Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","4587"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","4594"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Mertens, Jasmin"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T08:36:15Z"],["dc.date.available","2018-11-07T08:36:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Interferon regulatory factor-1 (IRF-1), a transcription regulator involved both in inducing and in mediating the effects of interferon, is encoded by a highly polymorphic gene in different ethnic populations. Some of these genetic variations have been described to be associated to disease traits in hepatitis C virus and in human immunodeficiency virus infection, including one single-nucleotide polymorphism rs2549009 within the promoter region. This study aimed at investigating the functional relevance of rs2549009 on IRF-1 transcriptional activity in peripheral blood mononuclear cells in its natural genomic environment. Haplotype-specific chromatin immunoprecipitation using antibodies directed against both the transcriptionally inactive and active RNA polymerase II (RNAPII) and allele-specific transcript quantification techniques were applied to ex vivo-derived samples from healthy heterozygous donors. Inactive serine 5 phosphorylated RNAPII was found to be preferentially bound to the rs2549009 A allele in all donors investigated. Active serine 2 phosphorylated (ser2-P) RNAPII, in contrast, was found to be precipitable, depending on the donor, preferentially either with the A or the G promoter variants or without any preference. The ratio of rs2549009 A/G promoter variants engaged by ser2-P RNAPII was closely related to the relative frequency of the respective IRF-1 transcripts, and relative allelic expression was found to be associated to total IRF-1 gene expression. These results provide evidence for a bidirectional IRF-1 gene expression imbalance that appears not to be solely controlled by rs2549009 in cis and may rely on a yet unidentified variant or haplotype or on environmental control in trans."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [MI 474/1-1]"],["dc.identifier.doi","10.1093/hmg/ddq386"],["dc.identifier.isi","000283930200004"],["dc.identifier.pmid","20846942"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18265"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0964-6906"],["dc.title","Functional relevance of the IRF-1 promoter polymorphism rs2549009 on transcriptional activity in a native genomic environment"],["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 Clinical Virology"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Wietzke-Braun, R."],["dc.contributor.author","Maenhardt, Larissa Bettina"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Uy, Angela"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T09:36:40Z"],["dc.date.available","2018-11-07T09:36:40Z"],["dc.date.issued","2006"],["dc.format.extent","S125"],["dc.identifier.isi","000239067300377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32668"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Symposium on Viral Hepatitis and Liver Disease"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","1386-6532"],["dc.title","Serological, clinical, and demographic correlates of the outcome of hepatitis C virus infection"],["dc.type","conference_abstract"],["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","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","50"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Virology"],["dc.bibliographiccitation.lastpage","58"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Meier, V."],["dc.contributor.author","Burger, E."],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:42:33Z"],["dc.date.available","2018-11-07T10:42:33Z"],["dc.date.issued","2003"],["dc.description.abstract","The treatment of choice for patients infected chronically with HCV is the combination of IFN-alpha and ribavirin. Monotherapy with ribavirin leads to a clinical and histological improvement, but its exact mechanism of action is unknown. Therefore, the effect of ribavirin on synthesis of inflammatory cytokines and on apoptosis in stimulated peripheral blood mononuclear cells (PBMCs) was investigated. PBMCs were isolated from the blood of HCV infected patients and from healthy volunteers. The effect of ribavirin on IFN-gamma and IL-1beta release in the supernatant of unstimulated and phytohemagglutinin (PHA) stimulated PBMCs was investigated by enzyme linked immunosorbent assay (ELISA). The effect on total DNA, RNA, and protein synthesis was analyzed by measurement of H-3-thymidine H-3-uridine and H-3-leucine incorporation into cellular macromolecules. Ribavirin led to a dose-dependent decrease of the IFN-gamma but an increase of IL-1beta release into the supernatant of PHA-stimulated PBMCs. At the same time, a dose-dependent decrease of total DNA, RNA, and protein synthesis in cultures of PHA-stimulated PBMCs was demonstrated. These effects could be compensated by the addition of equimolar amounts of guanosine. The rate of apoptotic CD45+ and CD14+ cells in PBMCs cultures increased in a dose-dependent manner. Our data suggest that ribavirin administration to chronically HCV-infected patients could lead to a decrease of the synthesis of proinflammatory cytokines (e.g., IFN-gamma) by an inhibition of total DNA-, RNA-, and protein-synthesis and by induction of apoptosis in the cells of the inflammatory infiltrate. Furthermore, ribavirin could influence the synthesis of viral particles in the hepatocytes. (C) 2003 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jmv.10264"],["dc.identifier.isi","000179585400007"],["dc.identifier.pmid","12436477"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46826"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0146-6615"],["dc.title","Ribavirin inhibits DNA, RNA, and protein synthesis in PHA-stimulated human peripheral blood mononuclear cells: Possible explanation for therapeutic efficacy in patients with chronic HCV infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","563"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Digestive and Liver Disease"],["dc.bibliographiccitation.lastpage","577"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Zocco, Maria Assunta"],["dc.contributor.author","Carloni, E."],["dc.contributor.author","Pescatori, M."],["dc.contributor.author","Saulnier, N."],["dc.contributor.author","Lupascu, A."],["dc.contributor.author","Nista, E. C."],["dc.contributor.author","Novi, M."],["dc.contributor.author","Candelli, M."],["dc.contributor.author","Cimica, Velasco"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Gasbarrini, G."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Gasbarrini, A."],["dc.date.accessioned","2018-11-07T09:27:36Z"],["dc.date.available","2018-11-07T09:27:36Z"],["dc.date.issued","2006"],["dc.description.abstract","Background and aim. Kupffer cells are intrasinusoidal space located macrophages with phagocytic capacity. Interferons are cytokines with antiviral, antiprolifierative and immunomodulatory activities which may influence the activity of Kupffer cells. Aim of this study was to evaluate Kupffer cell gene expression after interferon-a or interferon-gamma stimulation in order to investigate a link between these cytokines and macrophage activation. Methods. Rat Kupffer cells were cultured for 24 h and divided into three groups: unstimulated; stimulated with interferon-a and stimulated with interferon-gamma. After 8 h stimulation total RNA was extracted and processed according to Affymetrix protocols and hybridised on R34A microarray gene set. Data analyses was performed using Microarray Analysis Suite 5.0 software. Genes showing remarkably different expression in microarray analysis were confirmed by real-time PCR. Results. Nearly 4000 out of the 8800 genes represented in the array were expressed by Kupffer cells. Among these, interferon-alpha up-regulates 91 genes by over two-fold (antiviral, antigen processing and presentation, and tumour suppressor/proapoptotic genes) and down-regulates 72 genes by 50% or more. Interferon-gamma up-regulates 70 genes by over two-fold and down-regulates 78 genes by 50% or more. Most of the genes induced by interferon-a are also induced by interferon-gamma. Down-regulated genes include growth factors and genes involved in cell cycle/proliferation. Real-time PCR confirms the results of the array. Conclusion. Interferons directly target rat Kupffer cells and are involved in the regulation of a wide variety of genes. Their expression profile shed light onto molecular mechanism of Kupffer cells activation in specific pathways such as antiviral and antitumour processes. (c) 2006 Editrice Gastroenterologica Italiana S.H. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.dld.2006.04.015"],["dc.identifier.isi","000239777800007"],["dc.identifier.pmid","16807150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30579"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pacini Editore"],["dc.relation.issn","1590-8658"],["dc.title","Characterization of gene expression profile in rat Kupffer cells stimulated with IFN-alpha or IFN-gamma"],["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","38"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:39:47Z"],["dc.date.available","2018-11-07T10:39:47Z"],["dc.date.issued","2003"],["dc.format.extent","158"],["dc.identifier.doi","10.1016/S0168-8278(03)80809-7"],["dc.identifier.isi","000182174500536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46133"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","38th Annual Meeting of the European-Association-for-the-Study-of-the-Liver"],["dc.relation.eventlocation","ISTANBUL, TURKEY"],["dc.relation.issn","0168-8278"],["dc.title","Expression of the chemokine IP-10 correlates with the amount of hepatic IFN-gamma and IL-18 mRNA in chronic hepatitis C"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3884"],["dc.bibliographiccitation.issue","31"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","3890"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Askar, Eva"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T11:25:37Z"],["dc.date.available","2018-11-07T11:25:37Z"],["dc.date.issued","2009"],["dc.description.abstract","AIM: To analyze the correlation between CD14 rs2569190/C-159T single nucleotide polymorphism (SNP) and disease progression in chronic hepatitis C. METHODS: Liver biopsy specimens from a total of 137 and 349 patients with chronic hepatitis C were separately evaluated with respect to necroinflammatory activity (grading) and architectural changes (staging). In one group, further histological lesions characteristic for hepatitis C, hepatitis C virus subtypes, and biochemical parameters of liver disease were also investigated. Samples of genomic DNA were genotyped for the respective SNP by 5'-nuclease assays using fluorescent dye-labeled allele-specific probes. RESULTS: Genotype distribution did not deviate from the Hardy-Weinberg equilibrium. In the first group, patients homozygous for the variant allele T were found to be younger than C allele carriers (39.6 +/- 12.5 vs 45.7 +/- 11.5, P = 0.008). Among the histological lesions studied, portal lymphoid aggregates were more frequently observed among TT homozygotes than among C carriers (21/37 vs 32/100, P = 0.008). The presence of portal lymphoid aggregates was closely correlated with hepatic inflammation (P = 0.003) and with bile duct damage (P < 0.001). The degree of fibrosis, in contrast, was not found to be related to the CD14 gene C-159T polymorphism. CONCLUSION: The data suggest a possible relationship between CD14 C-159T polymorphism and the formation of portal lymphoid aggregates, but not liver fibrosis progression in chronic hepatitis C. (c) 2009 The WJG Press and Baishideng. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [474/1-1]; Damascus University, Syria"],["dc.identifier.doi","10.3748/wjg.15.3884"],["dc.identifier.isi","000269202900007"],["dc.identifier.pmid","19701968"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56666"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W J G Press"],["dc.relation.issn","1007-9327"],["dc.title","Endotoxin receptor CD14 gene variants and histological features in chronic HCV infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1213"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Hepatology"],["dc.bibliographiccitation.lastpage","1214"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T09:43:03Z"],["dc.date.available","2018-11-07T09:43:03Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1002/hep.26651"],["dc.identifier.isi","000331787500055"],["dc.identifier.pmid","23907789"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1527-3350"],["dc.relation.issn","0270-9139"],["dc.title","Relating Serum GGT to ALT Activity Enhances Its Predictability on Treatment Outcome in Chronic Hepatitis C"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","29"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Virology"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Monazahian, M."],["dc.contributor.author","Grethe, S."],["dc.contributor.author","Meier, V."],["dc.contributor.author","Thomssen, R."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:54:20Z"],["dc.date.available","2018-11-07T10:54:20Z"],["dc.date.issued","2000"],["dc.description.abstract","The hepatitis C virus (HCV) interferon-alpha (IFN-alpha) sensitivity-determining region (ISDR) has been shown to suppress double-stranded RNA-dependent protein kinase (PKR) activity in vitro in a yeast PKR expression system. Since variability of ISDR was shown to correlate with nonresponsiveness to IFN-alpha therapy in chronically HCV-infected patients, it has been suggested that prototype ISDR might be a viral inhibitor of cellular PKR. The present study evaluates the biological significance of ISDR variability in situ, relating it to PKR-mediated cellular antiviral responses within the liver. ISDR variability was determined in patients chronically infected with HCV genotypes 1a, 1b, and 3a by direct sequencing using liver-derived RNA preparations as starting material. As surrogate parameters for PKR-mediated cellular responses, hepatic endogenous IFN-alpha gene expression as well as MxA expression were analysed by a competitive, quantitative reverse transcription-polymerase chain reaction technique. Irrespectively of intra- or intergenotypic ISDR amino acid substitutions, ISDR variability was found not to correlate with endogenous hepatic IFN-alpha or with hepatic MxA gene expression. The data suggest that at least two prominent PKR-mediated cellular responses might be largely unaffected by HCV ISDR variability. J. Med. Virol. 61:29-36, 2000. (C) 2000 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/(SICI)1096-9071(200005)61:1<29::AID-JMV5>3.0.CO;2-C"],["dc.identifier.isi","000086206900005"],["dc.identifier.pmid","10745229"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49542"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0146-6615"],["dc.title","Lack of clinical evidence for involvement of hepatitis C virus interferon-alpha sensitivity-determining region variability in RNA-dependent protein kinase-mediated cellular antiviral responses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1437"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Hepatology"],["dc.bibliographiccitation.lastpage","1439"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Spengler, Ulrich"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:34:31Z"],["dc.date.available","2018-11-07T09:34:31Z"],["dc.date.issued","2014"],["dc.description.abstract","The molecular mechanisms that link IFN-lambda 3 genotypes to differential induction of interferon (IFN)-stimulated genes (ISGs) in the liver of patients with chronic hepatitis C (CHC) are not known. We measured the expression of IFN-lambda and of the specific IFN-lambda receptor chain (IFN-lambda R1) in 122 liver biopsies of patients with CHC and 53 control samples. The IFN-lambda 3 genotype was not associated with differential expression of IFN-lambda, but rather IFN-lambda R1. In a series of 30 primary human hepatocyte (PHH) samples, IFN-lambda R1 expression was low but could be induced with IFN-alpha. IFN-alpha-induced IFN-lambda R1 expression was significantly stronger in PHHs carrying the minor IFN-lambda 3 allele. The analysis of liver biopsies of patients with CHC revealed a strong association of high IFN-lambda R1 expression with elevated ISG expression, with IFN-lambda 3 minor alleles, and with nonresponse to pegylated IFN-alpha and ribavirin. The findings provide a missing link between the IFN-lambda 3 genotype and the associated phenotype of treatment nonresponse."],["dc.identifier.doi","10.1002/hep.27345"],["dc.identifier.isi","000342662100036"],["dc.identifier.pmid","25078395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32186"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1527-3350"],["dc.relation.issn","0270-9139"],["dc.title","Does the interferon-lambda rather than the interferon-alpha pathway determine the outcome of hepatitis C virus infection?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]