Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family
Identifieur interne : 003789 ( Istex/Corpus ); précédent : 003788; suivant : 003790Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family
Auteurs : Anja Hiller ; Johann M. Hagenah ; Ana Djarmati ; Katja Hedrich ; Kathrin Reetz ; Christiane Schneider-Gold ; Wolfgang Kress ; Alexander Münchau ; Christine KleinSource :
- Movement Disorders [ 0885-3185 ] ; 2007-01.
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Abstract
The phenotypic spectrum of PINK1‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. This finding suggests a role not only of homozygous but also of heterozygous PINK1 mutations in the development of parkinsonian signs and underlines the necessity to carefully investigate family members of affected mutation carriers. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21059
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ISTEX:B1CDA608BC05D3455858DFF0A2EEF4598D3240C2Le document en format XML
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Hagenah</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Djarmati, Ana" sort="Djarmati, Ana" uniqKey="Djarmati A" first="Ana" last="Djarmati">Ana Djarmati</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hedrich, Katja" sort="Hedrich, Katja" uniqKey="Hedrich K" first="Katja" last="Hedrich">Katja Hedrich</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Reetz, Kathrin" sort="Reetz, Kathrin" uniqKey="Reetz K" first="Kathrin" last="Reetz">Kathrin Reetz</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schneider Old, Christiane" sort="Schneider Old, Christiane" uniqKey="Schneider Old C" first="Christiane" last="Schneider-Gold">Christiane Schneider-Gold</name><affiliation><mods:affiliation>Department of Neurology, Georg‐August University, Göttingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kress, Wolfgang" sort="Kress, Wolfgang" uniqKey="Kress W" first="Wolfgang" last="Kress">Wolfgang Kress</name><affiliation><mods:affiliation>Department of Human Genetics, Julius‐Maximilians University, Würzburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Munchau, Alexander" sort="Munchau, Alexander" uniqKey="Munchau A" first="Alexander" last="Münchau">Alexander Münchau</name><affiliation><mods:affiliation>Department of Neurology, University of Hamburg, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B1CDA608BC05D3455858DFF0A2EEF4598D3240C2</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1002/mds.21059</idno><idno type="url">https://api.istex.fr/document/B1CDA608BC05D3455858DFF0A2EEF4598D3240C2/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">003789</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family</title><author><name sortKey="Hiller, Anja" sort="Hiller, Anja" uniqKey="Hiller A" first="Anja" last="Hiller">Anja Hiller</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hagenah, Johann M" sort="Hagenah, Johann M" uniqKey="Hagenah J" first="Johann M." last="Hagenah">Johann M. Hagenah</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Djarmati, Ana" sort="Djarmati, Ana" uniqKey="Djarmati A" first="Ana" last="Djarmati">Ana Djarmati</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hedrich, Katja" sort="Hedrich, Katja" uniqKey="Hedrich K" first="Katja" last="Hedrich">Katja Hedrich</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Reetz, Kathrin" sort="Reetz, Kathrin" uniqKey="Reetz K" first="Kathrin" last="Reetz">Kathrin Reetz</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schneider Old, Christiane" sort="Schneider Old, Christiane" uniqKey="Schneider Old C" first="Christiane" last="Schneider-Gold">Christiane Schneider-Gold</name><affiliation><mods:affiliation>Department of Neurology, Georg‐August University, Göttingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kress, Wolfgang" sort="Kress, Wolfgang" uniqKey="Kress W" first="Wolfgang" last="Kress">Wolfgang Kress</name><affiliation><mods:affiliation>Department of Human Genetics, Julius‐Maximilians University, Würzburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Munchau, Alexander" sort="Munchau, Alexander" uniqKey="Munchau A" first="Alexander" last="Münchau">Alexander Münchau</name><affiliation><mods:affiliation>Department of Neurology, University of Hamburg, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-01">2007-01</date><biblScope unit="vol">22</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="145">145</biblScope><biblScope unit="page" to="147">147</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B1CDA608BC05D3455858DFF0A2EEF4598D3240C2</idno><idno type="DOI">10.1002/mds.21059</idno><idno type="ArticleID">MDS21059</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PINK1</term><term>mutation carriers</term><term>phenotype</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The phenotypic spectrum of PINK1‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. This finding suggests a role not only of homozygous but also of heterozygous PINK1 mutations in the development of parkinsonian signs and underlines the necessity to carefully investigate family members of affected mutation carriers. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Anja Hiller MD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Johann M. Hagenah MD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Ana Djarmati MS</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Katja Hedrich PhD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Kathrin Reetz MD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Christiane Schneider‐Gold MD</name><affiliations><json:string>Department of Neurology, Georg‐August University, Göttingen, Germany</json:string></affiliations></json:item><json:item><name>Wolfgang Kress MD</name><affiliations><json:string>Department of Human Genetics, Julius‐Maximilians University, Würzburg, Germany</json:string></affiliations></json:item><json:item><name>Alexander Münchau MD</name><affiliations><json:string>Department of Neurology, University of Hamburg, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Christine Klein MD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>PINK1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mutation carriers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>phenotype</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The phenotypic spectrum of PINK1‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. 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No. Kl‐1134/2‐4;</note><note>Volkswagen Foundation - No. I/78 553;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family</title><author><persName><forename type="first">Anja</forename><surname>Hiller</surname><roleName type="degree">MD</roleName></persName><note type="biography">A.H. and J.M.H. contributed equally to this work.</note><affiliation>A.H. and J.M.H. contributed equally to this work.</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Johann M.</forename><surname>Hagenah</surname><roleName type="degree">MD</roleName></persName><note type="biography">A.H. and J.M.H. contributed equally to this work.</note><affiliation>A.H. and J.M.H. contributed equally to this work.</affiliation><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Ana</forename><surname>Djarmati</surname><roleName type="degree">MS</roleName></persName><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Katja</forename><surname>Hedrich</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Kathrin</forename><surname>Reetz</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Christiane</forename><surname>Schneider‐Gold</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Georg‐August University, Göttingen, Germany</affiliation></author><author><persName><forename type="first">Wolfgang</forename><surname>Kress</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Human Genetics, Julius‐Maximilians University, Würzburg, Germany</affiliation></author><author><persName><forename type="first">Alexander</forename><surname>Münchau</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Hamburg, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Christine</forename><surname>Klein</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany</p></note><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-01"></date><biblScope unit="vol">22</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="145">145</biblScope><biblScope unit="page" to="147">147</biblScope></imprint></monogr><idno type="istex">B1CDA608BC05D3455858DFF0A2EEF4598D3240C2</idno><idno type="DOI">10.1002/mds.21059</idno><idno type="ArticleID">MDS21059</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The phenotypic spectrum of PINK1‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. 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Julius‐Maximilians University, Würzburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Hamburg, Hamburg, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1"><i>PINK1</i></keyword><keyword xml:id="kwd2">mutation carriers</keyword><keyword xml:id="kwd3">phenotype</keyword></keywordGroup><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>Kl‐1134/2‐4</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Volkswagen Foundation</fundingAgency><fundingNumber>I/78 553</fundingNumber></fundingInfo><supportingInformation><p> This article includes Supplementary Video, available online at <url href="http://www.interscience.wiley.com/jpages/0885-3185/suppmat"> http://www.interscience.wiley.com/jpages/0885‐3185/suppmat </url></p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds21059:jws-mds"></mediaResource><caption>The early view short clip shows the Index Patient II.3 of the article only.Segment 1. Index Patient II.3, on phase: There are muscle jerks of the upper body, resulting in shoulder shrugging, bringing the shoulder forward and backward, thrusting of the trunk, and facial grimacing. These movements cease completely when asked to perform motor tasks and most probably represent tics. Finger tapping is irregular and hand movements are bradykinetic bilaterally but more pronounced on the right side. Stride length and velocity are normal when he is walking, and there is physiological arm swing, but his steps appear a bit wooden.Segment 2. Index Patient II.3, off phase: Eye blinding is increased, and there are several facial tics. Bradykinesia of both hands is more pronounced than in the on state. His gait is small‐stepped and shuffling with markedly reduced arm swing bilaterally.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The phenotypic spectrum of <i>PINK1</i>‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) <i>PINK1</i> mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. This finding suggests a role not only of homozygous but also of heterozygous <i>PINK1</i> mutations in the development of parkinsonian signs and underlines the necessity to carefully investigate family members of affected mutation carriers. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>A.H. and J.M.H. contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PINK1‐Associated Parkinsonism in 1 Family</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Phenotypic spectrum of PINK1‐associated parkinsonism in 15 mutation carriers from 1 family</title></titleInfo><name type="personal"><namePart type="given">Anja</namePart><namePart type="family">Hiller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><description>A.H. and J.M.H. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johann M.</namePart><namePart type="family">Hagenah</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><description>A.H. and J.M.H. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ana</namePart><namePart type="family">Djarmati</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katja</namePart><namePart type="family">Hedrich</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathrin</namePart><namePart type="family">Reetz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christiane</namePart><namePart type="family">Schneider‐Gold</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Georg‐August University, Göttingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfgang</namePart><namePart type="family">Kress</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Human Genetics, Julius‐Maximilians University, Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexander</namePart><namePart type="family">Münchau</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Hamburg, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><description>Correspondence: Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-01</dateIssued><dateCaptured encoding="w3cdtf">2005-12-09</dateCaptured><dateValid encoding="w3cdtf">2006-04-06</dateValid><copyrightDate encoding="w3cdtf">2007</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">1</extent><extent unit="tables">1</extent><extent unit="references">6</extent><extent unit="words">1562</extent></physicalDescription><abstract lang="en">The phenotypic spectrum of PINK1‐associated Parkinsonism was studied in a family with homozygous (n = 4) or heterozygous (n = 3) PINK1 mutations. All homozygous mutation carriers were definitely affected; the heterozygous carriers were asymptomatic but displayed unequivocal signs of probable or possible Parkinsonism. This finding suggests a role not only of homozygous but also of heterozygous PINK1 mutations in the development of parkinsonian signs and underlines the necessity to carefully investigate family members of affected mutation carriers. © 2006 Movement Disorder Society</abstract><note type="funding">Deutsche Forschungsgemeinschaft - No. Kl‐1134/2‐4; </note><note type="funding">Volkswagen Foundation - No. I/78 553; </note><subject lang="en"><genre>Keywords</genre><topic>PINK1</topic><topic>mutation carriers</topic><topic>phenotype</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> This article includes Supplementary Video, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmatSupporting Info Item: The early view short clip shows the Index Patient II.3 of the article only.Segment 1. Index Patient II.3, on phase: There are muscle jerks of the upper body, resulting in shoulder shrugging, bringing the shoulder forward and backward, thrusting of the trunk, and facial grimacing. These movements cease completely when asked to perform motor tasks and most probably represent tics. Finger tapping is irregular and hand movements are bradykinetic bilaterally but more pronounced on the right side. Stride length and velocity are normal when he is walking, and there is physiological arm swing, but his steps appear a bit wooden.Segment 2. Index Patient II.3, off phase: Eye blinding is increased, and there are several facial tics. Bradykinesia of both hands is more pronounced than in the on state. His gait is small‐stepped and shuffling with markedly reduced arm swing bilaterally. - </note><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>145</start><end>147</end><total>3</total></extent></part></relatedItem><identifier type="istex">B1CDA608BC05D3455858DFF0A2EEF4598D3240C2</identifier><identifier type="DOI">10.1002/mds.21059</identifier><identifier type="ArticleID">MDS21059</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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