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Periodontal microbiota and phospholipases: The Oral Infections and Vascular Disease Epidemiology Study (INVEST)

Identifieur interne : 002589 ( Pmc/Corpus ); précédent : 002588; suivant : 002590

Periodontal microbiota and phospholipases: The Oral Infections and Vascular Disease Epidemiology Study (INVEST)

Auteurs : Adrien Boillot ; Ryan T. Demmer ; Ziad Mallat ; Ralph L. Sacco ; David R. Jacobs ; Joelle Benessiano ; Alain Tedgui ; Tatjana Rundek ; Panos N. Papapanou ; Moïse Desvarieux

Source :

RBID : PMC:4862208

Abstract

Objective

Periodontal infections have been linked to cardiovascular disease, including atherosclerosis, and systemic inflammation has been proposed as a possible mediator. Secretory phospholipase A2 (s-PLA2) and Lipoprotein-associated PLA2 (Lp-PLA2) are inflammatory enzymes associated with athero-sclerosis. No data are available on the association between oral microbiota and PLA2s. We studied whether a relationship exists between periodontal microbiota and the activities of these enzymes.

Methods

The Oral Infection and Vascular Disease Epidemiology Study (INVEST) collected subgingival biofilms and serum samples from 593 dentate men and women (age 68.7 ± 8.6 years). 4561 biofilm samples were collected in the two most posterior teeth of each quadrant (average 7/participant) for quantitative assessment of 11 bacterial species using DNA–DNA checkerboard hybridization. Mean concentration of s-PLA2 and activities of s-PLA2 and Lp-PLA2 were regressed on tertiles of etiologic dominance (ED). ED is defined as the level of presumed periodontopathic species/combined level of all eleven species measured, and represents the relative abundance of periodontopathic organisms. Analyses were adjusted for age, sex, race/ethnicity, education, smoking, BMI, diabetes, LDL cholesterol and HDL cholesterol, and systolic blood pressure.

Results

Higher levels of s-PLA2 activity were observed across increasing tertiles of etiologic dominance (0.66 ± 0.04 nmol ml−1 min−1, 0.73 ± 0.04 nmol ml−1 min−1, 0.89 ± 0.04 nmol ml−1 min−1; p < 0.001), with also a trend of association between Lp-PLA2 activity and ED (p = 0.07), while s-PLA2 concentration was unrelated to ED.

Conclusion

Increasingly greater s-PLA2 activity at higher tertiles of etiologic dominance may provide a mechanistic explanatory link of the relationship between periodontal microbiota and vascular diseases. Additional studies investigating the role of s-PLA2 are needed.


Url:
DOI: 10.1016/j.atherosclerosis.2015.07.039
PubMed: 26282947
PubMed Central: 4862208

Links to Exploration step

PMC:4862208

Le document en format XML

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<nlm:aff id="A1"> Department of Periodontology, Rothschild Hospital (AP-HP); University Paris 7, 5 Rue Santerre, Paris, France</nlm:aff>
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<nlm:aff id="A2"> INSERM U1018, University of Versailles St Quentin. Centre for research in Epidemiology and Population Health, Villejuif, France</nlm:aff>
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<nlm:aff id="A5"> Department of Medicine, University of Cambridge, Cambridge, United Kingdom</nlm:aff>
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<name sortKey="Sacco, Ralph L" sort="Sacco, Ralph L" uniqKey="Sacco R" first="Ralph L." last="Sacco">Ralph L. Sacco</name>
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<nlm:aff id="A6"> Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA</nlm:aff>
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<name sortKey="Jacobs, David R" sort="Jacobs, David R" uniqKey="Jacobs D" first="David R." last="Jacobs">David R. Jacobs</name>
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<nlm:aff id="A7"> Department of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA</nlm:aff>
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<nlm:aff id="A8"> Department of Nutrition, University of Oslo, Oslo, Norway</nlm:aff>
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<name sortKey="Benessiano, Joelle" sort="Benessiano, Joelle" uniqKey="Benessiano J" first="Joelle" last="Benessiano">Joelle Benessiano</name>
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<name sortKey="Tedgui, Alain" sort="Tedgui, Alain" uniqKey="Tedgui A" first="Alain" last="Tedgui">Alain Tedgui</name>
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<nlm:aff id="A4"> Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France</nlm:aff>
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<name sortKey="Rundek, Tatjana" sort="Rundek, Tatjana" uniqKey="Rundek T" first="Tatjana" last="Rundek">Tatjana Rundek</name>
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<nlm:aff id="A6"> Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA</nlm:aff>
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<name sortKey="Papapanou, Panos N" sort="Papapanou, Panos N" uniqKey="Papapanou P" first="Panos N." last="Papapanou">Panos N. Papapanou</name>
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<nlm:aff id="A10"> Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA</nlm:aff>
</affiliation>
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<name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moïse" last="Desvarieux">Moïse Desvarieux</name>
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<nlm:aff id="A3"> Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA</nlm:aff>
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<affiliation>
<nlm:aff id="A11"> INSERM Epidemiology and Biostatistics Research Center, Sorbonne Paris Cité, INSERM UMR 1153, Paris, France</nlm:aff>
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<nlm:aff id="A1"> Department of Periodontology, Rothschild Hospital (AP-HP); University Paris 7, 5 Rue Santerre, Paris, France</nlm:aff>
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<nlm:aff id="A2"> INSERM U1018, University of Versailles St Quentin. Centre for research in Epidemiology and Population Health, Villejuif, France</nlm:aff>
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<name sortKey="Demmer, Ryan T" sort="Demmer, Ryan T" uniqKey="Demmer R" first="Ryan T." last="Demmer">Ryan T. Demmer</name>
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<nlm:aff id="A3"> Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA</nlm:aff>
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<name sortKey="Mallat, Ziad" sort="Mallat, Ziad" uniqKey="Mallat Z" first="Ziad" last="Mallat">Ziad Mallat</name>
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<nlm:aff id="A4"> Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France</nlm:aff>
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<affiliation>
<nlm:aff id="A5"> Department of Medicine, University of Cambridge, Cambridge, United Kingdom</nlm:aff>
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<name sortKey="Sacco, Ralph L" sort="Sacco, Ralph L" uniqKey="Sacco R" first="Ralph L." last="Sacco">Ralph L. Sacco</name>
<affiliation>
<nlm:aff id="A6"> Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA</nlm:aff>
</affiliation>
</author>
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<name sortKey="Jacobs, David R" sort="Jacobs, David R" uniqKey="Jacobs D" first="David R." last="Jacobs">David R. Jacobs</name>
<affiliation>
<nlm:aff id="A7"> Department of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A8"> Department of Nutrition, University of Oslo, Oslo, Norway</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Benessiano, Joelle" sort="Benessiano, Joelle" uniqKey="Benessiano J" first="Joelle" last="Benessiano">Joelle Benessiano</name>
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</affiliation>
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<name sortKey="Tedgui, Alain" sort="Tedgui, Alain" uniqKey="Tedgui A" first="Alain" last="Tedgui">Alain Tedgui</name>
<affiliation>
<nlm:aff id="A4"> Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France</nlm:aff>
</affiliation>
</author>
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<name sortKey="Rundek, Tatjana" sort="Rundek, Tatjana" uniqKey="Rundek T" first="Tatjana" last="Rundek">Tatjana Rundek</name>
<affiliation>
<nlm:aff id="A6"> Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Papapanou, Panos N" sort="Papapanou, Panos N" uniqKey="Papapanou P" first="Panos N." last="Papapanou">Panos N. Papapanou</name>
<affiliation>
<nlm:aff id="A10"> Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Desvarieux, Moise" sort="Desvarieux, Moise" uniqKey="Desvarieux M" first="Moïse" last="Desvarieux">Moïse Desvarieux</name>
<affiliation>
<nlm:aff id="A3"> Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A11"> INSERM Epidemiology and Biostatistics Research Center, Sorbonne Paris Cité, INSERM UMR 1153, Paris, France</nlm:aff>
</affiliation>
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<series>
<title level="j">Atherosclerosis</title>
<idno type="ISSN">0021-9150</idno>
<idno type="eISSN">1879-1484</idno>
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<front>
<div type="abstract" xml:lang="en">
<sec id="S1">
<title>Objective</title>
<p id="P1">Periodontal infections have been linked to cardiovascular disease, including atherosclerosis, and systemic inflammation has been proposed as a possible mediator. Secretory phospholipase A2 (s-PLA2) and Lipoprotein-associated PLA2 (Lp-PLA2) are inflammatory enzymes associated with athero-sclerosis. No data are available on the association between oral microbiota and PLA2s. We studied whether a relationship exists between periodontal microbiota and the activities of these enzymes.</p>
</sec>
<sec id="S2">
<title>Methods</title>
<p id="P2">The Oral Infection and Vascular Disease Epidemiology Study (INVEST) collected subgingival biofilms and serum samples from 593 dentate men and women (age 68.7 ± 8.6 years). 4561 biofilm samples were collected in the two most posterior teeth of each quadrant (average 7/participant) for quantitative assessment of 11 bacterial species using DNA–DNA checkerboard hybridization. Mean concentration of s-PLA2 and activities of s-PLA2 and Lp-PLA2 were regressed on tertiles of etiologic dominance (ED). ED is defined as the level of presumed periodontopathic species/combined level of all eleven species measured, and represents the relative abundance of periodontopathic organisms. Analyses were adjusted for age, sex, race/ethnicity, education, smoking, BMI, diabetes, LDL cholesterol and HDL cholesterol, and systolic blood pressure.</p>
</sec>
<sec id="S3">
<title>Results</title>
<p id="P3">Higher levels of s-PLA2 activity were observed across increasing tertiles of etiologic dominance (0.66 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
, 0.73 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
, 0.89 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
; p < 0.001), with also a trend of association between Lp-PLA2 activity and ED (p = 0.07), while s-PLA2 concentration was unrelated to ED.</p>
</sec>
<sec id="S4">
<title>Conclusion</title>
<p id="P4">Increasingly greater s-PLA2 activity at higher tertiles of etiologic dominance may provide a mechanistic explanatory link of the relationship between periodontal microbiota and vascular diseases. Additional studies investigating the role of s-PLA2 are needed.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article">
<pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-journal-id">0242543</journal-id>
<journal-id journal-id-type="pubmed-jr-id">890</journal-id>
<journal-id journal-id-type="nlm-ta">Atherosclerosis</journal-id>
<journal-id journal-id-type="iso-abbrev">Atherosclerosis</journal-id>
<journal-title-group>
<journal-title>Atherosclerosis</journal-title>
</journal-title-group>
<issn pub-type="ppub">0021-9150</issn>
<issn pub-type="epub">1879-1484</issn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">26282947</article-id>
<article-id pub-id-type="pmc">4862208</article-id>
<article-id pub-id-type="doi">10.1016/j.atherosclerosis.2015.07.039</article-id>
<article-id pub-id-type="manuscript">NIHMS757891</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Periodontal microbiota and phospholipases: The Oral Infections and Vascular Disease Epidemiology Study (INVEST)</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Boillot</surname>
<given-names>Adrien</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Demmer</surname>
<given-names>Ryan T.</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Mallat</surname>
<given-names>Ziad</given-names>
</name>
<xref ref-type="aff" rid="A4">d</xref>
<xref ref-type="aff" rid="A5">e</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Sacco</surname>
<given-names>Ralph L.</given-names>
</name>
<xref ref-type="aff" rid="A6">f</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Jacobs</surname>
<given-names>David R.</given-names>
</name>
<xref ref-type="aff" rid="A7">g</xref>
<xref ref-type="aff" rid="A8">h</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Benessiano</surname>
<given-names>Joelle</given-names>
</name>
<xref ref-type="aff" rid="A9">i</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Tedgui</surname>
<given-names>Alain</given-names>
</name>
<xref ref-type="aff" rid="A4">d</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Rundek</surname>
<given-names>Tatjana</given-names>
</name>
<xref ref-type="aff" rid="A6">f</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Papapanou</surname>
<given-names>Panos N.</given-names>
</name>
<xref ref-type="aff" rid="A10">j</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Desvarieux</surname>
<given-names>Moïse</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
<xref ref-type="aff" rid="A11">k</xref>
<xref ref-type="corresp" rid="CR1">*</xref>
</contrib>
</contrib-group>
<aff id="A1">
<label>a</label>
Department of Periodontology, Rothschild Hospital (AP-HP); University Paris 7, 5 Rue Santerre, Paris, France</aff>
<aff id="A2">
<label>b</label>
INSERM U1018, University of Versailles St Quentin. Centre for research in Epidemiology and Population Health, Villejuif, France</aff>
<aff id="A3">
<label>c</label>
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA</aff>
<aff id="A4">
<label>d</label>
Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France</aff>
<aff id="A5">
<label>e</label>
Department of Medicine, University of Cambridge, Cambridge, United Kingdom</aff>
<aff id="A6">
<label>f</label>
Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA</aff>
<aff id="A7">
<label>g</label>
Department of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA</aff>
<aff id="A8">
<label>h</label>
Department of Nutrition, University of Oslo, Oslo, Norway</aff>
<aff id="A9">
<label>i</label>
Service de Biochimie, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France</aff>
<aff id="A10">
<label>j</label>
Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA</aff>
<aff id="A11">
<label>k</label>
INSERM Epidemiology and Biostatistics Research Center, Sorbonne Paris Cité, INSERM UMR 1153, Paris, France</aff>
<author-notes>
<corresp id="CR1">
<label>*</label>
Corresponding author. Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th Street, Room 525, New York, NY 10032, USA.
<email>mdesvarieux@columbia.edu</email>
(M. Desvarieux).</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>11</day>
<month>2</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>22</day>
<month>7</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="ppub">
<month>10</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>10</day>
<month>5</month>
<year>2016</year>
</pub-date>
<volume>242</volume>
<issue>2</issue>
<fpage>418</fpage>
<lpage>423</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.atherosclerosis.2015.07.039</pmc-comment>
<abstract>
<sec id="S1">
<title>Objective</title>
<p id="P1">Periodontal infections have been linked to cardiovascular disease, including atherosclerosis, and systemic inflammation has been proposed as a possible mediator. Secretory phospholipase A2 (s-PLA2) and Lipoprotein-associated PLA2 (Lp-PLA2) are inflammatory enzymes associated with athero-sclerosis. No data are available on the association between oral microbiota and PLA2s. We studied whether a relationship exists between periodontal microbiota and the activities of these enzymes.</p>
</sec>
<sec id="S2">
<title>Methods</title>
<p id="P2">The Oral Infection and Vascular Disease Epidemiology Study (INVEST) collected subgingival biofilms and serum samples from 593 dentate men and women (age 68.7 ± 8.6 years). 4561 biofilm samples were collected in the two most posterior teeth of each quadrant (average 7/participant) for quantitative assessment of 11 bacterial species using DNA–DNA checkerboard hybridization. Mean concentration of s-PLA2 and activities of s-PLA2 and Lp-PLA2 were regressed on tertiles of etiologic dominance (ED). ED is defined as the level of presumed periodontopathic species/combined level of all eleven species measured, and represents the relative abundance of periodontopathic organisms. Analyses were adjusted for age, sex, race/ethnicity, education, smoking, BMI, diabetes, LDL cholesterol and HDL cholesterol, and systolic blood pressure.</p>
</sec>
<sec id="S3">
<title>Results</title>
<p id="P3">Higher levels of s-PLA2 activity were observed across increasing tertiles of etiologic dominance (0.66 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
, 0.73 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
, 0.89 ± 0.04 nmol ml
<sup>−1</sup>
min
<sup>−1</sup>
; p < 0.001), with also a trend of association between Lp-PLA2 activity and ED (p = 0.07), while s-PLA2 concentration was unrelated to ED.</p>
</sec>
<sec id="S4">
<title>Conclusion</title>
<p id="P4">Increasingly greater s-PLA2 activity at higher tertiles of etiologic dominance may provide a mechanistic explanatory link of the relationship between periodontal microbiota and vascular diseases. Additional studies investigating the role of s-PLA2 are needed.</p>
</sec>
</abstract>
<kwd-group>
<kwd>Periodontitis</kwd>
<kwd>Phospholipases</kwd>
<kwd>Cardiovascular diseases</kwd>
<kwd>Atherosclerosis</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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