Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue
Identifieur interne : 000F12 ( Istex/Corpus ); précédent : 000F11; suivant : 000F13Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue
Auteurs : Valérie Cochen ; Maria-Joao Ribeiro ; Jean-Paul Nguyen ; Jean-Marc Gurruchaga ; Gabriel Villafane ; Christian Loc'H ; Gilles Defer ; Yves Samson ; Marc Peschanski ; Philippe Hantraye ; Pierre Cesaro ; Philippe RemySource :
- Movement Disorders [ 0885-3185 ] ; 2003-08.
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Abstract
An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10463
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changes correlate with the amount of grafted tissue</title><author><name sortKey="Cochen, Valerie" sort="Cochen, Valerie" uniqKey="Cochen V" first="Valérie" last="Cochen">Valérie Cochen</name><affiliation><mods:affiliation>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Ribeiro, Maria Oao" sort="Ribeiro, Maria Oao" uniqKey="Ribeiro M" first="Maria-Joao" last="Ribeiro">Maria-Joao Ribeiro</name><affiliation><mods:affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Nguyen, Jean Aul" sort="Nguyen, Jean Aul" uniqKey="Nguyen J" first="Jean-Paul" last="Nguyen">Jean-Paul Nguyen</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</mods:affiliation></affiliation></author><author><name sortKey="Gurruchaga, Jean Arc" sort="Gurruchaga, Jean Arc" uniqKey="Gurruchaga J" first="Jean-Marc" last="Gurruchaga">Jean-Marc Gurruchaga</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation></author><author><name sortKey="Villafane, Gabriel" sort="Villafane, Gabriel" uniqKey="Villafane G" first="Gabriel" last="Villafane">Gabriel Villafane</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation></author><author><name sortKey="Loc H, Christian" sort="Loc H, Christian" uniqKey="Loc H C" first="Christian" last="Loc'H">Christian Loc'H</name><affiliation><mods:affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Defer, Gilles" sort="Defer, Gilles" uniqKey="Defer G" first="Gilles" last="Defer">Gilles Defer</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Service de Neurologie Déjerine, Caen, France</mods:affiliation></affiliation></author><author><name sortKey="Samson, Yves" sort="Samson, Yves" uniqKey="Samson Y" first="Yves" last="Samson">Yves Samson</name><affiliation><mods:affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Urgences Cérébro‐Vasculaires, CHU Pitié‐Salpétrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Peschanski, Marc" sort="Peschanski, Marc" uniqKey="Peschanski M" first="Marc" last="Peschanski">Marc Peschanski</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</mods:affiliation></affiliation></author><author><name sortKey="Hantraye, Philippe" sort="Hantraye, Philippe" uniqKey="Hantraye P" first="Philippe" last="Hantraye">Philippe Hantraye</name><affiliation><mods:affiliation>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Cesaro, Pierre" sort="Cesaro, Pierre" uniqKey="Cesaro P" first="Pierre" last="Cesaro">Pierre Cesaro</name><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</mods:affiliation></affiliation></author><author><name sortKey="Remy, Philippe" sort="Remy, Philippe" uniqKey="Remy P" first="Philippe" last="Remy">Philippe Remy</name><affiliation><mods:affiliation>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="2003-08">2003-08</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="928">928</biblScope><biblScope unit="page" to="932">932</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">27F23CAAF90303E367C943AB008DA5282B9F509F</idno><idno type="DOI">10.1002/mds.10463</idno><idno type="ArticleID">MDS10463</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CIT</term><term>PET</term><term>Parkinson</term><term>dopamine transporter</term><term>fetal transplantation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Valérie Cochen MD</name><affiliations><json:string>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</json:string></affiliations></json:item><json:item><name>Maria‐Joao Ribeiro MD, PhD</name><affiliations><json:string>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</json:string></affiliations></json:item><json:item><name>Jean‐Paul Nguyen MD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string><json:string>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</json:string></affiliations></json:item><json:item><name>Jean‐Marc Gurruchaga MD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string></affiliations></json:item><json:item><name>Gabriel Villafane MD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string></affiliations></json:item><json:item><name>Christian Loc'h BS</name><affiliations><json:string>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</json:string></affiliations></json:item><json:item><name>Gilles Defer MD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string><json:string>Service de Neurologie Déjerine, Caen, France</json:string></affiliations></json:item><json:item><name>Yves Samson MD</name><affiliations><json:string>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</json:string><json:string>Urgences Cérébro‐Vasculaires, CHU Pitié‐Salpétrière, Paris, France</json:string></affiliations></json:item><json:item><name>Marc Peschanski MD, PhD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string><json:string>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</json:string></affiliations></json:item><json:item><name>Philippe Hantraye PhD</name><affiliations><json:string>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</json:string></affiliations></json:item><json:item><name>Pierre Cesaro MD, PhD</name><affiliations><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</json:string><json:string>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</json:string></affiliations></json:item><json:item><name>Philippe Remy MD, PhD</name><affiliations><json:string>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</json:string><json:string>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</json:string><json:string>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</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>fetal transplantation</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>dopamine transporter</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CIT</value></json:item></subject><language><json:string>eng</json:string></language><abstract>An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119).We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</abstract><qualityIndicators><score>6.704</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1003</abstractCharCount><pdfWordCount>24094</pdfWordCount><pdfCharCount>154188</pdfCharCount><pdfPageCount>41</pdfPageCount><abstractWordCount>142</abstractWordCount></qualityIndicators><title>Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title><genre><json:string>Serial article</json:string></genre><host><volume>18</volume><pages><total>6</total><last>932</last><first>928</first></pages><issn><json:string>0885-3185</json:string></issn><issue>8</issue><subject><json:item><value>Brief 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xml:lang="en">Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2003</date></publicationStmt><notesStmt><note>Ministère de la Santé - No. PHRC‐96138;</note><note>Fondation pour la Recherche Médicale</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title><author><persName><forename type="first">Valérie</forename><surname>Cochen</surname><roleName type="degree">MD</roleName></persName><affiliation>Unité de Recherche Associée Commissariat à l'Energie Atomique (CEA)–Centre National de la Recherche Scientifique (CNRS) 2210, Orsay, France</affiliation></author><author><persName><forename type="first">Maria‐Joao</forename><surname>Ribeiro</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</affiliation></author><author><persName><forename type="first">Jean‐Paul</forename><surname>Nguyen</surname><roleName type="degree">MD</roleName></persName><affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</affiliation><affiliation>Institut National de la Santé et de la Recherche Médicale U421, Faculté de Médecine, Créteil, France</affiliation></author><author><persName><forename type="first">Jean‐Marc</forename><surname>Gurruchaga</surname><roleName type="degree">MD</roleName></persName><affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</affiliation></author><author><persName><forename type="first">Gabriel</forename><surname>Villafane</surname><roleName type="degree">MD</roleName></persName><affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</affiliation></author><author><persName><forename type="first">Christian</forename><surname>Loc'h</surname><roleName type="degree">BS</roleName></persName><affiliation>CEA, Direction des Sciences du Vivant/Département de Recherche Médicale, Service Hospitalier Frédéric Joliot, Orsay, France</affiliation></author><author><persName><forename type="first">Gilles</forename><surname>Defer</surname><roleName type="degree">MD</roleName></persName><affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</affiliation><affiliation>Service de 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There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. 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type="figureTotal" number="2"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="20"></count><count type="wordTotal" number="3166"></count></countGroup><titleGroup><title type="main" xml:lang="en">Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title><title type="short" xml:lang="en">Grafts in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Valérie</givenNames><familyName>Cochen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Maria‐Joao</givenNames><familyName>Ribeiro</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3 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type="main" xml:lang="en"><title type="main">Abstract</title><p>An erratum for this article appears in the January, 2004 issue of Movement Disorders (<accessionId ref="info:doi/10.1002/mds.10661">Mov Disord 2004;12:119</accessionId>).</p><p>We compared the striatal uptake of [<sup>18</sup>F]fluorodopa with [<sup>76</sup>Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [<sup>18</sup>F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [<sup>18</sup>F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [<sup>18</sup>F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Grafts in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue</title></titleInfo><name type="personal"><namePart type="given">Valérie</namePart><namePart type="family">Cochen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Unité de Recherche Associée 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Hospitalier Frédéric Joliot, Orsay, France</affiliation><affiliation>Département de Neurosciences, Centre Hospitalier Universitaire (CHU) Henri Mondor, AP‐HP et Faculté de Médecine Paris‐XII, Créteil, France</affiliation><description>Correspondence: URA CEA‐CNRS 2210, Service Hospitalier Frédéric Joliot, 91401 Orsay Cedex, France</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">2003-08</dateIssued><dateCaptured encoding="w3cdtf">2002-10-16</dateCaptured><dateValid encoding="w3cdtf">2003-01-15</dateValid><copyrightDate encoding="w3cdtf">2003</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">2</extent><extent unit="tables">1</extent><extent unit="references">20</extent><extent unit="words">3166</extent></physicalDescription><abstract lang="en">An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</abstract><note type="funding">Ministère de la Santé - No. PHRC‐96138; </note><note type="funding">Fondation pour la Recherche Médicale</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson</topic><topic>fetal transplantation</topic><topic>PET</topic><topic>dopamine transporter</topic><topic>CIT</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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