Oncostatin M acting via OSMR, augments the actions of IL-1 and TNF in synovial fibroblasts.
Identifieur interne : 003544 ( PubMed/Corpus ); précédent : 003543; suivant : 003545Oncostatin M acting via OSMR, augments the actions of IL-1 and TNF in synovial fibroblasts.
Auteurs : Benoit Le Goff ; Sofie Singbrant ; Brett A. Tonkin ; T John Martin ; Evange Romas ; Natalie A. Sims ; Nicole C. WalshSource :
- Cytokine [ 1096-0023 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Arthritis, Rheumatoid (genetics), Arthritis, Rheumatoid (pathology), Fibroblasts (metabolism), Gene Expression Regulation, Humans, Interleukin-1beta (genetics), Interleukin-1beta (metabolism), Mice, Inbred C57BL, Oncostatin M (metabolism), Osteoprotegerin (genetics), Osteoprotegerin (metabolism), RANK Ligand (genetics), RANK Ligand (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Receptors, Interleukin-1 (metabolism), Receptors, Oncostatin M (deficiency), Receptors, Oncostatin M (metabolism), Synovial Membrane (pathology), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , deficiency : Receptors, Oncostatin M.
- chemical , genetics : Interleukin-1beta, Osteoprotegerin, RANK Ligand, RNA, Messenger.
- genetics : Arthritis, Rheumatoid.
- metabolism : Fibroblasts, Interleukin-1beta, Oncostatin M, Osteoprotegerin, RANK Ligand, RNA, Messenger, Receptors, Interleukin-1, Receptors, Oncostatin M, Tumor Necrosis Factor-alpha.
- pathology : Arthritis, Rheumatoid, Synovial Membrane.
- Animals, Gene Expression Regulation, Humans, Mice, Inbred C57BL.
Abstract
To identify how the gp130-signaling cytokine oncostatin M (OSM), acting alone or in concert with IL-1β or TNFα, affects synovial fibroblast expression of genes relevant to inflammation and bone erosion in inflammatory arthritis.
DOI: 10.1016/j.cyto.2014.04.001
PubMed: 24767864
Links to Exploration step
pubmed:24767864Le document en format XML
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Tonkin</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Martin, T John" sort="Martin, T John" uniqKey="Martin T" first="T John" last="Martin">T John Martin</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Romas, Evange" sort="Romas, Evange" uniqKey="Romas E" first="Evange" last="Romas">Evange Romas</name><affiliation><nlm:affiliation>Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia; Department of Rheumatology, St Vincent's Hospital, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Sims, Natalie A" sort="Sims, Natalie A" uniqKey="Sims N" first="Natalie A" last="Sims">Natalie A. Sims</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Walsh, Nicole C" sort="Walsh, Nicole C" uniqKey="Walsh N" first="Nicole C" last="Walsh">Nicole C. Walsh</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia. 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Tonkin</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Martin, T John" sort="Martin, T John" uniqKey="Martin T" first="T John" last="Martin">T John Martin</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Romas, Evange" sort="Romas, Evange" uniqKey="Romas E" first="Evange" last="Romas">Evange Romas</name><affiliation><nlm:affiliation>Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia; Department of Rheumatology, St Vincent's Hospital, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Sims, Natalie A" sort="Sims, Natalie A" uniqKey="Sims N" first="Natalie A" last="Sims">Natalie A. Sims</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Walsh, Nicole C" sort="Walsh, Nicole C" uniqKey="Walsh N" first="Nicole C" last="Walsh">Nicole C. Walsh</name><affiliation><nlm:affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia. Electronic address: nwalsh@svi.edu.au.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cytokine</title><idno type="eISSN">1096-0023</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Arthritis, Rheumatoid (genetics)</term><term>Arthritis, Rheumatoid (pathology)</term><term>Fibroblasts (metabolism)</term><term>Gene Expression Regulation</term><term>Humans</term><term>Interleukin-1beta (genetics)</term><term>Interleukin-1beta (metabolism)</term><term>Mice, Inbred C57BL</term><term>Oncostatin M (metabolism)</term><term>Osteoprotegerin (genetics)</term><term>Osteoprotegerin (metabolism)</term><term>RANK Ligand (genetics)</term><term>RANK Ligand (metabolism)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, Interleukin-1 (metabolism)</term><term>Receptors, Oncostatin M (deficiency)</term><term>Receptors, Oncostatin M (metabolism)</term><term>Synovial Membrane (pathology)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptors, Oncostatin M</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-1beta</term><term>Osteoprotegerin</term><term>RANK Ligand</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Arthritis, Rheumatoid</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Fibroblasts</term><term>Interleukin-1beta</term><term>Oncostatin M</term><term>Osteoprotegerin</term><term>RANK Ligand</term><term>RNA, Messenger</term><term>Receptors, Interleukin-1</term><term>Receptors, Oncostatin M</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Arthritis, Rheumatoid</term><term>Synovial Membrane</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Regulation</term><term>Humans</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To identify how the gp130-signaling cytokine oncostatin M (OSM), acting alone or in concert with IL-1β or TNFα, affects synovial fibroblast expression of genes relevant to inflammation and bone erosion in inflammatory arthritis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24767864</PMID><DateCreated><Year>2014</Year><Month>05</Month><Day>21</Day></DateCreated><DateCompleted><Year>2014</Year><Month>12</Month><Day>30</Day></DateCompleted><DateRevised><Year>2014</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0023</ISSN><JournalIssue CitedMedium="Internet"><Volume>68</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Cytokine</Title><ISOAbbreviation>Cytokine</ISOAbbreviation></Journal><ArticleTitle>Oncostatin M acting via OSMR, augments the actions of IL-1 and TNF in synovial fibroblasts.</ArticleTitle><Pagination><MedlinePgn>101-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cyto.2014.04.001</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1043-4666(14)00096-9</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To identify how the gp130-signaling cytokine oncostatin M (OSM), acting alone or in concert with IL-1β or TNFα, affects synovial fibroblast expression of genes relevant to inflammation and bone erosion in inflammatory arthritis.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Synovial fibroblasts (SFs) were isolated from non-arthritic wild type (WT) or OSM receptor deficient (OSMR(-/-)) mice and stimulated with OSM, IL-1β or TNFα and their combinations. Cytokine gene expression was assessed by quantitative RT-PCR. ELISA, flow cytometry and immunohistochemistry identified protein expression. Gene expression patterns were confirmed in SFs isolated from patients with osteoarthritis (OASFs) and rheumatoid arthritis (RASFs).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Expression of OSM and its receptors, gp130, OSMR and LIFR, was increased in synovial tissue from the mouse antigen-induced arthritis model. In isolated WT mouse synovial fibroblasts OSM alone, or in synergy with IL-1β, or together with TNFα, potently induced expression of the pro-inflammatory cytokine IL-6. OSM also induced a sustained increase in mRNA levels of the pro-osteoclastic cytokine RANKL. Combining OSM with IL-1β, but not with TNFα, further increased RANKL expression. Importantly these effects of OSM were all dependent on the expression of OSMR. Furthermore, OSM also increased expression of its own receptors, gp130 and OSMR and the IL-1 receptor, IL1-R1; the latter effects were also observed in both human OASFs and RASFs.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Together our data suggests that OSM signaling via OSMR in SFs has the potential to contribute significantly to joint destruction in inflammatory arthritis. It not only induces expression of pro-inflammatory and pro-osteoclastic cytokines but can also augment its own actions and that of IL-1 by inducing expression of OSMR and IL-1R1.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le Goff</LastName><ForeName>Benoit</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; INSERM UMR-S957, Laboratoire Physiopathologie de la Resorption Osseuse, Nantes, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Singbrant</LastName><ForeName>Sofie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tonkin</LastName><ForeName>Brett A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>T John</ForeName><Initials>TJ</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romas</LastName><ForeName>Evange</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia; Department of Rheumatology, St Vincent's Hospital, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sims</LastName><ForeName>Natalie A</ForeName><Initials>NA</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Walsh</LastName><ForeName>Nicole C</ForeName><Initials>NC</Initials><AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, Melbourne, Australia; Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia. Electronic address: nwalsh@svi.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cytokine</MedlineTA><NlmUniqueID>9005353</NlmUniqueID><ISSNLinking>1043-4666</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053244">Osteoprotegerin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053245">RANK Ligand</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017472">Receptors, Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053677">Receptors, Oncostatin M</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>106956-32-5</RegistryNumber><NameOfSubstance UI="D053683">Oncostatin M</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001172" MajorTopicYN="N">Arthritis, Rheumatoid</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053683" MajorTopicYN="N">Oncostatin M</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053244" MajorTopicYN="N">Osteoprotegerin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053245" MajorTopicYN="N">RANK Ligand</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017472" MajorTopicYN="N">Receptors, Interleukin-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053677" MajorTopicYN="N">Receptors, Oncostatin M</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013583" MajorTopicYN="N">Synovial Membrane</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arthritis</Keyword><Keyword MajorTopicYN="N">IL-1</Keyword><Keyword MajorTopicYN="N">IL-6</Keyword><Keyword MajorTopicYN="N">Oncostatin M</Keyword><Keyword MajorTopicYN="N">Synovial fibroblast</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>12</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>02</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>04</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>12</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24767864</ArticleId><ArticleId IdType="pii">S1043-4666(14)00096-9</ArticleId><ArticleId IdType="doi">10.1016/j.cyto.2014.04.001</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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