Amanzada, Ahmad

[["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.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.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","561"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY"],["dc.bibliographiccitation.lastpage","570"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Rahman, Hazir"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Moriconi, Federico"],["dc.date.accessioned","2018-11-07T09:30:00Z"],["dc.date.available","2018-11-07T09:30:00Z"],["dc.date.issued","2013"],["dc.description.abstract","CD-68 is widely regarded as a selective marker for human monocytes and macrophages and is commonly used in human pathology studies. The purpose of this study was to investigate the expression of CD-68 in human peripheral blood mononuclear cells (PBMCs), neutrophil granulocytes (NGs) and in inflamed intestinal tissue samples for comparison. PBMCs and NGs were isolated from heparinized human blood samples. Intestinal biopsies were obtained during routine endoscopic procedures from patients with inflammatory bowel disease (IBD), e. g. ulcerative colitis and Crohn's disease. Gene and protein expression was analyzed by real-time RT-PCR, Western blot and immunohistochemistry. Both PBMCs and NGs preparations contained cells that were positive for CD-68 and either neutrophil elastase (NE), or myeloperoxidase (MPO). CD-68(+)/NE-/MPO- cells were regarded as monocytes. CD-68 mRNA expression was detected in PBMCs and NGs preparations. With Western blot and by performing immunoprecipitation of cell lysate, we could clearly detect CD-68 in NGs, U-937, THP-1, Hep-G2, Jurkat cells and PBMCs. Identification of inflammatory cells in acutely inflamed colonic mucosa obtained from patients with IBD revealed a strong accumulation of CD-68(+)/MPO+ cells compared to normal colonic mucosa. The uptake of the marker by phagocytosis was excluded by performing a double staining with CD-163/NE and CD-163/MPO in PBMCs, NGs cultures and in inflamed colonic mucosa. These results identify CD-68(+) NGs in peripheral blood and inflamed colonic mucosa. CD-68 is not only a marker for the macrophages-monocytes but also for NGs."],["dc.identifier.isi","000318571700002"],["dc.identifier.pmid","23573303"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31193"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","E-century Publishing Corp"],["dc.relation.issn","1936-2625"],["dc.title","Identification of CD68(+) neutrophil granulocytes in in vitro model of acute inflammation and inflammatory bowel disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","317"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Alimentary Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","318"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Schneider, S."],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:16:03Z"],["dc.date.available","2018-11-07T09:16:03Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1111/j.1365-2036.2011.04931.x"],["dc.identifier.isi","000298086600018"],["dc.identifier.pmid","22172087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27846"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0269-2813"],["dc.title","Enhancing predictive ability of IL28B-SNPs for SVR in HCV"],["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","1534"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Medical Virology"],["dc.bibliographiccitation.lastpage","1541"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Goralczyk, Armin Dietmar"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T09:21:04Z"],["dc.date.available","2018-11-07T09:21:04Z"],["dc.date.issued","2013"],["dc.description.abstract","The circulating 25-hydroxylated form of vitamin D-3, 25(OH)D, and serum ferritin concentrations have been described to be associated with disease progression in chronic hepatitis C. Both parameters also have been assessed with regard to treatment outcome, however, with divergent results. This study examined both the pre- and posttreatment serum concentrations of 25(OH)D and ferritin in 191 patients infected chronically with hepatitis C virus (HCV) type 1 with regard to liver inflammatory activity (grading), disease progression in terms of fibrosis (staging) and an antiviral treatment outcome. Mean pretreatment serum 25(OH)D and ferritin concentrations were 18 +/- 10ng/ml and 280 +/- 225 mu g/L, respectively. Multivariate analysis revealed lower pretreatment serum 25(OH)D and higher ferritin concentrations to be significantly related to both severity of inflammatory activity and of fibrotic alterations. Pretreatment serum ferritin concentration, furthermore, unlike 25(OH)D concentration, was found to be associated with a sustained virological response by uni- and multivariate analyses. A sustained virological response was featured by a significant increase in serum 25(OH)D levels (18 +/- 10ng/ml vs. 22 +/- 11ng/ml; P<0.01), a reduction of serum ferritin concentration (191 +/- 156 mu g/L vs. 103 +/- 63 mu g/L; P<0.001) and a normalization of serum alanine aminotransferase (ALT) and -glutamyl-transferase (-GT) activities. Taken together, decreased 25(OH)D and increased ferritin serum levels indicate the severity of hepatic inflammation and fibrosis in patients infected chronically with HCV type 1. Elevated ferritin, furthermore, was found to be an independent predictor for standard IFN-based therapy responsiveness. J. Med. Virol. 85:1534-1541, 2013. (c) 2013 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/jmv.23632"],["dc.identifier.isi","000321699700006"],["dc.identifier.pmid","23852677"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29029"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0146-6615"],["dc.title","Vitamin D status and serum ferritin concentration in chronic hepatitis C virus type 1 infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Hepatology"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:04:48Z"],["dc.date.available","2018-11-07T09:04:48Z"],["dc.date.issued","2012"],["dc.format.extent","619A"],["dc.identifier.isi","000310955602257"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25186"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","63rd Annual Meeting of the American-Association-for-the-Study-of-Liver-Diseases (AASLD)"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","0270-9139"],["dc.title","Characterization of the erythropoietin/erythropoietin receptor axis in a rat model of liver damage and cholangiocarcinoma development"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","American Journal of Hematology"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:05:15Z"],["dc.date.available","2018-11-07T09:05:15Z"],["dc.date.issued","2012"],["dc.format.extent","E107"],["dc.identifier.isi","000309065700054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25271"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","0361-8609"],["dc.title","CHARACTERIZATION OF THE ERYTHROPOIETIN/ ERYTHROPOIETIN RECEPTOR AXIS IN A RAT MODEL OF LIVER DAMAGE AND CHOLANGIOCARCINOMA DEVELOPMENT"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1208"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Medical Virology"],["dc.bibliographiccitation.lastpage","1216"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Schneider, Simon"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Suermann, Thomas"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:08:06Z"],["dc.date.available","2018-11-07T09:08:06Z"],["dc.date.issued","2012"],["dc.description.abstract","IL28B genotypes and virological response within 4 weeks are predictors of sustained virological response in patients infected with chronic hepatitis C virus (HCV) genotype 1 treated with antiviral dual combination therapy. The predictive value of early anemia (within 4 weeks) alone or in combination with the two other predictors has not been studied yet. A total of 305 pegylated interferon-a and ribavirin-treated patients with HCV genotype 1 were included in this study. Hemoglobin values at week 0, 4, 8, and 12 as well as the predictive efficiency of early anemia (hemoglobin value below the gender-specific lower limit: female?