Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL
Identifieur interne : 002718 ( Istex/Corpus ); précédent : 002717; suivant : 002719Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL
Auteurs : Robert S. Root-Bernstein ; Sheila Hobbs DewittSource :
- Genetica [ 0016-6707 ] ; 1995-03-01.
English descriptors
- KwdEn :
- Teeft :
- Acad, Aids, Aids patients, Allogeneic, Anal, Anal intercourse, Animal models, Antibody, Antibody pairs, Antigen, Antigenic, Antigenic mimicry, Antilymphocyte antibodies, Antisperm antibodies, Autoantibody, Autoimmune, Autoimmune phenomena, Autoimmune processes, Autoimmunity, Avium, Boca raton, Cics, Clin, Cofactor, Complementary, Complementary antigens, European study group, Fermentans, Fertilization antigen, Herpes, Herpes simplex virus, Heterosexual, Histone, Hobbs, Hoffmann, Hoffmann grant, Homology, Homosexual, Human histone, Human immunodeficiency virus, Human sperm, Idiotypic, Idiotypic antibody, Iiii, Immune, Immune complexes, Immune deficiency syndrome, Immune response, Immune responses, Immune suppression, Immune system, Immunodeficiency, Immunodeficiency syndrome, Immunol, Immunologic, Immunologic exposure, Immunological, Immunological exposure, Infection, Infectious agents, Large number, Lctas, Lymphocyte, Lymphocyte antigens, Lymphocyte proteins, Lymphocytotoxic, Lymphocytotoxic antibodies, Lymphocytotoxic autoimmunity, Macrophage, Mama theory, Mimic, Mimicry, Mitochondrial, Mitochondrial proteins, Molecular mimicry, Morrow, Mycobacteria, Mycobacterium avium, Mycoplasma, Nuclear proteins, Opportunistic infections, Pathogenesis, Platelet, Platelet glycoprotein, Polyclonal, Positive results, Precipitate, Precipitates model, Precipitation, Precursor, Proc, Protamine, Protein, Receptive anal intercourse, Receptor, Risk factors, Semen, Semen components, Seminal, Seminal fluid, Seminal plasma, Shearer, Shearer rabson, Significant homologies, Significant role, Sonnabend, Sperm, Sperm antibodies, Sperm antibody, Sperm polyclonal, Sperm proteins, Stricker, Such antibodies, Such autoimmunity, Syndrome, Transfusion, Westall, Wide range, Witkin, Word size.
Abstract
Abstract: More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.
Url:
DOI: 10.1007/BF01435006
Links to Exploration step
ISTEX:B610BE7B23CEB228A49A99E3AD78720791ACAE6FLe document en format XML
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Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>sperm</json:string><json:string>autoimmunity</json:string><json:string>immune</json:string><json:string>lymphocyte</json:string><json:string>semen</json:string><json:string>autoimmune</json:string><json:string>mycoplasma</json:string><json:string>lctas</json:string><json:string>histone</json:string><json:string>anal</json:string><json:string>lymphocytotoxic</json:string><json:string>antigenic</json:string><json:string>immunol</json:string><json:string>anal intercourse</json:string><json:string>homology</json:string><json:string>precipitation</json:string><json:string>hoffmann</json:string><json:string>immune 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Root-Bernstein</name><affiliations><json:string>Department of Physiology, Michigan State University, 48824, East Lansing, MI, USA</json:string></affiliations></json:item><json:item><name>Sheila Hobbs DeWitt</name><affiliations><json:string>Parke-Davis Pharmaceutical Research Division, 2800 Plymouth Road, 48106-1047, Ann Arbor, MI, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>AIDS</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>alloantigen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autoimmunity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lymphocytotoxic antibodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>semen</value></json:item></subject><articleId><json:string>BF01435006</json:string><json:string>Art10</json:string></articleId><arkIstex>ark:/67375/1BB-VT8QFT90-L</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.</abstract><qualityIndicators><score>10</score><pdfWordCount>14020</pdfWordCount><pdfCharCount>86990</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>24</pdfPageCount><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>255</abstractWordCount><abstractCharCount>1776</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL</title><pmid><json:string>7744257</json:string></pmid><genre><json:string>research-article</json:string></genre><host><title>Genetica</title><language><json:string>unknown</json:string></language><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><issn><json:string>0016-6707</json:string></issn><eissn><json:string>1573-6857</json:string></eissn><journalId><json:string>10709</json:string></journalId><volume>95</volume><issue>1-3</issue><pages><first>133</first><last>156</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Human Genetics</value></json:item><json:item><value>Microbial Genetics and Genomics</value></json:item><json:item><value>Plant Genetics & Genomics</value></json:item><json:item><value>Animal Genetics and Genomics</value></json:item></subject></host><namedEntities><unitex><date></date><geogName></geogName><orgName></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName></placeName><ref_url></ref_url><ref_bibl></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/1BB-VT8QFT90-L</json:string></ark><categories><wos><json:string>1 - 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Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Key words</head><item><term>AIDS</term></item><item><term>alloantigen</term></item><item><term>autoimmunity</term></item><item><term>lymphocytotoxic antibodies</term></item><item><term>semen</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Life Sciences</head><item><term>Human Genetics</term></item><item><term>Microbial Genetics and Genomics</term></item><item><term>Plant Genetics & Genomics</term></item><item><term>Animal Genetics and Genomics</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-01-27">Created</change><change when="1995-03-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-VT8QFT90-L/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Kluwer Academic Publishers</PublisherName><PublisherLocation>Dordrecht</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>10709</JournalID><JournalPrintISSN>0016-6707</JournalPrintISSN><JournalElectronicISSN>1573-6857</JournalElectronicISSN><JournalTitle>Genetica</JournalTitle><JournalSubTitle>An International Journal of Genetics and Evolution</JournalSubTitle><JournalAbbreviatedTitle>Genetica</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Life Sciences</JournalSubject><JournalSubject Type="Secondary">Human Genetics</JournalSubject><JournalSubject Type="Secondary">Microbial Genetics and Genomics</JournalSubject><JournalSubject Type="Secondary">Plant Genetics & Genomics</JournalSubject><JournalSubject Type="Secondary">Animal Genetics and Genomics</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>95</VolumeIDStart><VolumeIDEnd>95</VolumeIDEnd><VolumeIssueCount>3</VolumeIssueCount></VolumeInfo><Issue IssueType="Combined"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>3</IssueIDEnd><IssueArticleCount>14</IssueArticleCount><IssueHistory><CoverDate><Year>1995</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Kluwer Academic Publishers</CopyrightHolderName><CopyrightYear>1995</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art10"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01435006</ArticleID><ArticleDOI>10.1007/BF01435006</ArticleDOI><ArticleSequenceNumber>10</ArticleSequenceNumber><ArticleTitle Language="En">Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL</ArticleTitle><ArticleFirstPage>133</ArticleFirstPage><ArticleLastPage>156</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>3</Month><Day>22</Day></RegistrationDate><Received><Year>1994</Year><Month>1</Month><Day>27</Day></Received><Accepted><Year>1994</Year><Month>6</Month><Day>17</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Kluwer Academic Publishers</CopyrightHolderName><CopyrightYear>1995</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>10709</JournalID><VolumeIDStart>95</VolumeIDStart><VolumeIDEnd>95</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>3</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Robert</GivenName><GivenName>S.</GivenName><FamilyName>Root-Bernstein</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Sheila</GivenName><GivenName>Hobbs</GivenName><FamilyName>DeWitt</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Physiology</OrgDivision><OrgName>Michigan State University</OrgName><OrgAddress><Postcode>48824</Postcode><City>East Lansing</City><State>MI</State><Country>USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>Parke-Davis Pharmaceutical Research Division</OrgName><OrgAddress><Street>2800 Plymouth Road</Street><Postcode>48106-1047</Postcode><City>Ann Arbor</City><State>MI</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,<Emphasis Type="Italic">per se</Emphasis>, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>AIDS</Keyword><Keyword>alloantigen</Keyword><Keyword>autoimmunity</Keyword><Keyword>lymphocytotoxic antibodies</Keyword><Keyword>semen</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL</title></titleInfo><name type="personal"><namePart type="given">Robert</namePart><namePart type="given">S.</namePart><namePart type="family">Root-Bernstein</namePart><affiliation>Department of Physiology, Michigan State University, 48824, East Lansing, MI, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sheila</namePart><namePart type="given">Hobbs</namePart><namePart type="family">DeWitt</namePart><affiliation>Parke-Davis Pharmaceutical Research Division, 2800 Plymouth Road, 48106-1047, Ann Arbor, MI, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Kluwer Academic Publishers</publisher><place><placeTerm type="text">Dordrecht</placeTerm></place><dateCreated encoding="w3cdtf">1994-01-27</dateCreated><dateIssued encoding="w3cdtf">1995-03-01</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.</abstract><subject lang="en"><genre>Key words</genre><topic>AIDS</topic><topic>alloantigen</topic><topic>autoimmunity</topic><topic>lymphocytotoxic antibodies</topic><topic>semen</topic></subject><relatedItem type="host"><titleInfo><title>Genetica</title><subTitle>An International Journal of Genetics and Evolution</subTitle></titleInfo><titleInfo type="abbreviated"><title>Genetica</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">1995-03-01</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><subject><genre>Life Sciences</genre><topic>Human Genetics</topic><topic>Microbial Genetics and Genomics</topic><topic>Plant Genetics & Genomics</topic><topic>Animal Genetics and Genomics</topic></subject><identifier type="ISSN">0016-6707</identifier><identifier type="eISSN">1573-6857</identifier><identifier type="JournalID">10709</identifier><identifier type="IssueArticleCount">14</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1995</date><detail type="volume"><number>95</number><caption>vol.</caption></detail><detail type="issue"><number>1-3</number><caption>no.</caption></detail><extent unit="pages"><start>133</start><end>156</end></extent></part><recordInfo><recordOrigin>Kluwer Academic Publishers, 1995</recordOrigin></recordInfo></relatedItem><identifier type="istex">B610BE7B23CEB228A49A99E3AD78720791ACAE6F</identifier><identifier type="ark">ark:/67375/1BB-VT8QFT90-L</identifier><identifier type="DOI">10.1007/BF01435006</identifier><identifier type="ArticleID">BF01435006</identifier><identifier type="ArticleID">Art10</identifier><accessCondition type="use and reproduction" contentType="copyright">Kluwer Academic Publishers, 1995</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Kluwer Academic Publishers, 1995</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-VT8QFT90-L/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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