STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection
Identifieur interne : 000E06 ( Main/Corpus ); précédent : 000E05; suivant : 000E07STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection
Auteurs : Jacob Geday ; Karen Stergaard ; Erik Johnsen ; Albert GjeddeSource :
- Human Brain Mapping [ 1065-9471 ] ; 2009-01.
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Abstract
To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/hbm.20486
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ISTEX:9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection</title><author><name sortKey="Geday, Jacob" sort="Geday, Jacob" uniqKey="Geday J" first="Jacob" last="Geday">Jacob Geday</name><affiliation><mods:affiliation>PET‐Center, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey=" Stergaard, Karen" sort=" Stergaard, Karen" uniqKey=" Stergaard K" first="Karen" last=" Stergaard">Karen Stergaard</name><affiliation><mods:affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Johnsen, Erik" sort="Johnsen, Erik" uniqKey="Johnsen E" first="Erik" last="Johnsen">Erik Johnsen</name><affiliation><mods:affiliation>Neurosurgical Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Gjedde, Albert" sort="Gjedde, Albert" uniqKey="Gjedde A" first="Albert" last="Gjedde">Albert Gjedde</name><affiliation><mods:affiliation>PET‐Center, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/hbm.20486</idno><idno type="url">https://api.istex.fr/document/9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000E06</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection</title><author><name sortKey="Geday, Jacob" sort="Geday, Jacob" uniqKey="Geday J" first="Jacob" last="Geday">Jacob Geday</name><affiliation><mods:affiliation>PET‐Center, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey=" Stergaard, Karen" sort=" Stergaard, Karen" uniqKey=" Stergaard K" first="Karen" last=" Stergaard">Karen Stergaard</name><affiliation><mods:affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Johnsen, Erik" sort="Johnsen, Erik" uniqKey="Johnsen E" first="Erik" last="Johnsen">Erik Johnsen</name><affiliation><mods:affiliation>Neurosurgical Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Gjedde, Albert" sort="Gjedde, Albert" uniqKey="Gjedde A" first="Albert" last="Gjedde">Albert Gjedde</name><affiliation><mods:affiliation>PET‐Center, Aarhus University Hospitals, Denmark</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Brain Mapping</title><title level="j" type="abbrev">Hum. Brain Mapp.</title><idno type="ISSN">1065-9471</idno><idno type="eISSN">1097-0193</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-01">2009-01</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="112">112</biblScope><biblScope unit="page" to="121">121</biblScope></imprint><idno type="ISSN">1065-9471</idno></series><idno type="istex">9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750</idno><idno type="DOI">10.1002/hbm.20486</idno><idno type="ArticleID">HBM20486</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1065-9471</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PET</term><term>Parkinson</term><term>STN‐stimulation</term><term>VL</term><term>basalgangglia loop</term><term>clinical outcome</term><term>deactivation</term><term>flow</term><term>thalamus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jacob Geday</name><affiliations><json:string>PET‐Center, Aarhus University Hospitals, Denmark</json:string><json:string>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</json:string></affiliations></json:item><json:item><name>Karen Østergaard</name><affiliations><json:string>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</json:string></affiliations></json:item><json:item><name>Erik Johnsen</name><affiliations><json:string>Neurosurgical Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</json:string></affiliations></json:item><json:item><name>Albert Gjedde</name><affiliations><json:string>PET‐Center, Aarhus University Hospitals, Denmark</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>STN‐stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>flow</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VL</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>thalamus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deactivation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basalgangglia loop</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical outcome</value></json:item></subject><articleId><json:string>HBM20486</json:string></articleId><language><json:string>eng</json:string></language><abstract>To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. 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Brain Mapp.</title><idno type="pISSN">1065-9471</idno><idno type="eISSN">1097-0193</idno><idno type="DOI">10.1002/(ISSN)1097-0193</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-01"></date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="112">112</biblScope><biblScope unit="page" to="121">121</biblScope></imprint></monogr><idno type="istex">9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750</idno><idno type="DOI">10.1002/hbm.20486</idno><idno type="ArticleID">HBM20486</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson</term></item><item><term>STN‐stimulation</term></item><item><term>PET</term></item><item><term>flow</term></item><item><term>VL</term></item><item><term>thalamus</term></item><item><term>deactivation</term></item><item><term>basalgangglia loop</term></item><item><term>clinical outcome</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-04-08">Received</change><change when="2007-08-27">Registration</change><change when="2009-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-0193</doi><issn type="print">1065-9471</issn><issn type="electronic">1097-0193</issn><idGroup><id type="product" value="HBM"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="HUMAN BRAIN MAPPING">Human Brain Mapping</title><title type="short">Hum. 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affiliationRef="#af3"><personName><givenNames>Erik</givenNames><familyName>Johnsen</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Albert</givenNames><familyName>Gjedde</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DK" type="organization"><unparsedAffiliation>PET‐Center, Aarhus University Hospitals, Denmark</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DK" type="organization"><unparsedAffiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DK" type="organization"><unparsedAffiliation>Neurosurgical Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson</keyword><keyword xml:id="kwd2">STN‐stimulation</keyword><keyword xml:id="kwd3">PET</keyword><keyword xml:id="kwd4">flow</keyword><keyword xml:id="kwd5">VL</keyword><keyword xml:id="kwd6">thalamus</keyword><keyword xml:id="kwd7">deactivation</keyword><keyword xml:id="kwd8">basalgangglia loop</keyword><keyword xml:id="kwd9">clinical outcome</keyword></keywordGroup><fundingInfo><fundingAgency>Danish Parkinson Association</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Augustinus Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>GlaxoSmithKline A/S (Denmark)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Orion Pharma</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Novo Nordisk Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Institute of Experimental Clinical Research of the University of Aarhus</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Medical Research Council of Denmark</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Danish National Science Foundation</fundingAgency></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:10659471:media:hbm20486:HBM_20486_sm_suppinfofigB"></mediaResource><caption>Supporting Information Figure B</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:10659471:media:hbm20486:HBM_20486_sm_suppinfotableA"></mediaResource><caption>STN‐DBS settings in the 10 patients</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>STN‐Stimulation in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>STN‐stimulation in Parkinson's disease restores striatal inhibition of thalamocortical projection</title></titleInfo><name type="personal"><namePart type="given">Jacob</namePart><namePart type="family">Geday</namePart><affiliation>PET‐Center, Aarhus University Hospitals, Denmark</affiliation><affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</affiliation><description>Correspondence: PET‐Center and Neurological Department F, Aarhus Hospital, Aarhus University Hospitals, Noerrebrogade 44, 8000 Aarhus C, Denmark</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karen</namePart><namePart type="family">Østergaard</namePart><affiliation>Neurological Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Erik</namePart><namePart type="family">Johnsen</namePart><affiliation>Neurosurgical Department, Aarhus Hospital, Aarhus University Hospitals, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Albert</namePart><namePart type="family">Gjedde</namePart><affiliation>PET‐Center, Aarhus University Hospitals, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-01</dateIssued><dateCaptured encoding="w3cdtf">2007-04-08</dateCaptured><dateValid encoding="w3cdtf">2007-08-27</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">3</extent><extent unit="references">52</extent><extent unit="words">7533</extent></physicalDescription><abstract lang="en">To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN‐stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN‐stimulation with a 4‐h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.</abstract><note type="funding">Danish Parkinson Association</note><note type="funding">Augustinus Foundation</note><note type="funding">GlaxoSmithKline A/S (Denmark)</note><note type="funding">Orion Pharma</note><note type="funding">Novo Nordisk Foundation</note><note type="funding">Institute of Experimental Clinical Research of the University of Aarhus</note><note type="funding">Medical Research Council of Denmark</note><note type="funding">Danish National Science Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson</topic><topic>STN‐stimulation</topic><topic>PET</topic><topic>flow</topic><topic>VL</topic><topic>thalamus</topic><topic>deactivation</topic><topic>basalgangglia loop</topic><topic>clinical outcome</topic></subject><relatedItem type="host"><titleInfo><title>Human Brain Mapping</title></titleInfo><titleInfo type="abbreviated"><title>Hum. Brain Mapp.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information Figure B - STN‐DBS settings in the 10 patients - </note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1065-9471</identifier><identifier type="eISSN">1097-0193</identifier><identifier type="DOI">10.1002/(ISSN)1097-0193</identifier><identifier type="PublisherID">HBM</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>112</start><end>121</end><total>10</total></extent></part></relatedItem><identifier type="istex">9BFF2AF4B4382896A7269ECAFFBAA3E4C4A46750</identifier><identifier type="DOI">10.1002/hbm.20486</identifier><identifier type="ArticleID">HBM20486</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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