Diverse morphology of biliary atresia in an animal model
Identifieur interne : 000249 ( Istex/Corpus ); précédent : 000248; suivant : 000250Diverse morphology of biliary atresia in an animal model
Auteurs : Claus Petersen ; Sabine Grasshoff ; Liliana LucianoSource :
- Journal of Hepatology [ 0168-8278 ] ; 1997.
Abstract
Background/Aims: Extrahepatic biliary atresia can be simulated in Balb/c-mice which have been infected with rotavirus. Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children. Methods: Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy. Results: The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident. Conclusions: Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.
Url:
DOI: 10.1016/S0168-8278(98)80283-3
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Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children. Methods: Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy. Results: The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident. Conclusions: Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Claus Petersen</name><affiliations><json:string>Department of Pediatric Surgery, Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Sabine Grasshoff</name><affiliations><json:string>Department of Pediatric Surgery, Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Liliana Luciano</name><affiliations><json:string>Laboratory of Cell Biology and Electron Microscopy, Medical School, Hannover, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Animal model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Biliary atresia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pathology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rotavirus</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Background/Aims: Extrahepatic biliary atresia can be simulated in Balb/c-mice which have been infected with rotavirus. Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children. Methods: Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy. Results: The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident. Conclusions: Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.</abstract><qualityIndicators><score>5.617</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 850 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1550</abstractCharCount><pdfWordCount>2953</pdfWordCount><pdfCharCount>18197</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>222</abstractWordCount></qualityIndicators><title>Diverse morphology of biliary atresia in an animal model</title><pii><json:string>S0168-8278(98)80283-3</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>1</volume><editor><json:item><name>WT Mustard</name></json:item><json:item><name>MM Ravitch</name></json:item><json:item><name>WH Snyder</name></json:item><json:item><name>KJ Welch</name></json:item><json:item><name>CD Benson</name></json:item></editor><pages><last>740</last><first>732</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Pediatric Surgery</title></serie><host><volume>28</volume><pii><json:string>S0168-8278(00)X0018-9</json:string></pii><pages><last>607</last><first>603</first></pages><issn><json:string>0168-8278</json:string></issn><issue>4</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Journal of Hepatology</title><publicationDate>1998</publicationDate></host><categories><wos><json:string>GASTROENTEROLOGY & HEPATOLOGY</json:string></wos></categories><publicationDate>1997</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0168-8278(98)80283-3</json:string></doi><id>71C56AA3068DDAC51F5811274AE1D4D1A773AB72</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/71C56AA3068DDAC51F5811274AE1D4D1A773AB72/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/71C56AA3068DDAC51F5811274AE1D4D1A773AB72/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/71C56AA3068DDAC51F5811274AE1D4D1A773AB72/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/71C56AA3068DDAC51F5811274AE1D4D1A773AB72/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Diverse morphology of biliary atresia in an animal model</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Diverse morphology of biliary atresia in an animal model</title><author><persName><forename type="first">Claus</forename><surname>Petersen</surname></persName><note type="correspondence"><p>Correspondence: Claus Petersen, Department of Pediatric Surgery, Medical School of Hannover, Carl-Neuberg-Str. 1, 30625 Hannover, Germany. Tel: 49-511/532-9043. Fax: 49-511/532-9059.</p></note><affiliation>Department of Pediatric Surgery, Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Sabine</forename><surname>Grasshoff</surname></persName><affiliation>Department of Pediatric Surgery, Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Liliana</forename><surname>Luciano</surname></persName><affiliation>Laboratory of Cell Biology and Electron Microscopy, Medical School, Hannover, Germany</affiliation></author></analytic><monogr><title level="j">Journal of Hepatology</title><title level="j" type="abbrev">JHEPAT</title><idno type="pISSN">0168-8278</idno><idno type="PII">S0168-8278(00)X0018-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="603">603</biblScope><biblScope unit="page" to="607">607</biblScope></imprint></monogr><idno type="istex">71C56AA3068DDAC51F5811274AE1D4D1A773AB72</idno><idno type="DOI">10.1016/S0168-8278(98)80283-3</idno><idno type="PII">S0168-8278(98)80283-3</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background/Aims: Extrahepatic biliary atresia can be simulated in Balb/c-mice which have been infected with rotavirus. Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children. Methods: Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy. Results: The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident. Conclusions: Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Animal model</term></item><item><term>Biliary atresia</term></item><item><term>Pathology</term></item><item><term>Rotavirus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-12-03">Registration</change><change when="1997-11-17">Modified</change><change when="1997">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JHEPAT</jid><aid>98802833</aid><ce:pii>S0168-8278(98)80283-3</ce:pii><ce:doi>10.1016/S0168-8278(98)80283-3</ce:doi><ce:copyright type="unknown" year="1998"></ce:copyright></item-info><head><ce:title>Diverse morphology of biliary atresia in an animal model</ce:title><ce:author-group><ce:author><ce:given-name>Claus</ce:given-name><ce:surname>Petersen</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Sabine</ce:given-name><ce:surname>Grasshoff</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Liliana</ce:given-name><ce:surname>Luciano</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Pediatric Surgery, Medical School, Hannover, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Laboratory of Cell Biology and Electron Microscopy, Medical School, Hannover, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>*</ce:label><ce:text>Correspondence: Claus Petersen, Department of Pediatric Surgery, Medical School of Hannover, Carl-Neuberg-Str. 1, 30625 Hannover, Germany. Tel: 49-511/532-9043. Fax: 49-511/532-9059.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="28" month="7" year="1997"></ce:date-received><ce:date-revised day="17" month="11" year="1997"></ce:date-revised><ce:date-accepted day="3" month="12" year="1997"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para><ce:italic>Background/Aims:</ce:italic> Extrahepatic biliary atresia can be simulated in Balb/c-mice which have been infected with rotavirus. Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children.</ce:simple-para><ce:simple-para><ce:italic>Methods:</ce:italic> Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy.</ce:simple-para><ce:simple-para><ce:italic>Results:</ce:italic> The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident.</ce:simple-para><ce:simple-para><ce:italic>Conclusions:</ce:italic> Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Animal model</ce:text></ce:keyword><ce:keyword><ce:text>Biliary atresia</ce:text></ce:keyword><ce:keyword><ce:text>Pathology</ce:text></ce:keyword><ce:keyword><ce:text>Rotavirus</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Diverse morphology of biliary atresia in an animal model</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Diverse morphology of biliary atresia in an animal model</title></titleInfo><name type="personal"><namePart type="given">Claus</namePart><namePart type="family">Petersen</namePart><affiliation>Department of Pediatric Surgery, Medical School, Hannover, Germany</affiliation><description>Correspondence: Claus Petersen, Department of Pediatric Surgery, Medical School of Hannover, Carl-Neuberg-Str. 1, 30625 Hannover, Germany. Tel: 49-511/532-9043. Fax: 49-511/532-9059.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sabine</namePart><namePart type="family">Grasshoff</namePart><affiliation>Department of Pediatric Surgery, Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Liliana</namePart><namePart type="family">Luciano</namePart><affiliation>Laboratory of Cell Biology and Electron Microscopy, Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued><dateValid encoding="w3cdtf">1997-12-03</dateValid><dateModified encoding="w3cdtf">1997-11-17</dateModified><copyrightDate encoding="w3cdtf">1998</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">Background/Aims: Extrahepatic biliary atresia can be simulated in Balb/c-mice which have been infected with rotavirus. Irreversible occlusion of the common bile duct is the result of an inflammatory process of the whole biliary tract. The observations in this animal model are similar to extrahepatic biliary atresia in newborn children. The present study describes the wide range of morphological findings in mice and compares the results with several classifications of extrahepatic biliary atresia in children. Methods: Newborn Balb/c-mice were infected intraperitoneally with rhesus rotavirus; the pathological morphology of the extrahepatic bile ducts in 73 mice is described and illustrated by scanning electron microscopy. Results: The extension and localisation of atresia varied from short to interrupted or long-segment atresia, with or without prestenotic dilatation. The gallbladder was small and atretic, or appeared hydropic due to atresia of the common bile duct. The wide range of pathomorphological findings is the final stage of an inflammatory process. The morphological changes of the extrahepatic bile ducts do not fit any pattern, and no classification is evident. Conclusions: Most types of extrahepatic biliary atresia in children can be mimicked in this animal model. Comparing these observations with different classifications of extrahepatic biliary atresia in children, it must be asked if any classification of the disease is justified, having regard only to pathomorphological findings in the extrahepatic biliary tract.</abstract><subject><genre>Keywords</genre><topic>Animal model</topic><topic>Biliary atresia</topic><topic>Pathology</topic><topic>Rotavirus</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Hepatology</title></titleInfo><titleInfo type="abbreviated"><title>JHEPAT</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199804</dateIssued></originInfo><identifier type="ISSN">0168-8278</identifier><identifier type="PII">S0168-8278(00)X0018-9</identifier><part><date>199804</date><detail type="volume"><number>28</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>531</start><end>744</end></extent><extent unit="pages"><start>603</start><end>607</end></extent></part></relatedItem><identifier type="istex">71C56AA3068DDAC51F5811274AE1D4D1A773AB72</identifier><identifier type="DOI">10.1016/S0168-8278(98)80283-3</identifier><identifier type="PII">S0168-8278(98)80283-3</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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