Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.
Identifieur interne : 003B52 ( PubMed/Corpus ); précédent : 003B51; suivant : 003B53Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.
Auteurs : G E Salvi ; C E Brown ; K. Fujihashi ; H. Kiyono ; F W Smith ; J D Beck ; S. OffenbacherSource :
- Journal of periodontal research [ 0022-3484 ] ; 1998.
English descriptors
- KwdEn :
- Adult, Aged, Aggressive Periodontitis (immunology), Cross-Sectional Studies, Cytokines (analysis), Dentition, Dinoprostone (analysis), Female, Gingival Crevicular Fluid (immunology), Humans, Inflammation Mediators (analysis), Interferon-gamma (analysis), Interleukin-1 (analysis), Interleukin-2 (analysis), Interleukin-4 (analysis), Interleukin-6 (analysis), Jaw, Edentulous, Leukocytes, Mononuclear (immunology), Lipopolysaccharides (immunology), Male, Middle Aged, Monocytes (immunology), Periodontitis (immunology), RNA, Messenger (genetics), Th1 Cells (immunology), Th2 Cells (immunology), Tooth Loss (immunology), Tumor Necrosis Factor-alpha (analysis), Up-Regulation.
- MESH :
- chemical , analysis : Cytokines, Dinoprostone, Inflammation Mediators, Interferon-gamma, Interleukin-1, Interleukin-2, Interleukin-4, Interleukin-6, Tumor Necrosis Factor-alpha.
- chemical , genetics : RNA, Messenger.
- immunology : Aggressive Periodontitis, Gingival Crevicular Fluid, Leukocytes, Mononuclear, Lipopolysaccharides, Monocytes, Periodontitis, Th1 Cells, Th2 Cells, Tooth Loss.
- Adult, Aged, Cross-Sectional Studies, Dentition, Female, Humans, Jaw, Edentulous, Male, Middle Aged, Up-Regulation.
Abstract
Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.
PubMed: 9689617
Links to Exploration step
pubmed:9689617Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.</title><author><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G E" last="Salvi">G E Salvi</name><affiliation><nlm:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brown, C E" sort="Brown, C E" uniqKey="Brown C" first="C E" last="Brown">C E Brown</name></author><author><name sortKey="Fujihashi, K" sort="Fujihashi, K" uniqKey="Fujihashi K" first="K" last="Fujihashi">K. Fujihashi</name></author><author><name sortKey="Kiyono, H" sort="Kiyono, H" uniqKey="Kiyono H" first="H" last="Kiyono">H. Kiyono</name></author><author><name sortKey="Smith, F W" sort="Smith, F W" uniqKey="Smith F" first="F W" last="Smith">F W Smith</name></author><author><name sortKey="Beck, J D" sort="Beck, J D" uniqKey="Beck J" first="J D" last="Beck">J D Beck</name></author><author><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S" last="Offenbacher">S. Offenbacher</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9689617</idno><idno type="pmid">9689617</idno><idno type="wicri:Area/PubMed/Corpus">003B52</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003B52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.</title><author><name sortKey="Salvi, G E" sort="Salvi, G E" uniqKey="Salvi G" first="G E" last="Salvi">G E Salvi</name><affiliation><nlm:affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brown, C E" sort="Brown, C E" uniqKey="Brown C" first="C E" last="Brown">C E Brown</name></author><author><name sortKey="Fujihashi, K" sort="Fujihashi, K" uniqKey="Fujihashi K" first="K" last="Fujihashi">K. Fujihashi</name></author><author><name sortKey="Kiyono, H" sort="Kiyono, H" uniqKey="Kiyono H" first="H" last="Kiyono">H. Kiyono</name></author><author><name sortKey="Smith, F W" sort="Smith, F W" uniqKey="Smith F" first="F W" last="Smith">F W Smith</name></author><author><name sortKey="Beck, J D" sort="Beck, J D" uniqKey="Beck J" first="J D" last="Beck">J D Beck</name></author><author><name sortKey="Offenbacher, S" sort="Offenbacher, S" uniqKey="Offenbacher S" first="S" last="Offenbacher">S. Offenbacher</name></author></analytic><series><title level="j">Journal of periodontal research</title><idno type="ISSN">0022-3484</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aggressive Periodontitis (immunology)</term><term>Cross-Sectional Studies</term><term>Cytokines (analysis)</term><term>Dentition</term><term>Dinoprostone (analysis)</term><term>Female</term><term>Gingival Crevicular Fluid (immunology)</term><term>Humans</term><term>Inflammation Mediators (analysis)</term><term>Interferon-gamma (analysis)</term><term>Interleukin-1 (analysis)</term><term>Interleukin-2 (analysis)</term><term>Interleukin-4 (analysis)</term><term>Interleukin-6 (analysis)</term><term>Jaw, Edentulous</term><term>Leukocytes, Mononuclear (immunology)</term><term>Lipopolysaccharides (immunology)</term><term>Male</term><term>Middle Aged</term><term>Monocytes (immunology)</term><term>Periodontitis (immunology)</term><term>RNA, Messenger (genetics)</term><term>Th1 Cells (immunology)</term><term>Th2 Cells (immunology)</term><term>Tooth Loss (immunology)</term><term>Tumor Necrosis Factor-alpha (analysis)</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Cytokines</term><term>Dinoprostone</term><term>Inflammation Mediators</term><term>Interferon-gamma</term><term>Interleukin-1</term><term>Interleukin-2</term><term>Interleukin-4</term><term>Interleukin-6</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aggressive Periodontitis</term><term>Gingival Crevicular Fluid</term><term>Leukocytes, Mononuclear</term><term>Lipopolysaccharides</term><term>Monocytes</term><term>Periodontitis</term><term>Th1 Cells</term><term>Th2 Cells</term><term>Tooth Loss</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Cross-Sectional Studies</term><term>Dentition</term><term>Female</term><term>Humans</term><term>Jaw, Edentulous</term><term>Male</term><term>Middle Aged</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9689617</PMID><DateCompleted><Year>1998</Year><Month>10</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3484</ISSN><JournalIssue CitedMedium="Print"><Volume>33</Volume><Issue>4</Issue><PubDate><Year>1998</Year><Month>May</Month></PubDate></JournalIssue><Title>Journal of periodontal research</Title><ISOAbbreviation>J. Periodont. Res.</ISOAbbreviation></Journal><ArticleTitle>Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.</ArticleTitle><Pagination><MedlinePgn>212-25</MedlinePgn></Pagination><Abstract><AbstractText>Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Salvi</LastName><ForeName>G E</ForeName><Initials>GE</Initials><AffiliationInfo><Affiliation>University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>C E</ForeName><Initials>CE</Initials></Author><Author ValidYN="Y"><LastName>Fujihashi</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Kiyono</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>F W</ForeName><Initials>FW</Initials></Author><Author ValidYN="Y"><LastName>Beck</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Offenbacher</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="N"><Grant><GrantID>DE 10519</GrantID><Acronym>DE</Acronym><Agency>NIDCR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DE 12453</GrantID><Acronym>DE</Acronym><Agency>NIDCR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DE08228</GrantID><Acronym>DE</Acronym><Agency>NIDCR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Periodontal Res</MedlineTA><NlmUniqueID>0055107</NlmUniqueID><ISSNLinking>0022-3484</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007376">Interleukin-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>207137-56-2</RegistryNumber><NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>K7Q1JQR04M</RegistryNumber><NameOfSubstance UI="D015232">Dinoprostone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>D</CitationSubset><CitationSubset>IM</CitationSubset><CitationSubset>X</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010520" MajorTopicYN="N">Aggressive Periodontitis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003817" MajorTopicYN="N">Dentition</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015232" MajorTopicYN="N">Dinoprostone</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005883" MajorTopicYN="N">Gingival Crevicular Fluid</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="Y">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007375" MajorTopicYN="N">Interleukin-1</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007376" MajorTopicYN="N">Interleukin-2</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015847" MajorTopicYN="N">Interleukin-4</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007575" MajorTopicYN="N">Jaw, Edentulous</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010518" MajorTopicYN="N">Periodontitis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016388" MajorTopicYN="N">Tooth Loss</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>8</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>8</Month><Day>5</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>8</Month><Day>5</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9689617</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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