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.firstpage","1807"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","1821"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Xu, Min"],["dc.contributor.author","Seyhan, Hatice Ali"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Schultze, Frank Christian"],["dc.date.accessioned","2018-11-07T09:43:39Z"],["dc.date.available","2018-11-07T09:43:39Z"],["dc.date.issued","2014"],["dc.description.abstract","AIM: To explore lipocalin-2 (LCN-2) expression and its possible role and mechanism(s) of production in rat models of diet-inducible fatty liver. METHODS: Fatty liver was triggered in male Sprague-Dawley rats fed either with liquid Lieber-DeCarli (LDC) or LDC + 70% cal fructose (L-HFr) diet for 4 or 8 wk. Chow-nourished animals served as controls. Hepatic expression of LCN-2 and other metabolic and inflammatory mediators was assessed by quantitative reverse transcription polymerase chain reaction and Western blotting. Serum LCN-2, fasting leptin, and lipid profile were evaluated via Enzyme-Linked Immunosorbent Assay, Radioimmunoassay, and colorimetric assays, respectively. The localization of LCN-2 in the liver was detected by using immunofluorescence staining. Furthermore, HE stain was used to evaluate hepatic fat degeneration and inflammation. RESULTS: Both LDC-fed and L-HFr-fed rat histologically featured fatty liver. In the liver, mRNA transcriptions of Mcp-1, a2-m, Il-8 and Glut5 were increased in the L-HFr group at both time points (P < 0.001), while the transcription of Tlr4, Inos, and Tnf-alpha was significantly up-regulated at week 4. Interestingly, hepatic Lcn-2 expression was 90-fold at week 4 and 507-fold at week 8 higher in L-HFr-subjected rats vs control (P < 0.001). In contrast to HDL-cholesterol, systemic levels of LCN-2, fasting leptin and triglycerides were elevated in the L-HFr regimen (P < 0.001). Moreover, protein expression of hepatic LCN-2, CD14, phospho-MAPK, caspase-9, cytochrome c and 4-hydroxynonenal was increased in the L-HFr group. Conversely, the hepatic expression of PGC-1 alpha (a mitochondrial-biogenic protein) was reduced in the L-HFr category at week 8. The localization of LCN-2 in the liver was predominantly restricted to MPO+ granulocytes. CONCLUSION: Fructose diet up-regulates hepatic LCN-2 expression, which correlates with the increased indicators of oxidative stress and mitochondrial dysfunction. The LCN-2 may be involved in liver protection. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved."],["dc.description.sponsorship","Open Access Publikationsfonds 2014"],["dc.identifier.doi","10.3748/wjg.v20.i7.1807"],["dc.identifier.isi","000331966100016"],["dc.identifier.pmid","24587658"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10409"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34228"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Baishideng Publ Grp Co Ltd"],["dc.relation.issn","2219-2840"],["dc.relation.issn","1007-9327"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Diet high in fructose leads to an overexpression of lipocalin-2 in rat fatty liver"],["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 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.artnumber","e104220"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Xu, Min"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:36:45Z"],["dc.date.available","2018-11-07T09:36:45Z"],["dc.date.issued","2014"],["dc.description.abstract","Although both alcohol and fructose are particularly steatogenic, their long-term effect in the development of a metabolic syndrome has not been studied in vivo. Consumption of fructose generally leads to obesity, whereas ethanol can induce liver damage in the absence of overweight. Here, Sprague-Dawley rats were fed ad libitum for 28 days on five diets: chow (control), liquid Lieber-DeCarli (LDC) diet, LDC +30%J of ethanol (L-Et) or fructose (L-Fr), and LDC combined with 30%J ethanol and 30%J fructose (L-EF). Body weight (BW) and liver weight (LW) were measured. Blood and liver samples were harvested and subjected to biochemical tests, histopathological examinations, and RT-PCR. Alcohol-containing diets substantially reduced the food intake and BW (<= 3rd week), whereas fructose-fed animals had higher LW than controls ( P < 0.05). Additionally, leukocytes, plasma AST and leptin levels were the highest in the fructose-administered rats. Compared to the chow and LDC diets, the L-EF diet significantly elevated blood glucose, insulin, and total-cholesterol levels (also vs. the L-Et group). The albumin and Quick-test levels were the lowest, whereas ALT activity was the highest in the L-EF group. Moreover, the L-EF diet aggravated plasma triglyceride and reduced HDL-cholesterol levels more than 2.7-fold compared to the sum of the effects of the L-Et and L-Fr diets. The decreased hepatic insulin clearance in the L-EF group vs. control and LDC groups was reflected by a significantly decreased C-peptide: insulin ratio. All diets except the control caused hepatosteatosis, as evidenced by Nile red and H&E staining. Hepatic transcription of insulin receptor substrate-1/2 was mainly suppressed by the L-Fr and L-EF diets. The L-EF diet did not enhance the mitochondrial beta-oxidation of fatty acids (Cpt1 alpha and Ppar-alpha expressions) compared to the L-Et or L-Fr diet. Together, our data provide evidence for the coaction of ethanol and fructose with a high-fat-diet on dyslipidemia and insulin resistance-accompanied liver damage."],["dc.description.sponsorship","Open Access Publikationsfonds 2014"],["dc.identifier.doi","10.1371/journal.pone.0104220"],["dc.identifier.isi","000339993900050"],["dc.identifier.pmid","25101998"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10788"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32686"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Combination of Alcohol and Fructose Exacerbates Metabolic Imbalance in Terms of Hepatic Damage, Dyslipidemia, and Insulin Resistance in Rats"],["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","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.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"]]