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  <identifier identifierType="DOI">10.18453/rosdok_id00000675</identifier>
  <creators>
    <creator>
      <creatorName nameType="Personal">Hildebrandt, Anke</creatorName>
      <givenName>Anke</givenName>
      <familyName>Hildebrandt</familyName>
      <nameIdentifier nameIdentifierScheme="GND" schemeURI="http://d-nb.info/gnd/">http://d-nb.info/gnd/141580720</nameIdentifier>
    </creator>
  </creators>
  <titles>
    <title>Die Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen Leberversagens</title>
  </titles>
  <publisher>Universität Rostock</publisher>
  <publicationYear>2009</publicationYear>
  <resourceType resourceTypeGeneral="Text" />
  <subjects>
    <subject xml:lang="en" schemeURI="http://dewey.info/" subjectScheme="dewey">610 Medical sciences Medicine</subject>
  </subjects>
  <dates>
    <date dateType="Created">2009</date>
  </dates>
  <language>de</language>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="PURL">http://purl.uni-rostock.de/rosdok/id00000675</alternateIdentifier>
    <alternateIdentifier alternateIdentifierType="URN">urn:nbn:de:gbv:28-diss2010-0091-5</alternateIdentifier>
  </alternateIdentifiers>
  <descriptions>
    <description descriptionType="Abstract">We investigated whether a mutation in the ATPase subunit-8 gene exerts effects on the course of endotoxemic acute liver failure in mice. Wildtype and ATP8 mutant mice were challenged with D-galactosamine and E. coli lipopolysaccharide and studied 6 hrs thereafter. Induction of endotoxemic liver failure provoked marked liver damage, a drop of total adenosine nucleotide level and an increased malondialdehyde production. In contrast, ATP levels in livers ATP8 mutants remained significantly higher. As a net result, ATP8 mutant mice showed lower transaminase release and better survival rate.</description>
  </descriptions>
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