mycoreobjectrosdok_disshab_0000000458rosdok_disshab_0000000458rosdokdisshabrosdok_derivate_00000043082023-08-08T10:01:52.226Z2010-06-15T07:14:16.744Zadministratorpublished1rosdok_derivate_0000004308truetruederivate_types:fulltextVolltextfulltextwf_edit_epub wf_register_epubstate:publishedstate:publishedveröffentlichtpublishedrosdok/id0000067563043607XMODS updated during RosDok migration in June 2021DissertationHochschulschrift141580720AnkeHildebrandt1983-VerfasserInautDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensdeProf. Dr. med.BrigitteVollmarAkademischeR BetreuerIndgsProf. Dr. med. Dipl. Chem.JochenSchubertAkademischeR BetreuerIndgsApl. Prof. Dr. med.JohannesHoffmannAkademischeR BetreuerIndgs1029510660Universität RostockUniversitätsmedizinGrad-verleihende Institutiondgg10.18453/rosdok_id00000675http://purl.uni-rostock.de/rosdok/id00000675urn:nbn:de:gbv:28-diss2010-0091-5610 Medizin, GesundheitUniversitätsmedizinfrei zugänglich (Open Access)Lizenz Metadaten: CC0Nutzungsrechte erteiltalle Rechte vorbehaltenUniversität RostockRostock2009monographic20102009Universitätsbibliothek RostockRostock20102010We 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.SepsisMitochondriumATP-SynthaseUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000675doctype:epubdoctype:epubDokumenttypDocument typedoctype:epub.dissertationdoctype:epub.dissertationDissertationdoctoral thesisdiniPublType:doctoralThesis diniPublType2022:PhDThesis XMetaDissPlusThesisLevel:thesis.doctoralinfo:eu-repo/semantics/doctoralThesisdocumentnatureOfContent:ppn_105825778natureOfContent:ppn_105825778HochschulschriftdiniPublType2022:DoctoralThesisdiniPublType2022:DoctoralThesisDissertation oder HabilitationDoctoral thesisDRIVERdiniPublType2022:PhDThesisdiniPublType2022:PhDThesisDissertationPhD thesisKDSF (Pu34)XMetaDissPlusThesisLevel:thesis.doctoralXMetaDissPlusThesisLevel:thesis.doctoralDoktorarbeitdoctoral thesisrfc5646:derfc5646:deDeutschGermangerdeuSDNB:610SDNB:610610 Medizin, Gesundheit610 Medical sciences Medicineinstitution:unirostockinstitution:unirostockUniversität RostockUniversity of RostockUniversität RostockUniversität RostockUni.Rostockhttp://d-nb.info/gnd/38329-6institution:unirostock.umrinstitution:unirostock.umrUniversitätsmedizinUniversity MedicineUniversität Rostock. UniversitätsmedizinUniversitätsmedizinUni.Rostock.Fakultaet.MEDhttp://d-nb.info/gnd/1029510660accesscondition:openaccessaccesscondition:openaccessfrei zugänglich (Open Access)open accesshttp://purl.org/coar/access_right/c_abf2OAfreeinfo:eu-repo/semantics/openAccess[DE-28]Open Access$gControlled Vocabulary for Access Rights$uhttp://purl.org/coar/access_right/c_abf2licenseinfo:metadatalicenseinfo:metadataLizenzen für Metadatenlicenseinfo:metadata.cc0licenseinfo:metadata.cc0Lizenz Metadaten: CC0license metadata: CC0/creativecommons/p/zero/1.0/88x31.pnghttps://creativecommons.org/publicdomain/zero/1.0/licenseinfo:depositlicenseinfo:depositVeröffentlichungsgenehmigungpermission to storelicenseinfo:deposit.rightsgrantedlicenseinfo:deposit.rightsgrantedNutzungsrechte erteiltrights grantedlicenseinfo:worklicenseinfo:workWerkworklicenseinfo:work.rightsreservedlicenseinfo:work.rightsreservedalle Rechte vorbehaltenall rights reserved/creativecommons/r/reserved/0.9/88x31.png[DE-28]Urheberrechtsschutz 1.0$gRights Statements$uhttp://rightsstatements.org/vocab/InC/1.0/http://rightsstatements.org/vocab/InC/1.0/http://rightsstatements.org/vocab/InC/1.0/Die Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen Leberversagensgnd:141580720gnd:1029510660gnd:141580720gnd:1029510660rosdok_disshab_0000000458-d603432e39gnd:141580720Anke HildebrandtAnke Hildebrandtrosdok_disshab_0000000458-d603432e60Prof. Dr. med. Brigitte VollmarProf. Dr. med. Brigitte Vollmarrosdok_disshab_0000000458-d603432e72Prof. Dr. med. Dipl. Chem. Jochen SchubertProf. Dr. med. Dipl. Chem. Jochen Schubertrosdok_disshab_0000000458-d603432e84Apl. Prof. Dr. med. Johannes HoffmannApl. Prof. Dr. med. Johannes Hoffmannrosdok_disshab_0000000458-d603432e97gnd:1029510660Universität Rostock UniversitätsmedizinUniversität Rostock UniversitätsmedizinAnke HildebrandtProf. Dr. med. Brigitte VollmarProf. Dr. med. Dipl. Chem. Jochen SchubertApl. Prof. Dr. med. Johannes HoffmannUniversität Rostock UniversitätsmedizinAnke HildebrandtProf. Dr. med. Brigitte VollmarProf. Dr. med. Dipl. Chem. Jochen SchubertApl. Prof. Dr. med. Johannes HoffmannUniversität Rostock UniversitätsmedizinAnke HildebrandtRostockUniversität Rostockepub.dissertation10.18453/rosdok_id00000675http://purl.uni-rostock.de/rosdok/id00000675urn:nbn:de:gbv:28-diss2010-0091-5SepsisMitochondriumATP-SynthaseWe 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.20092009epub.dissertation1 Dissertation_Hildebrandt_2010.pdf 7949484 d463644740e4bbc2fc62f87581ba373c rosdok/id0000067563043607XMODS updated during RosDok migration in June 2021DissertationHochschulschrift141580720AnkeHildebrandt1983-VerfasserInautDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensdeProf. Dr. med.BrigitteVollmarAkademischeR BetreuerIndgsProf. Dr. med. Dipl. Chem.JochenSchubertAkademischeR BetreuerIndgsApl. Prof. Dr. med.JohannesHoffmannAkademischeR BetreuerIndgs1029510660Universität RostockUniversitätsmedizinGrad-verleihende Institutiondgg10.18453/rosdok_id00000675http://purl.uni-rostock.de/rosdok/id00000675urn:nbn:de:gbv:28-diss2010-0091-5610 Medizin, GesundheitUniversitätsmedizinfrei zugänglich (Open Access)Lizenz Metadaten: CC0Nutzungsrechte erteiltalle Rechte vorbehaltenUniversität RostockRostock2009monographic20102009Universitätsbibliothek RostockRostock20102010We 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.SepsisMitochondriumATP-SynthaseUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000675 2010-06-15T07:14:16.744Z 2023-08-08T10:01:52.226Z 2023-08-18T10:01:52.231Z {"identifier":"rosdok/id00000675","type":"local_id","additional":"","service":"MCRLocalID","created":"2018-06-30T12:45:12.420Z"} {"identifier":"http://purl.uni-rostock.de/rosdok/id00000675","type":"purl","additional":"","service":"RosDokPURL","created":"2018-06-30T12:45:12.534Z","registered":"2018-06-30T12:45:12.534Z"} {"identifier":"10.18453/rosdok_id00000675","type":"doi","additional":"","service":"RosDokDOI","created":"2018-06-30T12:45:13.872Z","registered":"2018-06-30T12:45:13.872Z"} {"identifier":"urn:nbn:de:gbv:28-diss2010-0091-5","type":"dnbUrn","additional":"","service":"RosDokURN","created":"2018-06-30T12:45:12.424Z","registered":"2010-07-02T02:25:07.397Z"} administratorfulltextfile/rosdok_disshab_0000000458/rosdok_derivate_0000004308/Dissertation_Hildebrandt_2010.pdfDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen Leberversagensgnd:141580720gnd:1029510660gnd:141580720gnd:1029510660rosdok_disshab_0000000458-d603432e39gnd:141580720Anke HildebrandtAnke Hildebrandtrosdok_disshab_0000000458-d603432e60Prof. Dr. med. Brigitte VollmarProf. Dr. med. Brigitte Vollmarrosdok_disshab_0000000458-d603432e72Prof. Dr. med. Dipl. Chem. Jochen SchubertProf. Dr. med. Dipl. Chem. Jochen Schubertrosdok_disshab_0000000458-d603432e84Apl. Prof. Dr. med. Johannes HoffmannApl. Prof. Dr. med. Johannes Hoffmannrosdok_disshab_0000000458-d603432e97gnd:1029510660Universität Rostock UniversitätsmedizinUniversität Rostock UniversitätsmedizinAnke HildebrandtProf. Dr. med. Brigitte VollmarProf. Dr. med. Dipl. Chem. Jochen SchubertApl. Prof. Dr. med. Johannes HoffmannUniversität Rostock UniversitätsmedizinAnke HildebrandtProf. Dr. med. Brigitte VollmarProf. Dr. med. Dipl. Chem. Jochen SchubertApl. Prof. Dr. med. Johannes HoffmannUniversität Rostock UniversitätsmedizinAnke HildebrandtRostockUniversität Rostockepub.dissertation10.18453/rosdok_id00000675http://purl.uni-rostock.de/rosdok/id00000675urn:nbn:de:gbv:28-diss2010-0091-5SepsisMitochondriumATP-SynthaseWe 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.20092009[xslt]Saxonrosdok/id00000675https://purl.uni-rostock.de/rosdok/id0000067563043607X10.18453/rosdok_id00000675urn:nbn:de:gbv:28-diss2010-0091-5Anke HildebrandtHildebrandt AnkeDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensDissertationdoctoral thesisUniversität Rostock, 2009We 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…Anke HildebrandtDie Mutation des mitochondrialen ATP8 Gens verbessert den hepatischen Energiestatus im murinen Modell des akuten septischen LeberversagensUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000675141580720AnkeHildebrandt1983-VerfasserInautProf. Dr. med.BrigitteVollmarAkademischeR BetreuerIndgsProf. Dr. med. Dipl. Chem.JochenSchubertAkademischeR BetreuerIndgsApl. Prof. Dr. med.JohannesHoffmannAkademischeR BetreuerIndgs1029510660Universität RostockUniversitätsmedizinGrad-verleihende Institutiondgg[doi]10.18453/rosdok_id00000675[purl]http://purl.uni-rostock.de/rosdok/id00000675[urn]urn:nbn:de:gbv:28-diss2010-0091-5open_access20092009epoch:21th_centuryrfc5646:dedoctype:epub.dissertationaccesscondition:openaccessSDNB:610institution:unirostock.umrstate:published