Neurogenetic diseases: molecular diagnosis and therapeutic approaches
Identifieur interne : 000681 ( Main/Corpus ); précédent : 000680; suivant : 000682Neurogenetic diseases: molecular diagnosis and therapeutic approaches
Auteurs : U. Müller ; B. GraeberSource :
- Journal of Molecular Medicine [ 0946-2716 ] ; 1996-02-01.
Abstract
Abstract: A neurogenetic disorder is defined as a clinical disease caused by a defect in one or more genes which affect the differentiation and function of the neuroectoderm and its derivatives. Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. Finally, some of the many obstacles are summarized that must be overcome before gene therapy becomes feasible in most monogenic neurological diseases.
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DOI: 10.1007/BF00196782
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neurogenetic diseases: molecular diagnosis and therapeutic approaches</title><author><name sortKey="Muller, U" sort="Muller, U" uniqKey="Muller U" first="U." last="Müller">U. Müller</name><affiliation><mods:affiliation>Institut für Humangenetik, Justus-Liebig-Universität, Schlangenzahl 14, D-35392, Giessen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Graeber, B" sort="Graeber, B" uniqKey="Graeber B" first="B." last="Graeber">B. Graeber</name><affiliation><mods:affiliation>Labor für Molekulare Neuropathologie, Institut für Neuropathologie, Ludwig-Maximilians Universität, Thalkirchner Strasse 36, D-80337, München, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:341A6BE94FF1D95FEDD7B1AD05D0BA1378CE0880</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1007/BF00196782</idno><idno type="url">https://api.istex.fr/document/341A6BE94FF1D95FEDD7B1AD05D0BA1378CE0880/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000681</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neurogenetic diseases: molecular diagnosis and therapeutic approaches</title><author><name sortKey="Muller, U" sort="Muller, U" uniqKey="Muller U" first="U." last="Müller">U. Müller</name><affiliation><mods:affiliation>Institut für Humangenetik, Justus-Liebig-Universität, Schlangenzahl 14, D-35392, Giessen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Graeber, B" sort="Graeber, B" uniqKey="Graeber B" first="B." last="Graeber">B. Graeber</name><affiliation><mods:affiliation>Labor für Molekulare Neuropathologie, Institut für Neuropathologie, Ludwig-Maximilians Universität, Thalkirchner Strasse 36, D-80337, München, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Molecular Medicine</title><title level="j" type="abbrev">J Mol Med</title><idno type="ISSN">0946-2716</idno><idno type="eISSN">1432-1440</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1996-02-01">1996-02-01</date><biblScope unit="volume">74</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="71">71</biblScope><biblScope unit="page" to="84">84</biblScope></imprint><idno type="ISSN">0946-2716</idno></series><idno type="istex">341A6BE94FF1D95FEDD7B1AD05D0BA1378CE0880</idno><idno type="DOI">10.1007/BF00196782</idno><idno type="ArticleID">Art2</idno><idno type="ArticleID">BF00196782</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0946-2716</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: A neurogenetic disorder is defined as a clinical disease caused by a defect in one or more genes which affect the differentiation and function of the neuroectoderm and its derivatives. Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. Finally, some of the many obstacles are summarized that must be overcome before gene therapy becomes feasible in most monogenic neurological diseases.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>U. Müller</name><affiliations><json:string>Institut für Humangenetik, Justus-Liebig-Universität, Schlangenzahl 14, D-35392, Giessen, Germany</json:string></affiliations></json:item><json:item><name>M. B. Graeber</name><affiliations><json:string>Labor für Molekulare Neuropathologie, Institut für Neuropathologie, Ludwig-Maximilians Universität, Thalkirchner Strasse 36, D-80337, München, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>AD : Alzheimer disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ALS : Amyotrophic lateral sclerosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>apoE : Apolipoprotein E</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>APP : Amyloid precursor protein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AR : Androgen receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DGGE : Denaturing gradient gel electrophoresis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DRPLA : Dentatorubral pallidoluysian atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HD : Huntington disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MJD : Machado-Joseph diseas</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NGF : Nerve growth factor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PCR : Polymerase chain reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PD : Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SBMA : Spinobulbar muscular atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SCA : Spinocerebellar ataxias</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SSCP : Single-strand conformation polymorphism</value></json:item></subject><articleId><json:string>Art2</json:string><json:string>BF00196782</json:string></articleId><language><json:string>eng</json:string></language><abstract>Abstract: A neurogenetic disorder is defined as a clinical disease caused by a defect in one or more genes which affect the differentiation and function of the neuroectoderm and its derivatives. Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. 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Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. Finally, some of the many obstacles are summarized that must be overcome before gene therapy becomes feasible in most monogenic neurological diseases.</p></abstract><textClass><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>AD</term><term>Alzheimer disease</term></item><item><term>ALS</term><term>Amyotrophic lateral sclerosis</term></item><item><term>apoE</term><term>Apolipoprotein E</term></item><item><term>APP</term><term>Amyloid precursor protein</term></item><item><term>AR</term><term>Androgen receptor</term></item><item><term>DGGE</term><term>Denaturing gradient gel electrophoresis</term></item><item><term>DRPLA</term><term>Dentatorubral pallidoluysian atrophy</term></item><item><term>HD</term><term>Huntington disease</term></item><item><term>MJD</term><term>Machado-Joseph diseas</term></item><item><term>NGF</term><term>Nerve growth factor</term></item><item><term>PCR</term><term>Polymerase chain reaction</term></item><item><term>PD</term><term>Parkinson disease</term></item><item><term>SBMA</term><term>Spinobulbar muscular atrophy</term></item><item><term>SCA</term><term>Spinocerebellar ataxias</term></item><item><term>SSCP</term><term>Single-strand conformation polymorphism</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Molecular Medicine</term></item><item><term>Internal Medicine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-06-29">Created</change><change when="1996-02-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/341A6BE94FF1D95FEDD7B1AD05D0BA1378CE0880/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" 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Neuropathologie</OrgDivision><OrgName>Ludwig-Maximilians Universität</OrgName><OrgAddress><Street>Thalkirchner Strasse 36</Street><Postcode>D-80337</Postcode><City>München</City><Country>Germany</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>A neurogenetic disorder is defined as a clinical disease caused by a defect in one or more genes which affect the differentiation and function of the neuroectoderm and its derivatives. Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. Finally, some of the many obstacles are summarized that must be overcome before gene therapy becomes feasible in most monogenic neurological diseases.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Expanding trinucleotide repeat</Keyword><Keyword>Gene therapy</Keyword><Keyword>Linkage mapping</Keyword><Keyword>Mutation analysis</Keyword><Keyword>Risk calculation</Keyword></KeywordGroup><AbbreviationGroup><Heading>Abbreviations</Heading><DefinitionList><DefinitionListEntry><Term><Emphasis Type="Italic">AD</Emphasis></Term><Description><Para>Alzheimer disease</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">ALS</Emphasis></Term><Description><Para>Amyotrophic lateral sclerosis</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">apoE</Emphasis></Term><Description><Para>Apolipoprotein E</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">APP</Emphasis></Term><Description><Para>Amyloid precursor protein</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">AR</Emphasis></Term><Description><Para>Androgen receptor</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">DGGE</Emphasis></Term><Description><Para>Denaturing gradient gel electrophoresis</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">DRPLA</Emphasis></Term><Description><Para>Dentatorubral pallidoluysian atrophy</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">HD</Emphasis></Term><Description><Para>Huntington disease</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">MJD</Emphasis></Term><Description><Para>Machado-Joseph diseas</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">NGF</Emphasis></Term><Description><Para>Nerve growth factor</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">PCR</Emphasis></Term><Description><Para>Polymerase chain reaction</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">PD</Emphasis></Term><Description><Para>Parkinson disease</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">SBMA</Emphasis></Term><Description><Para>Spinobulbar muscular atrophy</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">SCA</Emphasis></Term><Description><Para>Spinocerebellar ataxias</Para></Description></DefinitionListEntry><DefinitionListEntry><Term><Emphasis Type="Italic">SSCP</Emphasis></Term><Description><Para>Single-strand conformation polymorphism</Para></Description></DefinitionListEntry></DefinitionList></AbbreviationGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neurogenetic diseases: molecular diagnosis and therapeutic approaches</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neurogenetic diseases: molecular diagnosis and therapeutic approaches</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">U.</namePart><namePart type="family">Müller</namePart><affiliation>Institut für Humangenetik, Justus-Liebig-Universität, Schlangenzahl 14, D-35392, Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="given">B.</namePart><namePart type="family">Graeber</namePart><affiliation>Labor für Molekulare Neuropathologie, Institut für Neuropathologie, Ludwig-Maximilians Universität, Thalkirchner Strasse 36, D-80337, München, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="ReviewPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1995-06-29</dateCreated><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Abstract: A neurogenetic disorder is defined as a clinical disease caused by a defect in one or more genes which affect the differentiation and function of the neuroectoderm and its derivatives. Genetic findings in various neurogenetic disorders are discussed. Huntington disease, spinobulbar muscular atrophy, and the autosomal dominant cerebellar ataxias are examples of autosomal dominant disorders caused by the expansion of trinucleotides (CAG) within disease genes. The CAG expansions appear to result in a gain of gene function. Prenatal, presymptomatic, and differential diagnostic tests are based on the detection of the repeat expansions. Point mutations within disease genes result in many additional neurogenetic disorders. An autosomal dominant form of amyotrophic lateral sclerosis and various types of craniosynostotic syndromes are described. The mutations in the disease genes also appear to result in a gain of gene function. Molecular diagnosis in these disorders is based on the direct examination of the mutated gene by methods such as single-strand conformation polymorphism analysis, denaturing gradient gel electrophoresis, and direct DNA sequencing. In many neurogenetic disorders the disease gene has not yet been identified. Here molecular diagnosis relies on indirect approaches based on methods such as the analysis of linkage and of allelic association. Hereditary forms of dystonia are presented as examples. Common sporadic neurological disorders such as Alzheimer and Parkinson diseases frequently have multifactorial causes. Investigations into the molecular basis and the development of diagnostic tests in these two important diseases are discussed. At present no curative therapies exist in neurogenetic disorders. Gene therapeutic approaches, however, provide promise for a cure in at least some of these diseases. Basic principles of gene therapy are explained and attempts at gene therapy in Alzheimer and Parkinson diseases are described. Finally, some of the many obstacles are summarized that must be overcome before gene therapy becomes feasible in most monogenic neurological diseases.</abstract><note>Review</note><subject><genre>Abbreviations</genre><topic> AD : Alzheimer disease</topic><topic> ALS : Amyotrophic lateral sclerosis</topic><topic> apoE : Apolipoprotein E</topic><topic> APP : Amyloid precursor protein</topic><topic> AR : Androgen receptor</topic><topic> DGGE : Denaturing gradient gel electrophoresis</topic><topic> DRPLA : Dentatorubral pallidoluysian atrophy</topic><topic> HD : Huntington disease</topic><topic> MJD : Machado-Joseph diseas</topic><topic> NGF : Nerve growth factor</topic><topic> PCR : Polymerase chain reaction</topic><topic> PD : Parkinson disease</topic><topic> SBMA : Spinobulbar muscular atrophy</topic><topic> SCA : Spinocerebellar ataxias</topic><topic> SSCP : Single-strand conformation polymorphism</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Molecular Medicine</title></titleInfo><titleInfo type="abbreviated"><title>J Mol Med</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Molecular Medicine</topic><topic>Internal Medicine</topic></subject><identifier type="ISSN">0946-2716</identifier><identifier type="eISSN">1432-1440</identifier><identifier type="JournalID">109</identifier><identifier type="IssueArticleCount">7</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>1996</date><detail type="volume"><number>74</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="pages"><start>71</start><end>84</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></relatedItem><identifier type="istex">341A6BE94FF1D95FEDD7B1AD05D0BA1378CE0880</identifier><identifier type="DOI">10.1007/BF00196782</identifier><identifier type="ArticleID">Art2</identifier><identifier type="ArticleID">BF00196782</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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