Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","321"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Moriconi, Federico"],["dc.date.accessioned","2018-11-07T09:22:03Z"],["dc.date.available","2018-11-07T09:22:03Z"],["dc.date.issued","2013"],["dc.description.abstract","The liver is considered a radiosensitive organ. However, in rats, high single-dose irradiation (HDI) showed only mild effects. Consequences of fractionated irradiation (FI) in such an animal model have not been studied so far. Rats were exposed to selective liver FI (total dose 60 Gy, 2 Gy/day) or HDI (25 Gy) and were killed three months after the end of irradiation. To study acute effects, HDI-treated rats were additionally killed at several time points between 1 and 48 h. Three months after irradiation, no differences between FI and HDI treatment were found for macroscopically detectable small \"scars\" on the liver surface and for an increased number of neutrophil granulocytes distributed in the portal fields and through the liver parenchyma. As well, no changes in HE-stained tissues or clear signs of fibrosis were found around the portal vessels. Differences were seen for the number of bile ducts being increased in FI- but not in HDI-treated livers. Serum levels indicative of liver damage were determined for alkaline phosphatase (AP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase (gamma GT) and lactate dehydrogenase (LDH). A significant increase of AP was detected only after FI while HDI led to the significant increases of AST and LDH serum levels. By performing RT-PCR, we detected up-regulation of matrix metalloproteinases, MMP-2, MMP-9, MMP-14, and of their inhibitors, TIMP-1, TIMP-2 and TIMP-3, shortly after HDI, but not at 3 month after FI or HDI. Overall, we saw punctual differences after FI and HDI, and a diffuse formation of small scars at the liver surface. Lack of \"provisional clot\"-formation and absence of recruitment of mononuclear phagocytes could be one explanation for scar formation as incomplete repair response to irradiation."],["dc.identifier.doi","10.1007/s00411-013-0468-7"],["dc.identifier.isi","000322033000004"],["dc.identifier.pmid","23595725"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29250"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0301-634X"],["dc.title","Rat model of fractionated (2 Gy/day) 60 Gy irradiation of the liver: long-term effects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","162"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Radiation Research"],["dc.bibliographiccitation.lastpage","169"],["dc.bibliographiccitation.volume","169"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rave-Fraenk, Mararet"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:18:56Z"],["dc.date.available","2018-11-07T11:18:56Z"],["dc.date.issued","2008"],["dc.description.abstract","The aim of the study was to analyze the effect of a single irradiation on chemokine gene expression in the rat liver and in isolated rat hepatocytes. RNA extracted from livers and from hepatocytes within the first 48 h after irradiation was analyzed by real-time PCR and the Northern blot assay. The chemokine concentrations in the serum of irradiated rats were measured quantitatively by ELISA. A significant radiation-induced increase of CINC1, IP10, MCP1, MIP3 alpha, MIP3 beta, MIG and ITAC gene expression could be detected at the RNA level in the liver. CINC1, MCP1 and IP10 serum levels were significantly increased. In rat hepatocytes in vitro, only MIP3a showed a radiation-induced increase in expression, while CINC1, IP10, MIP3 beta, MIG, MIP1 alpha, ITAC and SDF1 RNA levels were significantly down-regulated. However, incubation of irradiated hepatocytes in vitro with either TNF-alpha, IL1 beta, or IL6 plus TNF-alpha led to up-regulation of MCP1, IP10 and MCP1 or CINC1 and MIP3 beta, respectively. Irradiation of the liver induces up-regulation of the genes of the main proinflammatory chemokines, probably through the action of locally synthesized proinflammatory cytokines. The reason for the lack of liver inflammation in this model has still to be clarified. (C) 2008 by Radiation Research Society."],["dc.identifier.doi","10.1667/RR1006.1"],["dc.identifier.isi","000252633000004"],["dc.identifier.pmid","18220462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55150"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Radiation Research Soc"],["dc.relation.issn","0033-7587"],["dc.title","Effect of radiation on gene expression of rat liver chemokines: In vivo and in vitro studies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","327"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European journal of gastroenterology & hepatology"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Haller, Florian"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Armbrust, Thomas"],["dc.contributor.author","Langer, Claus"],["dc.contributor.author","Füzesi, Laszlo"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2011-05-13T14:17:12Z"],["dc.date.accessioned","2021-10-27T13:10:51Z"],["dc.date.available","2011-05-13T14:17:12Z"],["dc.date.available","2021-10-27T13:10:51Z"],["dc.date.issued","2008"],["dc.description.abstract","INTRODUCTION: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. They are regarded as having relatively uniform histology, although their potential for malignant behavior varies. Despite a strong promoting role of tumor-infiltrating innate immune cells in neoplastic progression, the presence of immune cells in GISTs has not yet been studied. METHODS: A total of 47 untreated, c-kit-positive primary GISTs were immunohistochemically analyzed to distinguish histiocytic and dendritic cells (DCs) (KIM-1P, fascin, and CD68) from cells of lymphoplasmacellular origin (CD3, CD20, and CD56). Furthermore, the gene expression of proinflammatory cytokines was characterized by real-time, reverse transcription-PCR analysis of total RNA extracted from frozen tissue samples. RESULTS: KIM-1P+ cells were the dominant immune cells (851+/-295 cells/mm2) and were scattered among the tumor cells. Most of the KIM-1P+ cells showed cellular projections characteristic of DCs. Fascin positivity identified a subgroup of DCs. In comparison to KIM-1P+ cells, there were significantly fewer CD68+ macrophages (196+/-217 cells/mm2). CD3+ T cells were the dominant lymphocytes (201+/-331 cells/mm2), whereas B cells (60+/-126 cells/mm2) were few. On transcriptional level, a concomitant gene expression of cytokines for the classical acute phase cytokines TNF-alpha and IL-6 was missing, thus supporting the rather innate status of immune cells. CONCLUSION: GISTs contain, beside T lymphocytes, a high number of monocyte-derived cells, which we suggest are, at least in part, immature DCs. Together with the lack of gene expression of inflammatory cytokines in tumor tissue our results point to a possible 'symbiotic relationship' between the tumor and the local immune cells."],["dc.identifier.doi","10.1097/MEG.0b013e3282f3a403"],["dc.identifier.isi","000257628200013"],["dc.identifier.pmid","18334877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6331"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91538"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0954-691X"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.mesh","Adult"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Aged, 80 and over"],["dc.subject.mesh","Antigens, CD"],["dc.subject.mesh","Antigens, CD3"],["dc.subject.mesh","Antigens, Differentiation, Myelomonocytic"],["dc.subject.mesh","Cell Communication"],["dc.subject.mesh","Cell Transformation, Neoplastic"],["dc.subject.mesh","Cytokines"],["dc.subject.mesh","Dendritic Cells"],["dc.subject.mesh","Female"],["dc.subject.mesh","Gastrointestinal Stromal Tumors"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Phenotype"],["dc.subject.mesh","Proto-Oncogene Proteins c-kit"],["dc.subject.mesh","Stromal Cells"],["dc.title","Immune cells in primary gastrointestinal stromal tumors"],["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"]]

[["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Schneider, S."],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Reinhardt, Lars"],["dc.contributor.author","Wietzke-Braun, Perdita"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:11:32Z"],["dc.date.available","2018-11-07T09:11:32Z"],["dc.date.issued","2012"],["dc.format.extent","S426"],["dc.identifier.isi","000303241302190"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26741"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","47th Annual Meeting of the European-Association-for-the-Study-of-the-Liver (EASL)"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","0168-8278"],["dc.title","RATHER THE ALLELIC VARIATION OF IL28B BUT NOT OF CYP27B1 OR HCV GENOTYPE PREDICT SPONTANEOUS ELIMINATION OF HCV-INFECTION"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","337"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Shock"],["dc.bibliographiccitation.lastpage","345"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Ahmad, Ghayyor"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2018-11-07T09:41:37Z"],["dc.date.available","2018-11-07T09:41:37Z"],["dc.date.issued","2014"],["dc.description.abstract","Decreased serum and increased hepatic iron uptake is the hallmark of acute-phase (AP) response. Iron uptake is controlled by iron transport proteins such as transferrin receptors (TfRs) and lipocalin 2 (LCN-2). The current study aimed to understand the regulation of iron uptake in primary culture hepatocytes in the presence/absence of AP mediators. Rat hepatocytes were stimulated with different concentrations of iron alone (0.01, 0.1, 0.5 mM) and AP cytokines (interleukin 6 [IL-6], IL-1, tumor necrosis factor ) in the presence/absence of iron (FeCl3: 0.1 mM). Hepatocytes were harvested at different time points (0, 6, 12, 24 h). Total mRNA and proteins were extracted for reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. A significant iron uptake was detected with 0.1 mM iron administration with a maximum (133.37 +/- 4.82 mu g/g of protein) at 24 h compared with control and other iron concentrations. This uptake was further enhanced in the presence of AP cytokines with a maximum iron uptake (481 +/- 25.81 mu g/g of protein) after concomitant administration of IL-6 + iron to cultured hepatocytes. Concomitantly, gene expression of LCN-2 and ferritin subunits (light- and heavy-chain ferritin subunits) was upregulated by iron or/and AP cytokines with a maximum at 24 h both at mRNA and protein levels. In contrast, a decreased TfR1 level was detected by IL-6 and iron alone, whereas combination of iron and AP cytokines (mainly IL-6) abrogated the downregulation of TfR1. An increase in LCN-2 release into the supernatant of cultured hepatocytes was observed after addition of iron/AP cytokines into the medium. This increase in secretion was further enhanced by combination of IL-6 + iron. In conclusion, iron uptake is tightly controlled by already present iron concentration in the culture. This uptake can be further enhanced by AP cytokines, mainly by IL-6."],["dc.identifier.doi","10.1097/SHK.0000000000000107"],["dc.identifier.isi","000335648600011"],["dc.identifier.pmid","24365882"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33775"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1540-0514"],["dc.relation.issn","1073-2322"],["dc.title","REGULATION OF IRON UPTAKE IN PRIMARY CULTURE RAT HEPATOCYTES: THE ROLE OF ACUTE-PHASE CYTOKINES"],["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","56"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Schneider, S."],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Reinhardt, Lars"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:11:31Z"],["dc.date.available","2018-11-07T09:11:31Z"],["dc.date.issued","2012"],["dc.format.extent","S426"],["dc.identifier.isi","000303241302191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26740"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","47th Annual Meeting of the European-Association-for-the-Study-of-the-Liver (EASL)"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","0168-8278"],["dc.title","CHRONIC AND PROGRESSIVE HEPATITIS DUE TO GENOTYPE 1 HCV-INFECTION MODIFY VITAMIN-D-METABOLISM"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","177"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:14:00Z"],["dc.date.available","2018-11-07T09:14:00Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic inflammatory bowel diseases can be successfully treated with antibodies against the acute phase mediator TNF-alpha. The process of activation and of extravasation of inflammatory cells from the blood into the 'stressed' tissue site is controlled by cytokines and chemokines, which attract leukocytes and by adhesion molecules, which mediate their attachment and transmigration toward the affected cell(s). The changes in the gene expression of adhesion molecules taking place in those cells before attachment have been less investigated. Changes of PECAM-1, ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) gene expression were studied in phytohaemagglutinin (PHA)- and lipolysaccharide (LPS)-treated human peripheral blood leukocytes (PBLs), granulocytes and the human monocyte cell line U-937. Cells were treated either with PHA or with LPS in the presence or absence of infliximab and incubated with TNF-alpha, IFN-gamma and/or transforming growth factor beta (TGF-beta) and treated as above. Activation of PBLs by PHA or LPS treatment triggered a sharp upregulation of ICAM-1, VCAM-1 gene expression and a time-dependent downregulation of PECAM-1 gene expression reaching a minimum 4 h from start of the experiment. The anti-TNF-alpha antibody infliximab, by neutralizing TNF-alpha and IFN-gamma production, completely reversed PECAM-1 mRNA downregulation and ICAM-1 and VCAM-1 upregulation. Immunostaining of PBLs cytospins with antibodies against PECAM-1 and ICAM-1 confirmed RT-PCR and western blot results. PBLs IFN-gamma or TNF-alpha treatment downregulated PECAM-1 in parallel with the upregulation of ICAM-1 and VCAM-1 gene expression, whereas TGF-beta upregulated PECAM-1- and downregulated ICAM-1 and VCAM-1 gene expression counteracting the effect of TNF-alpha or IFN-gamma. Similar results were obtained in human U937 cells and in granulocyte cultures by TNF-alpha or IFN-gamma treatment. Taken together, these results suggest that infliximab, blocking TNF-alpha and IFN-gamma production, exerts its anti-inflammatory effect through inhibiting downregulation of PECAM-1 gene expression and upregulation of ICAM-1 and VCAM-1 expression in leukocytes of the peripheral blood. These results also suggest that TGF-beta may thus be of therapeutic importance as an anti-inflammatory agent. Laboratory Investigation (2012) 92, 166-177; doi:10.1038/labinvest.2011.160; published online 31 October 2011"],["dc.identifier.doi","10.1038/labinvest.2011.160"],["dc.identifier.isi","000299799700001"],["dc.identifier.pmid","22042082"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27298"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","The anti-TNF-alpha antibody infliximab indirectly regulates PECAM-1 gene expression in two models of in vitro blood cell activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","218"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Digestion"],["dc.bibliographiccitation.lastpage","227"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Goralczyk, Armin Dietmar"],["dc.contributor.author","Schneider, S."],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","van Thiel, D. H."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:14:47Z"],["dc.date.available","2018-11-07T09:14:47Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: Chronic hepatitis C virus genotype 1 (HCV-G1) infection is treated with pegylated interferon-a and ribavirin. Predictive factors for treatment success are even more important now as direct-acting antiviral agents are available. Methods: Clinical and laboratory parameters were analyzed by uni- and multivariate statistical means in 264 patients with HCV-G1 infections with regard to treatment outcome. Results:The overall sustained virological response (SVR) rate was 44%. Univariate analyses revealed SVRs to be associated with age, high alanine aminotransferase (ALT) and low gamma-glutamyltransferase (gamma-GT) serum activities, a low pretreatment gamma-GT/ALT ratio, rapid virological response (RVR), and absence of steatosis. Multivariate analyses unveiled IL28B rs12979860 genotype (CC vs. CT: OR = 2.8, CI: 1.5-4.9, p = 0.001; CC vs. TT: OR = 7.1, CI: 3.1-16.7, p < 0.001), low pretreatment gamma-GT/ALT ratio (OR = 2.5, CI: 1.7-3.3, p <0.001), age (OR = 0.96, CI: 0.94-0.98, p = 0.001) and RVR (OR = 4.18, CI: 2.85-8.65, p <0.001) to be significantly related to treatment outcome. Patients with the IL28B rs12979860 CC genotype and a low pretreatment gamma-GT/ALT ratio achieved the highest rate of a SVR with the highest predictive values (OR = 26.7, 95% CI: 10-71.1, p<0.0001). Conclusion: The pretreatment gamma-GT/ALT ratio significantly enhances the predictability of the IL28B genotype. Employing this combination will help to identify patients who will most likely benefit from an interferon-alpha-based combination therapy in a nontriaged ordinary setting. Copyright (C) 2012 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000339879"],["dc.identifier.isi","000310717600007"],["dc.identifier.pmid","22964578"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27501"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9867"],["dc.relation.issn","0012-2823"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","High Predictability of a Sustained Virological Response (87%) in Chronic Hepatitis C Virus Genotype 1 Infection Treatment by Combined IL28B Genotype Analysis and gamma-Glutamyltransferase/Alanine Aminotransferase Ratio: A Retrospective Single-Center Study"],["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"]]

[["dc.bibliographiccitation.artnumber","92"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Haller, Florian"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:16:07Z"],["dc.date.available","2018-11-07T11:16:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Prospero-related homeobox 1 (Prox1) transcription factor was described as a tumor-suppressor gene in liver tumors. In contrast, Prox1 knock out in murine embryos drastically reduces proliferation of hepatoblasts. Methods: We have studied the expression of Prox1 in normal liver, liver cirrhosis and peritumoral liver samples in comparison to hepatocellular (HCC) and cholangiocellular carcinoma (CCC) at mRNA, protein and functional levels. Results: Prox1 was found in hepatocytes of normal liver, while normal bile duct epithelial cells were negative. However, Prox1(+) cells, which co-expressed biliary epithelial makers and showed ductular morphology, could be detected within fibrotic septa of cirrhotic livers, and in both HCC and CCC. Two Prox1 mRNA isoforms (2.9 kb and 7.9 kb) were identified with a prevalence of the longer isoform in several HCC samples and the shorter in most CCC samples. Evidence was provided that Myc-associated zinc finger protein (MAZ) might significantly contribute to the gene expression of Prox1 in HCC, while neo-expression of Prox1 in CCC remains to be resolved. A point mutation in the prospero domain of Prox1 was found in one HCC sample. Conclusion: Our study shows dysregulation of Prox1 in liver cirrhosis, HCC and CCC, such as neo-expression in cells with biliary epithelial phenotype in liver cirrhosis, and in CCC. Altered Prox1 mRNA expression is partly regulated by MAZ, and mutation of the prospero domain in HCC indicates an involvement for Prox1 during tumor progression."],["dc.identifier.doi","10.1186/1471-2407-8-92"],["dc.identifier.isi","000255937600001"],["dc.identifier.pmid","18400094"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54521"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2407"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Altered regulation of Prox1-gene-expression in liver tumors"],["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"]]

[["dc.bibliographiccitation.firstpage","3296"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Digestive Diseases and Sciences"],["dc.bibliographiccitation.lastpage","3304"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Goralczyk, Armin"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:50:09Z"],["dc.date.available","2018-11-07T08:50:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Background and Aims The standard treatment regimen for chronic HCV genotype 3 (HCV-G3) hepatitis consists of PEGylated interferon-alpha (IFN-alpha) and ribavirin at varying doses ranging from 400 to 1,200 mg and results in response rates of 80%. However, this therapy has substantial side-effects including anemia, is teratogenic, and costly. To reduce the side-effects of therapy, the role of monotherapy consisting of only IFN-alpha was investigated. Methods A retrospective analysis of individual therapy courses of HCV-G3-infected patients who were treated with IFN-alpha(2a) monotherapy or a combination therapy with attention to the treatment outcome and the presence of IL28B rs12979860 and IL28B rs8099917 single-nucleotide polymorphism genotypes was performed. Conventional prognostic features in each case were assessed as well. Results In the study, 15/30 (50%) of patients treated with IFN-alpha(2a) monotherapy and 32/36 (89%) treated with combination therapy achieved a sustained virological response (SVR). In addition, 7/11 (64%) of those treated initially with monotherapy and subsequently with combination therapy achieved an SVR. An \"ultra-rapid\" virological response occurring within 2 weeks of initiation of therapy (p = 0.005), young age (< 40; p < 0.001) and low initial gamma-GT/ALT-ratio (p = 0.03) were associated with a SVR to IFN-alpha(2a) monotherapy. An SVR in those treated with combination therapy was found to be associated with a rapid virological response (RVR) (p = 0.03). The absence of histologic steatosis was associated with SVR in all patient groups (p = 0.01). Therapy duration (24 vs. 48 weeks) did not affect the SVR in either group. As expected, combination therapy resulted in more hematological side-effects than did monotherapy. Conclusions An \"ultra-rapid\" virological response, young age, low initial gamma-GT/ALT-ratio and absence of steatosis were each associated with an SVR in those receiving IFN-alpha(2a) monotherapy. Therefore, monotherapy in these patients should still be discussed independently of the existence of the IL28B polymorphisms."],["dc.identifier.doi","10.1007/s10620-011-1933-2"],["dc.identifier.isi","000296643400027"],["dc.identifier.pmid","21994136"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21634"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0163-2116"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Ultra-Rapid Virological Response, Young Age, Low gamma-GT/ALT-Ratio, and Absence of Steatosis Identify a Subgroup of HCV Genotype 3 Patients Who Achieve SVR with IFN-alpha(2a) Monotherapy"],["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"]]