Now showing 1 - 3 of 3
  • 2006Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","BMC Comparative hepatology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Meier, Volker"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Batusic, Danko"],["dc.contributor.author","Elmaouhoub, Abderrahim"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2019-07-09T11:41:48Z"],["dc.date.available","2019-07-09T11:41:48Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Alpha-fetoprotein (AFP) expression can resume in the adult liver under pathophysiological conditions. Orphan nuclear receptors were supposed to regulate AFP gene expression, in vitro. We were interested to study the expression of AFP and orphan nuclear receptors, in vivo. Results: The expression of AFP gene and orphan nuclear receptors in the liver was examined in different rat models: (a) fetal liver (b) liver regeneration [partial hepatectomy (PH) with and without 2-acetyl-aminofluren treatment (2-AAF)], (c) acute liver damage [treatment with CCl4] and (d) acute phase reaction treatment with turpentine oil]. After PH of 2-AAF treated rats, clusters of AFP positive cells occurred in the periportal region. In the Northern blot analysis, a positive hybridization signal for the full-length AFP-RNA was observed only in liver samples from 2-AAF treated rats after PH. In real-time PCR analysis, the full-length AFP-RNA was highly up regulated in the fetal liver (maximum at day 14: 21,500 fold); after PH of 2-AAF treated rats, the full-length AFPRNA was also up regulated up to 400 fold (day 7 after PH). The orphan nuclear receptors were down regulated at nearly each time points in all models, also at time point of up regulation of the AFP gene..."],["dc.identifier.doi","10.1186/1476-5926-5-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1241"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58515"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.subject.ddc","610"],["dc.title","Expression of AFP and Rev-Erb A/Rev-Erb B and N-CoR in fetal rat liver, liver injury and liver regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2007Journal Article
    [["dc.bibliographiccitation.artnumber","10"],["dc.bibliographiccitation.journal","BMC Gastroenterology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Mueller, Annegret"],["dc.date.accessioned","2018-11-07T11:04:05Z"],["dc.date.available","2018-11-07T11:04:05Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: While the mortality of esophageal surgery has decreased due to technological advancements, there is still a complication rate of about 30%. One of the main complications is the anastomotic leakage associated with a significant rate of morbidity and mortality. To close the leakage the efficacy of self-expanding stents (SES) has been shown in different studies. However, the high rate of stent migration limits the use of commercial available stents. In our case we were faced with the problem that the diameter of all available stents was too small to attach tightly to the mucosal wall of the esophagogastric anastomosis. Case presentation: We used, for the first time to our knowledge, a metal stent designed for colorectal application in an extensive anastomotic leak after esophageal resection in a patient with an esophageal cancer. After primary surgery with subtotal esohagectomy the anastomotic leak was stented endoscopically with a Polyflex self-expanding covered plastic stent after no response to intensive conventional management. Even though the stent was placed correctly, the diameter of the Polyflex stent was too small to attach onto the wall of the esophagogastric anastomosis. Again surgery was performed with a thoracal resection of the esophageal remnant and a hand made anastomosis. Unfortunately, again an anastomotic leak was detected soon after. To close the leak we decided to use a covered colorectal stent (Hanarostent) with an inner diameter of 30 mm. Sixteen weeks later the stent was extracted and complete mucosal healing of the esophageal leak was observed. Conclusion: The stent implantation with a large wide diameter offers a good chance to close more extensive leaks and prevent stent migration."],["dc.identifier.doi","10.1186/1471-230X-7-10"],["dc.identifier.fs","52491"],["dc.identifier.isi","000245455700001"],["dc.identifier.pmid","17367525"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1268"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51754"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-230X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.ddc","616"],["dc.title","Implantation of a colorectal stent as a therapeutic approach in the treatment of esophageal leakage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2008Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","BMC physiology"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Neubauer, Katrin"],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2019-07-10T08:12:56Z"],["dc.date.available","2019-07-10T08:12:56Z"],["dc.date.issued","2008"],["dc.description.abstract","Background and aim: The mechanisms of transmigration of inflammatory cells through the sinusoids are still poorly understood. This study aims to identify in vitro conditions (cytokine treatment) which may allow a better understanding of the changes in PECAM (platelet endothelial cell adhesion molecule)-1-gene-expression observed in vivo. Methods and results: In this study we show by immunohistochemistry, that there is an accumulation of ICAM-1 (intercellular cell adhesion molecule-1) and ED1 positive cells in necrotic areas of livers of CCl4-treated rats, whereas there are few PECAM-1 positive cells observable. After the administration of CCl4, we could detect an early rise of levels of IFN-? followed by an enhanced TGF-? protein level. As shown by Northern blot analysis and surface protein expression analysed by flow cytometry, IFN-?-treatment decreased PECAM-1-gene-expression in isolated SECs (sinusoidal endothelial cells) and mononuclear phagocytes (MNPs) in parallel with an increase in ICAM-1-gene-expression in a dose and time dependent manner. In contrast, TGF-?-treatment increased PECAM-1-expression. Additional administration of IFN-? to CCl4-treated rats and observations in IFN-?-/- mice confirmed the effect of IFN-? on PECAM-1 and ICAM-1-expression observed in vitro and increased the number of ED1-expressing cells 12 h after administration of the toxin.Conclusion: The early decrease of PECAM-1-expression and the parallel increase of ICAM-1-expression following CCl4-treatment is induced by elevated levels of IFN-? in livers and may facilitate adhesion and transmigration of inflammatory cells. The up-regulation of PECAM-1-expression in SECs and MNPs after TGF-?-treatment suggests the involvement of PECAM-1 during the recovery after liver damage."],["dc.identifier.fs","204399"],["dc.identifier.ppn","575631112"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61081"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1472-6793"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.title","Decrease of PECAM-1-gene-expression induced by proinflammatory cytokines IFN-Ú and IFN-» is reversed by TGF-Ø in sinusoidal endothelial cells and hepatic mononuclear phagocytes"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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