Onset and pre-onset studies to define the Huntington’s disease natural history
Identifieur interne : 002A25 ( Istex/Corpus ); précédent : 002A24; suivant : 002A26Onset and pre-onset studies to define the Huntington’s disease natural history
Auteurs : F. Squitieri ; M. Cannella ; P. Giallonardo ; V. Maglione ; C. Mariotti ; M. R. HaydenSource :
- Brain Research Bulletin [ 0361-9230 ] ; 2001.
English descriptors
Abstract
Huntington’s disease’s (HD) clinical history has not been defined yet. However, many aspects of the most confusing clinical stages, i.e., the first and last disease phases, including the symptom progression and the disease duration, have been better approached after discovery of the responsible gene. The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic in vivo models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.
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DOI: 10.1016/S0361-9230(01)00648-7
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ISTEX:15F32D0387E2F0031C413C67C5CE17E6434C7AA5Le document en format XML
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Squitieri</name><affiliation><mods:affiliation>E-mail: neurogen@neuromed.it</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</mods:affiliation></affiliation></author><author><name sortKey="Cannella, M" sort="Cannella, M" uniqKey="Cannella M" first="M." last="Cannella">M. Cannella</name><affiliation><mods:affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</mods:affiliation></affiliation></author><author><name sortKey="Giallonardo, P" sort="Giallonardo, P" uniqKey="Giallonardo P" first="P." last="Giallonardo">P. Giallonardo</name><affiliation><mods:affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</mods:affiliation></affiliation></author><author><name sortKey="Maglione, V" sort="Maglione, V" uniqKey="Maglione V" first="V." last="Maglione">V. 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However, many aspects of the most confusing clinical stages, i.e., the first and last disease phases, including the symptom progression and the disease duration, have been better approached after discovery of the responsible gene. The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic in vivo models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>F. Squitieri</name><affiliations><json:string>E-mail: neurogen@neuromed.it</json:string><json:string>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</json:string></affiliations></json:item><json:item><name>M. Cannella</name><affiliations><json:string>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</json:string></affiliations></json:item><json:item><name>P. Giallonardo</name><affiliations><json:string>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</json:string></affiliations></json:item><json:item><name>V. Maglione</name><affiliations><json:string>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</json:string></affiliations></json:item><json:item><name>C. Mariotti</name><affiliations><json:string>Division of Biochemistry and Genetics, Neurological Institute “C. Besta”, Milan, Italy</json:string></affiliations></json:item><json:item><name>M.R. 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The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic in vivo models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.</abstract><qualityIndicators><score>6.824</score><pdfWordCount>5235</pdfWordCount><pdfCharCount>32792</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>596 x 795 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>152</abstractWordCount><abstractCharCount>1025</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Onset and pre-onset studies to define the Huntington’s disease natural history</title><pii><json:string>S0361-9230(01)00648-7</json:string></pii><genre><json:string>review-article</json:string></genre><host><title>Brain Research Bulletin</title><language><json:string>unknown</json:string></language><publicationDate>2001</publicationDate><issn><json:string>0361-9230</json:string></issn><pii><json:string>S0361-9230(00)X0116-5</json:string></pii><volume>56</volume><issue>3–4</issue><pages><first>233</first><last>238</last></pages><genre><json:string>journal</json:string></genre><conference><json:item><name>Triplet Repeat Diseases Triplet Repeat Diseases</name></json:item></conference><editor><json:item><name>A. Poletti</name></json:item><json:item><name>A. Servadio</name></json:item><json:item><name>F. Taroni</name></json:item></editor></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0361-9230(01)00648-7</json:string></doi><id>15F32D0387E2F0031C413C67C5CE17E6434C7AA5</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/15F32D0387E2F0031C413C67C5CE17E6434C7AA5/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/15F32D0387E2F0031C413C67C5CE17E6434C7AA5/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/15F32D0387E2F0031C413C67C5CE17E6434C7AA5/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Onset and pre-onset studies to define the Huntington’s disease natural history</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©2001 Elsevier Science Inc.</p></availability><date>2001</date></publicationStmt><notesStmt><note type="content">FIG. 1: Linear correlation obtained by simple regression analysis plotting the age at onset (y-axis) with the CAG repeat expansion (x-axis; n = 464, r2 = 0.54, p = 0.0001). Subjects, clinical and genetic data is included in the Italian Huntington’s disease databank (Table 1 and [54]). The logarithm transformation of data improved the linear correlation between x-y variables. The age at onset was calculated considering the first motor symptom appearance. The CAG repeat number beyond 35 was considered abnormal according to the published data [2].</note><note type="content">FIG. 2: Linear correlation obtained by simple regression analysis plotting the age of first severe psychiatric manifestations (y-axis) with the CAG repeat expansion (x-axis; n = 35; r2 = 0.31; p = 0.0005). Clinical and genetic data is included in the Italian Huntington’s disease databank (Table 1 and [54]). We considered as severe psychiatric symptoms those clinical manifestations altering the normal life state (mean age = 37.3 ± 11.7 years; range, 15–60) [61]. Severe behavioural changes anticipating of one or more years the motor onset symptoms (range, 1–28 years; mean = 7.6 ± 7 years), were considered.</note><note type="content">TABLE 1: Age-of-onset predictability according to the lower and upper 95% confidence intervals (CI) per fixed number of CAG expanded repeats</note><note type="content">TABLE 2: Effect of the affected parent’s gender on intergenerational year-of-onset and CAG repeat changes and influence of the normal allele length on age at onset</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Onset and pre-onset studies to define the Huntington’s disease natural history</title><author xml:id="author-0000"><persName><forename type="first">F.</forename><surname>Squitieri</surname></persName><email>neurogen@neuromed.it</email><affiliation>Address for correspondence: Ferdinando Squitieri, M.D., Ph.D., Neurogenetics Unit, IRCCS Neuromed, Loc. Camerelle - 86077, Pozzilli (IS), Italy. Fax: +390865-927575</affiliation><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation></author><author xml:id="author-0001"><persName><forename type="first">M.</forename><surname>Cannella</surname></persName><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation></author><author xml:id="author-0002"><persName><forename type="first">P.</forename><surname>Giallonardo</surname></persName><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation></author><author xml:id="author-0003"><persName><forename type="first">V.</forename><surname>Maglione</surname></persName><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation></author><author xml:id="author-0004"><persName><forename type="first">C.</forename><surname>Mariotti</surname></persName><affiliation>Division of Biochemistry and Genetics, Neurological Institute “C. Besta”, Milan, Italy</affiliation></author><author xml:id="author-0005"><persName><forename type="first">M.R.</forename><surname>Hayden</surname></persName><affiliation>Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation></author><idno type="istex">15F32D0387E2F0031C413C67C5CE17E6434C7AA5</idno><idno type="DOI">10.1016/S0361-9230(01)00648-7</idno><idno type="PII">S0361-9230(01)00648-7</idno></analytic><monogr><title level="j">Brain Research Bulletin</title><title level="j" type="abbrev">BRB</title><idno type="pISSN">0361-9230</idno><idno type="PII">S0361-9230(00)X0116-5</idno><meeting><addName>Triplet Repeat Diseases</addName><addName>Triplet Repeat Diseases</addName></meeting><editor xml:id="book-author-0000"><persName>A. Poletti</persName></editor><editor xml:id="book-author-0001"><persName>A. Servadio</persName></editor><editor xml:id="book-author-0002"><persName>F. Taroni</persName></editor><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">56</biblScope><biblScope unit="issue">3–4</biblScope><biblScope unit="page" from="233">233</biblScope><biblScope unit="page" to="238">238</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Huntington’s disease’s (HD) clinical history has not been defined yet. However, many aspects of the most confusing clinical stages, i.e., the first and last disease phases, including the symptom progression and the disease duration, have been better approached after discovery of the responsible gene. The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic in vivo models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Predictive diagnosis</term></item><item><term>Clinical history</term></item><item><term>Onset symptoms</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/15F32D0387E2F0031C413C67C5CE17E6434C7AA5/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="GR1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="GR2"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="rev" xml:lang="en"><item-info><jid>BRB</jid><aid>6282</aid><ce:pii>S0361-9230(01)00648-7</ce:pii><ce:doi>10.1016/S0361-9230(01)00648-7</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science Inc.</ce:copyright></item-info><head><ce:title>Onset and pre-onset studies to define the Huntington’s disease natural history</ce:title><ce:author-group><ce:author><ce:given-name>F.</ce:given-name><ce:surname>Squitieri</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="COR1">∗</ce:cross-ref><ce:e-address>neurogen@neuromed.it</ce:e-address></ce:author><ce:author><ce:given-name>M.</ce:given-name><ce:surname>Cannella</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.</ce:given-name><ce:surname>Giallonardo</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>V.</ce:given-name><ce:surname>Maglione</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.</ce:given-name><ce:surname>Mariotti</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.R.</ce:given-name><ce:surname>Hayden</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>3</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>1</ce:label><ce:textfn>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>2</ce:label><ce:textfn>Division of Biochemistry and Genetics, Neurological Institute “C. Besta”, Milan, Italy</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>3</ce:label><ce:textfn>Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for correspondence: Ferdinando Squitieri, M.D., Ph.D., Neurogenetics Unit, IRCCS Neuromed, Loc. Camerelle - 86077, Pozzilli (IS), Italy. Fax: +390865-927575</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Huntington’s disease’s (HD) clinical history has not been defined yet. However, many aspects of the most confusing clinical stages, i.e., the first and last disease phases, including the symptom progression and the disease duration, have been better approached after discovery of the responsible gene. The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic <ce:italic>in vivo</ce:italic> models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Predictive diagnosis</ce:text></ce:keyword><ce:keyword><ce:text>Clinical history</ce:text></ce:keyword><ce:keyword><ce:text>Onset symptoms</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Onset and pre-onset studies to define the Huntington’s disease natural history</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Onset and pre-onset studies to define the Huntington’s disease natural history</title></titleInfo><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Squitieri</namePart><affiliation>E-mail: neurogen@neuromed.it</affiliation><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation><description>Address for correspondence: Ferdinando Squitieri, M.D., Ph.D., Neurogenetics Unit, IRCCS Neuromed, Loc. Camerelle - 86077, Pozzilli (IS), Italy. Fax: +390865-927575</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Cannella</namePart><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Giallonardo</namePart><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Maglione</namePart><affiliation>Neurogenetics Unit, Neurological Institute IRCCS “Neuromed”, Pozzilli (IS), Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Mariotti</namePart><affiliation>Division of Biochemistry and Genetics, Neurological Institute “C. Besta”, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.R.</namePart><namePart type="family">Hayden</namePart><affiliation>Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="Review article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Huntington’s disease’s (HD) clinical history has not been defined yet. However, many aspects of the most confusing clinical stages, i.e., the first and last disease phases, including the symptom progression and the disease duration, have been better approached after discovery of the responsible gene. The existence of accurate genetic tests, available for affected and pre-symptomatic subjects (i.e., mutation carriers) and the possibility to study transgenic in vivo models, are actually helping us to understand some of the aspects of HD clinical presentation. HD may present with motor symptoms other than chorea, the psychiatric manifestations may represent part of the clinical picture and cognitive deterioration may occur very early in the disease and depend on early cortical involvement. Pre-onset studies are of crucial importance in understanding the temporal sequence of the clinical events. This is also very important for future therapeutic strategies in those diseases initiating late in the life, such as HD.</abstract><note type="content">FIG. 1: Linear correlation obtained by simple regression analysis plotting the age at onset (y-axis) with the CAG repeat expansion (x-axis; n = 464, r2 = 0.54, p = 0.0001). Subjects, clinical and genetic data is included in the Italian Huntington’s disease databank (Table 1 and [54]). The logarithm transformation of data improved the linear correlation between x-y variables. The age at onset was calculated considering the first motor symptom appearance. The CAG repeat number beyond 35 was considered abnormal according to the published data [2].</note><note type="content">FIG. 2: Linear correlation obtained by simple regression analysis plotting the age of first severe psychiatric manifestations (y-axis) with the CAG repeat expansion (x-axis; n = 35; r2 = 0.31; p = 0.0005). Clinical and genetic data is included in the Italian Huntington’s disease databank (Table 1 and [54]). We considered as severe psychiatric symptoms those clinical manifestations altering the normal life state (mean age = 37.3 ± 11.7 years; range, 15–60) [61]. Severe behavioural changes anticipating of one or more years the motor onset symptoms (range, 1–28 years; mean = 7.6 ± 7 years), were considered.</note><note type="content">TABLE 1: Age-of-onset predictability according to the lower and upper 95% confidence intervals (CI) per fixed number of CAG expanded repeats</note><note type="content">TABLE 2: Effect of the affected parent’s gender on intergenerational year-of-onset and CAG repeat changes and influence of the normal allele length on age at onset</note><subject lang="en"><genre>Keywords</genre><topic>Predictive diagnosis</topic><topic>Clinical history</topic><topic>Onset symptoms</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research Bulletin</title></titleInfo><titleInfo type="abbreviated"><title>BRB</title></titleInfo><name type="conference"><namePart>Triplet Repeat Diseases</namePart><namePart>Triplet Repeat Diseases</namePart></name><name type="personal"><namePart>A. Poletti</namePart><role><roleTerm type="text">editor</roleTerm></role></name><name type="personal"><namePart>A. Servadio</namePart><role><roleTerm type="text">editor</roleTerm></role></name><name type="personal"><namePart>F. Taroni</namePart><role><roleTerm type="text">editor</roleTerm></role></name><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">20011101</dateIssued></originInfo><identifier type="ISSN">0361-9230</identifier><identifier type="PII">S0361-9230(00)X0116-5</identifier><part><date>20011101</date><detail type="issue"><title>Triplet Repeat Diseases</title></detail><detail type="volume"><number>56</number><caption>vol.</caption></detail><detail type="issue"><number>3–4</number><caption>no.</caption></detail><extent unit="issue pages"><start>159</start><end>410</end></extent><extent unit="pages"><start>233</start><end>238</end></extent></part></relatedItem><identifier type="istex">15F32D0387E2F0031C413C67C5CE17E6434C7AA5</identifier><identifier type="DOI">10.1016/S0361-9230(01)00648-7</identifier><identifier type="PII">S0361-9230(01)00648-7</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Elsevier Science Inc.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Inc., ©2001</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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