EdenteV2, Istex, Corpus, bibRecord, 000014

Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin

Identifieur interne : 000014 ( Istex/Corpus ); précédent : 000013; suivant : 000015

Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin

Auteurs : S. Offenbacher ; G. E. Salvi

Source :

Clinical Infectious Diseases [ 1058-4838 ] ; 1999-03.

RBID : ISTEX:002DE9BE995900CBB769CA23378914E5E9EE592D

Abstract

This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.

Url:

https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/pdf

DOI: 10.1086/515177

Links to Exploration step

ISTEX:002DE9BE995900CBB769CA23378914E5E9EE592D

Le document en format XML

<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
<author><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S." last="Offenbacher">S. Offenbacher</name>
<affiliation><mods:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</mods:affiliation>
</affiliation>
<affiliation><mods:affiliation>E-mail: steve_offenbacher@dentistry.unc.edu</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G. E." last="Salvi">G. E. Salvi</name>
<affiliation><mods:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:002DE9BE995900CBB769CA23378914E5E9EE592D</idno>
<date when="1999" year="1999">1999</date>
<idno type="doi">10.1086/515177</idno>
<idno type="url">https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000014</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000014</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a">Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
<author><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S." last="Offenbacher">S. Offenbacher</name>
<affiliation><mods:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</mods:affiliation>
</affiliation>
<affiliation><mods:affiliation>E-mail: steve_offenbacher@dentistry.unc.edu</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G. E." last="Salvi">G. E. Salvi</name>
<affiliation><mods:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Clinical Infectious Diseases</title>
<title level="j" type="abbrev">Clinical Infectious Diseases</title>
<idno type="ISSN">1058-4838</idno>
<idno type="eISSN">1537-6591</idno>
<imprint><publisher>The University of Chicago Press</publisher>
<date type="published" when="1999-03">1999-03</date>
<biblScope unit="volume">28</biblScope>
<biblScope unit="issue">3</biblScope>
<biblScope unit="page" from="505">505</biblScope>
<biblScope unit="page" to="513">513</biblScope>
</imprint>
<idno type="ISSN">1058-4838</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">1058-4838</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract">This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.</div>
</front>
</TEI>
<istex><corpusName>oup</corpusName>
<author><json:item><name>S. Offenbacher</name>
<affiliations><json:string>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</json:string>
<json:string>E-mail: steve_offenbacher@dentistry.unc.edu</json:string>
</affiliations>
</json:item>
<json:item><name>G. E. Salvi</name>
<affiliations><json:string>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</json:string>
</affiliations>
</json:item>
</author>
<arkIstex>ark:/67375/HXZ-KW6L9SBN-8</arkIstex>
<language><json:string>unknown</json:string>
</language>
<originalGenre><json:string>research-article</json:string>
</originalGenre>
<abstract>This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.</abstract>
<qualityIndicators><score>8.356</score>
<pdfWordCount>7010</pdfWordCount>
<pdfCharCount>42735</pdfCharCount>
<pdfVersion>1.4</pdfVersion>
<pdfPageCount>9</pdfPageCount>
<pdfPageSize>612 x 792 pts (letter)</pdfPageSize>
<refBibsNative>false</refBibsNative>
<abstractWordCount>113</abstractWordCount>
<abstractCharCount>803</abstractCharCount>
<keywordCount>0</keywordCount>
</qualityIndicators>
<title>Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
<pmid><json:string>10194068</json:string>
</pmid>
<genre><json:string>research-article</json:string>
</genre>
<host><title>Clinical Infectious Diseases</title>
<language><json:string>unknown</json:string>
</language>
<issn><json:string>1058-4838</json:string>
</issn>
<eissn><json:string>1537-6591</json:string>
</eissn>
<publisherId><json:string>cid</json:string>
</publisherId>
<volume>28</volume>
<issue>3</issue>
<pages><first>505</first>
<last>513</last>
</pages>
<genre><json:string>journal</json:string>
</genre>
</host>
<namedEntities><unitex><date><json:string>02-22-99</json:string>
<json:string>1986</json:string>
<json:string>1999</json:string>
<json:string>1989</json:string>
</date>
<geogName></geogName>
<orgName><json:string>Steven Offenbacher, Center for Oral and Systemic Diseases</json:string>
<json:string>University of North Carolina</json:string>
<json:string>Sigma Chemical</json:string>
<json:string>University of Berne</json:string>
<json:string>American Academy of Periodontology</json:string>
<json:string>National Institutes of Health</json:string>
<json:string>Department of Periodontology and Dental Research Center</json:string>
<json:string>Waters Inc.</json:string>
<json:string>Inus Systems, Tampa</json:string>
<json:string>Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA</json:string>
</orgName>
<orgName_funder></orgName_funder>
<orgName_provider></orgName_provider>
<persName><json:string>G. E. Salvi</json:string>
<json:string>Berne</json:string>
<json:string>Selection</json:string>
<json:string>In</json:string>
<json:string>Mølvig</json:string>
<json:string>Medicine</json:string>
<json:string>Switzerland</json:string>
<json:string>Powell</json:string>
<json:string>Figure</json:string>
<json:string>Although</json:string>
</persName>
<placeName><json:string>Marlborough</json:string>
<json:string>America</json:string>
<json:string>MA</json:string>
</placeName>
<ref_url></ref_url>
<ref_bibl><json:string>[14, 15]</json:string>
<json:string>[4]</json:string>
<json:string>[23]</json:string>
<json:string>[29]</json:string>
<json:string>[6]</json:string>
<json:string>Salvi et al. [8]</json:string>
<json:string>[22]</json:string>
<json:string>[10, 11]</json:string>
<json:string>[8]</json:string>
<json:string>[39]</json:string>
<json:string>[9, 11]</json:string>
<json:string>Collins et al. [13]</json:string>
<json:string>[32]</json:string>
<json:string>Gunsolley et al. [14]</json:string>
<json:string>[37, 38]</json:string>
<json:string>[3]</json:string>
<json:string>[31]</json:string>
<json:string>[24, 25]</json:string>
<json:string>[5]</json:string>
<json:string>[26]</json:string>
<json:string>Salvi et al. [9]</json:string>
<json:string>[41]</json:string>
<json:string>[8, 9, 16]</json:string>
<json:string>[36]</json:string>
<json:string>Shapira et al. [22]</json:string>
<json:string>[9]</json:string>
<json:string>[40]</json:string>
<json:string>Loe et al. [4]</json:string>
<json:string>[35]</json:string>
<json:string>[19]</json:string>
</ref_bibl>
<bibl></bibl>
</unitex>
</namedEntities>
<ark><json:string>ark:/67375/HXZ-KW6L9SBN-8</json:string>
</ark>
<categories><wos><json:string>science</json:string>
<json:string>microbiology</json:string>
<json:string>infectious diseases</json:string>
<json:string>immunology</json:string>
</wos>
<scienceMetrix><json:string>health sciences</json:string>
<json:string>biomedical research</json:string>
<json:string>microbiology</json:string>
</scienceMetrix>
<scopus><json:string>1 - Health Sciences</json:string>
<json:string>2 - Medicine</json:string>
<json:string>3 - Infectious Diseases</json:string>
<json:string>1 - Health Sciences</json:string>
<json:string>2 - Medicine</json:string>
<json:string>3 - Microbiology (medical)</json:string>
</scopus>
</categories>
<publicationDate>1999</publicationDate>
<copyrightDate>1999</copyrightDate>
<doi><json:string>10.1086/515177</json:string>
</doi>
<id>002DE9BE995900CBB769CA23378914E5E9EE592D</id>
<score>1</score>
<fulltext><json:item><extension>pdf</extension>
<original>true</original>
<mimetype>application/pdf</mimetype>
<uri>https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/pdf</uri>
</json:item>
<json:item><extension>zip</extension>
<original>false</original>
<mimetype>application/zip</mimetype>
<uri>https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
<respStmt><resp>Références bibliographiques récupérées via GROBID</resp>
<name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name>
</respStmt>
</titleStmt>
<publicationStmt><authority>ISTEX</authority>
<publisher scheme="https://publisher-list.data.istex.fr">The University of Chicago Press</publisher>
<availability><licence><p>© 1999 by the Infectious Diseases Society of America</p>
</licence>
<p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-GTWS0RDP-M">oup</p>
</availability>
<date>1999</date>
</publicationStmt>
<notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note>
<note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note>
</notesStmt>
<sourceDesc><biblStruct type="inbook"><analytic><title level="a">Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
<author xml:id="author-0000" corresp="yes"><persName><forename type="first">S.</forename>
<surname>Offenbacher</surname>
</persName>
<email>steve_offenbacher@dentistry.unc.edu</email>
<affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</affiliation>
</author>
<author xml:id="author-0001"><persName><forename type="first">G. E.</forename>
<surname>Salvi</surname>
</persName>
<affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</affiliation>
</author>
<idno type="istex">002DE9BE995900CBB769CA23378914E5E9EE592D</idno>
<idno type="ark">ark:/67375/HXZ-KW6L9SBN-8</idno>
<idno type="DOI">10.1086/515177</idno>
</analytic>
<monogr><title level="j">Clinical Infectious Diseases</title>
<title level="j" type="abbrev">Clinical Infectious Diseases</title>
<idno type="pISSN">1058-4838</idno>
<idno type="eISSN">1537-6591</idno>
<idno type="publisher-id">cid</idno>
<idno type="PublisherID-hwp">cid</idno>
<imprint><publisher>The University of Chicago Press</publisher>
<date type="published" when="1999-03"></date>
<biblScope unit="volume">28</biblScope>
<biblScope unit="issue">3</biblScope>
<biblScope unit="page" from="505">505</biblScope>
<biblScope unit="page" to="513">513</biblScope>
</imprint>
</monogr>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><creation><date>1999</date>
</creation>
<abstract><p>This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.</p>
</abstract>
</profileDesc>
<revisionDesc><change when="1999-03">Published</change>
<change xml:id="refBibs-istex" who="#ISTEX-API" when="2017-10-6">References added</change>
</revisionDesc>
</teiHeader>
</istex:fulltextTEI>
<json:item><extension>txt</extension>
<original>false</original>
<mimetype>text/plain</mimetype>
<uri>https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/fulltext/txt</uri>
</json:item>
</fulltext>
<metadata><istex:metadataXml wicri:clean="corpus oup, element #text not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0"</istex:xmlDeclaration>
<istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType>
<istex:document><article article-type="research-article">

<front>

<journal-meta>

<journal-id journal-id-type="hwp">cid</journal-id>

<journal-id journal-id-type="publisher-id">cid</journal-id>

<journal-title>Clinical Infectious Diseases</journal-title>

<abbrev-journal-title>Clinical Infectious Diseases</abbrev-journal-title>

<issn pub-type="ppub">1058-4838</issn>

<issn pub-type="epub">1537-6591</issn>

<publisher>

<publisher-name>The University of Chicago Press</publisher-name>

</publisher>

</journal-meta>

<article-meta>

<article-id pub-id-type="doi">10.1086/515177</article-id>

<article-categories>

<subj-group subj-group-type="heading">

<subject>Molecular Mechanisms of Microbial Host Cell Interactions in Periodontal Disease</subject>

</subj-group>

</article-categories>

<title-group>

<article-title>Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</article-title>

</title-group>

<contrib-group>

<contrib contrib-type="author" corresp="yes">

<name>

<surname>Offenbacher</surname>
<given-names>S.</given-names>

</name>
<xref ref-type="corresp"></xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Salvi</surname>
<given-names>G. E.</given-names>

</name>

</contrib>

<aff><institution>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center</institution>
, <addr-line>Chapel Hill, North Carolina, USA</addr-line>
</aff>

<aff><institution>University of Berne, School of Dental Medicine</institution>
, <addr-line>Berne, Switzerland</addr-line>
</aff>

</contrib-group>

<author-notes>

<corresp id="cor">Reprints or correspondence: Steven Offenbacher, Center for Oral and Systemic Diseases, University of North Carolina at Chapel Hill School of Dentistry, Department of Periodontology and Dental Research Center, CB #7455, DRC Building, Room 222, Chapel Hill, North Carolina 27599-7455 (<email>steve_offenbacher@dentistry.unc.edu</email>
).</corresp>

</author-notes>

<pub-date pub-type="ppub">

<month>3</month>

<year>1999</year>

</pub-date>

<volume>28</volume>

<issue>3</issue>

<fpage>505</fpage>

<lpage>513</lpage>

<copyright-statement>© 1999 by the Infectious Diseases Society of America</copyright-statement>

<copyright-year>1999</copyright-year>

<abstract>

<p>This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E<sub>2</sub>
 (PGE<sub>2</sub>
) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE<sub>2</sub>
, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.</p>

</abstract>

</article-meta>

</front>

</article>
</istex:document>
</istex:metadataXml>
<mods version="3.6"><titleInfo><title>Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA"><title>Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin</title>
</titleInfo>
<name type="personal" displayLabel="corresp"><namePart type="given">S.</namePart>
<namePart type="family">Offenbacher</namePart>
<affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</affiliation>
<affiliation>E-mail: steve_offenbacher@dentistry.unc.edu</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">G. E.</namePart>
<namePart type="family">Salvi</namePart>
<affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, Chapel Hill, North Carolina, USA, Berne, Switzerland</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre>
<originInfo><publisher>The University of Chicago Press</publisher>
<dateIssued encoding="w3cdtf">1999-03</dateIssued>
<copyrightDate encoding="w3cdtf">1999</copyrightDate>
</originInfo>
<abstract>This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.</abstract>
<relatedItem type="host"><titleInfo><title>Clinical Infectious Diseases</title>
</titleInfo>
<titleInfo type="abbreviated"><title>Clinical Infectious Diseases</title>
</titleInfo>
<genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre>
<identifier type="ISSN">1058-4838</identifier>
<identifier type="eISSN">1537-6591</identifier>
<identifier type="PublisherID">cid</identifier>
<identifier type="PublisherID-hwp">cid</identifier>
<part><date>1999</date>
<detail type="volume"><caption>vol.</caption>
<number>28</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>3</number>
</detail>
<extent unit="pages"><start>505</start>
<end>513</end>
</extent>
</part>
</relatedItem>
<identifier type="istex">002DE9BE995900CBB769CA23378914E5E9EE592D</identifier>
<identifier type="DOI">10.1086/515177</identifier>
<accessCondition type="use and reproduction" contentType="copyright">© 1999 by the Infectious Diseases Society of America</accessCondition>
<recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-GTWS0RDP-M">oup</recordContentSource>
<recordOrigin>© 1999 by the Infectious Diseases Society of America</recordOrigin>
</recordInfo>
</mods>
<json:item><extension>json</extension>
<original>false</original>
<mimetype>application/json</mimetype>
<uri>https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/metadata/json</uri>
</json:item>
</metadata>
<annexes><json:item><extension>pdf</extension>
<original>true</original>
<mimetype>application/pdf</mimetype>
<uri>https://api.istex.fr/document/002DE9BE995900CBB769CA23378914E5E9EE592D/annexes/pdf</uri>
</json:item>
</annexes>
<serie></serie>
</istex>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/EdenteV2/Data/Istex/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000014 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000014 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    EdenteV2
   |flux=    Istex
   |étape=   Corpus
   |type=    RBID
   |clé=     ISTEX:002DE9BE995900CBB769CA23378914E5E9EE592D
   |texte=   Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin
}}

This area was generated with Dilib version V0.6.32.
Data generation: Thu Nov 30 15:26:48 2017. Site generation: Tue Mar 8 16:36:20 2022

	Serveur d'exploration sur le patient édenté
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur le patient édenté

Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin

Induction of Prostaglandin Release from Macrophages by Bacterial Endotoxin

Source :

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri