Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism
Identifieur interne : 001654 ( Main/Corpus ); précédent : 001653; suivant : 001655Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism
Auteurs : Chin-Hsien Lin ; Wuh-Liang Hwu ; Shu-Chuan Chiang ; Chun-Hwei Tai ; Ruey-Meei WuSource :
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics [ 1552-4841 ] ; 2007-06-05.
English descriptors
- KwdEn :
Abstract
Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa‐responsive Parkinson's disease (PD) in familial cases, several of which were ethnic Chinese. To investigate the role of SCA2 and SCA3 mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of SCA2 and SCA3 genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. SCA2 gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and SCA3 gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either SCA2 or SCA3, although borderline CAG repeat number was detected in the SCA3 gene of four patients. Thus, mutations of SCA2 or SCA3 did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of SCA2 or SCA3 mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/ajmg.b.30427
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ISTEX:979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6Le document en format XML
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Genet.</title><idno type="ISSN">1552-4841</idno><idno type="eISSN">1552-485X</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-06-05">2007-06-05</date><biblScope unit="volume">144B</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="434">434</biblScope><biblScope unit="page" to="438">438</biblScope></imprint><idno type="ISSN">1552-4841</idno></series><idno type="istex">979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6</idno><idno type="DOI">10.1002/ajmg.b.30427</idno><idno type="ArticleID">AJMG30427</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1552-4841</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>SCA2</term><term>SCA3</term><term>Taiwanese</term><term>early‐onset parkinsonism</term><term>ethnic Chinese</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa‐responsive Parkinson's disease (PD) in familial cases, several of which were ethnic Chinese. To investigate the role of SCA2 and SCA3 mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of SCA2 and SCA3 genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. SCA2 gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and SCA3 gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either SCA2 or SCA3, although borderline CAG repeat number was detected in the SCA3 gene of four patients. Thus, mutations of SCA2 or SCA3 did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of SCA2 or SCA3 mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Chin‐Hsien Lin</name><affiliations><json:string>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Wuh‐Liang Hwu</name><affiliations><json:string>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Shu‐Chuan Chiang</name><affiliations><json:string>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Chun‐Hwei Tai</name><affiliations><json:string>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Ruey‐Meei Wu</name><affiliations><json:string>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>SCA2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SCA3</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>early‐onset parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Taiwanese</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ethnic Chinese</value></json:item></subject><articleId><json:string>AJMG30427</json:string></articleId><language><json:string>eng</json:string></language><abstract>Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa‐responsive Parkinson's disease (PD) in familial cases, several of which were ethnic Chinese. To investigate the role of SCA2 and SCA3 mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of SCA2 and SCA3 genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. SCA2 gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and SCA3 gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either SCA2 or SCA3, although borderline CAG repeat number was detected in the SCA3 gene of four patients. Thus, mutations of SCA2 or SCA3 did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of SCA2 or SCA3 mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>5.97</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1511</abstractCharCount><pdfWordCount>3162</pdfWordCount><pdfCharCount>20248</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>234</abstractWordCount></qualityIndicators><title>Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism</title><genre><json:string>article</json:string></genre><host><volume>144B</volume><publisherId><json:string>AJMG</json:string></publisherId><pages><total>5</total><last>438</last><first>434</first></pages><issn><json:string>1552-4841</json:string></issn><issue>4</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1552-485X</json:string></eissn><title>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><doi><json:string>10.1002/(ISSN)1552-485X</json:string></doi></host><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1002/ajmg.b.30427</json:string></doi><id>979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2007</date></publicationStmt><notesStmt><note type="content">*Please cite this article as follows: Lin C‐H, Hwu W‐L, Chiang S‐C, Tai C‐H, Wu R‐M. 2007. Lack of Mutations in Spinocerebellar Ataxia Type 2 and 3 Genes in a Taiwanese (Ethnic Chinese) Cohort of Familial and Early‐Onset Parkinsonism. Am J Med Genet Part B 144B:434–438.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism</title><author><persName><forename type="first">Chin‐Hsien</forename><surname>Lin</surname></persName><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">Wuh‐Liang</forename><surname>Hwu</surname></persName><affiliation>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">Shu‐Chuan</forename><surname>Chiang</surname></persName><affiliation>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">Chun‐Hwei</forename><surname>Tai</surname></persName><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">Ruey‐Meei</forename><surname>Wu</surname></persName><note type="correspondence"><p>Correspondence: Department of Neurology, National Taiwan University Hospital, No 7, Chung‐Shan South Road, Taipei 100, Taiwan.</p></note><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation></author></analytic><monogr><title level="j">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><title level="j" type="abbrev">Am. J. Med. Genet.</title><idno type="pISSN">1552-4841</idno><idno type="eISSN">1552-485X</idno><idno type="DOI">10.1002/(ISSN)1552-485X</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-06-05"></date><biblScope unit="volume">144B</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="434">434</biblScope><biblScope unit="page" to="438">438</biblScope></imprint></monogr><idno type="istex">979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6</idno><idno type="DOI">10.1002/ajmg.b.30427</idno><idno type="ArticleID">AJMG30427</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa‐responsive Parkinson's disease (PD) in familial cases, several of which were ethnic Chinese. To investigate the role of SCA2 and SCA3 mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of SCA2 and SCA3 genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. SCA2 gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and SCA3 gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either SCA2 or SCA3, although borderline CAG repeat number was detected in the SCA3 gene of four patients. Thus, mutations of SCA2 or SCA3 did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of SCA2 or SCA3 mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>SCA2</term></item><item><term>SCA3</term></item><item><term>early‐onset parkinsonism</term></item><item><term>Taiwanese</term></item><item><term>ethnic Chinese</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="2006-05-06">Received</change><change when="2006-08-02">Registration</change><change when="2007-06-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6/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)1552-485X</doi><issn type="print">1552-4841</issn><issn type="electronic">1552-485X</issn><idGroup><id type="product" value="AJMG"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="AMERICAN JOURNAL OF MEDICAL GENETICS PART B: NEUROPSYCHIATRIC GENETICS">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title><title type="short">Am. 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To investigate the role of <i>SCA2</i> and <i>SCA3</i> mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of <i>SCA2</i> and <i>SCA3</i> genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. <i>SCA2</i> gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and <i>SCA3</i> gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either <i>SCA2</i> or <i>SCA3</i>, although borderline CAG repeat number was detected in the <i>SCA3</i> gene of four patients. Thus, mutations of <i>SCA2</i> or <i>SCA3</i> did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of <i>SCA2</i> or <i>SCA3</i> mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Please cite this article as follows: Lin C‐H, Hwu W‐L, Chiang S‐C, Tai C‐H, Wu R‐M. 2007. Lack of Mutations in Spinocerebellar Ataxia Type 2 and 3 Genes in a Taiwanese (Ethnic Chinese) Cohort of Familial and Early‐Onset Parkinsonism. Am J Med Genet Part B 144B:434–438.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SCA2 and SCA3 in Early‐Onset and Familial Parkinsonism in Taiwanese</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Lack of mutations in spinocerebellar ataxia type 2 and 3 genes in a Taiwanese (ethnic Chinese) cohort of familial and early‐onset parkinsonism</title></titleInfo><name type="personal"><namePart type="given">Chin‐Hsien</namePart><namePart type="family">Lin</namePart><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wuh‐Liang</namePart><namePart type="family">Hwu</namePart><affiliation>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shu‐Chuan</namePart><namePart type="family">Chiang</namePart><affiliation>Pediatrics and Medical Genetics, College of Medicine, National Taiwan University Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chun‐Hwei</namePart><namePart type="family">Tai</namePart><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ruey‐Meei</namePart><namePart type="family">Wu</namePart><affiliation>Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><description>Correspondence: Department of Neurology, National Taiwan University Hospital, No 7, Chung‐Shan South Road, Taipei 100, Taiwan.</description><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">2007-06-05</dateIssued><dateCaptured encoding="w3cdtf">2006-05-06</dateCaptured><dateValid encoding="w3cdtf">2006-08-02</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">3</extent><extent unit="references">32</extent><extent unit="words">3873</extent></physicalDescription><abstract lang="en">Recent reports suggest that CAG triplet expansions of spinocerebellar ataxia type 2 and 3 (SCA2 and SCA3) genes are the cause of typical levodopa‐responsive Parkinson's disease (PD) in familial cases, several of which were ethnic Chinese. To investigate the role of SCA2 and SCA3 mutations in Chinese familial and early‐onset PD patients, we analyzed CAG triplet repeat expansions of SCA2 and SCA3 genes in a cohort of 73 Taiwanese/Ethnic Chinese familial and early‐onset PD patients [mean age at onset 42.70 ± 7.17 years (mean ± SD)]. Thirteen of them (17.8%) had positive family history. All patients received comprehensive clinical evaluation including a thorough neurological examination, laboratory tests, and neuroimaging studies to exclude secondary causes and atypical parkinsonism. The CAG repeat length in these genes was determined using polymerase chain reaction polyacrylamide gel electrophoresis. SCA2 gene CAG repeats ranged from 15 to 26 repeats with a median of 20, and SCA3 gene CAG repeats ranged from 15 to 40 with a median of 15. No long pathogenic repeats were found in either SCA2 or SCA3, although borderline CAG repeat number was detected in the SCA3 gene of four patients. Thus, mutations of SCA2 or SCA3 did not play a major role in familial or early‐onset PD in our study cohort. PD patients without autosomal dominant family history or obvious cerebellar ataxia should not be candidates for routine screening of SCA2 or SCA3 mutations for cost‐effectiveness. © 2007 Wiley‐Liss, Inc.</abstract><note type="content">*Please cite this article as follows: Lin C‐H, Hwu W‐L, Chiang S‐C, Tai C‐H, Wu R‐M. 2007. Lack of Mutations in Spinocerebellar Ataxia Type 2 and 3 Genes in a Taiwanese (Ethnic Chinese) Cohort of Familial and Early‐Onset Parkinsonism. Am J Med Genet Part B 144B:434–438.</note><subject lang="en"><genre>Keywords</genre><topic>SCA2</topic><topic>SCA3</topic><topic>early‐onset parkinsonism</topic><topic>Taiwanese</topic><topic>ethnic Chinese</topic></subject><relatedItem type="host"><titleInfo><title>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title></titleInfo><titleInfo type="abbreviated"><title>Am. J. Med. Genet.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1552-4841</identifier><identifier type="eISSN">1552-485X</identifier><identifier type="DOI">10.1002/(ISSN)1552-485X</identifier><identifier type="PublisherID">AJMG</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>144B</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>434</start><end>438</end><total>5</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>American Journal of Medical Genetics</title></titleInfo><identifier type="ISSN">0148-7299</identifier><identifier type="ISSN">1096-8628</identifier><part><date point="end">2004</date></part></relatedItem><identifier type="istex">979B08B7AD1BBC74D4AF87009B01B1D645E1C0C6</identifier><identifier type="DOI">10.1002/ajmg.b.30427</identifier><identifier type="ArticleID">AJMG30427</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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