Ramadori, Giuliano

[["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.volume","183"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hess, C. F."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T11:02:14Z"],["dc.date.available","2018-11-07T11:02:14Z"],["dc.date.issued","2007"],["dc.format.extent","49"],["dc.identifier.isi","000247071800131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.publisher.place","Munich"],["dc.relation.conference","13th Congress of the Deutschen-Gesellschaft-fur-Radioonkologie"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","0179-7158"],["dc.title","Radiation-induced reduced expression of Hsp27 in in vitro liver macrophages leads to apoptosis and release of TNF-alpha"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","301"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","311"],["dc.bibliographiccitation.volume","313"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","El-Armouche, H."],["dc.contributor.author","Aprigliano, Isabella"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:36:23Z"],["dc.date.available","2018-11-07T10:36:23Z"],["dc.date.issued","2003"],["dc.description.abstract","Hepatic stellate cells (HSCs), the pericytes of hepatic sinusoids, and liver myofibroblasts (rMFs), cells located in the portal field and around the pericentral area, are the principal fibrogenic cell types of the liver. In cases of liver damage HSCs undergo 'activation,' i.e., they acquire a myofibroblast-like appearance and synthesize huge amounts of extracellular matrix proteins (ECMs). Their proliferation ability, however, is a matter of debate. In fact, during culture the number of rat HSCs decreases, while DNA synthesis activity and DNA content per cell increase (4+/-0.6 times). Together with the decrease in cell number (60+/-19% at day 6 of primary culture compared to day 3), cell volume increases and many HSCs become multinuclear. On the other hand, in cultures of rMFs, cell number increases along with DNA synthesis, and these cells do not become multinuclear. 'Activated' HSCs produce higher levels of cyclin D-1 and E-1 transcripts than rMFs, which correlates with their increased levels of phosphorylated retinoblastoma (Rb) protein. In activated HSCs DNA synthesis seems to be associated with polyploidy and increase in cell volume, while DNA synthesis is followed by mitosis in rMFs."],["dc.identifier.doi","10.1007/s00441-003-0768-3"],["dc.identifier.isi","000185457000006"],["dc.identifier.pmid","12898209"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45309"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.title","Endoreplication and polyploidy in primary culture of rat hepatic stellate cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S479"],["dc.bibliographiccitation.journal","Radiotherapy and Oncology"],["dc.bibliographiccitation.lastpage","S480"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Thello, K."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Hess, C. F."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T09:13:58Z"],["dc.date.available","2018-11-07T09:13:58Z"],["dc.date.issued","2006"],["dc.identifier.isi","000242719101490"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27292"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.publisher.place","Clare"],["dc.relation.conference","Conference of the Spanish-Portuguese-and -Latin-American-Association"],["dc.relation.eventlocation","Leipzig, GERMANY"],["dc.relation.issn","0167-8140"],["dc.title","Irradiation leads to sensitization of hepatocytes to TNF-alpha- mediated apoptosis by upregulation of IKB expression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","388"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cellular Physiology"],["dc.bibliographiccitation.lastpage","398"],["dc.bibliographiccitation.volume","199"],["dc.contributor.author","Novosyadlyy, R."],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.date.accessioned","2018-11-07T10:48:32Z"],["dc.date.available","2018-11-07T10:48:32Z"],["dc.date.issued","2004"],["dc.description.abstract","Apart from hepatic stellate cells (HSC), liver myofibroblasts (MF) represent a second mesenchymal cell population involved in hepatic fibrogenesis. The IGF system including the insulin-like growth factors I and II (IGF-I, -II), their receptors (IGF-I receptor, IGF-IR; IGF-II/mannose 6-phosphate receptor, IGF-II/M6-PR), and six high affinity IGF binding proteins (IGFBPs) participate in the regulation of growth and differentiation of cells of the fibroblast lineage, possibly contributing to the fibrogenic process. The aim of this work was to study the expression and regulation of the IGF axis components in rat liver MF. Methods: Cultures of MF from passages I to 4 (P1-4) were studied. IGFBP secretion was analyzed by [I-125]-IGF-I ligand and immunoblotting. IGF-I, IGF-IR, IGF-II/M6-PR, and IGFBP messenger RNA (mRNA) expression was assessed by Northern blot hybridization. DNA synthesis was evaluated by 5-bromo-2'-deoxyuridine (BrdU) incorporation assay. Results: MF from PI to 4 constitutively expressed nnRNA transcripts specific for IGF-I, IGF-IR, and IGF-II/M6-PR. In MF, biosynthesis of IGFBP-3 and -2 was observed that was stimulated by IGF-I, insulin, and transforming growth factor P (TGF-beta), whereas platelet-derived growth factor (PDGF-BB) revealed inhibitory effects. IGF-I and to a lesser extent insulin increased DNA synthesis of MF. Simultaneous addition of recombinant human IGFBP-2 or -3 with IGF-I diminished the mitogenic effect of IGF-I on MF whereas preincubation of MF with IGFBP-2 or -3 further potentiated the IGF-I stimulated DNA synthesis. In conclusion, the present study demonstrates that the IGF axis may play a role in the regulation of MF proliferation in vitro which might be relevant in vivo for the process of fibrogenesis during acute and chronic liver injury. J. Cell. Physiol. 199: 388-398, 2004. (C) 2004 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jcp.10437"],["dc.identifier.isi","000221180200007"],["dc.identifier.pmid","15095286"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48218"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0021-9541"],["dc.title","Expression and regulation of the insulin-like growth factor axis components in rat liver myofibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","189"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiology"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","242"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Reuter, Felix"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:07:32Z"],["dc.date.available","2018-11-07T11:07:32Z"],["dc.date.issued","2007"],["dc.description.abstract","Purpose: To prospectively analyze hepcidin, hemojuvelin and ferro-portin-1 expression after x-irradiation or rat liver and isolated rat hepacocytes. Materials and Methods: The treatment of the rats and this study were improved by the local committee and the public authority on animal welfare. Rat livers in vivo and isolated rat hepatocytes in vitro were irradiated. The total number of rats in this study was 43. RNA extracted from livers (1, 3, 6, 12, 24, and 48 hours after irradiation) and from hepatocytes (1, 3, 6, 12, and 24 hours after irradiation) was analyzed with real-time polymerase chain reaction and Northern blot. Cytokines and prohepcidin in serum of irradiated rats were quantitatively detected with enzyme-linked immunosorbent assay. Sham-irradiated animals served as controls in all experiments. Differences between sham-irradiated and irradiated data groups were tested with anaylsis of variance and Dunnett post hoc test. Results: In vivo, a significant radiation-induced increase of hepcidin (P = .034), interleukin (IL) 1 beta (P = .008), IL-6 (P < .011), and tumor necrosis factor alpha (TNF-alpha) (P = .047) expression could be detected within the first 48 hours after irradiation. Expression of hemojuvelin (P = .008) and ferro-portin-1 (P = .002) was significantly decreased. Serum iron levels were decreased because of irradiation (P < .058); prohepcidin serum levels were increased (P = .05). In rat hepatocytes in vitro, hepcidin RNA levels were significantly downregulated after irradiation (P < .001). Incubation of irradiated hepatocytes with IL-1 beta, IL-6, or TNNF-alpha led to upregulation of hepcidin expression in vitro up to 6 hours after irradiation, with subsequent significant down-regulation for incubation with IL-1 beta (P < .001). Hemojuvelin expression behaved in a way opposite to that of hepcidin. Conclusion: x-Irradiation of the liver, induced changes of hepcidin gene expression that are probably induced by acute phase mediators produced within the liver, itself."],["dc.identifier.doi","10.1148/radiol.2421060083"],["dc.identifier.isi","243842500024"],["dc.identifier.pmid","17090718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52584"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Radiological Soc North America"],["dc.relation.issn","0033-8419"],["dc.title","x-irradiation in rat liver: Consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","431"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","443"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Elmaouhoub, Abderrahim"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:57:01Z"],["dc.date.available","2018-11-07T10:57:01Z"],["dc.date.issued","2007"],["dc.description.abstract","Synthesis of most of the plasma proteins is one of the main functions of the hepatocytes. Albumin synthesis is quantitatively the most abundant. In the present study we investigated albumin- and alpha-fetoprotein-gene-expression, and the function of the secretory apparatus during rat liver development. To this purpose we used the method of radioactive biosynthetic labeling of newly synthesized albumin and alpha-fetoprotein (AFP) to monitor the secretory capacity of endodermal cells derived from ventral foregut region (embryonic day 10, E10), and of embryonic and fetal hepatoblasts. Synthesis and secretion of albumin and AFP were already detected in the low numbered ventral foregut endodermal cells; fibrinogen synthesis was detectable in the E12 hepatoblasts, which were in higher number. The whole secretory machinery was functional from the earliest stages of liver development, and the speed of secretion was comparable with that of the adult hepatocytes. There was almost 4-fold increase of hepatoblasts cell volume in fetal stage compared with embryonic stage. The model used suggests that the hepatocyte secretory apparatus is already functional before the emergence of the liver bud. This is the first comparative report to analyze the hepatocyte secretory function, cell proliferation and cell volume during liver development."],["dc.identifier.doi","10.1007/s00418-007-0338-y"],["dc.identifier.isi","000249807600006"],["dc.identifier.pmid","17879097"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50146"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-119X"],["dc.relation.issn","0948-6143"],["dc.title","Kinetics of albumin- and alpha-fetoprotein-production during rat liver development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1822"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","The International Journal of Biochemistry & Cell Biology"],["dc.bibliographiccitation.lastpage","1832"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Ahmad, Ghayyor"],["dc.contributor.author","Sial, Gull Zareen Khan"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Batusic, Danko S."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:49:23Z"],["dc.date.available","2018-11-07T08:49:23Z"],["dc.date.issued","2011"],["dc.description.abstract","Lactoferrin (Ltf), an iron binding glycoprotein, is a pleiotropic molecule whose serum concentration increases under acute phase conditions. The physiological roles of this protein have been well elucidated, but the source and serum regulation of Ltf gene expression have not been investigated in detail as part of the acute phase reaction (APR). In the current work, the changes in hepatic Ltf-gene-expression during turpentine oil- (TO-) or LPS-induced APR were investigated. Ltf was upregulated at both the mRNA and protein levels in the liver of TO- and LPS-treated wild type (WT) mice. The pattern of induction however was different in both animal models indicating distinctive signalling patterns resulting in an acute phase reaction. Cytokines are the core regulators of APR. Among the major cytokines, IL-6 is an important signalling molecule, which also regulates iron homeostasis in response to an inflammatory situation. In this study, the administration of IL-6 induced Ltf gene expression in the liver of WT mice, in murine hepatocytes and in hepa 1-6 cells. Ltf-gene-expression was upregulated also in the liver of TO- and LPS-treated IL-6 knockout (KO) mice. The increase in serum Ltf after LPS injection was greater than after TO-injection both in WT and IL-6-KO mice. To evaluate the contribution of other acute phase cytokines in the regulation of Ltf-gene-expression in the liver, both in vitro and in vivo studies with IL-1 beta, TNF-alpha, or IFN-gamma were performed. The results demonstrate that TNF-alpha and IFN-gamma also upregulated Ltf-gene-expression, while IL-1 beta has no role in the regulation of Ltf-gene-expression. (C) 2011 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.biocel.2011.09.002"],["dc.identifier.isi","000297491700021"],["dc.identifier.pmid","21963450"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1357-2725"],["dc.title","Changes of hepatic lactoferrin gene expression in two mouse models of the acute phase reaction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","469"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","European Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","476"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Eisenbach, C."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","El-Armouche, H."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:45:54Z"],["dc.date.available","2018-11-07T10:45:54Z"],["dc.date.issued","2004"],["dc.description.abstract","The activated hepatic stellate cell (HSC) is an important fibrogenic cell type of the liver. Interferon-alpha (IFN-alpha) has recently been shown to elicit an antiapoptotic effect on activated HSC by a JAK-2-dependent inhibition of caspase-8 activation. As JAK-2 has so far been shown to be a member of the IFN-gamma signal transduction pathway we studied the effect of IFN-gamma on apoptosis as well as on its signaling in primary cultured rat HSC. IFN-gamma elicited a proapoptotic effect in activated HSC. The combination of both, IFN-gamma and IFN-alpha, however, completely cancelled each other's effect. No effect of the two cytokines on major members of apoptosis-regulating systems (CD95, CD95L, bcl-2, bax, bcl-xL, p53, p21(WAFI), p27, NFkappaB) could be observed. Western Blot analysis revealed that gene expression of the chaperone HSP70 was found to be downregulated by IFN-gamma but upregulated by IFN-alpha. The effect could be abrogated by administration of both. After transfection of activated HSC with a pCMV-HSP70 M expression vector the proapoptotic effect of IFN-gamma was cancelled. Using HSP70 antisense, the antiapoptotic effect of IFN-alpha was cancelled as well. However IFN-gamma had no effect on upregulation of JAK-2 and pJAK-2 by IFN-alpha. Taken together IFN-gamma and IFN-alpha exert opposite effects on apoptosis in HSC. This effect is mediated by their counteracting effect on HSP70 expression which acts antiapoptotic at the level of caspase-8."],["dc.identifier.doi","10.1078/0171-9335-00409"],["dc.identifier.isi","000224916400003"],["dc.identifier.pmid","15540463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47614"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Fischer Verlag"],["dc.relation.issn","0171-9335"],["dc.title","Interferon-gamma acts proapoptotic on hepatic stellate cells (HSC) and abrogates the antiapoptotic effect of interferon-alpha by an HSP70-dependant pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","G435"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","AJP Gastrointestinal and Liver Physiology"],["dc.bibliographiccitation.lastpage","G444"],["dc.bibliographiccitation.volume","283"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Matthes, N."],["dc.contributor.author","Neubauer, K."],["dc.contributor.author","Eisenbach, C."],["dc.contributor.author","El-Armouche, H."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:11:28Z"],["dc.date.available","2018-11-07T10:11:28Z"],["dc.date.issued","2002"],["dc.description.abstract","Hepatic stellate cells (HSC), particularly activated HSC, are thought to be the principle matrix-producing cell of the diseased liver. However, other cell types of the fibroblast lineage, especially the rat liver myofibroblasts (rMF), also have fibrogenic potential. A major difference between the two cell types is the different life span under culture conditions. Although nearly no spontaneous apoptosis could be shown in rMF cultures, 18 +/- 2% of the activated HSC (day 7) were apoptotic. Compared with activated HSC, CD95R was expressed in 70% higher amounts in rMF. CD95L could only be detected in activated HSC. Stimulation of the CD95 system by agonistic antibodies (1 ng/ml) led to apoptosis of all rMF within 2 h, whereas activated HSC were more resistant (5.3 h/ 40% of total cells). Although transforming growth factor-beta downregulated apoptosis in both activated HSC and rMF, tumor necrosis factor-alpha (TNF-alpha) upregulated apoptosis in rMF. Lack of spontaneous apoptosis and CD95L expression in rMF and the different reaction on TNF-alpha stimulation reveal that activated HSC and rMF belong to different cell populations."],["dc.identifier.doi","10.1152/ajpgi.00441.2001"],["dc.identifier.isi","000176842200023"],["dc.identifier.pmid","12121892"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40050"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","0193-1857"],["dc.title","Rat liver myofibroblasts and hepatic stellate cells differ in CD95-mediated apoptosis and response to TNF-alpha"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Novosiadlyy, R."],["dc.contributor.author","Aprigliano, Isabella"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Bordoni, V."],["dc.contributor.author","Elmaouhoub, Abderrahim"],["dc.contributor.author","Tripodi, Marco"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:36:26Z"],["dc.date.available","2018-11-07T10:36:26Z"],["dc.date.issued","2006"],["dc.format.extent","S73"],["dc.identifier.doi","10.1016/S0168-8278(06)80175-3"],["dc.identifier.isi","000237328100175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45324"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","41st Annual Meeting of the European-Association-for-the-Study-of-the-Liver"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","0168-8278"],["dc.title","Opposite effects of immortalized met murine hepatocytes on cell cycle and cell fate of rat liver hepatic stellate cells and liver myofibroblasts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]