Hernandez, D
Diede, SJ
Dauwerse, HG
Rafferty, I
van de Leemput, J
Forrest, SM
Gardner, RJM
Storey, E
van Ommen, GJB
Tapscott, SJ
Fischbeck, KH
Singleton, AB
AF Knight, Melanie A.
Hernandez, Dena
Diede, Scott J.
Dauwerse, Hans G.
Rafferty, Ian
van de Leemput, Joyce
Forrest, Susan M.
Gardner, R. J. McKinlay
Storey, Elsdon
van Ommen, Gert-Jan B.
Tapscott, Stephen J.
Fischbeck, Kenneth H.
Singleton, Andrew B.
TI A duplication at chromosome 11q12.2-11q12.3 is associated with
spinocerebellar ataxia type 20
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOMIC STRUCTURE; CDNA CLONING; GENE; LOCALIZATION; MUTATIONS; PROTEIN;
DISORDERS; AMPLIFICATION; EXPRESSION; DELETION
AB Spinocerebellar ataxia type 20 (SCA20) has been linked to chromosome 11q12, but the underlying genetic defect has yet to be identified. We applied single-nucleotide polymorphism genotyping to detect structural alterations in the genomic DNA of patients with SCA20. We found a 260 kb duplication within the previously linked SCA20 region, which was confirmed by quantitative polymerase chain reaction and fiber fluorescence in situ hybridization, the latter also showing its direct orientation. The duplication spans 10 known and 2 unknown genes, and is present in all affected individuals in the single reported SCA20 pedigree. While the mechanism whereby this duplication may be pathogenic remains to be established, we speculate that the critical gene within the duplicated segment may be DAGLA, the product of which is normally present at the base of Purkinje cell dendritic spines and contributes to the modulation of parallel fiber-Purkinje cell synapses.
C1 [Knight, Melanie A.; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Hernandez, Dena; Rafferty, Ian; van de Leemput, Joyce; Singleton, Andrew B.] NIA, Mol Genet Unit, NIH, Bethesda, MD 20892 USA.
[Diede, Scott J.] Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
[Diede, Scott J.; Tapscott, Stephen J.] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98104 USA.
[Dauwerse, Hans G.; van Ommen, Gert-Jan B.] Leiden Univ, Med Ctr, Dept Human & Clin Genet, Leiden, Netherlands.
[Forrest, Susan M.] Walter & Eliza Hall Inst Med Res, Australian Genome Res Facil, Melbourne, Vic 3050, Australia.
[Gardner, R. J. McKinlay; Storey, Elsdon] Genet Hlth Serv Victoria, Melbourne, Vic, Australia.
[Gardner, R. J. McKinlay] Royal Childrens Hosp, Murdoch Childrens Res Inst, Melbourne, Vic, Australia.
[Storey, Elsdon] Monash Univ, Dept Med Neurosci, Melbourne, Vic 3004, Australia.
RP Knight, MA (reprint author), NHGRI, Med Genet Branch, Sect Mol Neurogenet, NIH, Bldg 35,Room 1A105,35 Convent Dr,MSC 3708, Bethesda, MD 20894 USA.
EM knightme@mail.nih.gov
RI Singleton, Andrew/C-3010-2009; Storey, Elsdon/A-9889-2013; Diede,
Scott/G-2288-2012
OI Diede, Scott/0000-0001-5422-549X
FU Intramural Research Programs of the National Institute on Aging [1 Z01
AG000949-02]; National Institute of Neurological Disorders and Stroke;
National Institutes of Health, Department of Health and Human Services,
USA; NINDS Competitive Postdoctoral Fellowship; National Institute on
Aging [Z01 AG000957-05]; Pediatric Oncology Research Training Program,
National Institutes of Health [2T32CA009351-29]
FX The research was funded in part by the Intramural Research Programs of
the National Institute on Aging ( project number 1 Z01 AG000949-02) and
the National Institute of Neurological Disorders and Stroke, both of the
National Institutes of Health, Department of Health and Human Services,
USA. M. A. K. was supported by a NINDS Competitive Postdoctoral
Fellowship. The National Institute on Aging project number associated
with this work is Z01 AG000957-05. S. J. D. was supported by a Pediatric
Oncology Research Training Program, National Institutes of Health
2T32CA009351-29.
NR 34
TC 25
Z9 26
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 15
PY 2008
VL 17
IS 24
BP 3847
EP 3853
DI 10.1093/hmg/ddn283
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 377VQ
UT WOS:000261280300002
PM 18801880
ER
PT J
AU Douillard-Guilloux, G
Raben, N
Takikita, S
Batista, L
Caillaud, C
Richard, E
AF Douillard-Guilloux, Gaelle
Raben, Nina
Takikita, Shoichi
Batista, Lionel
Caillaud, Catherine
Richard, Emmanuel
TI Modulation of glycogen synthesis by RNA interference: towards a new
therapeutic approach for glycogenosis type II
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID ACID ALPHA-GLUCOSIDASE; ENZYME-REPLACEMENT THERAPY; DISEASE TYPE-II;
FINE STRUCTURAL ASPECTS; POMPE-DISEASE; GAUCHER-DISEASE; MUSCLE
GLYCOGEN; MOUSE MODEL; IN-VIVO; HEPATIC GLYCOGEN
AB Glycogen storage disease type II (GSDII) or Pompe disease is an autosomal recessive disorder caused by defects in the acid alpha-glucosidase gene, which leads to lysosomal glycogen accumulation and enlargement of the lysosomes mainly in cardiac and muscle tissues, resulting in fatal hypertrophic cardiomyopathy and respiratory failure in the most severely affected patients. Enzyme replacement therapy has already proven to be beneficial in this disease, but correction of pathology in skeletal muscle still remains a challenge. As substrate deprivation was successfully used to improve the phenotype in other lysosomal storage disorders, we explore here a novel therapeutic approach for GSDII based on a modulation of muscle glycogen synthesis. Short hairpin ribonucleic acids (shRNAs) targeted to the two major enzymes involved in glycogen synthesis, i.e. glycogenin (shGYG) and glycogen synthase (shGYS), were selected. C2C12 cells and primary myoblasts from GSDII mice were stably transduced with lentiviral vectors expressing both the shRNAs and the enhanced green fluorescent protein (EGFP) reporter gene. Efficient and specific inhibition of GYG and GYS was associated not only with a decrease in cytoplasmic and lysosomal glycogen accumulation in transduced cells, but also with a strong reduction in the lysosomal size, as demonstrated by confocal microscopy analysis. A single intramuscular injection of recombinant AAV-1 (adeno-associated virus-1) vectors expressing shGYS into newborn GSDII mice led to a significant reduction in glycogen accumulation, demonstrating the in vivo therapeutic efficiency. These data offer new perspectives for the treatment of GSDII and could be relevant to other muscle glycogenoses.
C1 [Caillaud, Catherine] Univ Paris 05, Dept Genet & Dev, Inst Cochin, CNRS,UMR 8104, F-75014 Paris, France.
[Douillard-Guilloux, Gaelle; Batista, Lionel; Caillaud, Catherine; Richard, Emmanuel] INSERM, U567, Paris, France.
[Raben, Nina; Takikita, Shoichi] NIH, Bethesda, MD 20892 USA.
RP Caillaud, C (reprint author), Univ Paris 05, Dept Genet & Dev, Inst Cochin, CNRS,UMR 8104, 24 Rue Faubourg St Jacques, F-75014 Paris, France.
EM catherine.caillaud@inserm.fr
FU INSERM; Association Vaincre les Maladies Lysosomales; VML; Association
Francaise contre les Myopathies; Genzyme (France); AFM
FX This work was supported by INSERM and the Association Vaincre les
Maladies Lysosomales (VML). E. R. was supported by post-doctoral
fellowships from VML and the Association Francaise contre les Myopathies
(AFM). G. D. was supported by doctoral fellowship from Genzyme (France)
and AFM.
NR 46
TC 19
Z9 19
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 15
PY 2008
VL 17
IS 24
BP 3876
EP 3886
DI 10.1093/hmg/ddn290
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 377VQ
UT WOS:000261280300005
PM 18782850
ER
PT J
AU Raben, N
Hill, V
Shea, L
Takikita, S
Baum, R
Mizushima, N
Ralston, E
Plotz, P
AF Raben, Nina
Hill, Victoria
Shea, Lauren
Takikita, Shoichi
Baum, Rebecca
Mizushima, Noboru
Ralston, Evelyn
Plotz, Paul
TI Suppression of autophagy in skeletal muscle uncovers the accumulation of
ubiquitinated proteins and their potential role in muscle damage in
Pompe disease
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID ACID ALPHA-GLUCOSIDASE; ENZYME REPLACEMENT THERAPY; GLYCOGEN AUTOPHAGY;
STORAGE-DISEASE; GENE-EXPRESSION; SELF-DIGESTION; NEWBORN RATS; MOUSE
MODEL; CELL-DEATH; MICE
AB The role of autophagy, a catabolic lysosome-dependent pathway, has recently been recognized in a variety of disorders, including Pompe disease, the genetic deficiency of the glycogen-degrading lysosomal enzyme acid-alpha glucosidase. Accumulation of lysosomal glycogen, presumably transported from the cytoplasm by the autophagic pathway, occurs in multiple tissues, but pathology is most severe in skeletal and cardiac muscle. Skeletal muscle pathology also involves massive autophagic buildup in the core of myofibers. To determine if glycogen reaches the lysosome via autophagy and to ascertain whether autophagic buildup in Pompe disease is a consequence of induction of autophagy and/or reduced turnover due to defective fusion with lysosomes, we generated muscle-specific autophagy-deficient Pompe mice. We have demonstrated that autophagy is not required for glycogen transport to lysosomes in skeletal muscle. We have also found that Pompe disease involves induction of autophagy but manifests as a functional deficiency of autophagy because of impaired autophagosomal-lysosomal fusion. As a result, autophagic substrates, including potentially toxic aggregate-prone ubiquitinated proteins, accumulate in Pompe myofibers and may cause profound muscle damage.
C1 [Raben, Nina; Hill, Victoria; Shea, Lauren; Takikita, Shoichi; Baum, Rebecca; Plotz, Paul] NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA.
[Ralston, Evelyn] NIAMSD, Light Imaging Sect, Off Sci & Technol, NIH, Bethesda, MD 20892 USA.
[Mizushima, Noboru] Tokyo Med & Dent Univ, Dept Physiol & Cell Biol, Tokyo, Japan.
RP Raben, N (reprint author), NIAMS, NIH, 50 S Dr,Bld 50-1345, Bethesda, MD 20892 USA.
EM rabenn@arb.niams.nih.gov
RI Mizushima, Noboru/C-3635-2009
OI Mizushima, Noboru/0000-0002-6258-6444
FU National Institutes of Health; CRADA; Genzyme Corporation (Framingham,
MA)
FX This research was supported by the Intramural Research Program of the
National Institute of Arthritis and Musculoskeletal and Skin Diseases of
the National Institutes of Health. S. T. was supported in part by a
CRADA between the NIH and Genzyme Corporation (Framingham, MA).
NR 60
TC 141
Z9 146
U1 1
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 15
PY 2008
VL 17
IS 24
BP 3897
EP 3908
DI 10.1093/hmg/ddn292
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 377VQ
UT WOS:000261280300007
PM 18782848
ER
PT J
AU Domene, S
Roessler, E
El-Jaick, KB
Snir, M
Brown, JL
Velez, JI
Bale, S
Lacbawan, F
Muenke, M
Feldman, B
AF Domene, Sabina
Roessler, Erich
El-Jaick, Kenia B.
Snir, Mirit
Brown, Jamie L.
Velez, Jorge I.
Bale, Sherri
Lacbawan, Felicitas
Muenke, Maximilian
Feldman, Benjamin
TI Mutations in the human SIX3 gene in holoprosencephaly are loss of
function
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID EYE DEVELOPMENT; FOREBRAIN DEVELOPMENT; MOLECULAR NATURE; NEURAL PLATE;
SINE-OCULIS; ZEBRAFISH; EXPRESSION; WNT; REPRESSOR; FAMILY
AB Holoprosencephaly (HPE) is the most common developmental anomaly of the human forebrain; however, the genetics of this heterogeneous and etiologically complex malformation is incompletely understood. Heterozygous mutations in SIX3, a transcription factor gene expressed in the anterior forebrain and eyes during early vertebrate development, have been frequently detected in human HPE cases. However, only a few mutations have been investigated with limited functional studies that would confirm a role in HPE pathogenesis. Here, we report the development of a set of robust and sensitive assays of human SIX3 function in zebrafish and apply these to the analysis of a total of 46 distinct mutations (19 previously published and 27 novel) located throughout the entire SIX3 gene. We can now confirm that 89% of these putative deleterious mutations are significant loss-of-function alleles. Since disease-associated single point mutations in the Groucho-binding eh1-like motif decreases the function in all assays, we can also confirm that this interaction is essential for human SIX3 co-repressor activity; we infer, in turn, that this function is important in HPE causation. We also unexpectedly detected truncated versions with partial function, yet missing a SIX3-encoded homeodomain. Our data indicate that SIX3 is a frequent target in the pathogenesis of HPE and demonstrate how this can inform the genetic counseling of families.
C1 [Feldman, Benjamin] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Bale, Sherri] GeneDx, Gaithersburg, MD 20877 USA.
RP Feldman, B (reprint author), NHGRI, Med Genet Branch, NIH, 35 Convent Dr,MSC 3717 Bldg 35,Room 1B-205, Bethesda, MD 20892 USA.
EM bfeldman@mail.nih.gov
OI Feldman, Benjamin/0000-0003-4838-8641
FU Division of Intramural Research; NHGRI; NIH, USA
FX This work was supported in part by the Division of Intramural Research,
NHGRI, NIH, USA.
NR 43
TC 29
Z9 30
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 15
PY 2008
VL 17
IS 24
BP 3919
EP 3928
DI 10.1093/hmg/ddn294
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 377VQ
UT WOS:000261280300009
PM 18791198
ER
PT J
AU Zhu, H
Glasgow, W
George, MD
Chrysovergis, K
Olden, K
Roberts, JD
Eling, T
AF Zhu, Hong
Glasgow, Wayne
George, Margaret D.
Chrysovergis, Kali
Olden, Kenneth
Roberts, John D.
Eling, Thomas
TI 15-Lipoxygenase-1 activates tumor suppressor p53 independent of
enzymatic activity
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE 15-lipoxygenase-1; the tumor suppressor p53; DNA-dependent protein
kinase; p53 phosphorylation; HCT-116 cells
ID COLORECTAL-CANCER CELLS; DAMAGE-INDUCED PHOSPHORYLATION; DEPENDENT
PROTEIN-KINASE; CARCINOMA CACO-2 CELLS; DRUG-INDUCED APOPTOSIS;
DOWN-REGULATION; EXPRESSION; 12-LIPOXYGENASE; OVEREXPRESSION;
IDENTIFICATION
AB 15-LOX-1 and its metabolites are involved in colorectal cancer. Recently, we reported that 15-LOX-1 overexpression in HCT-116 human colorectal cancer cells inhibited cell growth by induction of p53 phosphorylation (4). To determine whether the 15-LOX-1 protein or its metabolites are responsible for phosphorylation of p53 in HCT-116 cells, we used HCT-116 cells that expressed a mutant 15-LOX-1. The mutant 15-LOX-1 enzyme, with a substitution of Leu at residue His361, was devoid of enzymatic activity. HCT-116 cells transiently transfected with either native or mutant 15-LOX-1 showed an increase in p53 phosphorylation and an increase in the expression of downstream genes. Thus, 15-LOX-1 induces p53 phosphorylation independent of enzymatic activity. Treatment of A549 human lung carcinoma cells with IL-4 increased the expression of 15-LOX-1 and also increased the expression of downstream targets of p53. This confirmed that the activation of p53 was also observed in wild-type cells expressing physiological 15-LOX-1. Immunoprecipitation experiments revealed that 15-LOX-1 interacts with, and binds to, DNA-dependent protein kinase (DNA-PK). The binding of 15-LOX-1 to DNA-PK caused an approximate 3.0-fold enhancement in kinase activity, resulting in increased p53 phosphorylation at Ser15. Knockdown of DNA-PK by small interfering RN A (siRNA) significantly reduced p53 phosphorylation. Furthermore, confocal microscopy demonstrated a colocalization of 15-LOX and DNA-PK in the cells. We propose that the 15-LOX-1 protein binds to DNA-PK, increasing its kinase activity and results in downstream activation of the tumor suppressor p53, thus revealing a new mechanism by which lipoxygenases (LOX) may influence the phenotype of tumor cells. Published 2008 Wiley-Liss, Inc.
C1 [Zhu, Hong; Chrysovergis, Kali; Eling, Thomas] NIEHS, Mol Carcinogenesis Lab, NIH, Eicosanoid Biochem Sect,DHHS, Res Triangle Pk, NC 27709 USA.
[Glasgow, Wayne] Mercer Univ, Sch Med, Macon, GA 31207 USA.
[George, Margaret D.; Olden, Kenneth; Roberts, John D.] NIEHS, Metastasis Sect, Mol Carcinogenesis Lab, NIH,DHHS, Res Triangle Pk, NC USA.
RP Eling, T (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Eicosanoid Biochem Sect,DHHS, MD E4-09,111 TW Alexander Driver, Res Triangle Pk, NC 27709 USA.
EM eling@niehs.nih.gov
FU National Institute of Environmental Health Sciences, NIH (Intramural
Research Program)
FX Grant sponsor: National Institute of Environmental Health Sciences, NIH
(Intramural Research Program).
NR 42
TC 9
Z9 10
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 15
PY 2008
VL 123
IS 12
BP 2741
EP 2749
DI 10.1002/ijc.23855
PG 9
WC Oncology
SC Oncology
GA 375KO
UT WOS:000261112900003
PM 18785202
ER
PT J
AU Bluhm, E
McNeil, DE
Cnattingius, S
Gridley, G
El Ghormli, L
Fraumeni, JF
AF Bluhm, Elizabeth
McNeil, Dawn Elizabeth
Cnattingius, Sven
Gridley, Gloria
El ghormli, Laure
Fraumeni, Joseph F., Jr.
TI Prenatal and perinatal risk factors for neuroblastoma
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE neuroblastoma; prenatal; delayed effects; prenatal exposure; anemia;
case-control study
ID CHILDHOOD-CANCER; NEURO-BLASTOMA; BIRTH CHARACTERISTICS; MEDICATION USE;
CONGENITAL-ANOMALIES; YOUNG-CHILDREN; BRAIN-TUMORS; PREGNANCY;
ASSOCIATION; DEFECTS
AB Neuroblastoma is a rare embryonal tumor of childhood for which risk factors are not well known. Using a nested case-control design, we investigated prenatal, perinatal and neonatal risk factors in detail by linking 245 pediatric neuroblastoma cases identified in the Swedish Cancer Register diagnosed in the year 1973-1995 with the Swedish Medical Birth Register. Five living controls per case were randomly selected from the birth registry, matched by gender and age. Increased risks were associated with maternal anemia during pregnancy (odds ratio (OR) = 2.95, 95% confidence interval (CI): 1.53, 5.69), neonatal respiratory distress (OR = 3.61, 95% CI: 1.41, 9.24) and low (below or equal to 7) 1-min Apgar score (OR = 2.23, 95% CI: 1.41, 3.52). Increased risks were limited to cases diagnosed before 1 year of age. Markers of prenatal, perinatal and neonatal distress may be associated with neuroblastoma in infancy, but not with diagnoses at 1 year or above. Published 2008 Wiley-Liss, Inc.
C1 [Bluhm, Elizabeth] Washington Hosp Ctr, Gen Internal Med Sect, Washington, DC 20010 USA.
[Bluhm, Elizabeth] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[McNeil, Dawn Elizabeth] US FDA, Div Neurol Drug Prod, Silver Spring, MD USA.
[Cnattingius, Sven] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Gridley, Gloria] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[El ghormli, Laure] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Fraumeni, Joseph F., Jr.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Bluhm, E (reprint author), Washington Hosp Ctr, Gen Internal Med Sect, POB 1A-50,110 Irving St NW, Washington, DC 20010 USA.
EM elizabeth.c.bluhm@medstar.net
FU Intramural Research Program of the NIH, National Cancer Institute,
Division of Cancer Epidemiology and Genetics
FX Grant sponsor: Intramural Research Program of the NIH, National Cancer
Institute, Division of Cancer Epidemiology and Genetics.
NR 53
TC 14
Z9 14
U1 1
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 15
PY 2008
VL 123
IS 12
BP 2885
EP 2890
DI 10.1002/ijc.23847
PG 6
WC Oncology
SC Oncology
GA 375KO
UT WOS:000261112900021
PM 18798548
ER
PT J
AU Mirochnick, M
Best, BM
Stek, AM
Capparelli, E
Hu, CC
Burchett, SK
Holland, DT
Smith, E
Gaddipati, S
Read, JS
AF Mirochnick, Mark
Best, Brookie M.
Stek, Alice M.
Capparelli, Edmund
Hu, Chengcheng
Burchett, Sandra K.
Holland, Diane T.
Smith, Elizabeth
Gaddipati, Sreedhar
Read, Jennifer S.
CA PACTG 1026s Study Team
TI Lopinavir Exposure With an Increased Dose During Pregnancy
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV; lopinavir; mother-to-child transmission; pharmacokinetics;
pregnancy
ID INHIBITOR-EXPERIENCED PATIENTS; RITONAVIR; ANTIRETROVIRALS; WOMEN
AB Background: Use of standard adult lopinavir/ritonavir (LPV/RTV) closing (400/100 mg) during the third trimester of pregnancy results in reduced LPV exposure. The goal of this study was to determine LPV exposure during the third trimester of pregnancy and 2 weeks postpartum with a higher LPV/RTV dose.
Methods: The Pediatric AIDS Clinical Trials Group protocol 1026s is all ongoing, prospective, nonblinded study of antiretroviral pharmacokinetics in HIV-infected pregnant women that included a cohort receiving LPV/RTV 400/100 mg twice daily during the second trimester and 533/133 mg twice daily during the third trimester through 2 weeks postpartum. Intensive steady state 12-hour pharmacokinetic profiles were performed during the third trimester and at 2 weeks postpartum and were optional during the second trimester. LPV and RTV were measured by reverse-phase high-performance liquid chromatography with a detection limit of 0.09 mu g/mL.
Results: Twenty-six HIV-infected pregnant women were studied. Median LPV area under the plasma concentration-time curve (AUCs) for the second trimester, third trimester, and postpartum were 57, 88, and 152 respectively. Median minimum LPV concentrations were 1.9, 4.1, and 8.3 mu g/mL.
Conclusions: The higher LPV/RTV dose (533/133 mg) provided LPV exposure during the third trimester similar to the median AUC (80 mu g.h(-1).mL(-1)) in nonpregnant adults taking standard doses. However, the AUC on this increased dose at 2 weeks postpartum was considerably higher. These data Suggest that the higher LPV/RTV dose should be used in third trimester pregnant women; that it should be considered in second trimester pregnant women, especially those who are protease inhibitor experienced; and that postpartum LPV/RTV dosing can be reduced to standard closing by 2 weeks after delivery.
C1 [Mirochnick, Mark] Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA.
[Best, Brookie M.; Capparelli, Edmund; Holland, Diane T.] Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA.
[Best, Brookie M.; Capparelli, Edmund; Holland, Diane T.] Univ Calif San Diego, Sch Pharm, San Diego, CA USA.
[Best, Brookie M.; Capparelli, Edmund; Holland, Diane T.] Univ Calif San Diego, Sch Pharmaceut Sci, San Diego, CA USA.
[Stek, Alice M.] Univ So Calif, Sch Med, Dept Obstet & Gynecol, Los Angeles, CA 90033 USA.
[Hu, Chengcheng] Harvard Univ, Sch Publ Hlth, Stat & Data Anal Ctr, Boston, MA 02115 USA.
[Burchett, Sandra K.] Childrens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Smith, Elizabeth] NIAID, Bethesda, MD 20892 USA.
[Gaddipati, Sreedhar] Columbia Univ Coll Phys & Surg, Dept Obstet & Gynecol, New York, NY 10032 USA.
[Read, Jennifer S.] NICHHD, Pediat Adolescent & Maternal AIDS Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Mirochnick, M (reprint author), Boston Med Ctr, Yawkey 2N-06, Boston, MA 02118 USA.
EM markm@bu.edu
RI Hu, Chengcheng/A-8391-2017
FU Pediatric AIDS Clinical Trials Group; National Institute of Allergy and
Infections Diseases [U01 A104189, U01 A141089, UOI A127560-18, U01
AI32907]; General Clinical Research Center Units; National Center for
Research Resources [MOI RR00069, M01 RR00533, M01 RR01271];
Pediatric/Perinatal HIV Clinical Trials Network; National Institute of
Child Health and Human Development [N01-HD-3-3365]
FX Supported in part by the Pediatric AIDS Clinical Trials Group of the
National Institute of Allergy and Infections Diseases (Grants U01
A104189, U01 A141089, UOI A127560-18, and U01 AI32907), the General
Clinical Research Center Units funded by the National Center for
Research Resources (Grants MOI RR00069, M01 RR00533, and M01 RR01271),
and by the Pediatric/Perinatal HIV Clinical Trials Network of the
National Institute of Child Health and Human Development (Contract
N01-HD-3-3365).
NR 18
TC 46
Z9 46
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD DEC 15
PY 2008
VL 49
IS 5
BP 485
EP 491
DI 10.1097/QAI.0b013e318186edd0
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 376YN
UT WOS:000261219000004
PM 18989231
ER
PT J
AU Robertson, SM
Maldarelli, F
Natarajan, V
Formentini, E
Alfaro, RM
Penzak, SR
AF Robertson, Sarah M.
Maldarelli, Frank
Natarajan, Ven
Formentini, Elizabeth
Alfaro, Raul M.
Penzak, Scott R.
TI Efavirenz Induces CYP2B6-Mediated Hydroxylation of Bupropion in Healthy
Subjects
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE efavirenz; bupropion; metabolism; CYP2B6; drug interaction; induction
ID CYTOCHROME P4502B6 ACTIVITY; POTENTIAL-DRUG INTERACTIONS; IN-VITRO;
HUMAN LIVER; POPULATION PHARMACOKINETICS; CATALYTIC-ACTIVITY; CYP2B6;
METABOLISM; POLYMORPHISM; SUBSTRATE
AB Objective: To characterize the effect of efavirenz on bupropion hydroxylation as a marker of cytochrome P450 (CYP) 2136 activity in healthy subjects.
Methods: Thirteen subjects received a single oral dose of bupropion SR 150 mg before and after 2 weeks of efavirenz administration for comparison of bupropion and hydroxybupropion pharmacokinetics. Efavirenz plasma concentrations were also assessed. Subjects were genotyped for CYP2B6 (G516T, C1459T, and A785G), CYP3A4 (A-392G), CYP3A5 (A6986G), and multidrug resistance protein 1 (C3435T).
Results: The area under the concentration vs. time curve ratio of hydroxybupropion: bupropion increased 2.3-fold after efavirenz administration (P = 0.0001). Bupropion area under the concentration vs. time curve and C(max) decreased by 55% and 34%, respectively (P < 0.002). None of the CYP2B6 or CYP3A genotypes evaluated were associated with a difference in bupropion or efavirenz clearance. The 2 individuals homozygous for multidrug resistance protein 1 3435-T/T had 2.5- and 1.8-fold greater bupropion and efavirenz clearance, respectively, relative to C/C and C/T individuals (P < 0.05).
Conclusions: Our results confirm that efavirenz induces CYP2B6 enzyme activity in vivo, as demonstrated by an increase in bupropion hydroxylation after 2 weeks of efavirenz administration.
C1 [Robertson, Sarah M.] US FDA, Off Clin Pharmacol, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
[Maldarelli, Frank] Natl Canc Inst, HIV Drug Resistance Program, Frederick, MD USA.
[Natarajan, Ven] Natl Canc Inst, SAIC Frederick, Mol Cell Biol Lab, Frederick, MD USA.
[Formentini, Elizabeth] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Alfaro, Raul M.; Penzak, Scott R.] NIH, Clin Res Ctr, Dept Pharm, Bethesda, MD 20892 USA.
RP Robertson, SM (reprint author), US FDA, Off Clin Pharmacol, Ctr Drug Evaluat & Res, Bldg 21,Room 4653,10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM sarah.robertson@fda.hhs.gov
FU Society of Infectious Diseases Pharmacists/Pfizer Award; Research in
Infectious Disease Phamacotherapy
FX Supported by the Society of Infectious Diseases Pharmacists/Pfizer Award
for Research in Infectious Disease Phamacotherapy; awarded December
2005.
NR 39
TC 37
Z9 37
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD DEC 15
PY 2008
VL 49
IS 5
BP 513
EP 519
DI 10.1097/QAI.0b013e318183a425
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 376YN
UT WOS:000261219000008
PM 18989234
ER
PT J
AU Guanira, JV
Casper, C
Lama, JR
Morrow, R
Montano, SM
Caballero, P
Suarez, L
Whittington, WLH
Wald, A
Sanchez, J
Celum, C
AF Guanira, Juan V.
Casper, Corey
Lama, Javier R.
Morrow, Rhoda
Montano, Silvia M.
Caballero, Patricia
Suarez, Luis
Whittington, William L. H.
Wald, Anna
Sanchez, Jorge
Celum, Connie
CA Peruvian HIV Sentinel Surveillance
TI Prevalence and Correlates of Human Herpesvirus 8 Infection Among
Peruvian Men Who Have Sex With Men
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE human herpesvirus 8; homosexual men; HIV; Peru; sexually transmitted
infections
ID KAPOSIS-SARCOMA; TESTING STRATEGY; BLOOD-DONORS; RISK-FACTORS; HIV;
ANTIBODIES; SEROPREVALENCE; POPULATIONS; BRAZIL; HHV-8
AB Background: Infection with human herpesvirus 8 (HHV-8) is common among men who have sex with men (MSM) in North America and Europe and is also found to be endemic in some regions Of South America. Little is known about HHV-8 prevalence and its correlates among MSM in the Andean region.
Methods: We assessed HHV-8 seroprevalence among 497 MSM recruited for the 2002 Peruvian HIV sentinel surveillance program using a combined HHV-8 enzyme immunoassay and immunofluorescence assay algorithm. Logistic regression analysis was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs) to determine the association between selected covariates and HHV-8 scropositivity.
Results: One hundred thirty-one (66.5%, 95% CI 63.1%, to 69.9%) of 197 HIV-infected and 80 (26.7%, 95% CI 24.4% to 29.0%) of 300 HIV-uninfected MSM had serologic evidence of HHV-8 infection. Factors independently associated with HHV-8 infection were education < 12 years (OR 1.7, 95%) CI 1.1 to 2.7), anal receptive sex with the last partner (OR 2.0, 95% CI 1.2 to 3.3), self-reported sexually transmitted infection symptoms during the last year (OR 1.9, 95% CI 1.2 to 3.0), coinfection with HIV (OR 4.2, 95%, CI 2.8 to 6.4) and chronic hepatitis B (OR 4.9, 95% CI 1.5 to 15.8). MSM with long-standing HIV infection were more likely to have serologic evidence of HHV-8 infection when compared with men with recently acquired HIV (OR 3.8, 95% CI 1.7 to 9.1).
Conclusions: HHV-8 infection is common among both HIV-infected and HIV-negative MSM in Lima, Peru. HHV-8 scropositivity is correlated with anal receptive sex, self-reported sexually transmitted infection symptoms, and HIV infection among these MSM and thus seems to be sexually transmitted. HHV-8 infection seems to be acquired after HIV infection, Suggesting that future studies should evaluate the mode of HHV-8 transmission and prevention strategies among HIV-uninfected MSM.
C1 [Guanira, Juan V.; Lama, Javier R.; Sanchez, Jorge] Invest Med Salud INMENSA, Lima 14, Peru.
[Casper, Corey; Whittington, William L. H.; Wald, Anna; Celum, Connie] Univ Washington, Dept Med, Seattle, WA USA.
[Casper, Corey; Wald, Anna; Celum, Connie] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Casper, Corey] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Inst, Seattle, WA USA.
[Morrow, Rhoda; Wald, Anna] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA.
[Morrow, Rhoda] Childrens Hosp & Reg Med Ctr, Seattle, WA USA.
[Montano, Silvia M.] US Naval Med Res Ctr Detachment, Virol Program, Lima, Peru.
[Suarez, Luis] Minist Hlth Peru, Gen Directorate Epidemiol, Lima, Peru.
[Caballero, Patricia] NIH, Bethesda, MD 20892 USA.
[Celum, Connie] Univ Washington, Dept Global Hlth, Seattle, WA USA.
RP Guanira, JV (reprint author), Invest Med Salud INMENSA, Jose De La Torre Ugarte 166, Lima 14, Peru.
EM jguanira@inmensa.org
RI Wald, Anna/B-6272-2012; Valle, Ruben/A-7512-2013;
OI Wald, Anna/0000-0003-3486-6438; Guanira, Juan/0000-0002-2746-3086
FU The Fogarty International Center; University of Washington International
AIDS Research and Training Program; US National Institute of Health
Research [D43 TW000007]; 9th International Conference in Malignancies
[62787A S17 H B0002]
FX Supported by funds of The Fogarty International Center through the
University of Washington International AIDS Research and Training
Program and US National Institute of Health Research, Grant no D43
TW000007 and Work Unit number 62787A S17 H B0002. Presented in part at
the 9th International Conference in Malignancies
NR 22
TC 7
Z9 7
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD DEC 15
PY 2008
VL 49
IS 5
BP 557
EP 562
DI 10.1097/QAI.0b013e31818d5bf8
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 376YN
UT WOS:000261219000015
PM 18989224
ER
PT J
AU Gardel, ML
Sabass, B
Ji, L
Danuser, G
Schwarz, US
Waterman, CM
AF Gardel, Margaret L.
Sabass, Benedikt
Ji, Lin
Danuser, Gaudenz
Schwarz, Ulrich S.
Waterman, Clare M.
TI Traction stress in focal adhesions correlates biphasically with actin
retrograde flow speed
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID FLUORESCENT SPECKLE MICROSCOPY; CELL-MIGRATION; DYNAMICS; PROTRUSION;
FORCE
AB How focal adhesions (FAs) convert retrograde filamentous actin (F-actin) flow into traction stress on the extracellular matrix to drive cell migration is unknown. Using combined traction force and fluorescent speckle microscopy, we observed a robust biphasic relationship between F-actin speed and traction force. F-actin speed is inversely related to traction stress near the cell edge where FAs are formed and F-actin motion is rapid. In contrast, larger FAs where the F-actin speed is low are marked by a direct relationship between F-actin speed and traction stress. We found that the biphasic switch is determined by a threshold F-actin speed of 8-10 nm/s, independent of changes in FA protein density, age, stress magnitude, assembly/disassembly status, or subcellular position induced by pleiotropic perturbations to Rho family guanosine triphosphatase signaling and myosin II activity. Thus, F-actin speed is a fundamental regulator of traction force at FAs during cell migration.
C1 [Gardel, Margaret L.] Univ Chicago, Dept Phys, Chicago, IL 60637 USA.
[Sabass, Benedikt; Schwarz, Ulrich S.] Univ Heidelberg, BIOQUANT, D-69120 Heidelberg, Germany.
[Sabass, Benedikt; Schwarz, Ulrich S.] Univ Karlsruhe, Inst Zool, D-76131 Karlsruhe, Germany.
[Sabass, Benedikt; Schwarz, Ulrich S.] Karlsruhe Inst Technol, D-76131 Karlsruhe, Germany.
[Ji, Lin; Danuser, Gaudenz] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA.
[Waterman, Clare M.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Gardel, ML (reprint author), Univ Chicago, Dept Phys, Chicago, IL 60637 USA.
EM gardel@uchicago.edu; watermancm@nhlbi.nih.gov
RI Gardel, Margaret/D-1703-2012; Schwarz, Ulrich/K-4111-2014;
OI Schwarz, Ulrich/0000-0003-1483-640X; Waterman, Clare/0000-0001-6142-6775
FU National Institutes of Health (NIH)/National Heart, Lung, and Blood
Institute (C. M. Waterman); Burroughs Wellcome Fund Career Award at the
Scientific Interface; Jane Coffin Childs Fellowship; NIH Director's
Pioneer Award [DP10D00354]; Center for Modelling and Simulation in the
Biosciences at Heidelberg (U. S. Schwarz); [R01 GM71868]
FX This work was supported by the intramural research program of the
National Institutes of Health (NIH)/National Heart, Lung, and Blood
Institute (C. M. Waterman); Burroughs Wellcome Fund Career Award at the
Scientific Interface, Jane Coffin Childs Fellowship, and NIH Director's
Pioneer Award (DP10D00354) to M. L. Gardel; grant R01 GM71868 to G.
Danuser; and the Center for Modelling and Simulation in the Biosciences
at Heidelberg (U. S. Schwarz).
NR 26
TC 195
Z9 195
U1 0
U2 22
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 DEC 15
PY 2008
VL 183
IS 6
BP 999
EP 1005
DI 10.1083/jcb.200810060
PG 7
WC Cell Biology
SC Cell Biology
GA 384ZQ
UT WOS:000261783100007
PM 19075110
ER
PT J
AU Zhang, NG
Kuznetsov, SG
Sharan, SK
Li, KY
Rao, PH
Pati, D
AF Zhang, Nenggang
Kuznetsov, Sergey G.
Sharan, Shyam K.
Li, Kaiyi
Rao, Pulivarthi H.
Pati, Debananda
TI A handcuff model for the cohesin complex
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID SISTER-CHROMATID COHESION; DOUBLE-STRAND BREAKS;
SACCHAROMYCES-CEREVISIAE; CHROMOSOME ARMS; SILENT CHROMATIN; SMC
COMPLEXES; NIPPED-B; PROTEINS; ANAPHASE; RING
AB The cohesin complex is responsible for the accurate separation of sister chromatids into two daughter cells. Several models for the cohesin complex have been proposed, but the one-ring embrace model currently predominates the field. However, the static configuration of the embrace model is not flexible enough for cohesins to perform their functions during DNA replication, transcription, and DNA repair. We used coimmunoprecipitation, a protein fragment complement assay, and a yeast two-hybrid assay to analyze the protein-protein interactions among cohesin subunits. The results show that three of the four human cohesin core subunits (Smc1, Smc3, and Rad21) interact with themselves in an Scc3 (SA1/SA2)-dependent manner. These data support a two-ring handcuff model for the cohesin complex, which is flexible enough to establish and maintain sister chromatid cohesion as well as ensure the fidelity of chromosome segregation in higher eukaryotes.
C1 [Zhang, Nenggang; Li, Kaiyi; Rao, Pulivarthi H.; Pati, Debananda] Baylor Coll Med, Texas Childrens Canc Ctr, Dept Pediat Hematol Oncol, Houston, TX 77030 USA.
[Kuznetsov, Sergey G.; Sharan, Shyam K.] NCI, Ctr Canc Res, Mouse Canc Genet Program, Frederick, MD 21702 USA.
RP Pati, D (reprint author), Baylor Coll Med, Texas Childrens Canc Ctr, Dept Pediat Hematol Oncol, Houston, TX 77030 USA.
EM pati@bcm.tmc.edu
FU Baylor College of Medicine; National Cancer Institute [1RO1 CA109478]
FX This study was supported by Baylor College of Medicine startup funds and
a grant from the National Cancer Institute (1RO1 CA109478) awarded to D.
Pati.
NR 47
TC 72
Z9 75
U1 0
U2 7
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 DEC 15
PY 2008
VL 183
IS 6
BP 1019
EP 1031
DI 10.1083/jcb.200801157
PG 13
WC Cell Biology
SC Cell Biology
GA 384ZQ
UT WOS:000261783100009
PM 19075111
ER
PT J
AU Evdokimov, E
Sharma, P
Lockett, SJ
Lualdi, M
Kuehn, MR
AF Evdokimov, Evgenij
Sharma, Prashant
Lockett, Stephen J.
Lualdi, Margaret
Kuehn, Michael R.
TI Loss of SUMO1 in mice affects RanGAP1 localization and formation of PML
nuclear bodies, but is not lethal as it can be compensated by SUMO2 or
SUMO3
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE SUMO; RanGAP1; PML
ID UBIQUITIN-LIKE PROTEIN; MODIFIER SUMO-1; TARGET PROTEINS; PORE COMPLEX;
CANCER; UBC9; DYNAMICS; DESUMOYLATION; CONJUGATION; PROSTATE
AB Conjugation of the small ubiquitin-like modifier (SUMO) to target proteins regulates numerous biological processes and has been implicated in tumorigenesis and metastasis. The three SUMO isoforms in vertebrates, SUMO1 and the highly similar SUMO2 and SUMO3, can be conjugated to unique as well as overlapping subsets of target proteins. Yet, it is still not clear whether roles for each family member are distinct or whether redundancy exists. Here we describe a mutant mouse line that completely lacks SUMO1, but surprisingly is viable and lacks any overt phenotype. Our study points to compensatory utilization of SUMO2 and/or SUMO3 for sumoylation of SUMO1 targets. The ability of SUMO isoforms to substitute for one another has important implications for rational targeting of the SUMO pathway.
C1 [Evdokimov, Evgenij; Sharma, Prashant; Kuehn, Michael R.] NCI, Lab Prot Dynam & Signaling, NIH, Frederick, MD 21702 USA.
[Lockett, Stephen J.] SAIC Frederick, Adv Technol Program, Opt Microscopy & Anal Lab, Frederick, MD 21702 USA.
[Lualdi, Margaret] SAIC Frederick, Lab Anim Sci Program, Frederick, MD 21702 USA.
RP Kuehn, MR (reprint author), NCI, Lab Prot Dynam & Signaling, NIH, Frederick, MD 21702 USA.
EM mkuehn@mail.nih.gov
RI Kuehn, Michael/A-4573-2014
OI Kuehn, Michael/0000-0002-7703-9160
FU Intramural NIH HHS; NCI NIH HHS [N01-CO-12400]
NR 46
TC 61
Z9 62
U1 1
U2 4
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD DEC 15
PY 2008
VL 121
IS 24
BP 4106
EP 4113
DI 10.1242/jcs.038570
PG 8
WC Cell Biology
SC Cell Biology
GA 379EE
UT WOS:000261378700013
PM 19033381
ER
PT J
AU Scheidweiler, KB
Barnes, AJ
Huestis, MA
AF Scheidweiler, Karl B.
Barnes, Allan J.
Huestis, Marilyn A.
TI A validated gas chromatographic-electron impact ionization mass
spectrometric method for methamphetamine, methylenedioxymethamphetamine
(MDMA), and metabolites in mouse plasma and brain
SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL
AND LIFE SCIENCES
LA English
DT Article
DE Methylenedioxymethamphetamine; Methamphetamine; Gas chromatography; Mass
spectrometry; Tissue; Mouse
ID TRANSPORTER KNOCKOUT MICE; NITRIC-OXIDE SYNTHASE;
3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; INDUCED NEUROTOXICITY; MAIN
METABOLITES; URINARY-EXCRETION; DEFICIENT MICE; DESIGNER DRUGS; NULL
MUTATION; AMPHETAMINE
AB A method was developed and fully validated for simultaneous quantification of methamphetamine (MAMP), amphetamine, hydroxy-methamphetamine, methylenedioxymethamphetamine (MDMA, ecstasy), methylenedioxyamphetamine, 3-hydroxy-4-methoxy-methamphetamine, and 3-hydroxy-4-methoxy-amphetamine in 100 mu L mouse plasma and 7.5 mg brain. Solid phase extraction and gas chromatography-electron impact ionization mass spectrometry in selected-ion monitoring mode achieved plasma linear ranges of 10-20 to 20,000 ng/mL and 0.1-0.2 to 200 ng/mg in brain. Recoveries were greater than 91%, bias 92.3-110.4%, and imprecision less than 5.3% coefficient of variation. This method was used for measuring MAMP and MDMA and metabolites in plasma and brain during mouse neurotoxicity studies. Published by Elsevier B.V.
C1 [Scheidweiler, Karl B.; Barnes, Allan J.; Huestis, Marilyn A.] NIDA, Intramural Res Program, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, Intramural Res Program, NIH, Biomed Res Ctr, 251 Bayview Blvd,Suite 200,Room 05a-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU Intramural Research Program of the National Institute on Drug Abuse;
National Institutes of Health
FX The authors thank the co-investigators of the MAMP and MDMA
neurotoxicity study conducted at the Intramural Research Program,
National Institute on Drug Abuse, jean Lud Cadet and Bruce Ladenheim for
generously providing mouse plasma and brain specimens for proof of
method. This research was supported by the Intramural Research Program
of the National Institute on Drug Abuse, National Institutes of Health.
NR 51
TC 15
Z9 16
U1 0
U2 1
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 DEC 15
PY 2008
VL 876
IS 2
BP 266
EP 276
DI 10.1016/j.jchromb.2008.11.001
PG 11
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 386PM
UT WOS:000261895100018
PM 19026602
ER
PT J
AU Huter, EN
Stummvoll, GH
DiPaolo, RJ
Glass, DD
Shevach, EM
AF Huter, Eva N.
Stummvoll, Georg H.
DiPaolo, Richard J.
Glass, Deborah D.
Shevach, Ethan M.
TI Cutting Edge: Antigen-Specific TGF beta-Induced Regulatory T Cells
Suppress Th17-Mediated Autoimmune Disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID DENDRITIC CELLS; GASTRITIS; PREVENT; TH17
AB CD4(+) T cells from the TCR transgenic TxA23 mouse recognize a peptide from the H/K-ATPase alpha-chain. When TxA23 CD4(+) thymocytes are differentiated into Th1, Th2, and Th17 lines, all three subpopulations induced autoimmune gastritis (AIG) upon transfer into nu/nu recipients. The induction of AIG by naive T cells or by Th1 or Th2 cell lines could be prevented by the cotransfer of polyclonal Foxp3(+) T regulatory cells (nTreg), whereas Th17-induced AIG was resistant to suppression. We compared the capacity of different types of Treg to suppress Th17-mediated AIG. Cotransfer of either nTreg or polyclonal TGF beta-induced Treg (iTreg) did not prevent AIG, while cotransfier of TGF beta-induced Ag-specific TxA23 iTreg completely prevented the development of disease. Ag-specific iTreg were able to suppress Th17-mediated disease when injected 6 days after the Th17 effectors. The implications of these results for the use of Treg for the cellular biotherapy of autoimmune disease are discussed. The Journal of Immunology, 2008, 181: 8209-8213.
C1 [Huter, Eva N.; Glass, Deborah D.; Shevach, Ethan M.] NIAID, Immunol Lab, Cellular Immunol Sect, NIH, Bethesda, MD 20892 USA.
[Stummvoll, Georg H.] Med Univ Vienna, Dept Rheumatol, Vienna, Austria.
[DiPaolo, Richard J.] St Louis Univ, Sch Med, St Louis, MO 63104 USA.
RP Shevach, EM (reprint author), NIAID, Immunol Lab, Cellular Immunol Sect, NIH, Bldg 10,Room 11N315, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
FU Intramural NIH HHS [ZIA AI000224-28]
NR 13
TC 81
Z9 82
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8209
EP 8213
PG 5
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000007
PM 19050237
ER
PT J
AU Chen, QY
Cannons, JL
Paton, JC
Akiba, H
Schwartzberg, PL
Snapper, CM
AF Chen, Quanyi
Cannons, Jennifer L.
Paton, James C.
Akiba, Hisaya
Schwartzberg, Pamela L.
Snapper, Clifford M.
TI A Novel ICOS-Independent, but CD28-and SAP-Dependent, Pathway of T
Cell-Dependent, Polysaccharide-Specific Humoral Immunity in Response to
Intact Streptococcus pneumoniae versus Pneumococcal Conjugate Vaccine
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID LINKED LYMPHOPROLIFERATIVE DISEASE; ZONE B-CELLS; IN-VIVO
ANTIPOLYSACCHARIDE; IG ISOTYPE RESPONSES; MARGINAL-ZONE; LYMPH-NODE;
ANTIPROTEIN RESPONSES; MECHANISM DISTINCT; ANTIBODY-RESPONSES;
GERMINAL-CENTERS
AB Polysaccharide (PS)- and protein-specific murine IgG responses to intact Streptococcus pneumoniae (Pn) are both dependent on CD4(+) T cell help, B7-dependent costimulation, and CD40/CD40 ligand interactions. However, the primary PS-specific, relative to protein-specific, IgG response terminates more rapidly, requires a shorter period of T cell help and B7-dependent costimulation, and fails to generate memory. In light of the critical role for ICOS/ICOS ligand interactions in sustaining T cell-dependent Ig responses and promoting germinal center reactions, we hypothesized that this interaction was nonessential for PS-specific IgG responses to Pn. We now demonstrate that ICOS(-/-), relative to wild-type, mice elicit a normal PS-specific IgG isotype response to Pn, despite marked inhibition of both the primary and secondary IgG anti-protein (i.e., PspA, PspC, and PsaA) response. A blocking anti-ICOS ligand mAb injected during primary Pn immunization inhibits both the primary anti-protein response and the generation of protein-specific memory, but has no effect when injected during secondary immunization. In contrast to Pn, both PS-and protein-specific IgG responses to a pneumococcal conjugate vaccine are inhibited in ICOS(-/-) mice. ICOS(-/-) mice immunized with intact Pn or conjugate exhibit nearly complete abrogation in germinal center formation. Finally, although mice that lack the adaptor molecule SAP (SLAM-associated protein) resemble ICOS-/- mice (and can exhibit decreased ICOS expression), we observe that the PS-specific, as well as protein-specific, IgG responses to both Pn and conjugate are markedly defective in SAP(-/-) mice. These data define a novel T cell-, SAP-, and B7-dependent, but ICOS-independent, extrafollicular pathway of Ig induction. The Journal of Immunology, 2008, 181: 8258-8266.
C1 [Chen, Quanyi; Snapper, Clifford M.] Uniformed Serv Univ Hlth Sci, Dept Pathol, Bethesda, MD 20814 USA.
[Cannons, Jennifer L.; Schwartzberg, Pamela L.] Natl Human Genome Res Inst, NIH, Bethesda, MD 20814 USA.
[Paton, James C.] Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA, Australia.
[Akiba, Hisaya] Juntendo Univ, Sch Med, Dept Immunol, Tokyo 113, Japan.
RP Snapper, CM (reprint author), Uniformed Serv Univ Hlth Sci, Dept Pathol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM csnapper@usuhs.mil
RI Paton, James/A-9920-2008
FU National Institutes of Health [1R01 AI49192]; Uniformed Services
University of the Health Sciences Dean's Research; Education Endowment
Fund; National Human Genome Research Institute
FX This study wits supported by National Institutes of Health Grants 1R01
AI49192 (to C.M.S.) and the Uniformed Services University of the Health
Sciences Dean's Research and Education Endowment Fund (to C.M.S.) and by
funding from the intramural program of the National Human Genome
Research Institute (to P.L.S.).
NR 65
TC 23
Z9 24
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8258
EP 8266
PG 9
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000012
PM 19050242
ER
PT J
AU Yamazaki, T
Yang, XO
Chung, Y
Fukunaga, A
Nurieva, R
Pappu, B
Martin-Orozco, N
Kang, HS
Ma, L
Panopoulos, AD
Craig, S
Watowich, SS
Jetten, AM
Tian, Q
Dong, C
AF Yamazaki, Tomohide
Yang, Xuexian O.
Chung, Yeonseok
Fukunaga, Atsushi
Nurieva, Roza
Pappu, Bhanu
Martin-Orozco, Natalia
Kang, Hong Soon
Ma, Li
Panopoulos, Athanasia D.
Craig, Suzanne
Watowich, Stephanie S.
Jetten, Anton M.
Tian, Qiang
Dong, Chen
TI CCR6 Regulates the Migration of Inflammatory and Regulatory T Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID GROWTH-FACTOR-BETA; AUTOIMMUNE INFLAMMATION; IL-17-PRODUCING CELLS;
IMMUNE-RESPONSES; HELPER-CELLS; ROR-GAMMA; LINEAGE; DIFFERENTIATION;
RECEPTOR; CYTOKINE
AB Th17 and regulatory T (Treg) cells play opposite roles in autoimmune diseases. However, the mechanisms underlying their proper migration to inflammatory tissues are unclear. In this study, we report that these two T cell subsets both express CCR6. CCR6 expression in Th17 cells is regulated by TGF-beta and requires two nuclear receptors, ROR alpha and ROR gamma. Th17 cells also express the CCR6 ligand CCL20, which is induced synergistically by TGF-beta and IL-6, which requires STAT3, ROR gamma and IL-21. Th17 cells, by producing CCL20, promote migration of Th17 and Treg cells in vitro in a CCR6-dependent manner. Lack of CCR6 in Th17 cells reduces the severity of experimental autoimmune encephalomyelitis and Th17 and Treg recruitment into inflammatory tissues. Similarly, CCR6 on Treg cells is also important for their recruitment into inflammatory tissues. Our data indicate an important role of CCR6 in Treg and Th17 cell migration. The Journal of Immunology, 2008, 181: 8391-8401.
C1 [Yamazaki, Tomohide; Yang, Xuexian O.; Chung, Yeonseok; Fukunaga, Atsushi; Nurieva, Roza; Pappu, Bhanu; Martin-Orozco, Natalia; Panopoulos, Athanasia D.; Watowich, Stephanie S.; Dong, Chen] Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
[Kang, Hong Soon; Jetten, Anton M.] Natl Inst Environm Sci, Cell Biol Sect, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
[Ma, Li; Tian, Qiang] Inst Syst Biol, Seattle, WA 98103 USA.
RP Dong, C (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
EM cdong@mdanderson.org
RI dong, chen /B-3181-2009; Martin Orozco, Natalia/E-4794-2010;
OI dong, chen /0000-0002-0084-9130; Jetten, Anton/0000-0003-0954-4445;
Chung, Yeonseok/0000-0001-5780-4841; Watowich,
Stephanie/0000-0003-1969-659X
FU National Institutes of Health; National Institute on Environmental
Health Sciences; Leukemia and Lymphoma Society; Anderson Cancer Center;
Gillson Longenbaugh Foundation; Odyssey Program; Kimberly-Clark
Foundation Award for Scientific Achievement at MD Anderson Cancer Center
FX This work was supported by research grants from the National Institutes
of Health (to C.D.), an Intramural Research Program of the National
Institute on Environmental Health Sciences, National Institutes of
Health (to A.M.J.), the Leukemia and Lymphoma Society (to C.D.) and M.D.
Anderson Cancer Center (to C.D. and S.S.W.), and the Gillson Longenbaugh
Foundation (to S.S.W.). T.Y. received a fellowship from the Odyssey
Program and The Kimberly-Clark Foundation Award for Scientific
Achievement at MD Anderson Cancer Center. R.N. is a recipient of a
Scientist Development Grant from the American Heart Association. C.D. is
a Trust Fellow of the MD Anderson Cancer Center, a Cancer Research
Institute Investigator, a Leukemia and Lymphoma Society Scholar, and an
American Lung Association Career Investigator.
NR 45
TC 203
Z9 212
U1 1
U2 7
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8391
EP 8401
PG 11
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000026
PM 19050256
ER
PT J
AU Yarovinsky, F
Hieny, S
Sher, A
AF Yarovinsky, Felix
Hieny, Sara
Sher, Alan
TI Recognition of Toxoplasma gondii by TLR11 Prevents Parasite-Induced
Immunopathology
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TOLL-LIKE RECEPTORS; NATURAL-KILLER-CELLS; IFN-GAMMA;
ACUTE-PANCREATITIS; DENDRITIC CELLS; IMMUNE-SYSTEM; RESISTANCE;
INFECTION; PATHOGENS; IL-12
AB TLRs are thought to play a critical role in self/non-self discrimination by sensing microbial infections and initiating both innate and adaptive immunity. In this study, we demonstrate that in the absence of TLR11, a major TLR involved in recognition of Toxoplasma gondii, infection with this protozoan parasite induces an abnormal immunopathological response consisting of pancreatic tissue destruction, fat necrosis, and systemic elevations in inflammatory reactants. We further show that this immunopathology is the result of non-TLR dependent activation of IFN-gamma secretion by NK cells in response to the infection. These findings reveal that in addition to triggering host resistance to infection, TLR recognition can be critical for the prevention of pathogen-induced immune destruction of self tissue. The Journal of Immunology, 2008,181: 8478-8484.
C1 [Yarovinsky, Felix] Univ Texas SW Med Ctr Dallas, Dept Immunol, Dallas, TX 75390 USA.
[Yarovinsky, Felix; Hieny, Sara; Sher, Alan] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Yarovinsky, F (reprint author), Univ Texas SW Med Ctr Dallas, Dept Immunol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Felix.Yarovinsky@UTSouthwestern.edu
FU National Institute of Allergy and Infectious Diseases intramural
program; University of Texas Southwestern Medical Center Endowed
Scholars Program
FX This project was supported (in part) by the National Institute of
Allergy and Infectious Diseases intramural program and by the University
of Texas Southwestern Medical Center Endowed Scholars Program.
NR 28
TC 18
Z9 24
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8478
EP 8484
PG 7
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000035
PM 19050265
ER
PT J
AU Furuichi, K
Gao, JL
Horuk, R
Wada, T
Kaneko, S
Murphy, PM
AF Furuichi, Kengo
Gao, Ji-Liang
Horuk, Richard
Wada, Takashi
Kaneko, Shuichi
Murphy, Philip M.
TI Chemokine Receptor CCR1 Regulates Inflammatory Cell Infiltration after
Renal Ischemia-Reperfusion Injury
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MICE; NEUTROPHIL; FIBROSIS; FAILURE; KIDNEY; MACROPHAGES; DEFICIENCY;
MIGRATION; SURVIVAL; DISEASE
AB Neutrophils and macrophages rapidly infiltrate the kidney after renal ischemia-reperfusion injury, however specific molecular recruitment mechanisms have not been fully delineated for these cell types. Here we provide genetic and pharmacologic evidence supporting a positive role for the chemokine receptor CCR1 in macrophage and neutrophil infiltration in a 7 day mouse model of renal ischemia-reperfusion injury. By day 7, injured kidneys from mice lacking CCR1 contained 35% fewer neutrophils and 45% fewer macrophages than injured kidneys from wild-type control mice. Pretreatment of wild-type mice with the specific CCR1 antagonist BX471 also suppressed neutrophil and macrophage infiltration in the model. Injured kidneys from mice lacking CCR1 also had reduced content of the CCR1 ligands CCL3 (MIP-1 alpha) and CCL5 (RANTES) compared with injured kidneys from wild-type controls, suggesting a leukocyte source for these inflammatory chemokines and existence of a CCR1-dependent positive feedback loop for leukocyte infiltration in the model. Local leukocyte proliferation and apoptosis were detected after injury, but were not dependent on CCR1. Also, the extent of necrotic and fibrotic damage and decline in renal function in injured kidneys was similar in wild-type and CCR1-deficient mice. Thus, CCR1 appears to regulate trafficking of macrophages and neutrophils to kidney in a mouse model of renal ischemia-reperfusion injury, however this activity does not appear to affect tissue injury. The Journal of Immunology, 2008, 181: 8670-8676.
C1 [Furuichi, Kengo; Gao, Ji-Liang; Murphy, Philip M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Furuichi, Kengo; Wada, Takashi; Kaneko, Shuichi] Kanazawa Univ, Lab Med Dis Control & Homeostasis, Div Blood Purificat, Kanazawa, Ishikawa, Japan.
[Horuk, Richard] Dept Immunol, Richmond, CA 94806 USA.
RP Murphy, PM (reprint author), NIAID, Lab Mol Immunol, NIH, Bldg 10,Room 11N113, Bethesda, MD 20892 USA.
EM pmm@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 37
TC 47
Z9 51
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8670
EP 8676
PG 7
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000057
PM 19050287
ER
PT J
AU Starosta, V
Pazdrak, K
Boldogh, I
Svider, T
Kurosky, A
AF Starosta, Vitaliy
Pazdrak, Konrad
Boldogh, Istvan
Svider, Tetyana
Kurosky, Alexander
TI Lipoxin A(4) Counterregulates GM-CSF Signaling in Eosinophilic
Granulocytes
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID COLONY-STIMULATING FACTOR; ASPIRIN-TRIGGERED LIPOXIN; NF-KAPPA-B;
TYROSINE PHOSPHORYLATION; GEL-ELECTROPHORESIS; HUMAN NEUTROPHILS; CELL
LINE; ACTIVATION; INFLAMMATION; SPECTRIN
AB Eosinophils are granulated leukocytes that are involved in many inflammation-associated pathologies including airway inflammation in asthma. Resolution of eosinophilic inflammation and return to homeostasis is in part due to endogenous chemical mediators, for example, lipoxins, resolvins, and protectins. Lipoxins are endogenous eicosanoids that demonstrate antiinflammatory activity and are synthesized locally at sites of inflammation. In view of the importance of lipoxins (LXs) in resolving inflammation, we investigated the molecular basis of LXA(4) action on eosinophilic granulocytes stimulated with GM-CSF employing the eosinophilic leukemia cell line EoL-1 as well as peripheral blood eosinophils. We report herein that LXA(4) (1-100 nM) decreased protein tyrosine phosphorylation in EoL-1 cells stimulated with GM-CSF. Additionally, the expression of a number of GM-CSF-induced cytokines was inhibited by LXA(4) in a dose-dependent manner. Furthermore, using a proteomics approach involving mass spectrometry and immunoblot analysis we identified 11 proteins that were tyrosine phosphorylated after GM-CSF stimulation and whose phosphorylation was significantly inhibited by LXA(4) pretreatment. Included among these 11 proteins were alpha-fodrin (non-erythroid spectrin) and actin. Microscopic imaging showed that treatment of EoL-1 cells or blood eosinophils with GM-CSF resulted in the reorganization of actin and the translocation of alpha-fodrin from the cytoplasm to the plasma membrane. Importantly, alpha-fodrin translocation was prevented by LXA(4) but actin reorganization was not. Thus, the mechanism of LXA(4) action likely involves prevention of activation of eosinophilic granulocytes by GM-CSF through inhibition of protein tyrosine phosphorylation and modification of some cytoskeletal components. The Journal of Immunology, 2008, 181: 8688-8699.
C1 [Starosta, Vitaliy; Pazdrak, Konrad; Kurosky, Alexander] Univ Texas Galveston, Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA.
[Boldogh, Istvan] Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Svider, Tetyana; Kurosky, Alexander] Univ Texas Galveston, Med Branch, NHLBI, Prote Ctr, Galveston, TX 77555 USA.
RP Kurosky, A (reprint author), Univ Texas Galveston, Med Branch, Dept Biochem & Mol Biol, 301 Univ Blvd, Galveston, TX 77555 USA.
EM akurosky@utmb.edu
FU National Institutes of Health National Heart, Lung, and Blood
Institute's Proteomics Initiative [N01-HV-28184]; National Institute for
Environmental Health Sciences Center [P30-ES006676]; National Institute
of Allergy and Infectious Diseases [P01 AI062885]
FX This study was supported by the National Institutes of Health National
Heart, Lung, and Blood Institute's Proteomics Initiative N01-HV-28184
(to A.K.), National Institute for Environmental Health Sciences Center
Grant P30-ES006676 (to J. Halpert), National Institute of Allergy and
Infectious Diseases Grant P01 AI062885 (to A. Brasier) and a James W.
McLaughlin postdoctoral fellowship grant to V. Starosta.
NR 50
TC 23
Z9 23
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8688
EP 8699
PG 12
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000059
PM 19050289
ER
PT J
AU Miura, K
Zhou, H
Moretz, SE
Diouf, A
Thera, MA
Dolo, A
Doumbo, O
Malkin, E
Diemert, D
Miller, LH
Mullen, GED
Longli, CA
AF Miura, Kazutoyo
Zhou, Hong
Moretz, Samuel E.
Diouf, Ababacar
Thera, Mahamadou A.
Dolo, Amagana
Doumbo, Ogobara
Malkin, Elissa
Diemert, David
Miller, Louis H.
Mullen, Gregory E. D.
Longli, Carole A.
TI Comparison of Biological Activity of Human Anti-Apical Membrane
Antigen-1 Antibodies Induced by Natural Infection and Vaccination
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; BLOOD-STAGE MALARIA; MEROZOITE SURFACE
PROTEIN-1; DOMAIN-III; RECOMBINANT; CANDIDATE; SPECIFICITY; PROTECTION;
RESPONSES; MONKEYS
AB Vaccines represent a significant potential means of decreasing global morbidity and mortality due to malaria. Clinical trials in the United States with Plasmodium falciparum Apical Membrane Antigen 1 (AMA1) showed that the vaccine induced biologically active Abs judged by an in vitro parasite growth inhibition assay (GIA). However, the same vaccine in Malian adults did not increase biological activity, although it elevated ELISA titers. Because GIA has been used to evaluate the biological activity of Abs induced by blood stage malarial vaccine candidates, we explored this discrepancy in this study. We affinity purified AMA1-specific Abs from both U.S. vaccinees and nonvaccinated individuals living in a malaria-endemic area of Mali and performed ELISA and GIA. Both AMA1-specifc Abs induced by vaccination (U.S.) and by natural infection (Mali) have comparable biological activity in GIA when the ELISA titer is normalized. However, a fraction of Malians' IgG that did not bind to AMA1 protein (Mali-non-AMA1 IgG) reduced the biological activity of the AMA1 Abs from U.S. vaccinees; in contrast, U.S.-non-AMA1 IgGs did not show a reduction of the biological activity. Further investigation revealed that the reduction was due to malaria-specitic IgGs in the Mali-non-AMA1 IgGs. The fact that both U.S.- and Mali-AMA1-specific Abs showed comparable biological activity supports further development of AMA1-based vaccines. However, the reduction of biological activity of AMA1-specific Ab by other malaria-specific IgGs likely explains the limited effect on growth-inhibitory activity of Abs induced by AMA1 vaccination in Malian adults and may complicate efforts to develop a blood stage malaria vaccine. The Journal of Immunology, 2008, 181: 8776-8783.
C1 [Miura, Kazutoyo; Malkin, Elissa; Diemert, David; Miller, Louis H.; Mullen, Gregory E. D.] NIAID, Malaria Vaccine Dev Branch, NIH, Bethesda, MD 20892 USA.
[Zhou, Hong; Moretz, Samuel E.; Diouf, Ababacar; Longli, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Thera, Mahamadou A.; Dolo, Amagana; Doumbo, Ogobara] Univ Bamako, Dept Hematol & Parasitol, Malaria Res & Training Ctr, Bamako, Mali.
RP Miura, K (reprint author), 12441 Parklawn Dr,Twinbrook 2,Room 107, Rockville, MD 20852 USA.
EM kmiura@niaid.nih.gov
FU PATH/Malaria Vaccine Initiative; National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This study was funded in part by the PATH/Malaria Vaccine Initiative and
the Intramural program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health.
NR 31
TC 39
Z9 39
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 2008
VL 181
IS 12
BP 8776
EP 8783
PG 8
WC Immunology
SC Immunology
GA 382CQ
UT WOS:000261583000069
PM 19050299
ER
PT J
AU Hadigan, C
AF Hadigan, Colleen
TI Peroxisome Proliferator-Activated Receptor gamma Agonists and the
Treatment of HIV-Associated Lipoatrophy: Unraveling the Molecular
Mechanism of Their Shortcomings
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Editorial Material
ID REVERSE-TRANSCRIPTASE INHIBITORS; PLACEBO-CONTROLLED TRIAL; INFECTED
PATIENTS; DOUBLE-BLIND; MITOCHONDRIAL TOXICITY; ANTIRETROVIRAL-THERAPY;
ADIPOSE-TISSUE; LIPODYSTROPHY; ROSIGLITAZONE; ANALOG
C1 NIAID, NIH, Immunoregulat Lab, Bethesda, MD 20892 USA.
RP Hadigan, C (reprint author), NIAID, NIH, Immunoregulat Lab, 10 Ctr Dr,Bldg 10 Rm 11C 103, Bethesda, MD 20892 USA.
EM hadiganc@niaid.nih.gov
NR 17
TC 4
Z9 4
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 15
PY 2008
VL 198
IS 12
BP 1729
EP 1731
DI 10.1086/593180
PG 3
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 376QB
UT WOS:000261197000001
PM 18954262
ER
PT J
AU Jensen, TB
Gottwein, JM
Scheel, TKH
Hoegh, AM
Eugen-Olsen, J
Bukh, J
AF Jensen, Tanja B.
Gottwein, Judith M.
Scheel, Troels K. H.
Hoegh, Anne M.
Eugen-Olsen, Jesper
Bukh, Jens
TI Highly Efficient JFH1-Based Cell-Culture System for Hepatitis C Virus
Genotype 5a: Failure of Homologous Neutralizing-Antibody Treatment to
Control Infection
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT 58th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY NOV 02-06, 2007
CL Boston, MA
SP Amer Assoc Study Liver Dis
ID SCAVENGER RECEPTOR-BI; SEQUENCE-ANALYSIS; IN-VITRO; DETERMINANTS;
ENHANCEMENT; RECOMBINANT; PERSISTENCE; INTERFERON; CHALLENGE; CLEARANCE
AB Background. Recently, a hepatitis C virus (HCV) cell-culture system was developed that employed strain JFH1 ( genotype 2a), and JFH1-based intra-and intergenotypic recombinants now permit functional studies of the structural genes ( Core, E1, and E2), p7, and NS2 of genotypes 1-4. The goal was to adapt the system to employ genotype 5. Methods. Huh7.5 cells infected with SA13/JFH1, containing Core-NS2 of strain SA13 ( genotype 5a), were monitored for Core expression and for supernatant infectivity and HCV-RNA titers. Adaptive mutations of SA13/JFH1 were identified by sequence analysis of recovered genomes and reverse-genetic studies. Receptor blockage was performed with anti-CD81 and anti-SR-BI. For neutralization experiments, SA13/JFH1 or JFH1-based viruses of other genotypes were incubated with patient sera. Results. SA13/JFH1 with NS2 and NS3 mutations yielded infectivity titers > 10(5) TCID(50)/mL. Infection with SA13/JFH1 was inhibited by CD81 blocking and SR-BI blocking, respectively, and by preincubation with genotype 5a chronic-phase patient sera. Such sera had varying cross-genotype neutralization potential. However, preincubation and treatment with homologous neutralizing antibodies could not control SA13/JFH1 infection in culture. Conclusion. The SA13/JFH1 culture permits genotype 5a-specific studies of Core-NS2 function and interfering agents. The ability of HCV to spread in vivo during treatment with neutralizing antibodies was confirmed in vitro.
C1 [Jensen, Tanja B.; Gottwein, Judith M.; Scheel, Troels K. H.; Eugen-Olsen, Jesper; Bukh, Jens] Copenhagen Univ Hosp, Dept Infect Dis, Copenhagen Hepatitis C Program CO HEP, DK-2650 Hvidovre, Denmark.
[Jensen, Tanja B.; Gottwein, Judith M.; Scheel, Troels K. H.; Eugen-Olsen, Jesper; Bukh, Jens] Copenhagen Univ Hosp, Clin Res Ctr, DK-2650 Hvidovre, Denmark.
[Hoegh, Anne M.] Copenhagen Univ Hosp, Dept Clin Microbiol, DK-2650 Hvidovre, Denmark.
[Scheel, Troels K. H.; Bukh, Jens] Univ Copenhagen, Dept Int Hlth Immunol & Microbiol, Fac Hlth Sci, Copenhagen, Denmark.
[Bukh, Jens] NIAID, Hepatitis Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Bukh, J (reprint author), Copenhagen Univ Hosp, Dept Infect Dis, Copenhagen Hepatitis C Program CO HEP, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark.
EM jbukh@niaid.nih.gov
OI Eugen-Olsen, jesper/0000-0002-4630-4275; Scheel,
Troels/0000-0003-1545-4067
NR 35
TC 63
Z9 64
U1 0
U2 6
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD DEC 15
PY 2008
VL 198
IS 12
BP 1756
EP 1765
DI 10.1086/593021
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 376QB
UT WOS:000261197000003
PM 19032070
ER
PT J
AU Horkay, F
Basser, PJ
AF Horkay, Ferenc
Basser, Peter J.
TI Ionic and pH Effects on the Osmotic Properties and Structure of
Polyelectrolyte Gels
SO JOURNAL OF POLYMER SCIENCE PART B-POLYMER PHYSICS
LA English
DT Article
DE neutron scattering; osmotic pressure; phase behavior; phase transition;
polyelectrolyte gel; polyelectrolytes; small-angle neutron scattering
ID PHYSIOLOGICAL SALT-SOLUTIONS; ANGLE NEUTRON-SCATTERING; POLYMER-CHAIN;
POLYACRYLATE HYDROGELS; PHASE-TRANSITION; THERMODYNAMIC OBSERVATIONS;
COLLAPSE; SWOLLEN; NETWORKS; BEHAVIORS
AB We investigate the effects of salt concentration and pH on neutralized poly(acrylic acid) (PAA) gels in near physiological salt solutions. Either adding calcium ions or decreasing the pH is found to induce reversible volume transitions but the nature of these transitions seems to be different. For example, the osmotic pressure exhibits a simple power law dependence on the concentration as the transition is approached in both systems, but the power law exponent it is substantially different in the two cases. On decreasing the pH the value of n gradually increases from 2.1 (at pH = 7) to 3.2 (at pH = 1). By contrast, n decreases with increasing calcium ion concentration from 2.1 (in 100 mM NaCl solution) to 1.6 (0.8 mM CaCl(2) ill 100 mM NaCl solution). In both systems, a strong increase of the small-angle neutron scattering intensity (SANS) is observed near the volume transition. The SANS results reveal that calcium ions favor the formation of linearly aligned regions in PAA gels. (C) 2008 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 46: 2803-2810, 2008
C1 [Horkay, Ferenc; Basser, Peter J.] NICHD, Sect Tissue Biophys & Biomimet, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA.
RP Horkay, F (reprint author), NICHD, Sect Tissue Biophys & Biomimet, Lab Integrat & Med Biophys, NIH, 13 S Dr, Bethesda, MD 20892 USA.
EM horkay@helix.nih.gov
RI Basser, Peter/H-5477-2011
FU Intramural Research Program of the NICHD, NIH; National Institute of
Standards and Technology; U.S. Department of Commerce; National Science
Foundation [DMR-0454672]
FX This research was supported by the Intramural Research Program of the
NICHD, NIH. The authors acknowledge the support of the National
Institute of Standards and Technology, U.S. Department of Commerce, in
providing the neutron research facilities used in this work. This work
utilized facilities supported in part by the National Science Foundation
under Agreement No. DMR-0454672. The authors are grateful to Dr. Jack F.
Douglas (NIST) for helpful comments.
NR 35
TC 3
Z9 3
U1 4
U2 24
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-6266
J9 J POLYM SCI POL PHYS
JI J. Polym. Sci. Pt. B-Polym. Phys.
PD DEC 15
PY 2008
VL 46
IS 24
BP 2803
EP 2810
DI 10.1002/polb.21590
PG 8
WC Polymer Science
SC Polymer Science
GA 383WQ
UT WOS:000261705400016
PM 20016687
ER
PT J
AU Regenold, WT
Phatak, P
Makley, MJ
Stone, RD
Kling, MA
AF Regenold, William T.
Phatak, Pornima
Makley, Michael J.
Stone, Roger D.
Kling, Mitchel A.
TI Cerebrospinal fluid evidence of increased extra-mitochondrial glucose
metabolism implicates mitochondrial dysfunction in multiple sclerosis
disease progression
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article
DE Multiple sclerosis; Metabolism; Mitochondrial; Polyol; Lactate; Glucose;
Energy; Progression; Degeneration
ID MAGNETIC-RESONANCE SPECTROSCOPY; CENTRAL-NERVOUS-SYSTEM; STROKE-LIKE
EPISODES; LACTIC-ACIDOSIS; AXONAL DEGENERATION; POLYOLS; DNA; LACTATE;
PLASMA; ENCEPHALOMYOPATHY
AB In contrast to relapse, the mechanisms of multiple sclerosis (MS) disease progression are less understood and appear not to be exclusively inflammatory in nature. In this pilot study we investigated the relationship between disturbed CNS energy metabolism and MS disease progression. We tested the hypothesis that cerebrospinal fluid (CSF) concentrations of sorbitol, fructose, and lactate, all metabolites of extramitochondrial glucose metabolism, would be elevated in secondary progressive (SP) MS patients and would be associated with worsening neurologic disability. We measured metabolite concentrations by gas chromatographic/mass spectrometric and enzymatic methods in archived CSF samples from 85 MS patients [31 relapsing-remitting (RR) and 54 SP patients] and 18 healthy controls. We found that concentrations of all three metabolites, but not concentrations of glucose or myoinositol, were significantly increased in CSF from SP and, to a lesser degree, RR patients, compared to controls. Furthermore, CSF concentrations of sorbitol and fructose (polyol pathway metabolites), but not lactate (anaerobic glycolysis metabolite), correlated positively and significantly with Expanded Disability Status Scale (EDSS) score, an index of neurologic disability in MS patients. We conclude that extra-mitochondrial glucose metabolism is increased in MS patients and is associated with disease progression evidenced by increasing EDSS score. As extra-mitochondrial glucose metabolism increases with impaired mitochondrial metabolism of glucose, these findings implicate mitochondrial dysfunction in the pathogenesis of MS disease progression. CSF metabolic profiling may be useful in clarifying the role of mitochondrial pathology in progression and in targeting and monitoring therapies for disease progression that aim to preserve or boost mitochondrial glucose metabolism. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Regenold, William T.; Phatak, Pornima] Univ Maryland, Sch Med, Dept Psychiat, Div Geriatr Psychiat, Baltimore, MD 21201 USA.
[Regenold, William T.; Phatak, Pornima] Baltimore Vet Affairs Med Ctr, Res Serv, Baltimore, MD 21201 USA.
[Makley, Michael J.] Univ Maryland, Sch Med, Dept Neurol, Comprehens Multiple Sclerosis Ctr Baltimore, Baltimore, MD 21201 USA.
[Stone, Roger D.] Natl Inst Neurol Disorders & Stroke, Neuroimmunol Branch, Bethesda, MD USA.
[Kling, Mitchel A.] Wyeth Pharmaceut, Div Clin Translat Med, Madison, NJ USA.
[Kling, Mitchel A.] NIMH, Clin Neuroendocrinol Branch, Bethesda, MD 20892 USA.
RP Regenold, WT (reprint author), Univ Maryland, Sch Med, Dept Psychiat, Div Geriatr Psychiat, Baltimore, MD 21201 USA.
EM wregenol@psych.umaryland.edu
RI Kling, Mitchel/F-4152-2010
OI Kling, Mitchel/0000-0002-2232-1409
FU National Multiple Sclerosis Society [PP0932]; Intramural Research
Program of the NIH; NINDS
FX The authors thank the individuals who generously donated their CSF; Lisa
McFarland, M.S. for GC-MS technical assistance; Andrew P. Goldberg, M.D.
and the Baltimore VAMC GRECC for extended loan of the GC-MS system;
Roland Martin, M.D. and Laura Tranquill, M.S. of the NINDS
Neuroimmunology Branch, for assistance in providing CSF samples for a
preliminary Study; W.W. Tourtelotte, M.D., Ph.D. and staff at the Human
Brain and Spinal Fluid Resource Center for assistance with samples and
clinical information; and the National Multiple Sclerosis Society for
funding this study with a Pilot Research Project Award (PP0932) to
W.T.R. This research was also supported in part by the Intramural
Research Program of the NIH, NINDS.
NR 46
TC 29
Z9 29
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD DEC 15
PY 2008
VL 275
IS 1-2
BP 106
EP 112
DI 10.1016/j.jns.2008.07.032
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 384MO
UT WOS:000261749100019
PM 18783801
ER
PT J
AU Darugar, Q
Kim, H
Gorelick, RJ
Landes, C
AF Darugar, Qusai
Kim, Hannah
Gorelick, Robert J.
Landes, Christy
TI Human T-Cell Lymphotropic Virus Type 1 Nucleocapsid Protein-Induced
Structural Changes in Transactivation Response DNA Hairpin Measured by
Single-Molecule Fluorescence Resonance Energy Transfer
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NUCLEIC-ACID-CHAPERONE; HIV-1 REVERSE TRANSCRIPTION; ZINC-FINGER
STRUCTURES; PLUS-STRAND TRANSFER; COMPLEMENTARY SEQUENCE; SECONDARY
STRUCTURE; BINDING-PROPERTIES; RNA; LEUKEMIA; MECHANISM
AB Time-resolved single-molecule fluorescence spectroscopy was used to study the human T-cell lymphotropic virus type 1 (HTLV-1) nucleocapsid protein (NC) chaperone activity compared to that of the human immunodeficiency virus type 1 (HIV-1) NC protein. HTLV-1 NC contains two zinc fingers, each having a CCHC binding motif similar to HIV-1 NC. HIV-1 NC is required for recognition and packaging of the viral RNA and is also a nucleic acid chaperone protein that facilitates nucleic acid restructuring during reverse transcription. Because of similarities in structures between the two retroviruses, we have used single-molecule fluorescence energy transfer to investigate the chaperoning activity of the HTLV-1 NC protein. The results indicate that the HTLV-1 NC protein induces structural changes by opening the transactivation response (TAR) DNA hairpin to an even greater extent than HIV-1 NC. However, unlike HIV-1 NC, HTLV-1 NC does not chaperone the strand-transfer reaction involving TAR DNA. These results suggest that, despite its effective destabilization capability, HTLV-1 NC is not as effective at overall chaperone function as is its HIV-1 counterpart.
C1 [Darugar, Qusai; Kim, Hannah; Landes, Christy] Univ Houston, Dept Chem, Houston, TX 77204 USA.
[Gorelick, Robert J.] NCI Frederick, SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick, MD 21702 USA.
RP Landes, C (reprint author), Univ Houston, Dept Chem, 136 Fleming, Houston, TX 77204 USA.
EM cflandes@uh.edu
RI Landes, Christy/I-5501-2014
FU National Cancer Institute; National Institutes of Health [N01-CO-12400]
FX We thank the University of Houston and the Texas Center for
Superconductivity for new faculty startup funds. This study has been
funded in whole or in part with federal funds from the National Cancer
Institute, National Institutes of Health, under contract N01-CO-12400.;
The content of this publication does not necessarily reflect the views
or policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U. S. Government.
NR 56
TC 16
Z9 16
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC 15
PY 2008
VL 82
IS 24
BP 12164
EP 12171
DI 10.1128/JVI.01158-08
PG 8
WC Virology
SC Virology
GA 376DS
UT WOS:000261164000017
PM 18829758
ER
PT J
AU Bukreyev, A
Yang, LJ
Fricke, J
Cheng, L
Ward, JM
Murphy, BR
Collins, PL
AF Bukreyev, Alexander
Yang, Lijuan
Fricke, Jens
Cheng, Lily
Ward, Jerrold M.
Murphy, Brian R.
Collins, Peter L.
TI The Secreted Form of Respiratory Syncytial Virus G Glycoprotein Helps
the Virus Evade Antibody-Mediated Restriction of Replication by Acting
as an Antigen Decoy and through Effects on Fc Receptor-Bearing
Leukocytes
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RECOMBINANT VACCINIA VIRUS; CYSTEINE-RICH REGION; G-PROTEIN;
INFLUENZA-VIRUS; INFECTED-CELLS; EBOLA-VIRUS; SOLUBLE GLYCOPROTEIN;
ATTACHMENT PROTEIN; GENETIC DIVERSITY; COTTON RATS
AB Respiratory syncytial virus (RSV) readily infects and reinfects during infancy and throughout life, despite maternal antibodies and immunity from prior infection and without the need for significant antigenic change. RSV has two neutralization antigens, the F and G virion glycoproteins. G is expressed in both membrane-bound (mG) and secreted (sG) forms. We investigated whether sG might act as a decoy for neutralizing antibodies by comparing the in vitro neutralization of wild-type (wt) RSV versus recombinant mG RSV expressing only mG. wt RSV indeed was less susceptible than mG RSV to monovalent G-specific and polyvalent RSV-specific antibodies, whereas susceptibility to F-specific antibodies was equivalent. This difference disappeared when the virus preparations were purified to remove sG. Thus, sG appears to function as a neutralization decoy. We evaluated this effect in vivo in mice by comparing the effects of passively transferred antibodies on the pulmonary replication of wt RSV versus mG RSV. Again, wt RSV was less sensitive than mG RSV to G-specific and RSV-specific antibodies; however, a similar difference was also observed with F-specific antibodies. This confirmed that sG helps wt RSV evade the antibody-dependent restriction of replication but indicated that in mice, it is not acting primarily as a decoy for G-specific antibodies, perhaps because sG is produced in insufficient quantities in this poorly permissive animal. Rather, we found that the greater sensitivity of mG versus wt RSV to the antiviral effect of passively transferred RSV antibodies required the presence of inflammatory cells in the lung and was Fc gamma receptor dependent. Thus, sG helps RSV escape the antibody-dependent restriction of replication via effects as an antigen decoy and as a modulator of leukocytes bearing Fc gamma receptors.
C1 [Bukreyev, Alexander; Yang, Lijuan; Fricke, Jens; Murphy, Brian R.; Collins, Peter L.] NIAID, LID, NIH, Bethesda, MD 20892 USA.
[Cheng, Lily; Ward, Jerrold M.] NIAID, Infect Dis Pathogenesis Sect, Comparat Med Branch, NIH, Bethesda, MD 20892 USA.
RP Bukreyev, A (reprint author), NIAID, LID, NIH, 50 S Dr,Room 6505, Bethesda, MD 20892 USA.
EM abukreyev@nih.gov
FU NIAID
FX This project was funded as part of the NIAID intramural program.
NR 55
TC 61
Z9 65
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC 15
PY 2008
VL 82
IS 24
BP 12191
EP 12204
DI 10.1128/JVI.01604-08
PG 14
WC Virology
SC Virology
GA 376DS
UT WOS:000261164000020
PM 18842713
ER
PT J
AU Howard, AR
Senkevich, TG
Moss, B
AF Howard, Amanda R.
Senkevich, Tatiana G.
Moss, Bernard
TI Vaccinia Virus A26 and A27 Proteins Form a Stable Complex Tethered to
Mature Virions by Association with the A17 Transmembrane Protein
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID A-TYPE INCLUSION; INTRACELLULAR MOVEMENT; CELL-SURFACE; ESSENTIAL
COMPONENT; MEMBRANE-PROTEIN; GENE; IDENTIFICATION; POLYPEPTIDES;
MICROTUBULES; PARTICLES
AB During vaccinia virus replication, mature virions (MVs) are wrapped with cellular membranes, transported to the periphery, and exported as extracellular virions (EVs) that mediate spread. The A26 protein is unusual in that it is present in MVs but not EVs. This distribution led to a proposal that A26 negatively regulates wrapping. A26 also has roles in the attachment of MVs to the cell surface and incorporation of MVs into proteinaceous A-type inclusions in some orthopoxvirus species. However, A26 lacks a transmembrane domain, and nothing is known regarding how it associates with the MV, regulates incorporation of the MV into inclusions, and possibly prevents EV formation. Here, we provide evidence that A26 forms a disulfide-bonded complex with A27 that is anchored to the MV through a noncovalent interaction with the A17 transmembrane protein. In the absence of A27, A26 was unstable, and only small amounts were detected. The interaction of A26 with A27 depended on a C-terminal segment of A26 with 45% amino acid identity to A27. Deletion of A26 failed to enhance EV formation by vaccinia virus, as had been predicted. Nevertheless, the interaction of A26 and A27 may have functional significance, since each is thought to mediate binding to cells through interaction with laminin and heparan sulfate, respectively. We also found that A26 formed a noncovalent complex with A25, a truncated form of the cowpox virus A-type inclusion matrix protein. The latter association suggests a mechanism for incorporation of virions into A-type inclusions in other orthopoxvirus strains.
C1 [Howard, Amanda R.; Senkevich, Tatiana G.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, 33 N Dr,MSC 3210, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU Division of Intramural Research; NIAID; NIH
FX The research was supported by the Division of Intramural Research,
NIAID, NIH.
NR 38
TC 23
Z9 27
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC 15
PY 2008
VL 82
IS 24
BP 12384
EP 12391
DI 10.1128/JVI.01524-08
PG 8
WC Virology
SC Virology
GA 376DS
UT WOS:000261164000038
PM 18842719
ER
PT J
AU Yuste, E
Bixby, J
Lifson, J
Sato, S
Johnson, W
Desrosiers, R
AF Yuste, Eloisa
Bixby, Jacqueline
Lifson, Jeffrey
Sato, Shuji
Johnson, Welkin
Desrosiers, Ronald
TI Glycosylation of gp41 of Simian Immunodeficiency Virus Shields Epitopes
That Can Be Targets for Neutralizing Antibodies
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID N-LINKED GLYCANS; EXTRACELLULAR ENVELOPE GLYCOPROTEIN; TYPE-1 ENVELOPE;
IN-VIVO; V3 LOOP; MACROPHAGE TROPISM; RESISTANCE; CD4; INFECTION; HIV-1
AB Human immunodeficiency virus type 1 and simian immunodeficiency virus possess three closely spaced, highly conserved sites for N-linked carbohydrate attachment in the extracellular domain of the transmembrane protein gp41. We infected rhesus monkeys with a variant of cloned SIVmac239 lacking the second and third sites or with a variant strain lacking all three of SIVmac239's glycosylation sites in gp41. For each mutation, asparagine (N) in the canonical N-X-S/T recognition sequence for carbohydrate attachment was changed to the structurally similar glutamine such that two nucleotide changes would be required for a reversion of the mutated codon. By 16 weeks, experimentally infected monkeys made antibodies that neutralized the mutant viruses to high titers. Such antibodies were not observed in monkeys infected with the parental virus. Thus, new specificities were revealed as a result of the carbohydrate attachment mutations, and antibodies of these specificities had neutralizing activity. Unlike monkeys infected with the parental virus, monkeys infected with the mutant viruses made antibodies that reacted with peptides corresponding to the sequences in this region. Furthermore, there was strong selective pressure for the emergence of variant sequences in this region during the course of infection. By analyzing the neutralization profiles of sequence variants, we were able to define three mutations (Q625R, K631N, and Q634H) in the region of the glycosylation site mutations that conferred resistance to neutralization by plasma from the monkeys infected with mutant virus. Based on the reactivity of antibodies to peptides in this region and the colocalization of neutralization escape mutations, we conclude that N-linked carbohydrates in the ectodomain of the transmembrane protein shield underlying epitopes that would otherwise be the direct targets of neutralizing antibodies.
C1 [Yuste, Eloisa; Bixby, Jacqueline; Sato, Shuji; Johnson, Welkin; Desrosiers, Ronald] Harvard Univ, New England Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA.
[Lifson, Jeffrey] NCI, Frederick Canc Res Facil, Frederick, MD USA.
RP Desrosiers, R (reprint author), Harvard Univ, New England Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, 1 Pine Hill Dr,Box 9102, Southborough, MA 01772 USA.
EM ronald_desrosiers@hms.harvard.edu
FU U. S. Public Health Service [AI025328, AI150421]; NEPRC [AI057039,
RR00168]; National Cancer Institute, National Institutes of Health
[N01-CO12400]
FX This work was supported by U. S. Public Health Service grants AI025328
and AI150421 to R. D., AI057039 to W. J., and RR00168 to the NEPRC; by
an award from the International AIDS Vaccine Initiative; and in part
with federal funds from the National Cancer Institute, National
Institutes of Health, under contract N01-CO12400.
NR 39
TC 11
Z9 13
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC 15
PY 2008
VL 82
IS 24
BP 12472
EP 12486
DI 10.1128/JVI.01382-08
PG 15
WC Virology
SC Virology
GA 376DS
UT WOS:000261164000047
PM 18829751
ER
PT J
AU Day, PM
Lowy, DR
Schiller, JT
AF Day, Patricia M.
Lowy, Douglas R.
Schiller, John T.
TI Heparan Sulfate-Independent Cell Binding and Infection with
Furin-Precleaved Papillomavirus Capsids
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PROPROTEIN CONVERTASES; HUMAN KERATINOCYTES; NEUTRALIZATION; EXPRESSION;
CLEAVAGE; PROTEIN; L2; ACTIVATION; MECHANISMS; GENERATION
AB Papillomavirus infection normally involves virion binding to cell surface heparan sulfate proteoglycans (HSPGs). However, we found that human papillomavirus type 16 pseudovirions efficiently bound and infected cells lacking HSPGs if their L2 capsid protein was precleaved by furin, a cellular protease required for infection. The inability of pseudovirions to efficiently bind and infect cultured primary keratinocytes was also overcome by furin precleavage, suggesting that the defect involves altered HSPG modification. We conclude that the primary function of HSPG binding is to enable cell surface furin cleavage of L2 and that binding to a distinct cell surface receptor(s) is a subsequent step of papillomavirus infection.
C1 [Day, Patricia M.; Lowy, Douglas R.; Schiller, John T.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
RP Day, PM (reprint author), NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
EM pmd@nih.gov
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 27
TC 69
Z9 71
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC 15
PY 2008
VL 82
IS 24
BP 12565
EP 12568
DI 10.1128/JVI.01631-08
PG 4
WC Virology
SC Virology
GA 376DS
UT WOS:000261164000055
PM 18829767
ER
PT J
AU Wurster, AL
Pazin, MJ
AF Wurster, Andrea L.
Pazin, Michael J.
TI BRG1-Mediated Chromatin Remodeling Regulates Differentiation and Gene
Expression of T Helper Cells
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID TRANSCRIPTION FACTOR GATA-3; LOCUS-CONTROL REGION; ACTIVATED
PROTEIN-KINASE; TH2 CELLS; HISTONE ACETYLATION; CYTOKINE GENES; CUTTING
EDGE; SWI/SNF COMPLEX; BAF COMPLEX; PROMOTER
AB During T helper cell differentiation, distinct programs of gene expression play a key role in defining the immune response to an environmental challenge. How chromatin remodeling events at the associated cytokine loci control differentiation is not known. We found that the ATP-dependent remodeling enzyme subunit BRG1 was required for T helper 2 (Th2) differentiation and Th2 cytokine transcription. BRG1 binding to cytokine genes was regulated by the extent of differentiation, the extent of activation, and cell fate. BRG1 was required for some features of the chromatin structure in target genes (DNase I hypersensitivity and histone acetylation), suggesting that BRG1 remodeling activity was directly responsible for changes in gene expression. NFAT and STAT6 activity were required for BRG1 recruitment to the Th2 locus control region, and STAT6 associated with BRG1 in a differentiation-inducible manner, suggesting direct recruitment of BRG1 to the bound loci. Together, these findings suggest BRG1 interprets differentiation signals and plays a causal role in gene regulation, chromatin structure, and cell fate.
C1 [Wurster, Andrea L.; Pazin, Michael J.] NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
RP Pazin, MJ (reprint author), NIA, Cellular & Mol Biol Lab, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM pazinm@mail.nih.gov
OI Pazin, Michael/0000-0002-7561-3640
FU National Institutes of Health; National Institute on Aging
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging.
NR 68
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Z9 42
U1 1
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC 15
PY 2008
VL 28
IS 24
BP 7274
EP 7285
DI 10.1128/MCB.00835-08
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376EO
UT WOS:000261166900002
PM 18852284
ER
PT J
AU Galliher-Beckley, AJ
Williams, JG
Collins, JB
Cidlowski, JA
AF Galliher-Beckley, Amy Jo
Williams, Jason Grant
Collins, Jennifer Brady
Cidlowski, John Anthony
TI Glycogen Synthase Kinase 3 beta-Mediated Serine Phosphorylation of the
Human Glucocorticoid Receptor Redirects Gene Expression Profiles
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID TRANSCRIPTIONAL ACTIVATION; NUCLEAR RECEPTORS; CELL-SURVIVAL; TARGET
GENES; PROTEIN; MECHANISMS; IDENTIFICATION; KINASE-3-BETA; INHIBITION;
ISOFORMS
AB Aberrant glycogen synthase kinase 3 beta (GSK-3 beta) activity is associated with the progression of several pathological conditions such as diabetes, Alzheimer's, and cancer. GSK-3 beta regulates cellular processes by directly phosphorylating metabolic enzymes and transcription factors. Here, we discovered a new target for GSK-3 beta phosphorylation: the human glucocorticoid receptor (GR). Glucocorticoid signaling is essential for life and regulates diverse biological functions from cell growth to metabolism to apoptosis. Specifically, we found hormone-dependent GR phosphorylation on serine 404 by GSK-3 beta. Cells expressing a GR that is incapable of GSK-3 beta phosphorylation had a redirection of the global transcriptional response to hormone, including the activation of additional signaling pathways, in part due to the altered ability of unphosphorylatable GR to recruit transcriptional cofactors CBP/p300 and the p65 (RelA) subunit of NF-kappa B. Furthermore, GSK-3 beta-mediated GR phosphorylation inhibited glucocorticoid-dependent NF-kappa B transrepression and attenuated the glucocorticoid-dependent cell death of osteoblasts. Collectively, our results describe a novel convergence point of the GSK-3 beta and the GR pathways, resulting in altered hormone-regulated signaling. Our results also provide a mechanism by which GSK-3 beta activity can dictate how cells will ultimately respond to glucocorticoids.
C1 [Galliher-Beckley, Amy Jo; Cidlowski, John Anthony] NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Williams, Jason Grant] NIEHS, Struct Biol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Collins, Jennifer Brady] NIEHS, Microarray Ctr, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH,Dept Hlth & Human Serv, POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
FU NIH National Institute of Environmental Health Sciences [Z01E5090057-12]
FX This research was supported by the Intramural Research Program of the
NIH National Institute of Environmental Health Sciences
(Z01E5090057-12).
NR 49
TC 61
Z9 61
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC 15
PY 2008
VL 28
IS 24
BP 7309
EP 7322
DI 10.1128/MCB.00808-08
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376EO
UT WOS:000261166900005
PM 18838540
ER
PT J
AU Kotekar, AS
Weissman, JD
Gegonne, A
Cohen, H
Singer, DS
AF Kotekar, Aparna S.
Weissman, Jocelyn D.
Gegonne, Anne
Cohen, Helit
Singer, Dinah S.
TI Histone Modifications, but Not Nucleosomal Positioning, Correlate with
Major Histocompatibility Complex Class I Promoter Activity in Different
Tissues In Vivo
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID NF-KAPPA-B; STIMULATED RESPONSE ELEMENT; GENE-EXPRESSION;
NUCLEAR-FACTOR; GENOME-WIDE; TRANSCRIPTIONAL COACTIVATOR; PREFERENTIAL
ACCESSIBILITY; SACCHAROMYCES-CEREVISIAE; REGULATORY REGIONS; PHO5
PROMOTER
AB To examine the role of chromatin in transcriptional regulation of the major histocompatibility complex (MHC) class I gene, we determined nucleosome occupancy and positioning, histone modifications, and H2A.Z occupancy across its regulatory region in murine tissues that have widely different expression levels. Surprisingly, nucleosome occupancy and positioning were indistinguishable between the spleen, kidney, and brain. In all three tissues, the 200 bp upstream of the transcription start site had low nucleosome occupancy. In contrast, nuclease hypersensitivity, histone modifications, and H2A.Z occupancy showed tissue-specific differences. Thus, tissue-specific differences in MHC class I transcription correlate with histone modifications and not nucleosomal organization. Further, activation of class I transcription by gamma interferon or its inhibition by alpha-amanitin did not alter nucleosome occupancy, positioning, nuclease hypersensitivity, histone modifications, or H2A.Z occupancy in any of the tissues examined. Thus, chromatin remodeling was not required to dynamically modulate transcriptional levels. These findings suggest that the MHC class I promoter remains poised and accessible to rapidly respond to infection and environmental cues.
C1 [Kotekar, Aparna S.; Weissman, Jocelyn D.; Gegonne, Anne; Cohen, Helit; Singer, Dinah S.] NCI, Mol Regulat Sect, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Singer, DS (reprint author), NCI, Mol Regulat Sect, Expt Immunol Branch, NIH, Bldg 10,Rm 4B-36, Bethesda, MD 20892 USA.
EM dinah.singer@nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 65
TC 9
Z9 9
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC 15
PY 2008
VL 28
IS 24
BP 7323
EP 7336
DI 10.1128/MCB.00889-08
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376EO
UT WOS:000261166900006
PM 18809568
ER
PT J
AU Pilon, AM
Arcasoy, MO
Dressman, HK
Vayda, SE
Maksimova, YD
Sangerman, JI
Gallagher, PG
Bodine, DM
AF Pilon, Andre M.
Arcasoy, Murat O.
Dressman, Holly K.
Vayda, Serena E.
Maksimova, Yelena D.
Sangerman, Jose I.
Gallagher, Patrick G.
Bodine, David M.
TI Failure of Terminal Erythroid Differentiation in EKLF-Deficient Mice Is
Associated with Cell Cycle Perturbation and Reduced Expression of E2F2
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID KRUPPEL-LIKE FACTOR; CHROMATIN REMODELING COMPLEX; TRANSCRIPTION FACTOR
EKLF; BETA-GLOBIN PROMOTER; LOCUS-CONTROL REGION; FETAL HEMOGLOBIN;
S-PHASE; GENE; ERYTHROPOIESIS; MATURATION
AB Erythroid Kruppel-like factor (EKLF) is a Kruppel-like transcription factor identified as a transcriptional activator and chromatin modifier in erythroid cells. EKLF-deficient (Eklf(-/-)) mice die at day 14.5 of gestation from severe anemia. In this study, we demonstrate that early progenitor cells fail to undergo terminal erythroid differentiation in Eklf(-/-) embryos. To discover potential EKLF target genes responsible for the failure of erythropoiesis, transcriptional profiling was performed with RNA from wild-type and Eklf(-/-) early erythroid progenitor cells. These analyses identified significant perturbation of a network of genes involved in cell cycle regulation, with the critical regulator of the cell cycle, E2f2, at a hub. E2f2 mRNA and protein levels were markedly decreased in Eklf(-/-) early erythroid progenitor cells, which showed a delay in the G(1)-to-S-phase transition. Chromatin immunoprecipitation analysis demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo. Consistent with the role of EKLF as a chromatin modifier, EKLF binding sites in the E2f2 promoter were located in a region of EKLF-dependent DNase I sensitivity in early erythroid progenitor cells. We propose a model in which EKLF-dependent activation and modification of the E2f2 locus is required for cell cycle progression preceding terminal erythroid differentiation.
C1 [Pilon, Andre M.; Vayda, Serena E.; Bodine, David M.] NHGRI, Hematopoiesis Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Pilon, Andre M.] George Washington Univ, Med Ctr, Dept Biochem & Mol Biol, Washington, DC 20037 USA.
[Arcasoy, Murat O.] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Dressman, Holly K.] CIEMAS, Duke Inst Genome Sci & Policy 2177B, Durham, NC 27708 USA.
[Maksimova, Yelena D.; Sangerman, Jose I.; Gallagher, Patrick G.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA.
RP Bodine, DM (reprint author), NHGRI, Hematopoiesis Sect, Genet & Mol Biol Branch, NIH, 49 Convent Dr,MSC-4442,Bldg 49,Room 4A04, Bethesda, MD 20892 USA.
EM tedyaz@mail.nih.gov
FU NHGRI [RO1 DK62039, RO1 HL65448, T32 HD07094]
FX This study was supported by grants RO1 DK62039 and RO1 HL65448 (P.G.G.)
and T32 HD07094 (J.I.S.) and by NHGRI intramural funds.
NR 43
TC 54
Z9 54
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC 15
PY 2008
VL 28
IS 24
BP 7394
EP 7401
DI 10.1128/MCB.01087-08
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376EO
UT WOS:000261166900012
PM 18852285
ER
PT J
AU Zeuner, KE
Peller, M
Knutzen, A
Hallett, M
Deuschl, G
Siebner, HR
AF Zeuner, Kirsten E.
Peller, Martin
Knutzen, Arne
Hallett, Mark
Deuschl, Guenther
Siebner, Hartwig R.
TI Motor Re-Training Does Not Need to Be Task Specific to Improve Writer's
Cramp
SO MOVEMENT DISORDERS
LA English
DT Article
DE focal hand dystonia; writer's cramp; kinematic analysis; training;
writing; immobilization
ID FOCAL HAND DYSTONIA; 1-YEAR FOLLOW-UP; BOTULINUM TOXIN; PATHOPHYSIOLOGY;
PERFORMANCE
AB Previous studies showed a beneficial effect of motor re-training in task-specific hand dystonia. Here we examined whether re-training needs to specifically focus on the task affected by dystonia. 21 patients with writer's cramp were randomly assigned to two types of re-training: One group of patients trained drawing and writing movements using a pen attached to the bottom of a finger splint. The second group used therapeutic putty to train finger movements without exercises of drawing and writing movements. Training lasted for 8 weeks. Before re-training, affected hand and forearm were immobilized for 4 weeks to facilitate the responsiveness to re-training. Dystonia was assessed during handwriting using the Writer's Cramp Rating Scale. Although no clinical improvement was observed immediately after immobilization, 8 weeks of re-training improved task-specific dystonia relative to baseline (P = 0.005). Both training modalities were equally effective. More severely affected patients benefited most. There was no correlation between disease duration and the individual treatment response. Retraining also improved hand function as indexed by the Ann Dystonia Disability Scale (P = 0.008). Kinematic handwriting analysis showed that re-training lowered vertical force level and enhanced the fluency of handwriting. We conclude that re-training does not need to specifically focus on the task affected by dystonia to be clinically effective. (c) 2008 Movement Disorder Society
C1 [Zeuner, Kirsten E.] Univ Kiel, Dept Neurol, Neurozentrum, D-24105 Kiel, Germany.
[Siebner, Hartwig R.] NeuroImageNord Kiel Hamburg Lubeck, Lubeck, Germany.
[Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Zeuner, KE (reprint author), Univ Kiel, Dept Neurol, Neurozentrum, Schittenhelmstr 10, D-24105 Kiel, Germany.
EM k.zeuner@neurologie.uni-kiel.de
RI Deuschl, Gunther/A-7986-2010; Siebner, Hartwig/G-4052-2016
FU Deutsche Forschungsgemeinschaft [DE 438/7-1, 7-2]; Federal Ministry of
Education and Research [01 GO 0511]
FX This work has been supported by the Deutsche Forschungsgemeinschaft to
G. Deuschl and H. Siebner (grant DE 438/7-1 and 7-2). H.R. Siebner was
supported by a structural grant sponsored by the Federal Ministry of
Education and Research to Neuro-ImageNord (grant 01 GO 0511). We greatly
appreciate the patients and normal volunteers for participating in this
study. We would like to thank Dirk Dressler, MD. Department of Neurology
at the University of Rostock, Alexander Munchau, MD. Department of
Neurology at, the University of Hamburg, Lars Timmermann, MD and Markus
Butz, PhD, Department of Neurology, University of Dusseldorf for
referring patients to us. The corresponding author had full access to
all of the data in the study and takes responsibility for the integrity
of the data and the accuracy of the data analysis.
NR 26
TC 22
Z9 22
U1 1
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD DEC 15
PY 2008
VL 23
IS 16
BP 2319
EP 2327
DI 10.1002/mds.22222
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 391PG
UT WOS:000262244600005
PM 18816801
ER
PT J
AU Daly, JW
Garraffo, HM
Spande, TF
Yeh, HJC
Peltzer, PM
Cacivio, PM
Baldo, JD
Faivovich, J
AF Daly, John W.
Garraffo, H. Martin
Spande, Thomas F.
Yeh, Herman J. C.
Peltzer, Paola M.
Cacivio, Pedro M.
Baldo, J. Diego
Faivovich, Julian
TI Indolizidine 239Q and quinolizidine 275I. Major alkaloids in two
Argentinian bufonid toads (Melanophryniscus)
SO TOXICON
LA English
DT Article
DE Alkaloids; Ants; Bufonidae; Dietary arthropods; Mass spectrometry; Mites
ID DART FROGS DENDROBATIDAE; RED-BELLIED TOADS; POISON FROGS;
PAPIERCHROMATOGRAPHISCHE PRUFUNG; DIET SPECIALIZATION; ARTHROPOD SOURCE;
AMPHIBIAN SKIN; COSTA-RICA; TETRODOTOXIN; BUFADIENOLIDES
AB Alkaloid profiles in skin of poison frogs/toads (Dendrobatidae, Mantellidae, Bufonidae, and Myobatrachidae) are highly dependent on diet and hence on the nature of habitat. Extracts of the two species of toads (Melanophryniscus kiappenbachi and Melanophryniscus cupreuscapularis) from similar habitats in the Corrientes/Chaco Provinces of Argentina have similar profiles of alkaloids, which differ considerably in profiles from other Metanophryniscus species from Brazil, Uruguay and Argentina. Structures of two major alkaloids 239Q (1) and 275I (2) were determined by mass, FTIR, and NMR spectral analysis as 5Z9Z-3-(1-hydroxybutyl)-5-propylindolizidine and 6Z,10E-4,6-di(pent-4-enyl) quinolizidine, respectively. A third alkaloid, 249F (3), is postulated to be a homopumiliotoxin with an unprecedented conjugated exocyclic diene moiety. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Daly, John W.; Garraffo, H. Martin; Spande, Thomas F.; Yeh, Herman J. C.] NIDDKD, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA.
[Peltzer, Paola M.] ESS FBCB UNL, Fac Bioquim & Ciencias Biol, CONICET, RA-3000 Santa Fe, Argentina.
[Baldo, J. Diego] Univ Nacl Misiones, CONICET, Lab Genet Evolut, Fac Ciencias Exactas Quim & Nat,Dept Genet, Posadas, Misiones, Argentina.
[Cacivio, Pedro M.] Consejo Nacl Invest Cient & Tecn, Museo Argentina Ciencias Nat, Div Herpetol, RA-1405 Buenos Aires, DF, Argentina.
[Faivovich, Julian] Univ Estadual Paulista, Inst Biociencias, Dept Zool, BR-13506900 Sao Paulo, Brazil.
RP Garraffo, HM (reprint author), NIDDKD, Bioorgan Chem Lab, NIH, DHHS, 9000 Rockville Pike,Bldg 8,Room 1A24, Bethesda, MD 20892 USA.
EM garraffo@helix.nih.gov
OI Baldo, Diego/0000-0003-2382-0872
FU NIDDK; PMP; JDB; CONICET (Consejo Nacional de Investigaciones
Cientificas y Tecnicas); PICT (Proyecto de Investigacion Cientifica y
Tecnologica) [2006 223]; FAPESP (Fundaco de Amparo a Pesquisa do Estado
de Sao Paulo) [2005/56756-0, 2006/562088-5]
FX We thank Ralph Saporito for valuable suggestions and references. Work at
NIH was supported by intramural funds of NIDDK. PMP, JDB, and JF thank
Rafael C. Lajmanovich, CONICET (Consejo Nacional de Investigaciones
Cientificas y Tecnicas) and PICT (Proyecto de Investigacion Cientifica y
Tecnologica) 2006 223. JF thanks FAPESP (Fundaco de Amparo a Pesquisa do
Estado de Sao Paulo) processes 2005/56756-0 and 2006/562088-5.
NR 64
TC 26
Z9 26
U1 1
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0041-0101
J9 TOXICON
JI Toxicon
PD DEC 15
PY 2008
VL 52
IS 8
BP 858
EP 870
DI 10.1016/j.toxicon.2008.08.016
PG 13
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 388XN
UT WOS:000262053700005
PM 18848574
ER
PT J
AU Aldhous, P
Gahl, W
AF Aldhous, Peter
Gahl, William
TI Dr House's caring alter ego
SO NEW SCIENTIST
LA English
DT Editorial Material
C1 [Gahl, William] US Natl Human Genome Res Inst, Bethesda, MD USA.
[Gahl, William] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU REED BUSINESS INFORMATION LTD
PI SUTTON
PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND
SN 0262-4079
J9 NEW SCI
JI New Sci.
PD DEC 13
PY 2008
VL 200
IS 2686
BP 44
EP 45
DI 10.1016/S0262-4079(08)63163-2
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 391BQ
UT WOS:000262208200032
ER
PT J
AU Robbiani, DF
Bothmer, A
Callen, E
Reina-San-Martin, B
Dorsett, Y
Difilippantonio, S
Bolland, DJ
Chen, HT
Corcoran, AE
Nussenzweig, A
Nussenzweig, MC
AF Robbiani, Davide F.
Bothmer, Anne
Callen, Elsa
Reina-San-Martin, Bernardo
Dorsett, Yair
Difilippantonio, Simone
Bolland, Daniel J.
Chen, Hua Tang
Corcoran, Anne E.
Nussenzweig, Andre
Nussenzweig, Michel C.
TI AID Is Required for the Chromosomal Breaks in c-myc that Lead to
c-myc/IgH Translocations
SO CELL
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; SINGLE-STRANDED-DNA; CYTIDINE DEAMINASE AID;
HEAVY-CHAIN LOCUS; CENTER B-CELLS; SOMATIC HYPERMUTATION;
BURKITT-LYMPHOMA; IN-VIVO; ANTIBODY DIVERSIFICATION; MURINE
PLASMACYTOMAS
AB Chromosomal translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromosomes. One of the most well characterized oncogenic translocations juxtaposes c-myc and the immunoglobulin heavy-chain locus (IgH) and is found in Burkitt's lymphomas in humans and plasmacytomas in mice. DNA breaks in IgH leading to c-myc/IgH translocations are created by activation-induced cytidine deaminase ( AID) during antibody class switch recombination or somatic hypermutation. However, the source of DNA breaks at c-myc is not known. Here, we provide evidence for the c-myc promoter region being required in targeting AID-mediated DNA damage to produce DSBs in c-myc that lead to c-myc/IgH translocations in primary B lymphocytes. Thus, in addition to producing somatic mutations and DNA breaks in antibody genes, AID is also responsible for the DNA lesions in oncogenes that are required for their translocation.
C1 [Robbiani, Davide F.; Bothmer, Anne; Reina-San-Martin, Bernardo; Dorsett, Yair; Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
[Nussenzweig, Michel C.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10065 USA.
[Callen, Elsa; Difilippantonio, Simone; Chen, Hua Tang; Nussenzweig, Andre] NCI, NIH, Expt Immunol Branch, Bethesda, MD 20892 USA.
[Bolland, Daniel J.; Corcoran, Anne E.] Babraham Inst, Lab Chromatin & Gene Express, Cambridge CB22 3AT, England.
RP Nussenzweig, MC (reprint author), Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
EM nussen@mail.rockefeller.edu
RI Reina-San-Martin, Bernardo/I-9484-2016
OI Reina-San-Martin, Bernardo/0000-0003-2083-6166
FU NIH; National Cancer Institute; Center for Cancer Research; Leukemia and
Lymphoma Society; Howard Hughes Medical Institute Investigator
FX All members of the Nussenzweig lab for discussions. Dr. Barry Stoddard (
Fred Hutchinson Cancer Research Center, Seattle) for suggestions on
catalytically inactive I-SceI*. The Rockefeller University Gene
Targeting Facility, Klara Velinzon, and Tamara Shengelia for FACSorting,
Matthias Muellenbeck and Nancy Wong for technical assistance, and David
Bosque and Tom Eisenreich for help in managing the mouse colonies. The
work was supported in part by NIH grants to M. C. N. The A. N. lab was
supported by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research. D. F. R. is a Fellow of the
Leukemia and Lymphoma Society, and M. C. N. is a Howard Hughes Medical
Institute Investigator.
NR 77
TC 222
Z9 227
U1 1
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD DEC 12
PY 2008
VL 135
IS 6
BP 1028
EP 1038
DI 10.1016/j.cell.2008.09.062
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 382ZB
UT WOS:000261642800019
PM 19070574
ER
PT J
AU Kachirskaia, I
Shi, XB
Yamaguchi, H
Tanoue, K
Wen, H
Wang, EW
Appella, E
Gozani, O
AF Kachirskaia, Ioulia
Shi, Xiaobing
Yamaguchi, Hiroshi
Tanoue, Kan
Wen, Hong
Wang, Evelyn W.
Appella, Ettore
Gozani, Or
TI Role for 53BP1 Tudor Domain Recognition of p53 Dimethylated at Lysine
382 in DNA Damage Signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HISTONE H4; METHYLATION; METHYLTRANSFERASE; REPRESSION; PR-SET7; BREAKS;
SET8
AB Modification of histone proteins by lysine methylation is a principal chromatin regulatory mechanism (Shi, Y., and Whet-stine, J. R. (2007) Mol. Cell 25, 1-14). Recently, lysine methylation has been shown also to play a role in regulating non-histone proteins, including the tumor suppressor protein p53 (Huang, J., and Berger, S. L. (2008) Curr. Opin. Genet. Dev. 18, 152-158). Here, we identify a novel p53 species that is dimethylated at lysine 382 (p53K382me2) and show that the tandem Tudor domain of the DNA damage response mediator 53BP1 acts as an "effector" for this mark. We demonstrate that the 53BP1 tandem Tudor domain recognizes p53K382me2 with a selectivity relative to several other protein lysine methylation sites and saturation states. p53K382me2 levels increase with DNA damage, and recognition of this modification by 53BP1 facilitates an interaction between p53 and 53BP1. The generation of p53K382me2 promotes the accumulation of p53 protein that occurs upon DNA damage, and this increase in p53 levels requires 53BP1. Taken together, our study identifies a novel p53 modification, demonstrates a new effector function for the 53BP1 tandem Tudor domain, and provides insight into how DNA damage signals are transduced to stabilize p53.
C1 [Kachirskaia, Ioulia; Shi, Xiaobing; Gozani, Or] Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
[Yamaguchi, Hiroshi; Tanoue, Kan; Appella, Ettore] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Wen, Hong; Wang, Evelyn W.] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA.
RP Gozani, O (reprint author), Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
EM ogozani@stanford.edu
FU National Institutes of Health [GM079641]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant GM079641 (to O.G.) and the Intramural Research Program of
the National Institutes of Health (to E. A. and H. Y.). The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 20
TC 47
Z9 50
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 DEC 12
PY 2008
VL 283
IS 50
BP 34660
EP 34666
DI 10.1074/jbc.M806020200
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 380MF
UT WOS:000261469100021
PM 18840612
ER
PT J
AU Burd, CJ
Kinyamu, HK
Miller, FW
Archer, TK
AF Burd, Craig J.
Kinyamu, H. Karimi
Miller, Frederick W.
Archer, Trevor K.
TI UV Radiation Regulates Mi-2 through Protein Translation and Stability
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HISTONE DEACETYLASE; REMODELING COMPLEX; P53 TRANSLATION; MUSCLE
DISEASE; BREAST-CANCER; CHROMATIN; DERMATOMYOSITIS; AUTOANTIBODIES;
EXPRESSION; MYOSITIS
AB Dermatomyositis (DM) is an autoimmune disease, which is often accompanied by the development of disease-specific autoantibodies directed against the SNF2-superfamily helicase, Mi-2. Recent evidence suggests that ultraviolet radiation exposure may be an important risk factor for the development of not only the disease but also specific autoimmunity against Mi-2. Consequently, we investigated the effects of ultraviolet radiation on Mi-2 protein expression. We observed an increase in protein levels upon ultraviolet radiation exposure in cell culture systems. These changes in expression occur quite rapidly, are maximized just 1 h following exposure, and are unique to Mi-2 when compared with other members of the NuRD complex. Changes in protein levels are not mediated through transcriptional mechanisms. Treatment results in a more efficiently translated message through regulatory elements in the 5'-UTR region of the transcript. Investigation into protein half-life further demonstrated increased stability of Mi-2 following UV exposure. Taken together, we describe a system by which Mi-2 protein expression can be quickly increased following UV exposure and then maintained up to 16 h later. These data provide a novel regulation of an important transcriptional regulator and provide insight into the possible mechanisms of the development of DM and associated autoantibodies.
C1 [Burd, Craig J.; Kinyamu, H. Karimi; Archer, Trevor K.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Miller, Frederick W.] NIEHS, Environm Autoimmunity Grp, Off Clin Res, NIH, Res Triangle Pk, NC 27709 USA.
RP Archer, TK (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, MD D4-01,POB 12233, Res Triangle Pk, NC 27709 USA.
EM archer1@niehs.nih.gov
OI Miller, Frederick/0000-0003-2831-9593; Burd, Craig/0000-0002-6899-6751
FU Intramural Research Program of the NIEHS [Z01 ES071006-09]; National
Institutes of Health
FX This work was supported, in whole or in part, by Program Grant Z01
ES071006-09 in the Intramural Research Program of the NIEHS, National
Institutes of Health. The costs of publication of this article were
defrayed in part by the payment of page charges. This article must
therefore be hereby marked "advertisement" in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact.
NR 33
TC 23
Z9 23
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 12
PY 2008
VL 283
IS 50
BP 34976
EP 34982
DI 10.1074/jbc.M805383200
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 380MF
UT WOS:000261469100054
PM 18922793
ER
PT J
AU Sauna, ZE
Bohn, SS
Rutledge, R
Dougherty, MP
Cronin, S
May, L
Xia, D
Ambudkar, SV
Golin, J
AF Sauna, Zuben E.
Bohn, Sherry Supernavage
Rutledge, Robert
Dougherty, Michael P.
Cronin, Susan
May, Leopold
Xia, Di
Ambudkar, Suresh V.
Golin, John
TI Mutations Define Cross-talk between the N-terminal Nucleotide-binding
Domain and Transmembrane Helix-2 of the Yeast Multidrug Transporter Pdr5
POSSIBLE CONSERVATION OF A SIGNALING INTERFACE FOR COUPLING ATP
HYDROLYSIS TO DRUG TRANSPORT
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CASSETTE ABC TRANSPORTER; SACCHAROMYCES-CEREVISIAE; CANDIDA-ALBICANS;
P-GLYCOPROTEIN; ENCODING GENE; RESISTANCE; PROTEIN; EFFLUX; MECHANISM;
CDR1P
AB The yeast Pdr5 multidrug transporter is an important member of the ATP-binding cassette superfamily of proteins. We describe a novel mutation (S558Y) in transmembrane helix 2 of Pdr5 identified in a screen for suppressors that eliminated Pdr5-mediated cycloheximide hyper-resistance. Nucleotides as well as transport substrates bind to the mutant Pdr5 with an affinity comparable with that for wild-type Pdr5. Wild-type and mutant Pdr5s show ATPase activity with comparable K(m(ATP)) values. Nonetheless, drug sensitivity is equivalent in the mutant pdr5 and the pdr5 deletion. Finally, the transport substrate clotrimazole, which is a noncompetitive inhibitor of Pdr5 ATPase activity, has a minimal effect on ATP hydrolysis by the S558Y mutant. These results suggest that the drug sensitivity of the mutant Pdr5 is attributable to the uncoupling of NTPase activity and transport. We screened for amino acid alterations in the nucleotide-binding domains that would reverse the phenotypic effect of the S558Y mutation. A second-site mutation, N242K, located between the Walker A and signature motifs of the N-terminal nucleotide-binding domain, restores significant function. This region of the nucleotide-binding domain interacts with the transmembrane domains via the intracellular loop-1 (which connects transmembrane helices 2 and 3) in the crystal structure of Sav1866, a bacterial ATP-binding cassette drug transporter. These structural studies are supported by biochemical and genetic evidence presented here that interactions between transmembrane helix 2 and the nucleotide-binding domain, via the intracellular loop-1, may define at least part of the translocation pathway for coupling ATP hydrolysis to drug transport.
C1 [Bohn, Sherry Supernavage; Dougherty, Michael P.; Golin, John] Catholic Univ Amer, Dept Biol, Washington, DC 20064 USA.
[May, Leopold] Catholic Univ Amer, Dept Chem, Washington, DC 20064 USA.
[Sauna, Zuben E.; Rutledge, Robert; Xia, Di; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Cronin, Susan] Immaculata Univ, Dept Biol, Immaculata, PA 19345 USA.
RP Golin, J (reprint author), Catholic Univ Amer, Dept Biol, McCort Ward Bldg 103, Washington, DC 20064 USA.
EM golin@cua.edu
FU National Institutes of Health (Intramural Research Program, Center for
Cancer Research, NCI); National Institutes of Health [GM07721]
FX Supported by National Institutes of Health Grant GM07721.
NR 36
TC 37
Z9 37
U1 0
U2 4
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 DEC 12
PY 2008
VL 283
IS 50
BP 35010
EP 35022
DI 10.1074/jbc.M806446200
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 380MF
UT WOS:000261469100058
PM 18842589
ER
PT J
AU Choi, E
Han, C
Park, I
Lee, B
Jin, S
Choi, H
Kim, DH
Park, ZY
Eddy, EM
Cho, C
AF Choi, Eunyoung
Han, Cecil
Park, Inju
Lee, Boyeon
Jin, Sora
Choi, Heejin
Kim, Do Han
Park, Zee Yong
Eddy, Edward M.
Cho, Chunghee
TI A Novel Germ Cell-specific Protein, SHIP1, Forms a Complex with
Chromatin Remodeling Activity during Spermatogenesis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HISTONE-DEACETYLASES; MOUSE SPERMATOGENESIS; VALPROIC ACID;
CO-REPRESSOR; SANT DOMAIN; N-COR; MEIOSIS; HSP70-2; GENES;
IDENTIFICATION
AB To determine the mechanisms of spermatogenesis, it is essential to identify and characterize germ cell-specific genes. Here we describe a protein encoded by a novel germ cell-specific gene, Mm. 290718/ZFP541, identified from the mouse spermatocyte UniGene library. Theprotein contains specific motifs and domains potentially involved in DNA binding and chromatin reorganization. An antibody against Mm. 290718/ZFP541 revealed the existence of the protein in testicular spermatogenic cells (159 kDa) but not testicular and mature sperm. Immunostaining analysis of cells at various stages of spermatogenesis consistently showed that the protein is present in spermatocytes and round spermatids only. Transfection assays and immunofluorescence studies indicate that the protein is localized specifically in the nucleus. Proteomic analyses performed to explore the functional characteristics of Mm. 290718/ZFP541 showed that the protein forms a unique complex. Other major components of the complex included histone deacetylase 1 (HDAC1) and heat-shock protein A2. Disappearance of Mm. 290718/ZFP541 was highly correlated with hyperacetylation in spermatids during spermatogenesis, and specific domains of the protein were involved in the regulation of interactions and nuclear localization of HDAC1. Furthermore, we found that premature hyperacetylation, induced by an HDAC inhibitor, is associated with an alteration in the integrity of Mm. 290718/ZFP541 in spermatogenic cells. Our results collectively suggest that the Mm. 290718/ZFP541 complex is implicated in chromatin remodeling during spermatogenesis, and we provide further information on the previously unknown molecular mechanism. Consequently, we re-designate Mm. 290718/ZFP541 as "SHIP1" representing spermatogenic cell HDAC-interacting protein 1.
C1 [Choi, Eunyoung; Han, Cecil; Park, Inju; Lee, Boyeon; Jin, Sora; Choi, Heejin; Kim, Do Han; Park, Zee Yong; Cho, Chunghee] Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea.
[Choi, Eunyoung; Han, Cecil; Park, Inju; Lee, Boyeon; Jin, Sora; Choi, Heejin; Kim, Do Han; Park, Zee Yong; Cho, Chunghee] Gwangju Inst Sci & Technol, Res Ctr Biomol Nanotechnol, Kwangju 500712, South Korea.
[Eddy, Edward M.] NIEHS, Gamete Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Cho, C (reprint author), Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea.
EM choch@gist.ac.kr
FU National Institutes of Health [ZO1 ES070077]; Korea Science and
Engineering Foundation [RO1-2007-000-20116]; Korean Systems Biology
Research Grant [M10503010001-06N0301-00110]; GIST Systems Biology
Infrastructure Establishment
FX This work was supported, in whole or in part, by National Institutes of
Health Grant ZO1 ES070077 ( Project 1, Intramural Research Program,
NIEHS). This work was also supported by the Korea Science and
Engineering Foundation Grant RO1-2007-000-20116, Korean Systems Biology
Research Grant M10503010001-06N0301-00110, and GIST Systems Biology
Infrastructure Establishment grant. The costs of publication of this
article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 36
TC 19
Z9 23
U1 1
U2 4
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 DEC 12
PY 2008
VL 283
IS 50
BP 35283
EP 35294
DI 10.1074/jbc.M805590200
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 380MF
UT WOS:000261469100084
PM 18849567
ER
PT J
AU Zhou, Z
Feng, HQ
Ghirlando, R
Bai, YW
AF Zhou, Zheng
Feng, Hanqiao
Ghirlando, Rodolfo
Bai, Yawen
TI The High-Resolution NMR Structure of the Early Folding Intermediate of
the Thermus thermophilus Ribonuclease H
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE protein folding intermediate; protein folding; NMR structure; hydrogen
exchange; protein engineering
ID STATE HYDROGEN-EXCHANGE; 2-STATE PROTEINS; NATIVE-STATE; DENATURED
STATE; RATE PREDICTION; CONTACT ORDER; CHAIN-LENGTH; PATHWAY;
EQUILIBRIUM; MECHANISM
AB Elucidation of the high-resolution structures of folding intermediates is a necessary but difficult step toward the ultimate understanding of the mechanism of protein folding. Here, using hydrogen-exchange-directed protein engineering, we populated the folding intermediate of the Thermus thermophilus ribonuclease H, which forms before the rate-limiting transition state, by removing the unfolded regions of the intermediate, including an alpha-helix and two beta-strands (51 folded residues). Using multidimensional NMR, we solved the structure of this intermediate mimic to an atomic resolution (backbone rmsd, 0.51 angstrom). It has a native-like backbone topology and shows some local deviations from the native structure, revealing that the structure of the folded region of an early folding intermediate can be as well defined as the native structure. The topological parameters calculated from the structures of the intermediate mimic and the native state predict that the intermediate should fold on a millisecond time scale or less and form much faster than the native state. Other factors that may lead to the slow folding of the native state and the accumulation of the intermediate before the rate-limiting transition state are also discussed. Published by Elsevier Ltd.
C1 [Zhou, Zheng; Feng, Hanqiao; Bai, Yawen] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Ghirlando, Rodolfo] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Bai, YW (reprint author), NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM yawen@helix.nih.gov
RI Ghirlando, Rodolfo/A-8880-2009
FU National Cancer Institute; National Institute of Diabetes and Digestive
and Kidney Diseases; National Institutes of Health
FX We thank Walter Englander and Tobin Sosnick for their critical comments.
This work is supported by the intramural research program of National
Cancer Institute and National Institute of Diabetes and Digestive and
Kidney Diseases, National Institutes of Health.
NR 55
TC 14
Z9 14
U1 0
U2 5
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 DEC 12
PY 2008
VL 384
IS 2
BP 531
EP 539
DI 10.1016/j.jmb.2008.09.044
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 377TC
UT WOS:000261272500018
PM 18848567
ER
PT J
AU Khan, J
Benoliel, R
Herzberg, U
Mannes, AJ
Caudle, RM
Young, A
Eliav, E
AF Khan, Junad
Benoliel, Rafael
Herzberg, Uri
Mannes, Andrew J.
Caudle, Robert M.
Young, Andrew
Eliav, Eli
TI Bite force and pattern measurements for dental pain assessment in the
rat
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE Dental Pain; Bite force; Bite pattern
ID MASSETER INHIBITORY PERIODS; TOOTH-PULP STIMULATION; MECHANICAL
ALLODYNIA; IRREVERSIBLE PULPITIS; TRIGEMINAL PAIN; DISCRIMINATION;
ENDURANCE; MODEL
AB We present simple method to assess dental pain in the awake rat. Using a sensitive strain gauge we examined changes in bite strength and bite pattern in rats following dental injury. Rats with dental injury displayed a significant reduction in mean peak bite strength and an altered bite cluster pattern. Both changes in the dental injury rats were reversed by an analgesic dose of morphine, and this could be reversed with naloxone. These changes were not observed in naive control animals. This simple method significantly improves our ability to evaluate dental pain syndromes. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Khan, Junad; Young, Andrew; Eliav, Eli] Univ Med & Dent New Jersey, Dept Diagnost Sci, Div Orofacial Pain,New Jersey Dent Sch, Suzan & Robert Carmel Endowed Chair Algesiol, Newark, NJ 07103 USA.
[Benoliel, Rafael] Hadassah Hebrew Univ, Fac Med Dent, Dept Oral Med, Jerusalem, Israel.
[Herzberg, Uri] Johnson & Johnson Med Device Grp, Ctr Biomat & Adv Technol, Somerville, NJ USA.
[Mannes, Andrew J.] NIDCR, DASS, CC PNSB, NIH,DHH, Bethesda, MD USA.
[Caudle, Robert M.] Univ Florida, Coll Dent, Dept Oral & Maxillofacial Surg, Gainesville, FL USA.
RP Eliav, E (reprint author), Univ Med & Dent New Jersey, Dept Diagnost Sci, Div Orofacial Pain,New Jersey Dent Sch, Suzan & Robert Carmel Endowed Chair Algesiol, 110 Bergen St, Newark, NJ 07103 USA.
EM eliavel@umdnj.edu
RI Rastelli, Marcio/B-8034-2011;
OI Mannes, Andrew/0000-0001-5834-5667
FU Intramural NIH HHS [Z99 CL999999]
NR 23
TC 5
Z9 5
U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD DEC 12
PY 2008
VL 447
IS 2-3
BP 175
EP 178
DI 10.1016/j.neulet.2008.70.008
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 381PV
UT WOS:000261549300017
PM 18926882
ER
PT J
AU Krueger, F
Grafman, J
McCabe, K
AF Krueger, Frank
Grafman, Jordan
McCabe, Kevin
TI Neural correlates of economic game playing
SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Review
DE neuroeconomics; game theory; trust; reward; social; functional magnetic
resonance imaging; oxytocin
ID ANTERIOR CINGULATE CORTEX; TEMPORO-PARIETAL JUNCTION; RIGHT PREFRONTAL
CORTEX; MIXED-STRATEGY GAME; THEORY-OF-MIND; DECISION-MAKING;
PERSPECTIVE-TAKING; COMPETITIVE GAME; ULTIMATUM GAME; SHARED
REPRESENTATIONS
AB The theory of games provides a mathematical formalization of strategic choices, which have been studied in both economics and neuroscience, and more recently has become the focus of neuroeconomics experiments with human and non-human actors. This paper reviews the results from a number of game experiments that establish a unitary system for forming subjective expected utility maps in the brain, and acting on these maps to produce choices. Social situations require the brain to build an understanding of the other person using neuronal mechanisms that share affective and intentional mental states. These systems allow subjects to better predict other players' choices, and allow them to modify their subjective utility maps to value pro-social strategies. New results for a trust game are presented, which show that the trust relationship includes systems common to both trusting and trustworthy behaviour, but they also show that the relative temporal positions of first and second players require computations unique to that role.
C1 [Krueger, Frank; McCabe, Kevin] George Mason Univ, Ctr Study Neuroecon, Fairfax, VA 22030 USA.
[Krueger, Frank; Grafman, Jordan] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
RP McCabe, K (reprint author), George Mason Univ, Ctr Study Neuroecon, 4400 Univ Dr,MSN 1G3, Fairfax, VA 22030 USA.
EM kmccabe@gmu.edu
FU NINDS; CNS/NINDS/NIH
FX The authors are grateful to N. Armstrong, J. Moll, M. Strenziok and R.
Zahn for their help in various stages of the fMRI experiment. The work
was supported in part by a postdoctoral NINDS competitive fellowship
award to F. K. and the Intramural Research Program of the CNS/NINDS/NIH.
NR 122
TC 30
Z9 32
U1 20
U2 40
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8436
J9 PHILOS T R SOC B
JI Philos. Trans. R. Soc. B-Biol. Sci.
PD DEC 12
PY 2008
VL 363
IS 1511
BP 3859
EP 3874
DI 10.1098/rstb.2008.0165
PG 16
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 371WY
UT WOS:000260864600009
PM 18829425
ER
PT J
AU Boon, K
Tomfohr, JK
Bailey, NW
Garantziotis, S
Li, ZW
Brass, DM
Maruoka, S
Hollingsworth, JW
Schwartz, DA
AF Boon, Kathy
Tomfohr, John K.
Bailey, Nathaniel W.
Garantziotis, Stavros
Li, Zhuowei
Brass, David M.
Maruoka, Shuichiro
Hollingsworth, John W.
Schwartz, David A.
TI Evaluating genome-wide DNA methylation changes in mice by Methylation
Specific Digital Karyotyping
SO BMC GENOMICS
LA English
DT Article
ID EPIGENETIC CHANGES; DISEASE; SUSCEPTIBILITY; EPIGENOMICS; COREST; GENES
AB Background: The study of genome-wide DNA methylation changes has become more accessible with the development of various array-based technologies though when studying species other than human the choice of applications are limited and not always within reach. In this study, we adapted and tested the applicability of Methylation Specific Digital Karyotyping (MSDK), a non-array based method, for the prospective analysis of epigenetic changes after perinatal nutritional modifications in a mouse model of allergic airway disease. MSDK is a sequenced based method that allows a comprehensive and unbiased methylation profiling. The method generates 21 base pairs long sequence tags derived from specific locations in the genome. The resulting tag frequencies determine in a quantitative manner the methylation level of the corresponding loci.
Results: Genomic DNA from whole lung was isolated and subjected to MSDK analysis using the methylation-sensitive enzyme Not I as the mapping enzyme and Nla III as the fragmenting enzyme. In a pair wise comparison of the generated mouse MSDK libraries we identified 158 loci that are significantly differentially methylated (P-value = 0.05) after perinatal dietary changes in our mouse model. Quantitative methylation specific PCR and sequence analysis of bisulfate modified genomic DNA confirmed changes in methylation at specific loci. Differences in genomic MSDK tag counts for a selected set of genes, correlated well with changes in transcription levels as measured by real-time PCR. Furthermore serial analysis of gene expression profiling demonstrated a dramatic difference in expressed transcripts in mice exposed to perinatal nutritional changes.
Conclusion: The genome-wide methylation survey applied in this study allowed for an unbiased methylation profiling revealing subtle changes in DNA methylation in mice maternally exposed to dietary changes in methyl-donor content. The MSDK method is applicable for mouse models of complex human diseases in a mixed cell population and might be a valuable technology to determine whether environmental exposures can lead to epigenetic changes.
C1 [Boon, Kathy; Tomfohr, John K.; Bailey, Nathaniel W.; Garantziotis, Stavros; Brass, David M.; Maruoka, Shuichiro; Schwartz, David A.] NHLBI, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
[Li, Zhuowei; Brass, David M.; Hollingsworth, John W.] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Schwartz, David A.] Natl Jewish Hlth, Denver, CO 80206 USA.
[Schwartz, David A.] Univ Colorado, Hlth Sci Ctr, Denver, CO 80206 USA.
RP Boon, K (reprint author), NHLBI, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
EM boonc@mail.nih.gov; tomfohr@gmail.com; getnatbailey@gmail.com;
garantziotis@niehs.nih.gov; zhuowei.li@duke.edu; david.brass@duke.edu;
maruokas@niehs.nih.gov; holli017@mc.duke.edu; schwartzd@njc.org
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU NIEHS; NHLBI Intramural Research Programs [HL091335]
FX This work was supported by NIEHS and NHLBI Intramural Research Programs
(DAS) and HL091335 (JWH).
NR 25
TC 3
Z9 3
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD DEC 11
PY 2008
VL 9
AR 598
DI 10.1186/1471-2164-9-598
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 403VC
UT WOS:000263109100003
PM 19077247
ER
PT J
AU Pierson, TC
AF Pierson, Theodore C.
TI Waste Not, Want Not: A Viral RNA Degradation Product Modulates West Nile
Virus Pathogenesis
SO CELL HOST & MICROBE
LA English
DT Editorial Material
ID BODIES; CELLS
AB In this issue of Cell Host & Microbe, Pijlman et al. define the structure and mechanism of generation of a small viral noncoding RNA present in flavivirus-infected cells that has a marked impact on the fate of infected cells and virulence in vivo.
C1 NIH, Viral Pathogenesis Sect, Viral Dis Lab, Bethesda, MD 20892 USA.
RP Pierson, TC (reprint author), NIH, Viral Pathogenesis Sect, Viral Dis Lab, Bethesda, MD 20892 USA.
EM piersontc@mail.nih.gov
NR 9
TC 2
Z9 2
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD DEC 11
PY 2008
VL 4
IS 6
BP 512
EP 513
DI 10.1016/j.chom.2008.11.004
PG 2
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 388GB
UT WOS:000262007200004
PM 19064251
ER
PT J
AU Neckers, L
Tatu, U
AF Neckers, Len
Tatu, Utpal
TI Molecular Chaperones in Pathogen Virulence: Emerging New Targets for
Therapy
SO CELL HOST & MICROBE
LA English
DT Review
ID HEAT-SHOCK-PROTEIN; HUMAN EPITHELIAL-CELLS; NF-KAPPA-B;
PLASMODIUM-FALCIPARUM; DRUG-RESISTANCE; LISTERIA-MONOCYTOGENES;
HELICOBACTER-PYLORI; GENE-EXPRESSION; LEISHMANIA-DONOVANI; HSP90
INHIBITORS
AB Infectious organisms have to cope with demanding and rapidly changing environments during establishment in the host. This is particularly relevant for pathogens that utilize different hosts to complete their life cycle. In addition to homeotic environmental challenges, other stressful factors, such as oxidative bursts, are often triggered in response to infection. It is not surprising that many successful pathogens have developed robust chaperone systems to conquer the stressful environments in the host. In addition to discussing ingenious ways by which pathogens have utilized chaperones, the potential of exploiting pathogen chaperones as drug targets is also discussed.
C1 [Tatu, Utpal] Indian Inst Sci, Dept Biochem, Bangalore 560012, Karnataka, India.
[Neckers, Len] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Tatu, U (reprint author), Indian Inst Sci, Dept Biochem, Bangalore 560012, Karnataka, India.
EM tatu@biochem.iisc.ernet.in
FU Intramural NIH HHS [Z01 SC010074-12]; NCI NIH HHS [Z01 BC011032-01]
NR 75
TC 41
Z9 42
U1 0
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD DEC 11
PY 2008
VL 4
IS 6
BP 519
EP 527
DI 10.1016/j.chom.2008.10.011
PG 9
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 388GB
UT WOS:000262007200005
PM 19064253
ER
PT J
AU Peterson, MM
Mack, JL
Hall, PR
Alsup, AA
Alexander, SM
Sully, EK
Sawires, YS
Cheung, AL
Otto, M
Gresham, HD
AF Peterson, M. Michal
Mack, Jessica L.
Hall, Pamela R.
Alsup, Anny A.
Alexander, Susan M.
Sully, Erin K.
Sawires, Youhanna S.
Cheung, Ambrose L.
Otto, Michael
Gresham, Hattie D.
TI Apolipoprotein B Is an Innate Barrier against Invasive Staphylococcus
aureus Infection
SO CELL HOST & MICROBE
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; LOW-DENSITY-LIPOPROTEIN; IN-VIVO;
CRITICALLY-ILL; PLASMA-LIPOPROTEINS; ACUTE-INFLAMMATION; VIRULENCE;
METABOLISM; ACTIVATION; DEATH
AB Staphylococcus aureus is both a colonizer of humans and a cause of severe invasive infections. Although the genetic basis for phenotype switching from colonizing to invasive has received significant study, knowledge of host factors that antagonize the switch is limited. We show that VLDL and LDL lipoproteins interfere with this switch by antagonizing the S. aureus agr quorum-sensing system that upregulates genes required for invasive infection. The mechanism of antagonism entails binding of the major structural protein of these lipoproteins, apolipoprotein B, to an S. aureus autoinducing pheromone, preventing attachment of this pheromone to the bacteria and subsequent signaling through its receptor, AgrC. Mice deficient in plasma apolipoprotein 13, either genetically or pharmacologically, are more susceptible to invasive agr+ bacterial infection, but not to infection with an agr deletion mutant. Therefore, apolipoprotein B at homeostatic levels in blood is an essential innate defense effector against invasive S. aureus infection.
C1 [Peterson, M. Michal; Mack, Jessica L.; Hall, Pamela R.; Alsup, Anny A.; Alexander, Susan M.; Sully, Erin K.; Sawires, Youhanna S.; Gresham, Hattie D.] Univ New Mexico, Sch Med, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA.
[Peterson, M. Michal; Mack, Jessica L.; Hall, Pamela R.; Alsup, Anny A.; Alexander, Susan M.; Sully, Erin K.; Sawires, Youhanna S.; Gresham, Hattie D.] Albuquerque Vet Affairs Med Ctr, Res Serv, Albuquerque, NM 87108 USA.
[Hall, Pamela R.] Univ New Mexico, Sch Med, Dept Pathol, Albuquerque, NM 87131 USA.
[Cheung, Ambrose L.] Dartmouth Med Sch, Dept Microbiol, Hanover, NH 03755 USA.
[Otto, Michael] NIAID, Rocky Mt Lab, NIH, Hamilton, MT 59840 USA.
RP Gresham, HD (reprint author), Univ New Mexico, Sch Med, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA.
EM hgresham@salud.unm.edu
RI Hall, Pamela/O-5402-2016;
OI Hall, Pamela/0000-0003-2367-3382; Otto, Michael/0000-0002-2222-4115
FU NIAID NIH HHS [R01 AI064926-01, AI 37142, AI 47441, AI-064926, R01
AI037142, R01 AI047441, R01 AI064926, R01 AI064926-02, R01 AI064926-03,
R01 AI064926-04, T32 AI007538]
NR 49
TC 68
Z9 71
U1 0
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD DEC 11
PY 2008
VL 4
IS 6
BP 555
EP 566
DI 10.1016/j.chom.2008.10.001
PG 12
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 388GB
UT WOS:000262007200008
PM 19064256
ER
PT J
AU Giubellino, A
Shi, ZD
Jenkins, LMM
Worthy, KM
Bindu, LK
Athauda, G
Peruzzi, B
Fisher, RJ
Appella, E
Burke, TR
Bottaro, DP
AF Giubellino, Alessio
Shi, Zhen-Dan
Jenkins, Lisa M. Miller
Worthy, Karen M.
Bindu, Lakshman K.
Athauda, Gagani
Peruzzi, Benedetta
Fisher, Robert J.
Appella, Ettore
Burke, Terrence R., Jr.
Bottaro, Donald P.
TI Selectivity and Mechanism of Action of a Growth Factor Receptor-Bound
Protein 2 Src Homology 2 Domain Binding Antagonist
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID FOCAL-ADHESION KINASE; SH2 DOMAIN; GRB2; P21-ACTIVATED-KINASE-1;
INHIBITION; LIGANDS; CANCER
AB We have shown previously that a potent synthetic antagonist of growth factor receptor-bound protein 2 (Grb2) Src homology 2 (SH2) domain binding (1) blocks growth factor stimulated motility, invasion, and angiogenesis in cultured cell models, as well as tumor metastasis in animals. To characterize the selectivity of I for the SH2 domain of Grb2 over other proteins containing similar structural binding motifs, we synthesized a biotinylated derivative (3) that retained high affinity Grb2 SH2 domain binding and potent biological activity. To investigate the selectivity of 1 and 3 for Grb2, the biotinylated antagonist 3 was used to immobilize target proteins from cell extracts for subsequent identification by mass spectrometry. Nonspecific binding was identified in parallel using a biotinylated analogue that lacked a single critical binding determinant. The mechanism of action of the antagonist was further characterized by immunoprecipitation, immunoblotting, and light microscopy. This approach to defining protein binding antagonist selectivity and molecular basis of action should be widely applicable in drug development.
C1 [Bottaro, Donald P.] NCI, Urol Oncol Branch, CCR, Bethesda, MD 20892 USA.
[Jenkins, Lisa M. Miller; Appella, Ettore] NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
[Shi, Zhen-Dan; Burke, Terrence R., Jr.] NCI, Med Chem Lab, Frederick, MD 21702 USA.
[Worthy, Karen M.; Bindu, Lakshman K.; Fisher, Robert J.] SAIC Frederick Inc, Prot Chem Lab, Frederick, MD 21702 USA.
RP Bottaro, DP (reprint author), NCI, Urol Oncol Branch, CCR, Bldg 10 CRC 1,W Room 3961,10 Ctr Drivem MSC 1107, Bethesda, MD 20892 USA.
EM dbottaro@helix.nih.gov
RI Fisher, Robert/B-1431-2009; Bottaro, Donald/F-8550-2010; Burke,
Terrence/N-2601-2014;
OI Bottaro, Donald/0000-0002-5057-5334; Giubellino,
Alessio/0000-0002-5352-0662
FU NIH, National Cancer Institute, Center for Cancer Research
[N01-CO-12400]
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. This project
has been funded in part with federal funds from the National Cancer
Institute, National Institutes of Health, under Contract N01-CO-12400.
The content of this publication does not necessarily reflect the views
or policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government.
NR 28
TC 7
Z9 8
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 DEC 11
PY 2008
VL 51
IS 23
BP 7459
EP 7468
DI 10.1021/jm800523u
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 379XG
UT WOS:000261429100014
PM 18989951
ER
PT J
AU Gupte, A
Boshoff, HI
Wilson, DJ
Neres, J
Labello, NP
Somu, RV
Xing, CG
Barry, CE
Aldrich, CC
AF Gupte, Amol
Boshoff, Helena I.
Wilson, Daniel J.
Neres, Joao
Labello, Nicholas P.
Somu, Ravindranadh V.
Xing, Chengguo
Barry, Clifton E., III
Aldrich, Courtney C.
TI Inhibition of Siderophore Biosynthesis by 2-Triazole Substituted
Analogues of 5'-O-[N-(Salicyl)sulfamoyl]adenosine: Antibacterial
Nucleosides Effective against Mycobacterium tuberculosis
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID ANTITUBERCULAR AGENTS; PEPTIDE SYNTHETASES; COUPLING REACTIONS; RECEPTOR
AGONISTS; IRON ACQUISITION; TERMINAL ALKYNES; FACILE SYNTHESIS; AZIDES;
ENZYME; DOMAIN
AB The synthesis, biochemical, and biological evaluation of a systematic series of 2-triazole derivatives of 5'-O-[N-(salicyl)sulfamoyl]adenosine (Sal-AMS) are described as inhibitors of aryl acid adenylating enzymes (AAAE) involved in siderophore biosynthesis by Mycobacterium tuberculosis. Structure-activity relationships revealed a remarkable ability to tolerate a wide range of substituents at the 4-position of the triazole moiety, and a majority of the Compounds possessed subnanomolar apparent inhibition constants. However, the in vitro potency did not always translate into whole cell biological activity against M. tuberculosis, suggesting that intrinsic resistance plays an important role in the observed activities. Additionally, the well-known valence tautomerism between 2-azidopurines and their fused tetrazole counterparts led to an unexpected facile acylation of the purine N-6 amino group.
C1 [Gupte, Amol; Wilson, Daniel J.; Neres, Joao; Labello, Nicholas P.; Somu, Ravindranadh V.; Aldrich, Courtney C.] Univ Minnesota, Acad Hlth Ctr, Ctr Drug Design, Minneapolis, MN 55455 USA.
[Boshoff, Helena I.; Barry, Clifton E., III] NIAID, TB Res Sect, Bethesda, MD 20892 USA.
[Xing, Chengguo] Univ Minnesota, Dept Med Chem, Minneapolis, MN 55455 USA.
RP Aldrich, CC (reprint author), Univ Minnesota, Acad Hlth Ctr, Ctr Drug Design, Minneapolis, MN 55455 USA.
EM aldri015@umn.edu
RI Barry, III, Clifton/H-3839-2012; Neres, Joao/A-1241-2011
OI Neres, Joao/0000-0003-4488-2423
FU NIH [R01A1070219]; Center for Drug Design; Academic Health Center;
University of Minnesota; NIH, National Institute of Allergy and
Infectious Disease
FX This research was supported by a grant from the NIH (Grant R01A1070219)
and funding from the Center for Drug Design, Academic Health Center,
University of Minnesota to C.C.A. This research was supported in part by
the Intramural Research Program of the NIH, National Institute of
Allergy and Infectious Disease. We thank the Minnesota Supercomputing
Institute for computing time.
NR 42
TC 59
Z9 60
U1 1
U2 13
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 DEC 11
PY 2008
VL 51
IS 23
BP 7495
EP 7507
DI 10.1021/jm8008037
PG 13
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 379XG
UT WOS:000261429100018
PM 19053762
ER
PT J
AU Andreani, A
Burnelli, S
Granaiola, M
Leoni, A
Locatelli, A
Morigi, R
Rambaldi, M
Varoli, L
Calonghi, N
Cappadone, C
Voltattomi, M
Zini, M
Stefanelli, C
Masotti, L
Shoemaker, RH
AF Andreani, Aldo
Burnelli, Silvia
Granaiola, Massimiliano
Leoni, Alberto
Locatelli, Alessandra
Morigi, Rita
Rambaldi, Mirella
Varoli, Lucilla
Calonghi, Natalia
Cappadone, Concettina
Voltattomi, Manuela
Zini, Maddalena
Stefanelli, Claudio
Masotti, Lanfranco
Shoemaker, Robert H.
TI Antitumor Activity of New Substituted
3-(5-Imidazo[2,1-b]thiazolylmethylene)-2-indolinones and
3-(5-Imidazo[2,1-b]thiadiazolylmethylene)-2-indolinones: Selectivity
against Colon Tumor Cells and Effect on Cell Cycle-Related Events
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID DERIVATIVES; CANCER; POLYAMINES
AB The synthesis of new 3-(5-imidazo[2,1-b]thiazolylmethylene)-2-indolinones and 3-(5-imidazo[2,1-b]thiadiazolylmethylene)-2-indolinones is reported. The antitumor activity was evaluated according to the protocols available at the National Cancer Institute (NCI), Bethesda, MD. To investigate the mechanism of action of the most potent antitumor agent of this series, its effect on growth of HT-29 colon carcinoma cells was studied. Its ability to inhibit cellular proliferation was mediated by cell cycle arrest at the G2/M phase, accompanied by inhibition of ornithine decarboxylase (ODC), the limiting enzyme of polyamine synthesis, and followed by induction of apoptosis.
C1 [Andreani, Aldo; Burnelli, Silvia; Granaiola, Massimiliano; Leoni, Alberto; Locatelli, Alessandra; Morigi, Rita; Rambaldi, Mirella; Varoli, Lucilla] Univ Bologna, Dipartimento Sci Farmaceut, I-40126 Bologna, Italy.
[Calonghi, Natalia; Cappadone, Concettina; Zini, Maddalena; Stefanelli, Claudio; Masotti, Lanfranco] Univ Bologna, Dipartimento Biochim G Moruzzi, I-40126 Bologna, Italy.
[Voltattomi, Manuela] Univ Bologna, CIRB, I-40127 Bologna, Italy.
[Shoemaker, Robert H.] NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21702 USA.
RP Andreani, A (reprint author), Univ Bologna, Dipartimento Sci Farmaceut, Via Belmeloro 6, I-40126 Bologna, Italy.
EM aldo.andreani@unibo.it
OI STEFANELLI, CLAUDIO/0000-0001-5864-2178; LEONI,
ALBERTO/0000-0001-8528-8207
FU MIUR-COFIN
FX This work was supported by a grant from MIUR-COFIN 2006. We are grateful
to NCI for the antitumor tests and to CIRB for the use of confocal
microscope and flow cytometer.
NR 23
TC 31
Z9 32
U1 0
U2 1
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 DEC 11
PY 2008
VL 51
IS 23
BP 7508
EP 7513
DI 10.1021/jm800827q
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 379XG
UT WOS:000261429100019
PM 19006285
ER
PT J
AU Yoo, CB
Valente, R
Congiatu, C
Gavazza, F
Angel, A
Siddiqui, MA
Jones, PA
McGuigan, C
Marquez, VE
AF Yoo, Christine B.
Valente, Rocco
Congiatu, Costantino
Gavazza, Federica
Angel, Annette
Siddiqui, Maqbool A.
Jones, Peter A.
McGuigan, Christopher
Marquez, Victor E.
TI Activation of p16 Gene Silenced by DNA Methylation in Cancer Cells by
Phosphoramidate Derivatives of 2 '-Deoxyzebularine
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID EPIGENETICALLY BASED STRATEGY; 2,3-DIDEHYDRO-2,3-DIDEOXYADENOSINE D4A;
CYTIDINE DEAMINASE; UNIQUE MOLECULE; ZEBULARINE; INHIBITION;
CHEMOTHERAPY; CONVERSION; MECHANISM; THERAPY
AB We report herein the application of the phosphoramidate ProTide technology to improve the metabolism of the DNA methytransferase inhibitor, zebularine (Z). Zebularine is a riboside that must undergo a complex metabolic transformation before reaching the critical 2'-deoxyzebularine 5'-triphosphate (dZTP). Because 2'-deoxyzebularine (dZ) is not phosphorylated and therefore inactive, the ProTide strategy was employed to bypass the lack of phosphorylation of dZ and the inefficient reduction of zebularine 5'-diphosphate by ribonucleotide-diphosphate reductase required for zebularine. Several compounds were identified as more potent inhibitors of DNA methylation and stronger inducers of p16 tumor suppressor gene than zebularine. However, their activity was dependent on the administration of thymidine to overcome the potent inhibition of thymidylate synthase (TS) and deoxycytidine monophosphate (dCMP) deaminase by dZMP, which deprives cells of essential levels of thymidine. Intriguingly, the activity of the ProTides was cell line-dependent, and activation of p16 was manifest only in Cf-Pac-1 pancreatic ductal adenocarcinoma. cells.
C1 [Yoo, Christine B.; Jones, Peter A.] Univ So Calif, Dept Biochem, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Yoo, Christine B.; Jones, Peter A.] Univ So Calif, Dept Mol Biol, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Valente, Rocco; Congiatu, Costantino; Gavazza, Federica; Angel, Annette; McGuigan, Christopher] Cardiff Univ, Welsh Sch Pharm, Cardiff CF10 3XF, S Glam, Wales.
[Siddiqui, Maqbool A.; Marquez, Victor E.] NIH, Natl Canc Inst, Ctr Canc Res, Med Chem Lab, Frederick, MD 21702 USA.
RP Jones, PA (reprint author), Univ So Calif, Dept Biochem, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
EM jones_p@cent.hsc.usc.edu; mcguigan@cf.ac.uk; marquezv@mail.nih.gov
RI McGuigan, Chris/P-1580-2014
OI McGuigan, Chris/0000-0001-8409-710X
FU NIH, Center for Cancer Research, NCI-Frederick
FX This research was supported in part by the Intramural Research Program
of the NIH, Center for Cancer Research, NCI-Frederick.
NR 28
TC 13
Z9 14
U1 0
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 DEC 11
PY 2008
VL 51
IS 23
BP 7593
EP 7601
DI 10.1021/jm8005965
PG 9
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 379XG
UT WOS:000261429100028
PM 19006382
ER
PT J
AU Bredemeyer, AL
Helmink, BA
Innes, CL
Calderon, B
McGinnis, LM
Mahowald, GK
Gapud, EJ
Walker, LM
Collins, JB
Weaver, BK
Mandik-Nayak, L
Schreiber, RD
Allen, PM
May, MJ
Paules, RS
Bassing, CH
Sleckman, BP
AF Bredemeyer, Andrea L.
Helmink, Beth A.
Innes, Cynthia L.
Calderon, Boris
McGinnis, Lisa M.
Mahowald, Grace K.
Gapud, Eric J.
Walker, Laura M.
Collins, Jennifer B.
Weaver, Brian K.
Mandik-Nayak, Laura
Schreiber, Robert D.
Allen, Paul M.
May, Michael J.
Paules, Richard S.
Bassing, Craig H.
Sleckman, Barry P.
TI DNA double-strand breaks activate a multi-functional genetic program in
developing lymphocytes
SO NATURE
LA English
DT Article
ID NF-KAPPA-B; LEAKY SCID PHENOTYPE; V(D)J RECOMBINATION; LYMPHOID ORGANS;
IONIZING-RADIATION; BONE-MARROW; ATM; EXPRESSION; DAMAGE;
DIFFERENTIATION
AB DNA double- strand breaks are generated by genotoxic agents and by cellular endonucleases as intermediates of several important physiological processes. The cellular response to genotoxic DNA breaks includes the activation of transcriptional programs known primarily to regulate cell- cycle checkpoints and cell survival(1-5). DNA double- strand breaks are generated in all developing lymphocytes during the assembly of antigen receptor genes, a process that is essential for normal lymphocyte development. Here we show that in murine lymphocytes these physiological DNA breaks activate a broad transcriptional program. This program transcends the canonical DNA double- strand break response and includes many genes that regulate diverse cellular processes important for lymphocyte development. Moreover, the expression of several of these genes is regulated similarly in response to genotoxic DNA damage. Thus, physiological DNA double- strand breaks provide cues that can regulate cell- type- specific processes not directly involved in maintaining the integrity of the genome, and genotoxic DNA breaks could disrupt normal cellular functions by corrupting these processes.
C1 [Bredemeyer, Andrea L.; Helmink, Beth A.; Calderon, Boris; McGinnis, Lisa M.; Mahowald, Grace K.; Gapud, Eric J.; Walker, Laura M.; Weaver, Brian K.; Mandik-Nayak, Laura; Schreiber, Robert D.; Allen, Paul M.; Sleckman, Barry P.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Innes, Cynthia L.; Collins, Jennifer B.; Paules, Richard S.] NIEHS, Environm Stress & Canc Grp, Res Triangle Pk, NC 27709 USA.
[Innes, Cynthia L.; Collins, Jennifer B.; Paules, Richard S.] NIEHS, Microarray Grp, Res Triangle Pk, NC 27709 USA.
[May, Michael J.] Univ Penn, Sch Vet Med, Philadelphia, PA 19104 USA.
[Bassing, Craig H.] Univ Penn, Sch Med, Childrens Hosp Philadelphia, Ctr Childhood Canc Res,Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Bassing, Craig H.] Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
RP Sleckman, BP (reprint author), Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
EM Sleckman@immunology.wustl.edu
RI Schreiber, Robert/A-1276-2013;
OI Schreiber, Robert/0000-0001-6311-0432; Bredemeyer,
Andrea/0000-0003-2970-5998; May, Michael/0000-0002-2485-3716; Calderon,
Boris/0000-0003-1575-0739
FU National Institutes of Health [AI47829]; Washington University
Department of Pathology and Immunology; Department of Pathology and
Center for Childhood Cancer Research of the Children's Hospital of
Philadelphia; Abramson Family Cancer Research Institute; National
Institute of Environmental Health Sciences; Research Scholar Award from
the American Cancer Society
FX We thank J. Bednarski, B. Van Honten andM. Diaz for critical review of
the manuscript, F. W. Alt for providing us with the Artemis 2/2 mice and
D. Ballard for providing us with the I kappa B alpha-Delta N construct.
This research is supported by the National Institutes of Health (NIH,
grant AI47829) and the Washington University Department of Pathology and
Immunology ( to B.P.S.); the Department of Pathology and Center for
Childhood Cancer Research of the Children's Hospital of Philadelphia,
and the Abramson Family Cancer Research Institute (to C.H.B.); and the
intramural research program of the NIH, National Institute of
Environmental Health Sciences (to R.S.P.). B.P.S. is a recipient of a
Research Scholar Award from the American Cancer Society. C.H.B. is a Pew
Scholar in the Biomedical Sciences. A.L.B. is supported by a
post-doctoral training grant from the NIH.
NR 38
TC 65
Z9 69
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD DEC 11
PY 2008
VL 456
IS 7223
BP 819
EP U113
DI 10.1038/nature07392
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 381TX
UT WOS:000261559900055
PM 18849970
ER
PT J
AU Mattson, MP
Gleichmann, M
Cheng, A
AF Mattson, Mark P.
Gleichmann, Marc
Cheng, Aiwu
TI Mitochondria in Neuroplasticity and Neurological Disorders
SO NEURON
LA English
DT Review
ID AMYOTROPHIC-LATERAL-SCLEROSIS; CYTOCHROME-C RELEASE; APOPTOSIS-INDUCING
FACTOR; FOCAL CEREBRAL-ISCHEMIA; PERMEABILITY TRANSITION PORE;
EXCITOTOXIC NEURONAL DEATH; MAJOR DEPRESSIVE DISORDER; AMYLOID PRECURSOR
PROTEIN; SYNUCLEIN TRANSGENIC MICE; CEREBELLAR GRANULE CELLS
AB Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function. Mitochondria are highly dynamic organelles that divide, fuse, and move purposefully within axons and dendrites. Major functions of mitochondria in neurons include the regulation of Ca(2+) and redox signaling, developmental and synaptic plasticity, and the arbitration of cell survival and death. The importance of mitochondria in neurons is evident in the neurological phenotypes in rare diseases caused by mutations in mitochondrial genes. Mitochondria-mediated oxidative stress, perturbed Ca(2+) homeostasis, and apoptosis may also contribute to the pathogenesis of prominent neurological diseases including Alzheimer's, Parkinson's, and Huntington's diseases; stroke; annyotrophic lateral sclerosis; and psychiatric disorders. Advances in understanding the molecular and cell biology of mitochondria are leading to novel approaches for the prevention and treatment of neurological disorders.
C1 [Mattson, Mark P.; Gleichmann, Marc; Cheng, Aiwu] Natl Inst Aging Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), Natl Inst Aging Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Mattson, Mark/F-6038-2012
FU National Institute on Aging Intramural Research Program of the NIH
FX The authors thank KC Alexander for preparing the illustrations for the
Figures of this manuscript. This work was supported by the National
Institute on Aging Intramural Research Program of the NIH.
NR 206
TC 344
Z9 352
U1 3
U2 53
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD DEC 11
PY 2008
VL 60
IS 5
BP 748
EP 766
DI 10.1016/j.neuron.2008.10.010
PG 19
WC Neurosciences
SC Neurosciences & Neurology
GA 384LQ
UT WOS:000261746700008
PM 19081372
ER
PT J
AU Schoen, RE
Pinsky, PF
AF Schoen, Robert E.
Pinsky, Paul F.
TI Five-Year Risk of Colorectal Neoplasia after Negative Colonoscopy
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID SCREENING COLONOSCOPY; SURVEILLANCE
C1 [Schoen, Robert E.] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA.
[Pinsky, Paul F.] NCI, Bethesda, MD 20892 USA.
RP Schoen, RE (reprint author), Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA.
EM rschoen@pitt.edu
NR 5
TC 0
Z9 0
U1 0
U2 0
PU MASSACHUSETTS MEDICAL SOC
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 DEC 11
PY 2008
VL 359
IS 24
BP 2611
EP 2611
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 381KG
UT WOS:000261534200018
PM 19073983
ER
PT J
AU Jeang, KT
AF Jeang, Kuan-Teh
TI The 2008 Retrovirology Prize: Ben Berkhout and his RNA world
SO RETROVIROLOGY
LA English
DT Editorial Material
ID HIV-1; SCIENCE; GENOME; LIFE; WINS
AB Ben Berkhout wins the 2008 Retrovirology Prize.
C1 NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM kjeang@niaid.nih.gov
RI Jeang, Kuan-Teh/A-2424-2008
NR 11
TC 4
Z9 4
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD DEC 11
PY 2008
VL 5
AR 113
DI 10.1186/1742-4690-5-113
PG 5
WC Virology
SC Virology
GA 394JI
UT WOS:000262442600001
PM 19077224
ER
PT J
AU Bianco, C
Mysliwiec, M
Watanabe, K
Mancino, M
Nagaoka, T
Gonzales, M
Salomon, DS
AF Bianco, Caterina
Mysliwiec, Margaret
Watanabe, Kazuhide
Mancino, Mario
Nagaoka, Tadahiro
Gonzales, Monica
Salomon, David S.
TI Activation of a Nodal-independent signaling pathway by Cripto-1 mutants
with impaired activation of a Nodal-dependent signaling pathway
SO FEBS LETTERS
LA English
DT Article
DE Cripto-1; Nodal; Glypican-1; Fucosylation; Mammary epithelial cell
ID MAMMARY EPITHELIAL-CELLS; FUCOSYLATION
AB Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway.
C1 [Bianco, Caterina; Mysliwiec, Margaret; Watanabe, Kazuhide; Mancino, Mario; Nagaoka, Tadahiro; Gonzales, Monica; Salomon, David S.] NCI, Mammary Biol & Tumorigenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Salomon, DS (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, NIH, 37 Convent Dr,Bldg 37,Room 1112, Bethesda, MD 20892 USA.
EM biancoc@mail.nih.gov; salomond@mail.nih.gov
OI Nagaoka, Tadahiro/0000-0002-9391-0243
FU NIH; NCI; CCR
FX We would like to thank Pamela Stanley (Albert Einstein College of
Medicine, New York) for generously providing the Cripto-1 mutant
plasmids. We would like to thank Christina Baraty for her excellent
technical assistance. This work was supported by Intramural Research
program of the NIH, NCI, CCR.
NR 16
TC 7
Z9 8
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD DEC 10
PY 2008
VL 582
IS 29
BP 3997
EP 4002
DI 10.1016/j.febslet.2008.10.052
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 377ES
UT WOS:000261235100006
PM 19013461
ER
PT J
AU Chriqui, JF
Tynan, M
Agurs-Collins, T
Masse, LC
AF Chriqui, Jamie F.
Tynan, Michael
Agurs-Collins, Tanya
Masse, Louise C.
TI Will web-based research suffice when collecting US school district
policies? The case of physical education and school-based nutrition
policies
SO INTERNATIONAL JOURNAL OF BEHAVIORAL NUTRITION AND PHYSICAL ACTIVITY
LA English
DT Article
ID STATE POLICY; SOFT DRINKS; OVERWEIGHT; PREVALENCE; OBESITY; HEALTH;
ADOLESCENTS; CHILDREN; IMPACT; RATES
AB Background: Recognizing the growing childhood overweight problem, a number of school-based strategies, including policy approaches, have been proposed and are being implemented to address the problem considering the amount of time children spend in schools. This paper describes the results of a pilot study that tested approaches to collecting U. S. school district policy information regarding physical education and nutrition requirements that can inform efforts by policy makers, researchers, advocates and others interested in collecting school district-level obesity-related policies that are typically not systematically available from a "one stop" source.
Methods: Sixty local school districts representing six states were selected for conducting the district policy research, with larger, urban school districts over-sampled to facilitate collection of policies from districts representing a larger proportion of the public school population in each study state. The six states within which the pilot districts were located were chosen based on the variability in their physical education and school-based nutrition policy and geographic and demographic diversity. Web research and a mail canvass of the study districts was conducted between January and May 2006 to obtain all relevant policies. An additional field collection effort was conducted in a sample of districts located in three study states to test the extent to which field collection would yield additional information.
Results: Policies were obtained from 40 (67%) of the 60 districts, with policies retrieved via both Web and mail canvass methods in 16 (27%) of the districts, and were confirmed to not exist in 10 (17%) of the districts. Policies were more likely to be retrieved from larger, urban districts, whereas the smallest districts had no policies available on the Web. In no instances were exactly the same policies retrieved from the two sources. Physical education policies were slightly more prevalent than nutrition policies.
Conclusion: Collection of U.S. local school district policies requires a multi-pronged approach. Web research and mail canvasses will likely yield different types of policy information. Given the variance in district-level Web site presence, researchers and others interested in obtaining district physical education and nutrition-related policies should consider supplementing Web research with more direct methods.
C1 [Chriqui, Jamie F.] Univ Illinois, Inst Hlth Res & Policy, Chicago, IL 60608 USA.
[Chriqui, Jamie F.] MayaTech Corp, Silver Spring, MD 20910 USA.
[Agurs-Collins, Tanya] NCI, Bethesda, MD 20852 USA.
[Masse, Louise C.] Univ British Columbia, Dept Pediat, CCHR Ctr Community Child Hlth Res, Vancouver, BC V6H 3V4, Canada.
RP Chriqui, JF (reprint author), Univ Illinois, Inst Hlth Res & Policy, 1747 W Roosevelt Rd,MC 275, Chicago, IL 60608 USA.
EM jchriqui@uic.edu; mtynan01@yahoo.com; collinsta@mail.nih.gov;
lmasse@cw.bc.ca
FU NCI [N02-PC-444006, 263-MQ-515012]
FX Support for this project was provided by the NCI to The MayaTech
Corporation through contract numbers N02-PC-444006 and 263-MQ-515012.
The authors would like to gratefully acknowledge the research assistance
provided by Carissa Holmes, Shelby Eidson, J.D., and Jim Igoe, M.A.,
M.L.S.. Michael Tynan and Jim Igoe were employed by MayaTech at the time
of their contribution. Additionally, the authors would like to
acknowledge the input provided by Drs. Amy Yaroch and Audie Autienza at
NCI as part of a larger study framework of which this study was a part
and Anna Sandavol, M. P. H. at the University of Illinois at Chicago,
Institute for Health Research and Policy who assisted with field-based
collection in one of our study states. The views presented in this paper
are those of the authors and do not, necessarily, reflect those of the
U.S. Department of Health and Human Services or any of the authors'
employers.
NR 28
TC 2
Z9 2
U1 2
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5868
J9 INT J BEHAV NUTR PHY
JI Int. J. Behav. Nutr. Phys. Act.
PD DEC 10
PY 2008
VL 5
AR 64
DI 10.1186/1479-5868-5-64
PG 9
WC Nutrition & Dietetics; Physiology
SC Nutrition & Dietetics; Physiology
GA 405PY
UT WOS:000263237900001
PM 19077186
ER
PT J
AU Kato, GJ
Gladwin, MT
AF Kato, Gregory J.
Gladwin, Mark T.
TI Evolution of Novel Small-Molecule Therapeutics Targeting Sickle Cell
Vasculopathy
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID MICROVASCULAR ENDOTHELIAL-CELLS; OXIDE SYNTHASE INHIBITOR; NITRIC-OXIDE;
PULMONARY-HYPERTENSION; ADHESION MOLECULES; PLATELET ACTIVATION; HEME
OXYGENASE-1; ASYMMETRIC DIMETHYLARGININE; ISCHEMIA-REPERFUSION;
VASOOCCLUSIVE CRISIS
AB A 34- year- old African American woman with sickle cell disease and history of relatively severe hemolysis, chronic leg ulcers, and mild pulmonary hypertension presented with a new ischemic stroke. Recent research has suggested a syndrome of hemolysis- associated vasculopathy in patients with sickle cell disease, which features severe hemolytic anemia and leads to scavenging of nitric oxide and its biochemical precursor L- arginine. This diminished bioavailability of nitric oxide promotes a hemolysis-vascular dysfunction syndrome, which includes pulmonary hypertension, cutaneous leg ulceration, priapism, and ischemic stroke. Additional correlates of this vasculopathy include activation of endothelial cell adhesion molecules, platelets, and the vascular protectant hemeoxygenase- 1. Some known risk factors for atherosclerosis are also associated with sickle cell vasculopathy, including low levels of apolipoprotein AI and high levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase. Identification of dysregulated vascular biology pathways in sickle vasculopathy has provided a focus for new clinical trials for therapeutic intervention, including inhaled nitric oxide, sodium nitrite, L- arginine, phosphodiesterase- 5 inhibitors, niacin, inhaled carbon monoxide, and endothelin receptor antagonists. This article reviews the pathophysiology of sickle vasculopathy and the results of preliminary clinical trials of novel small- molecule therapeutics directed at abnormal vascular biology in patients with sickle cell disease.
C1 [Kato, Gregory J.] NHLBI, Dept Crit Care Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Dept Med, Pittsburgh, PA USA.
[Gladwin, Mark T.] Hemostasis & Vasc Biol Res Inst, Pittsburgh, PA USA.
RP Kato, GJ (reprint author), NHLBI, Dept Crit Care Med, Ctr Clin, NIH, 10 Ctr Dr,MSC 1476,Bldg 10 CRC,Room 5-5140, Bethesda, MD 20892 USA.
EM gkato@mail.nih.gov
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU Department of Intramural Research of the NIH Clinical Center; National
Heart, Lung, and Blood Institute; Institute of Transfusion Medicine;
Hemophilia Center of Western Pennsylvania; NIH Collaborative Research
and Development Agreement
FX Drs Kato and Gladwin have been supported by intramural funds from the
Department of Intramural Research of the NIH Clinical Center and the
National Heart, Lung, and Blood Institute (NHLBI). Dr Gladwin currently
receives support from the Institute of Transfusion Medicine, the
Hemophilia Center of Western Pennsylvania, and grant support through an
NIH Collaborative Research and Development Agreement of inhaled nitric
oxide gas with Ikaria.
NR 82
TC 43
Z9 45
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD DEC 10
PY 2008
VL 300
IS 22
BP 2638
EP 2646
DI 10.1001/jama.2008.598
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 380YW
UT WOS:000261503000023
PM 19066384
ER
PT J
AU Hahn, T
McCarthy, PL
Zhang, MJ
Wang, D
Arora, M
Frangoul, H
Gale, RP
Hale, GA
Horan, J
Isola, L
Maziarz, RT
van Rood, JJ
Gupta, V
Halter, J
Reddy, V
Tiberghien, P
Litzow, M
Anasetti, C
Pavletic, S
Ringden, O
AF Hahn, Theresa
McCarthy, Philip L., Jr.
Zhang, Mei-Jie
Wang, Dan
Arora, Mukta
Frangoul, Haydar
Gale, Robert Peter
Hale, Gregory A.
Horan, John
Isola, Luis
Maziarz, Richard T.
van Rood, Jon J.
Gupta, Vikas
Halter, Joerg
Reddy, Vijay
Tiberghien, Pierre
Litzow, Mark
Anasetti, Claudio
Pavletic, Stephen
Ringden, Olle
TI Risk Factors for Acute Graft-Versus-Host Disease After Human Leukocyte
Antigen-Identical Sibling Transplants for Adults With Leukemia
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; TOTAL-BODY IRRADIATION; STEM-CELL
TRANSPLANTATION; CHRONIC MYELOID-LEUKEMIA; RANDOMIZED-TRIAL;
CYCLOSPORINE CONCENTRATION; PREPARATIVE REGIMEN; BUSULFAN-CYTOXAN;
FRENCH-SOCIETY; SURVIVAL
AB Purpose
Acute graft-versus-host disease (GVHD) causes substantial morbidity and mortality after human leukocyte antigen (HLA)-identical sibling transplants. No large registry studies of acute GVHD risk factors have been reported in two decades. Risk factors may have changed in this interval as transplant-related techniques have evolved.
Patients and Methods
Acute GVHD risk factors were analyzed in 1,960 adults after HLA-identical sibling myeloablative transplant for acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), or chronic myeloid leukemia (CML) reported by 226 centers worldwide to the Center for International Blood and Marrow Transplant Research from 1995 to 2002. Outcome was measured as time from transplant to onset of grade 2 to 4 acute GVHD, with death without acute GVHD as a competing risk.
Results
Cumulative incidence of grade 2 to 4 acute GVHD was 35% (95% CI, 33% to 37%). In multivariable analyses, factors significantly associated with grade 2 to 4 acute GVHD were cyclophosphamide + total-body irradiation versus busulfan + cyclophosphamide (relative risk [RR] = 1.4; P < .0001), blood cell versus bone marrow grafts in patients age 18 to 39 years (RR = 1.43; P = .0023), recipient age 40 and older versus age 18 to 39 years receiving bone marrow grafts (RR = 1.44; P = .0005), CML versus AML/ALL (RR = 1.35; P = .0003), white/Black versus Asian/Hispanic race (RR = 1.54; P = .0003), Karnofsky performance score less than 90 versus 90 to 100 (RR = 1.27; P = .014), and recipient/donor cytomegalovirus-seronegative versus either positive (RR = 1.20; P = .04). Stratification by disease showed the same significant predictors of grade 2 to 4 acute GVHD for CML; however, KPS and cytomegalovirus serostatus were not significant predictors for AML/ALL.
Conclusion
This analysis confirmed several previously reported risk factors for grade 2 to 4 acute GVHD. However, several new factors were identified whereas others are no longer significant. These new data may facilitate individualized risk estimates and raise several interesting biologic questions.
C1 [Hahn, Theresa] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
Med Coll Wisconsin, Milwaukee, WI 53226 USA.
Univ Minnesota, Minneapolis, MN USA.
Mayo Clin, Rochester, MN USA.
Vanderbilt Univ, Nashville, TN USA.
St Jude Childrens Hosp, Memphis, TN 38105 USA.
Emory Univ, Atlanta, GA 30322 USA.
Mt Sinai Med Ctr, New York, NY 10029 USA.
Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
Leiden Univ, Med Ctr, Leiden, Netherlands.
Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
Univ Basel Hosp, CH-4031 Basel, Switzerland.
Florida Hosp, Inst Canc, Orlando, FL USA.
Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
Univ Franche Comte, F-25030 Besancon, France.
NCI, Bethesda, MD 20892 USA.
Karolinska Univ Hosp, Stockholm, Sweden.
RP Hahn, T (reprint author), Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
EM Theresa.hahn@roswellpark.org
RI Halter, Joerg/C-9487-2012
FU American Society for Blood and Marrow Transplantation
FX Support information appears in the Acknowledgment. American Society for
Blood and Marrow Transplantation provided research support to T. H.
NR 27
TC 86
Z9 88
U1 2
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 10
PY 2008
VL 26
IS 35
BP 5728
EP 5734
DI 10.1200/JCO.2008.17.6545
PG 7
WC Oncology
SC Oncology
GA 381IC
UT WOS:000261528200013
PM 18981462
ER
PT J
AU Dean, RM
Fry, T
Mackall, C
Steinberg, SM
Hakim, F
Fowler, D
Odom, J
Foley, J
Gress, R
Bishop, MR
AF Dean, Robert M.
Fry, Terry
Mackall, Crystal
Steinberg, Seth M.
Hakim, Fran
Fowler, Daniel
Odom, Jeanne
Foley, Jason
Gress, Ronald
Bishop, Michael R.
TI Association of Serum Interleukin-7 Levels With the Development of Acute
Graft-Versus-Host Disease
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION;
PERIPHERAL-BLOOD; RISK-FACTORS; T-CELLS; IL-7; ENGRAFTMENT;
DIFFERENTIATION; RECONSTITUTION; HOMEOSTASIS
AB Purpose
Morbidity from acute graft-versus-host disease (GVHD) limits the success of allogeneic hematopoietic stem-cell transplantation (HSCT) to treat malignancy. Interleukin-7 (IL-7), the principal homeostatic cytokine for T cells, is required for acute GVHD in murine models. In contrast to inflammatory cytokines (eg, IL-2, tumor necrosis factor alpha), IL-7 has not been studied extensively in the clinical transplant setting relative to its relationship with acute GVHD.
Patients and Methods
We evaluated the association of serum IL-7 levels with acute GVHD in 31 patients who were uniformly treated in a prospective clinical trial with reduced-intensity allogeneic HSCT from human leukocyte antigen-identical siblings. GVHD prophylaxis consisted of cyclosporine and methotrexate. Serum IL-7 levels and lymphocyte populations were determined at enrollment, the day of transplantation before the allograft infusion, and at specified intervals through 12 months post-transplantation.
Results
As expected, IL-7 levels were inversely correlated with T-cell populations (P < .00001). Acute GVHD was significantly associated with higher IL-7 levels at day +7 (P = .01) and day +14 (P = .00003) post-transplantation as well as with the allograft CD34(+) cell dose (P = .01). IL-7 levels at day +14 also correlated with the severity of acute GVHD (P < .0001). In logistic regression models, these factors were highly sensitive (up to 86%) and specific (100%) for classifying whether patients developed acute GVHD.
Conclusion
These data support preclinical observations that IL-7 plays a critical role in inducing acute GVHD and provide a rational basis for novel approaches to prevent and treat acute GVHD through modulation of the IL-7 pathway.
C1 Cleveland Clin Fdn, Taussig Canc Inst, Cleveland, OH 44195 USA.
[Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
RP Bishop, MR (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bldg 10-CRC,Room 4-3152,10 Ctr Dr, Bethesda, MD 20892 USA.
EM mbishop@mail.nih.gov
FU Center for Cancer Research; National Cancer Institute; National
Institutes of Health
FX Supported by the Intramural Research Program of the Center for Cancer
Research, National Cancer Institute, National Institutes of Health.
NR 31
TC 50
Z9 51
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 10
PY 2008
VL 26
IS 35
BP 5735
EP 5741
DI 10.1200/JCO.2008.17.1314
PG 7
WC Oncology
SC Oncology
GA 381IC
UT WOS:000261528200014
PM 19001329
ER
PT J
AU Vale, C
Tierney, JF
Stewart, LA
Brady, M
Dinshaw, K
Jakobsen, A
Parmar, MKB
Thomas, G
Trimble, T
Alberts, DS
Chen, HW
Cikaric, S
Eifel, PJ
Garipagaoglu, M
Keys, H
Kantardzic, N
Lal, P
Lanciano, R
Leborgne, F
Lorvidhaya, V
Onishi, H
Pearcey, RG
Pras, E
Roberts, K
Rose, PG
Thomas, G
Whitney, CW
AF Vale, Claire
Tierney, Jayne F.
Stewart, Lesley A.
Brady, Mark
Dinshaw, Ketayun
Jakobsen, Anders
Parmar, Mahesh K. B.
Thomas, Gillian
Trimble, Ted
Alberts, David S.
Chen, Hongwei
Cikaric, Slobodan
Eifel, Patricia J.
Garipagaoglu, Melahat
Keys, Henry
Kantardzic, Nermina
Lal, Punita
Lanciano, Rachelle
Leborgne, Felix
Lorvidhaya, Vicharn
Onishi, Hiroshi
Pearcey, Robert G.
Pras, Elizabeth
Roberts, Kenneth
Rose, Peter G.
Thomas, Gillian
Whitney, Charles W.
CA Chemoradiotherapy Cervical Canc
TI Reducing Uncertainties About the Effects of Chemoradiotherapy for
Cervical Cancer: A Systematic Review and Meta-Analysis of Individual
Patient Data From 18 Randomized Trials
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID GYNECOLOGIC-ONCOLOGY-GROUP; RADIATION-THERAPY; CONCURRENT CHEMOTHERAPY;
PELVIC RADIATION; UTERINE CERVIX; RADICAL RADIOTHERAPY;
ADVANCED-CARCINOMA; MITOMYCIN-C; CISPLATIN; INFUSION
AB Background
After a 1999 National Cancer Institute (NCI) clinical alert was issued, chemoradiotherapy has become widely used in treating women with cervical cancer. Two subsequent systematic reviews found that interpretation of the benefits was complicated, and some important clinical questions were unanswered.
Patients and Methods
We initiated a meta-analysis seeking updated individual patient data from all randomized trials to assess the effect of chemoradiotherapy on all outcomes. We prespecified analyses to investigate whether the effect of chemoradiotherapy differed by trial or patient characteristics.
Results
On the basis of 13 trials that compared chemoradiotherapy versus the same radiotherapy, there was a 6% improvement in 5-year survival with chemoradiotherapy (hazard ratio [HR] = 0.81, P < .001). A larger survival benefit was seen for the two trials in which chemotherapy was administered after chemoradiotherapy. There was a significant survival benefit for both the group of trials that used platinum-based (HR = 0.83, P = .017) and non-platinum-based (HR = 0.77, P < .009) chemoradiotherapy, but no evidence of a difference in the size of the benefit by radiotherapy or chemotherapy dose or scheduling was seen. Chemoradiotherapy also reduced local and distant recurrence and progression and improved disease-free survival. There was a suggestion of a difference in the size of the survival benefit with tumor stage, but not across other patient subgroups. Acute hematologic and GI toxicity was increased with chemoradiotherapy, but data were too sparse for an analysis of late toxicity.
Conclusion
These results endorse the recommendations of the NCI alert, but also demonstrate their applicability to all women and a benefit of non-platinum-based chemoradiotherapy. Furthermore, although these results suggest an additional benefit from adjuvant chemotherapy, this requires testing in randomized trials.
C1 [Vale, Claire; Tierney, Jayne F.] Med Res Council Clin Trials Unit, Meta Anal Grp, London NW1 2DA, England.
[Thomas, Gillian; Thomas, Gillian] Toronto Sunnybrook Canc Ctr, Toronto, ON, Canada.
[Trimble, Ted] NCI, Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Alberts, David S.] Arizona Canc Ctr, Tucson, AZ USA.
[Eifel, Patricia J.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Keys, Henry] Albany Med Coll, Albany, NY 12208 USA.
[Lanciano, Rachelle] Delaware Cty Mem Hosp, Drexel Hill, PA USA.
[Lorvidhaya, Vicharn] Chiang Mai Univ, Chiang Mai, Thailand.
[Onishi, Hiroshi] Univ Yamanashi, Yamanashi, Japan.
[Pearcey, Robert G.] Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada.
[Pearcey, Robert G.] Univ Alberta, Edmonton, AB, Canada.
[Pras, Elizabeth] Univ Med Ctr Groningen, Groningen, Netherlands.
[Pras, Elizabeth] Univ Groningen, NL-9700 AB Groningen, Netherlands.
[Roberts, Kenneth] Yale Univ, Sch Med, New Haven, CT USA.
[Rose, Peter G.] Cleveland Clin, Cleveland, OH 44106 USA.
[Whitney, Charles W.] Christiana Care Hlth Syst, Wilmington, DE USA.
RP Vale, C (reprint author), Med Res Council Clin Trials Unit, Meta Anal Grp, 222 Euston Rd, London NW1 2DA, England.
EM cv@ctu.mrc.ac.uk
FU United Kingdom Medical Research Council; United Kingdom National
Coordinating Centre for Research Capacity Development
FX Supported by the United Kingdom Medical Research Council and the United
Kingdom National Coordinating Centre for Research Capacity Development
(C. V.).
NR 52
TC 256
Z9 263
U1 0
U2 16
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 10
PY 2008
VL 26
IS 35
BP 5802
EP 5812
DI 10.1200/JCO.2008.16.4368
PG 11
WC Oncology
SC Oncology
GA 381IC
UT WOS:000261528200024
ER
PT J
AU Yao, LS
Vogeli, B
Ying, JF
Bax, A
AF Yao, Lishan
Voegeli, Beat
Ying, Jinfa
Bax, Ad
TI NMR Determination of Amide N-H Equilibrium Bond Length from Concerted
Dipolar Coupling Measurements
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID RESIDUAL DIPOLAR; CONSERVATIVE MUTAGENESIS; BACKBONE DYNAMICS;
PROTEIN-STRUCTURE; RELAXATION; UBIQUITIN; SPECTROSCOPY
AB The N-H bond Length in backbone peptide groups of the protein GB3 has been studied by liquid-crystal NMR, using five structurally conserved mutants of this protein. In the absence of additional information, the impact of dynamic fluctuations of the N-H vector orientation on the (15)N-(1)H dipolar interaction cannot be separated from a change in N-H bond length. However, a change in N-H bond length directly impacts the orientation of C-H vectors in the peptide group, and simultaneous analysis of (13)C'-H(N) and (15)N-H(N) residual dipolar couplings, measured under five different alignment orientations, permits modelfree determination of the average equilibrium N-H bond length in GB3, yielding r(NH)(eq) = 1.008 +/- 0.006 angstrom. Anharmonicity of the bond stretching results in a slightly longer time-averaged bond length < r(NH)> = 1.015 +/- 0.006 angstrom, and an effective bond Length r(eff) = < r(NH)(-3)>(-1/3) = 1.023 +/- 0.006 angstrom pertinent for NMR relaxation analysis, not including the impact of zero-point or other angular fluctuations in N-H orientation. Using a reference frame defined by the backbone C degrees-C' vectors of the protein, angular fluctuations for N-H vectors in elements of secondary structure are approximately 1.5-fold larger for out-of-plane fluctuations than motions within the peptide plane and not much larger than anticipated on the basis of quantum mechanical analysis of their zero-point librations.
C1 [Yao, Lishan; Voegeli, Beat; Ying, Jinfa; Bax, Ad] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Bax, A (reprint author), NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM bax@nih.gov
RI Yao, Lishan /C-6961-2009; yao, lishan/H-3662-2012
OI yao, lishan/0000-0003-1797-922X
FU NIDDK, NIH; NTH
FX This work was supported in part by the Intramural Research Program of
the NIDDK, NIH, and by the Intramural AIDS-Targeted Antiviral Program of
the Office of the Director, NTH. We thank D.A. Torchia for useful
discussions.
NR 17
TC 61
Z9 61
U1 0
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD DEC 10
PY 2008
VL 130
IS 49
BP 16518
EP +
DI 10.1021/ja805654f
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA 406UK
UT WOS:000263320200037
PM 19049453
ER
PT J
AU Yamanaka, S
Zahanich, I
Wersto, RP
Boheler, KR
AF Yamanaka, Satoshi
Zahanich, Ihor
Wersto, Robert P.
Boheler, Kenneth R.
TI Enhanced Proliferation of Monolayer Cultures of Embryonic Stem (ES)
Cell-Derived Cardiomyocytes Following Acute Loss of Retinoblastoma
SO PLOS ONE
LA English
DT Article
AB Background: Cardiomyocyte (CM) cell cycle analysis has been impeded because of a reliance on primary neonatal cultures of poorly proliferating cells or chronic transgenic animal models with innate compensatory mechanisms.
Methodology/Principal Findings: We describe an in vitro model consisting of monolayer cultures of highly proliferative embryonic stem (ES) cell-derived CM. Following induction with ascorbate and selection with puromycin, early CM cultures are >98% pure, and at least 85% of the cells actively proliferate. During the proliferative stage, cells express high levels of E2F3a, B-Myb and phosphorylated forms of retinoblastoma (Rb), but with continued cultivation, cells stop dividing and mature functionally. This developmental transition is characterized by a switch from slow skeletal to cardiac TnI, an increase in binucleation, cardiac calsequestrin and hypophosphorylated Rb, a decrease in E2F3, B-Myb and atrial natriuretic factor, and the establishment of a more negative resting membrane potential. Although previous publications suggested that Rb was not necessary for cell cycle control in heart, we find following acute knockdown of Rb that this factor actively regulates progression through the G1 checkpoint and that its loss promotes proliferation at the expense of CM maturation.
Conclusions/Significance: We have established a unique model system for studying cardiac cell cycle progression, and show in contrast to previous reports that Rb actively regulates both cell cycle progression through the G1 checkpoint and maturation of heart cells. We conclude that this in vitro model will facilitate the analysis of cell cycle control mechanisms of CMs.
C1 [Yamanaka, Satoshi; Zahanich, Ihor; Boheler, Kenneth R.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
[Wersto, Robert P.] NIA, NIH, Resource Res Branch, Bethesda, MD 20892 USA.
RP Yamanaka, S (reprint author), NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
EM bohelerk@grc.nia.nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging (KRB, RPW). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 70
TC 13
Z9 13
U1 0
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 10
PY 2008
VL 3
IS 12
AR e3896
DI 10.1371/journal.pone.0003896
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436ZS
UT WOS:000265455700006
PM 19066628
ER
PT J
AU Lusa, L
Korn, EL
McShane, LM
AF Lusa, Lara
Korn, Edward L.
McShane, Lisa M.
TI A class comparison method with filtering-enhanced variable selection for
high-dimensional data sets
SO STATISTICS IN MEDICINE
LA English
DT Article
DE multiple testing methods; multivariate permutation methods;
high-dimensional data; microarrays; variable filtering
ID DIFFERENTIALLY EXPRESSED GENES; MICROARRAY EXPERIMENTS; BREAST-CANCER;
LYMPHOCYTES; POPULATION; PROFILES
AB High-throughput molecular analysis technologies can produce thousands of measurements for each of the assayed samples. A common scientific question is to identify the variables whose distribution differ between some pre-specified classes (i.e. are differentially expressed). The statistical cost of examining thousands of variables is related to the risk of identifying many variables that truly are not differentially expressed, and many different multiple testing strategies have been used for the analysis of high-dimensional data sets to control the number of these false positives. An approach that is often used in practice to reduce the multiple comparisons problem is to lessen the number of comparisons being performed by filtering out variables that are considered non-informative 'before' the analysis. However, deciding which and how many variables should be filtered out can be highly arbitrary, and different filtering strategies can result in different variables being identified as differentially expressed. We propose the filtering-enhanced variable selection (FEVS) method, a new multiple testin strategy for identifying differentially expressed variables. This method identifies differentially expressed variables by combining the results obtained using a variety of filtering methods, instead of using a pre-specified filtering method or trying to identify an optimal filtering of the variables prior to class comparison analysis. We prove that the FEVS method probabilistically controls the the number of false discoveries, and we show with a set of simulations and an example form the literature that FEVS can be useful for gaining sensitivity for the detection of truly differentially expressed variables. Published in 2008 by John Wiley & Sons. Ltd.
C1 [Lusa, Lara] Univ Ljubljana, Dept Med Informat, Ljubljana 61000, Slovenia.
[Korn, Edward L.; McShane, Lisa M.] NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Lusa, L (reprint author), Univ Ljubljana, Dept Med Informat, Ljubljana 61000, Slovenia.
EM Lara.Lusa@mf.uni-lj.si
RI Lusa, Lara/C-6692-2015
OI Lusa, Lara/0000-0002-8981-2421
NR 22
TC 5
Z9 5
U1 0
U2 4
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD DEC 10
PY 2008
VL 27
IS 28
BP 5834
EP 5849
DI 10.1002/sim.3405
PG 16
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 375VZ
UT WOS:000261143200003
PM 18781559
ER
PT J
AU Cornwell, BR
Carver, FW
Coppola, R
Johnson, L
Alvarez, R
Grillona, C
AF Cornwell, Brian R.
Carver, Frederick W.
Coppola, Richard
Johnson, Linda
Alvarez, Ruben
Grillona, Christian
TI Evoked amygdala responses to negative faces revealed by adaptive MEG
beamformers
SO BRAIN RESEARCH
LA English
DT Article
DE Adaptive beamformer; Amygdala; Anger; Facial expression; Fear;
Magnetoencephalography
ID SPATIALLY-FILTERED MAGNETOENCEPHALOGRAPHY; RECONSTRUCTING SPATIOTEMPORAL
ACTIVITIES; HUMAN HIPPOCAMPAL; BRAIN; ACTIVATION; EMOTION; TASK;
SYNCHRONIZATION; LATERALIZATION; RECOGNITION
AB Adaptive beamformer analyses of magnetoencephalograms (MEG) have shown promise as a method for functional imaging of cortical processes. Although recent evidence is encouraging, it is unclear whether these methods can both localize and reconstruct the time course of activity in subcortical structures such as the amygdala. Fourteen healthy participants (7 women) performed a perceptual matching task of negative emotional faces (angry and fearful) and geometric shapes that was designed for functional magnetic resonance imaging (fMRI) studies to maximize amygdala activation. Neuromagnetic data were collected with a 275-channel whole-head magnetometer, and event-related adaptive beamformer analyses were conducted to estimate broadband evoked responses to faces and shapes across the whole brain in 7 mm steps. Group analyses revealed greater left amygdala. activity to faces over shapes, both when face-matching and shape-matching trials were presented in separate blocks and when they were randomly intermixed. This finding was replicated in a second experiment with 7 new participants (3 women). Virtual sensor time series showed clear evoked responses in the left amygdala. and left fusiform gyrus in both runs and experiments. We conclude that amygdala activity can be resolved from MEGs with adaptive beamformers with temporal resolution superior to other neuroimaging modalities. This demonstration should encourage the use of MEG for elucidating functional networks mediating fear-related neural phenomena that likely unfold rapidly in time across cortical and subcortical structures. Published by Elsevier B.V.
C1 [Cornwell, Brian R.; Johnson, Linda; Alvarez, Ruben; Grillona, Christian] NIMH, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA.
[Carver, Frederick W.; Coppola, Richard] NIMH, Magnetoencephalog Core Facil, NIH, Bethesda, MD 20892 USA.
RP Cornwell, BR (reprint author), NIMH, Mood & Anxiety Disorders Program, NIH, 15 North Dr,MSC 2670, Bethesda, MD 20892 USA.
EM cornwellb@mail.nih.gov
FU National Institute of Mental Health
FX This research was supported by the intramural research program at the
National Institute of Mental Health. We would like to thank Arter Biggs
for his assistance in obtaining MRIs from participants. We are grateful
to Stephen Robinson (Neuromagnetism Laboratory, Department of Neurology,
Henry Ford Hospital, Detroit, MI) for developing the SAMerf program that
we used for event-related beamformer analysis.
NR 38
TC 47
Z9 50
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD DEC 9
PY 2008
VL 1244
BP 103
EP 112
DI 10.1016/j.brainres.2008.09.068
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 384YH
UT WOS:000261779600011
PM 18930036
ER
PT J
AU Kikuchi, J
Kinoshita, I
Shimizu, Y
Oizumi, S
Nishimura, M
Birrer, MJ
Dosaka-Akita, H
AF Kikuchi, J.
Kinoshita, I.
Shimizu, Y.
Oizumi, S.
Nishimura, M.
Birrer, M. J.
Dosaka-Akita, H.
TI Simultaneous blockade of AP-1 and phosphatidylinositol 3-kinase pathway
in non-small cell lung cancer cells
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE AP-1; phosphatidylinositol 3-kinase pathway; non-small cell lung cancer;
LY294002; TAM67
ID ANCHORAGE-INDEPENDENT GROWTH; DOMINANT-NEGATIVE MUTANT; C-JUN; CYCLIN-A;
UP-REGULATION; RAT1A CELLS; THERAPEUTIC STRATEGY; EPITHELIAL-CELLS;
KINASE-ACTIVITY; RAT-1A CELLS
AB c-Jun is a major constituent of AP-1 transcription factor that transduces multiple mitogen growth signals, and it is frequently overexpressed in non-small cell lung cancers (NSCLCs). Earlier, we showed that blocking AP-1 by the overexpression of a c-Jun dominant-negative mutant, TAM67, inhibited NSCLC cell growth. The phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathway is important in transformation, proliferation, survival and metastasis of NSCLC cells. In this study, we used NCI-H1299 Tet-on clone cells that express TAM67 under the control of inducible promoter to determine the effects of inhibition of AP-1 and PI3K on cell growth. The PI3K inhibitor, LY294002, produced a dose-dependent inhibition of growth in H1299 cells and that inhibition was enhanced by TAM67. TAM67 increased dephosphorylation of Akt induced by LY294002 and reduced the TPA response element DNA-binding of phosphorylated c-Jun. TAM67 increased G1 cell cycle blockade induced by LY294002, which was partially associated with cyclin A decrease and p27(Kip1) accumulation. Furthermore, TAM67 and LY294002 act, at least additively, to inhibit anchorage-independent growth of the H1299 cells. These results suggest that AP-1 and PI3K/Akt pathways play an essential role in the growth of some NSCLC cells.
C1 [Kinoshita, I.] Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Kita Ku, Sapporo, Hokkaido 0608638, Japan.
[Kikuchi, J.; Oizumi, S.; Nishimura, M.] Hokkaido Univ, Grad Sch Med, Dept Med 1, Sapporo, Hokkaido 0608638, Japan.
[Birrer, M. J.] NCI, Cell & Canc Biol Branch, Bethesda, MD 20892 USA.
RP Kinoshita, I (reprint author), Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Kita Ku, North 15,West 7, Sapporo, Hokkaido 0608638, Japan.
EM kinoshii@med.hokudai.ac.jp
RI Shimizu, Yasushi/D-8057-2012; Akita, Hirotoshi/E-1356-2012; Nishimura,
Masaharu/A-4062-2012
NR 45
TC 14
Z9 16
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD DEC 9
PY 2008
VL 99
IS 12
BP 2013
EP 2019
DI 10.1038/sj.bjc.6604782
PG 7
WC Oncology
SC Oncology
GA 382QI
UT WOS:000261620100008
PM 19018257
ER
PT J
AU Frankel, DS
Meigs, JB
Massaro, JM
Wilson, PWF
O'Donnell, CJ
D'Agostino, RB
Tofler, GH
AF Frankel, David S.
Meigs, James B.
Massaro, Joseph M.
Wilson, Peter W. F.
O'Donnell, Christopher J.
D'Agostino, Ralph B.
Tofler, Geoffrey H.
TI Von Willebrand Factor, Type 2 Diabetes Mellitus, and Risk of
Cardiovascular Disease The Framingham Offspring Study
SO CIRCULATION
LA English
DT Article
DE von Willebrand factor; diabetes mellitus; insulin resistance;
cardiovascular diseases; epidemiology
ID CORONARY-HEART-DISEASE; APPARENTLY HEALTHY-MEN; C-REACTIVE PROTEIN;
FUTURE MYOCARDIAL-INFARCTION; EDINBURGH ARTERY; ENDOTHELIAL DYSFUNCTION;
VONWILLEBRAND-FACTOR; PLASMA-CONCENTRATION; INSULIN-RESISTANCE;
HEMOSTATIC MARKERS
AB Background-Von Willebrand factor (vWF) is inconsistently associated with cardiovascular disease (CVD). This might be explained by associations of vWF with type 2 diabetes mellitus and insulin resistance.
Methods and Results-We tested whether vWF predicted incident CVD in 3799 Framingham Offspring Study participants, and in particular, among those with type 2 diabetes mellitus or insulin resistance. During 11 years of follow-up, 351 participants developed CVD. In proportional hazards models (with adjustment for age, sex, blood pressure, smoking, body mass index, total and high-density lipoprotein cholesterol, and treatment with aspirin, insulin, antihypertensives, and lipid-lowering medications) with the lowest quartile of the vWF distribution as the referent, the hazard ratio (HR) for CVD was 0.94 in the second quartile, 0.98 in the third, and 1.32 in the highest (P = 0.04 for trend). Additional adjustment for type 2 diabetes mellitus or insulin resistance (homeostasis model) partially attenuated the association (multivariable HRs for top quartile 1.28 and 1.21, respectively). We then stratified the models by diabetes status or the homeostasis model of insulin resistance distribution (top quartile versus lower 3 quartiles). vWF was associated with CVD among participants with diabetes mellitus (HR for top quartile relative to bottom 1.47, P = 0.04 for trend) but not among nondiabetic participants (HR 1.15, P = 0.5) and similarly among insulin-resistant (HR 1.50, P = 0.01) but not insulin-sensitive (HR 1.02, P = 0.9) participants.
Conclusions-Higher levels of vWF were associated with risk of CVD in people with type 2 diabetes mellitus or insulin resistance, which suggests that vWF may be a risk factor unique to these populations. (Circulation. 2008; 118: 2533-2539.)
C1 [Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Frankel, David S.] Univ Penn, Dept Med, Div Cardiovasc Med, Philadelphia, PA 19104 USA.
[Massaro, Joseph M.; O'Donnell, Christopher J.; D'Agostino, Ralph B.] NHLBI, Framingham, MA USA.
[Wilson, Peter W. F.] Emory Univ, Sch Med, Dept Med, Div Cardiol, Atlanta, GA USA.
[Massaro, Joseph M.; D'Agostino, Ralph B.] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
[Tofler, Geoffrey H.] Royal N Shore Hosp, Sydney, NSW, Australia.
RP Meigs, JB (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM jmeigs@partners.org
OI Massaro, Joseph/0000-0002-2682-4812
FU American Heart Association [92011960]; National Heart, Lung, and Blood
Institute's Framingham Heart Study [N01-HC-25195]
FX This study was supported by a Grant-in-Aid from the American Heart
Association (No. 92011960 to Dr Massaro) and by the National Heart,
Lung, and Blood Institute's Framingham Heart Study (contract No.
N01-HC-25195).
NR 49
TC 47
Z9 50
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD DEC 9
PY 2008
VL 118
IS 24
BP 2533
EP 2539
DI 10.1161/CIRCULATIONAHA.108.792986
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 381CJ
UT WOS:000261512400008
PM 19029465
ER
PT J
AU Song, MH
Aravind, L
Muller-Reichert, T
O'Connell, KF
AF Song, Mi Hye
Aravind, L.
Mueller-Reichert, Thomas
O'Connell, Kevin F.
TI The Conserved Protein SZY-20 Opposes the Plk4-Related Kinase ZYG-1 to
Limit Centrosome Size
SO DEVELOPMENTAL CELL
LA English
DT Article
ID DE-NOVO FORMATION; CAENORHABDITIS-ELEGANS; C-ELEGANS; CENTRIOLE
DUPLICATION; PERICENTRIOLAR MATERIAL; DROSOPHILA SPD-2; VERTEBRATE
CELLS; MESSENGER-RNAS; IN-VIVO; RECRUITMENT
AB Microtubules are organized by the centrosome, a dynamic organelle that exhibits changes in both size and number during the cell cycle. Here we show that SZY-20, a putative RNA-binding protein, plays a critical role in limiting centrosome size in C. elegans. SZY-20 localizes in part to centrosomes and in its absence centrosomes possess increased levels of centriolar and pericentriolar components including gamma-tubulin and the centriole duplication factors ZYG-1 and SPD-2. These enlarged centrosomes possess normal centrioles, nucleate more microtubules, and fail to properly direct a number of microtubule-dependent processes. Depletion of ZYG-1 restores normal centrosome size and function to szy-20 mutants, whereas loss of szy-20 suppresses the centrosome duplication defects in both zyg-1 and spd-2 mutants. Our results describe a pathway that determines centrosome size and implicate centriole duplication factors in this process.
C1 [Song, Mi Hye; O'Connell, Kevin F.] NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20894 USA.
[Aravind, L.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
[Mueller-Reichert, Thomas] Max Planck Inst Mol Cell Biol & Genet MPI CBG, D-01307 Dresden, Germany.
RP Song, MH (reprint author), NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20894 USA.
EM mihyesong@mail.nih.gov; kevino@intra.niddk.nih.gov
OI Song, Mi Hye/0000-0001-8326-6602
FU National Institutes Health (NIH); National Institute of Diabetes and
Digestive and Kidney Diseases
FX We thank So Jung Kim and O'Connell lab members for their support; David
Weisblat, Andy Golden, Bob Goldstein, Nick Miliaras, and Nina Peel for
comments on the manuscript; Harold Smith, Martin Srayko, Alexander
Dammerman, Anion Audhya, Karen Oegema, Ken Kemphues, and Yuji Kohara for
reagents; and In-Geol Choi and Kevin Eliceiri for technical assistance.
Some strains were provided by The Caenorhabditis Genetics Center and The
National Bioresource Project, Japan. This work was supported by the
Intramural Research Program of the National Institutes Health (NIH) and
by the National Institute of Diabetes and Digestive and Kidney Diseases.
NR 45
TC 26
Z9 32
U1 1
U2 4
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 DEC 9
PY 2008
VL 15
IS 6
BP 901
EP 912
DI 10.1016/j.devcel.2008.09.018
PG 12
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 382US
UT WOS:000261631500013
PM 19081077
ER
PT J
AU Ottman, R
Rosenberger, L
Bagic, A
Kamberakis, K
Ritzl, EK
Wohlschlager, AM
Shamim, S
Sato, S
Liew, C
Gaillard, WD
Wiggs, E
Berl, MM
Reeves-Tyers, P
Baker, EH
Butman, JA
Theodore, WH
AF Ottman, R.
Rosenberger, L.
Bagic, A.
Kamberakis, K.
Ritzl, E. K.
Wohlschlager, A. M.
Shamim, S.
Sato, S.
Liew, C.
Gaillard, W. D.
Wiggs, E.
Berl, M. M.
Reeves-Tyers, P.
Baker, E. H.
Butman, J. A.
Theodore, W. H.
TI Altered language processing in autosomal dominant partial epilepsy with
auditory features
SO NEUROLOGY
LA English
DT Article
ID TEMPORAL-LOBE EPILEPSY; IDIOPATHIC PARTIAL EPILEPSY; SPORADIC PARTIAL
EPILEPSY; APHASIC SEIZURES; LGI1 MUTATIONS; TOPIRAMATE TREATMENT;
CHROMOSOME 10Q; FUNCTIONAL MRI; GENE; FAMILIES
AB Background: Autosomal dominant partial epilepsy with auditory features (ADPEAF) is an idiopathic focal epilepsy syndrome with auditory symptoms or receptive aphasia as major ictal manifestations, frequently associated with mutations in the leucine-rich, glioma inactivated 1 (LGI1) gene. Although affected subjects do not have structural abnormalities detected on routine MRI, a lateral temporal malformation was identified through high resolution MRI in one family. We attempted to replicate this finding and to assess auditory and language processing in ADPEAF using fMRI and magnetoencephalography (MEG).
Methods: We studied 17 subjects (10 affected mutation carriers, 3 unaffected carriers, 4 noncarriers) in 7 ADPEAF families, each of which had a different LGI1 mutation. Subjects underwent high-resolution structural MRI, fMRI with an auditory description decision task (ADDT) and a tone discrimination task, and MEG. A control group comprising 26 volunteers was also included.
Results: We found no evidence of structural abnormalities in any of the 17 subjects. On fMRI with ADDT, subjects with epilepsy had significantly less activation than controls. On MEG with auditory stimuli, peak 2 auditory evoked field latency was significantly delayed in affected individuals compared to controls.
Conclusions: These findings do not support the previous report of a lateral temporal malformation in autosomal dominant partial epilepsy with auditory features (ADPEAF). However, our fMRI and magnetoencephalography data suggest that individuals with ADPEAF have functional impairment in language processing. Neurology (R) 2008;71:1973-1980
C1 [Ottman, R.; Kamberakis, K.] Columbia Univ, GH Sergievsky Ctr, New York, NY 10032 USA.
[Ottman, R.; Kamberakis, K.] Columbia Univ, Dept Epidemiol, New York, NY 10032 USA.
[Ottman, R.] Columbia Univ, Dept Neurol, New York, NY 10032 USA.
[Ottman, R.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Rosenberger, L.; Bagic, A.; Ritzl, E. K.; Wohlschlager, A. M.; Shamim, S.; Gaillard, W. D.; Wiggs, E.; Reeves-Tyers, P.; Theodore, W. H.] NINDS, Clin Epidemiol Sect, Bethesda, MD 20892 USA.
[Bagic, A.; Sato, S.] NINDS, EEG Sect, Bethesda, MD 20892 USA.
[Berl, M. M.] George Washington Univ, Sch Med, Childrens Natl Med Ctr, Dept Neurosci, Washington, DC USA.
[Baker, E. H.; Butman, J. A.] NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
RP Ottman, R (reprint author), Columbia Univ, GH Sergievsky Ctr, 630 W 168th St,P&S Box 16, New York, NY 10032 USA.
EM ro6@columbia.edu
RI Butman, John/A-2694-2008; Ottman, Ruth/O-2371-2013;
OI Butman, John/0000-0002-1547-9195
FU NIH [R01NS036319, R01NS043472]; NINDS Division of Intramural Research
FX Supported by NIH grants R01NS036319 and R01NS043472 (to R.O.), and the
NINDS Division of Intramural Research.
NR 39
TC 12
Z9 13
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD DEC 9
PY 2008
VL 71
IS 24
BP 1973
EP 1980
DI 10.1212/01.wnl.0000336923.29538.5b
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 381CN
UT WOS:000261512900008
PM 19064878
ER
PT J
AU Kagaayi, J
Gray, RH
Brahmbhatt, H
Kigozi, G
Nalugoda, F
Wabwire-Mangen, F
Serwadda, D
Sewankambo, N
Ddungu, V
Ssebagala, D
Sekasanvu, J
Kigozi, G
Makumbi, F
Kiwanuka, N
Lutalo, T
Reynolds, SJ
Wawer, MJ
AF Kagaayi, Joseph
Gray, Ronald H.
Brahmbhatt, Heena
Kigozi, Godfrey
Nalugoda, Fred
Wabwire-Mangen, Fred
Serwadda, David
Sewankambo, Nelson
Ddungu, Veronica
Ssebagala, Darix
Sekasanvu, Joseph
Kigozi, Grace
Makumbi, Fredrick
Kiwanuka, Noah
Lutalo, Tom
Reynolds, Steven J.
Wawer, Maria J.
TI Survival of Infants Born to HIV-Positive Mothers, by Feeding Modality,
in Rakai, Uganda
SO PLOS ONE
LA English
DT Article
AB Background: Data comparing survival of formula-fed to breast-fed infants in programmatic settings are limited. We compared mortality and HIV-free of breast and formula-fed infants born to HIV-positive mothers in a program in rural, Rakai District Uganda.
Methodology/Principal Findings: One hundred eighty two infants born to HIV-positive mothers were followed at one, six and twelve months postpartum. Mothers were given infant-feeding counseling and allowed to make informed choices as to whether to formula-feed or breast-feed. Eligible mothers and infants received antiretroviral therapy (ART) if indicated. Mothers and their newborns received prophylaxis for prevention of mother-to-child HIV transmission (pMTCT) if they were not receiving ART. Infant HIV infection was detected by PCR (Roche Amplicor 1.5) during the follow-up visits. Kaplan Meier time-to-event methods were used to compare mortality and HIV-free survival. The adjusted hazard ratio (Adjusted HR) of infant HIV-free survival was estimated by Cox regression. Seventy-five infants (41%) were formula-fed while 107 (59%) were breast-fed. Exclusive breast-feeding was practiced by only 25% of breast-feeding women at one month postpartum. The cumulative 12-month probability of infant mortality was 18% (95% CI = 11%-29%) among the formula-fed compared to 3% (95% CI = 1%-9%) among the breast-fed infants (unadjusted hazard ratio (HR) = 6.1(95% CI = 1.7-21.4, P-value<0.01). There were no statistically significant differentials in HIV-free survival by feeding choice (86% in the formula-fed compared to 96% in breast-fed group (Adjusted RH = 2.8[ 95% CI = 0.67-11.7, P-value = 0.16]
Conclusions/Significance: Formula-feeding was associated with a higher risk of infant mortality than breastfeeding in this rural population. Our findings suggest that formula-feeding should be discouraged in similar African settings.
C1 [Kigozi, Godfrey; Nalugoda, Fred; Ddungu, Veronica] Rakai Hlth Sci Program, Dept Clin Res Studies, Entebbe, Uganda.
[Gray, Ronald H.; Brahmbhatt, Heena; Wawer, Maria J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Populat, Family & Reproduct Hlth, Baltimore, MD 21218 USA.
[Wabwire-Mangen, Fred; Makumbi, Fredrick; Kiwanuka, Noah] Makerere Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Kampala, Uganda.
[Serwadda, David] Makerere Univ, Sch Publ Hlth, Dept Dis Control, Kampala, Uganda.
[Sewankambo, Nelson] Makerere Univ, Sch Med, Dept Med, Clin Epidemiol Unit, Kampala, Uganda.
[Ssebagala, Darix; Sekasanvu, Joseph; Lutalo, Tom] Rakai Hlth Sci Program, Dept Biostat & Data Management, Entebbe, Uganda.
[Kigozi, Grace] Rakai Hlth Sci Program, Dept Quality Control & Quality Assurance, Entebbe, Uganda.
[Reynolds, Steven J.] Johns Hopkins Univ, Sch Med, Div Infect Dis, Baltimore, MD 21218 USA.
[Reynolds, Steven J.] NIAID, NIH, Div Intramural Res, Lab Immunoregulat, Bethesda, MD USA.
RP Kagaayi, J (reprint author), Rakai Hlth Sci Program, Dept Clin Res Studies, Entebbe, Uganda.
EM jkagayi@rhsp.org
OI Sewankambo, Nelson/0000-0001-9362-053X
FU National Institute of Child Health and Human Development(NICHD);
Presidential Emergency Plan for AIDS Relief(PEPFAR)
FX National Institute of Child Health and Human Development(NICHD).
Presidential Emergency Plan for AIDS Relief(PEPFAR). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 18
TC 43
Z9 43
U1 1
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 9
PY 2008
VL 3
IS 12
AR e3877
DI 10.1371/journal.pone.0003877
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436ZP
UT WOS:000265455200003
PM 19065270
ER
PT J
AU Malone, JH
Fontenot, BE
AF Malone, John H.
Fontenot, Brian E.
TI Patterns of Reproductive Isolation in Toads
SO PLOS ONE
LA English
DT Article
ID FROG RANA-RUGOSA; HALDANES RULE; POSTZYGOTIC ISOLATION; HYBRID
INVIABILITY; CHARACTER DISPLACEMENT; HETEROGAMETIC SEX; GENE-EXPRESSION;
MOLECULAR SYSTEMATICS; CENTRARCHID FISHES; DARWINS COROLLARY
AB Understanding the general features of speciation is an important goal in evolutionary biology, and despite significant progress, several unresolved questions remain. We analyzed an extensive comparative dataset consisting of more than 1900 crosses between 92 species of toads to infer patterns of reproductive isolation. This unique dataset provides an opportunity to examine the strength of reproductive isolation, the development and sex ratios of hybrid offspring, patterns of fertility and infertility, and polyploidization in hybrids all in the context of genetic divergence between parental species. We found that the strength of intrinsic postzygotic isolation increases with genetic divergence, but relatively high levels of divergence are necessary before reproductive isolation is complete in toads. Fertilization rates were not correlated to genetic divergence, but hatching success, the number of larvae produced, and the percentage of tadpoles reaching metamorphosis were all inversely related with genetic divergence. Hybrids between species with lower levels of divergence developed to metamorphosis, while hybrids with higher levels of divergence stopped developing in gastrula and larval stages. Sex ratios of hybrid offspring were biased towards males in 70% of crosses and biased towards females in 30% of crosses. Hybrid females from crosses between closely related species were completely fertile, while approximately half (53%) of hybrid males were sterile, with sterility predicted by genetic divergence. The degree of abnormal ploidy in hybrids was positively related to genetic divergence between parental species, but surprisingly, polyploidization had no effect on patterns of asymmetrical inviability. We discuss explanations for these patterns, including the role of Haldane's rule in toads and anurans in general, and suggest mechanisms generating patterns of reproductive isolation in anurans.
C1 [Malone, John H.; Fontenot, Brian E.] Univ Texas, Dept Biol, Arlington, TX USA.
RP Malone, JH (reprint author), NIDDKD, Cellular & Dev Biol Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM malonej@niddk.nih.gov
NR 89
TC 34
Z9 35
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 9
PY 2008
VL 3
IS 12
AR e3900
DI 10.1371/journal.pone.0003900
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436ZP
UT WOS:000265455200012
PM 19065271
ER
PT J
AU Manji, H
McEwen, BS
AF Manji, Husseini
McEwen, Bruce S.
TI Reply to Schmidt et al.: The long and the short of BAG1
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Editorial Material
ID GLUCOCORTICOID-RECEPTOR
C1 [McEwen, Bruce S.] Rockefeller Univ, New York, NY 10021 USA.
[Manji, Husseini] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
RP McEwen, BS (reprint author), Rockefeller Univ, 1230 York Ave, New York, NY 10021 USA.
EM mcewen@mail.rockefeller.edu
NR 4
TC 0
Z9 0
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 9
PY 2008
VL 105
IS 49
BP E102
EP E102
DI 10.1073/pnas.0810014105
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 383XB
UT WOS:000261706600102
ER
PT J
AU Jiang, BM
Gentsch, JR
Glass, RI
AF Jiang, Baoming
Gentsch, Jon R.
Glass, Roger I.
TI Inactivated rotavirus vaccines: A priority for accelerated vaccine
development
SO VACCINE
LA English
DT Review
DE Rotavirus; Vaccine; Parenteral; Intussusception
ID VIRUS-LIKE PARTICLES; PROTECTIVE IMMUNITY; GNOTOBIOTIC PIGS;
INTRAMUSCULAR IMMUNIZATION; ANTIBODIES; MICE; GASTROENTERITIS;
IMMUNOGENICITY; EFFICACY; SAFETY
AB Live oral rotavirus vaccines have proven to be generally safe and effective to prevent severe dehydrating diarrhea among children in high and some middle income countries. However, concerns linger about rare but severe adverse events, Such as intussusception and their efficacy against the full range of rotavirus serotypes. More importantly, live oral vaccines have been less immunogenic and results of trails to assess their efficacy in poor children of both Africa and Asia will not be available for 2-3 years. This review describes the rationale for developing an inactivated rotavirus vaccine (IRV) as ail alternative approach should live oral vaccines not work well in these challenging populations. Studies have demonstrated the protective role of serum antibody in animals and children and the robust serum antibody response and protection against rotavirus infection in animal models following parenteral immunization with IRV. Four years after licensing the first new generation of rotavirus vaccine, we still remain several years away from knowing how well they work in the target populations. Research to develop alternative approaches should be fostered as an insurance policy to protect against suboptimal efficacy of Unanticipated adverse events that Could hinder global immunization and protection of all children. Published by Elsevier Ltd.
C1 [Jiang, Baoming; Gentsch, Jon R.; Glass, Roger I.] Ctr Dis Control & Prevent, Div Viral Dis, Atlanta, GA USA.
[Glass, Roger I.] NIH, Fogarty Int Ctr, Bethesda, MD USA.
RP Jiang, BM (reprint author), Natl Ctr Immunizat & Resp Dis, Gastroenteritis & Resp Viruses Lab Branch, Mailstop G04,1600 Clifton Rd, Atlanta, GA 30333 USA.
EM bxj4@cdc.gov
NR 38
TC 32
Z9 36
U1 0
U2 1
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 DEC 9
PY 2008
VL 26
IS 52
BP 6754
EP 6758
DI 10.1016/j.vaccine.2008.10.008
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 386QT
UT WOS:000261898400007
PM 18951937
ER
EF