Malik, Ihtzaz Ahmed

[["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","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.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.artnumber","257"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Bosio, Patrizia"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz A."],["dc.date.accessioned","2019-07-09T11:45:17Z"],["dc.date.available","2019-07-09T11:45:17Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: After orthotopic liver transplantation (OLT) for hepatocellular carcinoma (HCC), recurrent HCC mostly develops within 2 years. All cases of de novo HCC described so far occurred later than 2 years after OLT. Prevention of post-transplantation HCC has usually been tried to achieve by curing or controlling recurrent liver disease. This has been rationale for treatment with interferon (IFN)/ribavirin of HCV-recurrence in patients after OLT, transplanted for advanced HCV-induced liver disease and/or HCC. The availability of new and more efficient drugs has improved chances also for previously difficult-to-treat HCV-positive patients. CASE PRESENTATION: A 75 year-old male patient who had undergone OLT for decompensated HCV-cirrhosis in 2009, and bilio-digestive surgery in 2011 under tracrolimus (0.5 mg/day) and prednisone (5 mg/day) immunosuppressive therapy, started to receive antiviral treatment for recurrent HCV-infection of graft with 200 mg/day ribavirin in combination with ledipasvir and sofosbuvir by the end of October 2015. Because of multiple side effects (anemia, asthenia, infections, and reduction of kidney functions - palliated by treatment with erythropoietin), treatment was stopped after 16 weeks. At the third control, a minimal increase in alpha-fetoprotein (AFP) serum level to 10 μg/L was measured 8 months after therapy, whereas both liver sonography and serum transaminases were normal. The patient's general condition; however, remained poor, and a magnetic resonance imaging (MRI) of abdomen was performed 2 months later. A nodule of 3 cm in diameter with a pseudocapsule was found centrally in the liver. The patient had to be hospitalized for recurrent infections of the lung, overt ascites and peritonitis. Rapid tumor growth (10 cm) was detected during last stay in hospital (April 2017), concomitant with a rise of AFP-serum levels to 91 μg/L. The family decided to take the patient home, and best supportive care was provided by a general practitioner, local nurses and the patient's dedicated wife until his death. CONCLUSION: Before treating OLT patients with HCV graft reinfection one should not only consider possible advantages of newly effective antiviral-therapies, but also life expectancy and possible side effects (difficult to manage at an outpatient service basis), including severe disadvantages such as the development of HCC."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1186/s12885-018-4175-2"],["dc.identifier.pmid","29510685"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15129"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15090"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59200"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2407"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Case report: 8 years after liver transplantation: de novo hepatocellular carcinoma 8 months after HCV clearance through IFN-free antiviral therapy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Radiation Oncology*Biology*Physics"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:54:45Z"],["dc.date.available","2018-11-07T08:54:45Z"],["dc.date.issued","2011"],["dc.format.extent","960"],["dc.identifier.doi","10.1016/j.ijrobp.2011.01.072"],["dc.identifier.isi","000291711700044"],["dc.identifier.pmid","21621123"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22740"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0360-3016"],["dc.title","IN REGARD TO \"RADIATION-INDUCED LIVER FIBROSIS IS MITIGATED BY GENE THERAPY INHIBITING TRANSFORMING GROWTH FACTOR-beta SIGNALLING IN THE RAT\" BY SHI-SUO DU ET AL. (INT J RADIAT ONCOL BIOL PHYS 2010;78:1513-1523)"],["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","460"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","185"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz"],["dc.contributor.author","Ahmad, Ghayyor"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Vorwerk, Hilke"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T08:28:35Z"],["dc.date.available","2018-11-07T08:28:35Z"],["dc.date.issued","2009"],["dc.description.abstract","Background and Purpose: Migration of leukocytes into tissue is a key element of innate and adaptive immunity. An animal study showed that liver irradiation, in spite of induction of chemokine gene expression, does not Lead to recruitment of Leukocytes into the parenchyma. The aim of this study was to analyze gene expression of adhesion molecules, which mediate leukocyte recruitment into organs, in irradiated rat liver in vivo and rat hepatocytes in vitro. Material and Methods: Rat livers in vivo were irradiated selectively at 25 Gy. Isolated hepatocytes in vitro were irradiated at 8 Gy. RNA extracted within 48 h after irradiation in vivo and in vitro was analyzed by real-time PCR (polymerase chain reaction) and Northern blot. Adhesion molecule concentration in serum was measured by ELISA (enzyme-linked immunosorbent assay). Cryostat sections of livers were used for immunohistology. Results: Significant radiation-induced increase of ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), JAM-1 (junctional adhesion molecule-1), beta(1)-integrin, beta(2)-integrin, E-cadherin, and P-selectin gene expression could be detected in vivo, white PECAM-1 (platelet-endothelial cell adhesion molecule-1) gene expression remained unchanged. In vitro, beta(1)-integrin, JAM-1, and ICAM-2 showed a radiation-induced increased expression, whereas the Levels of P-selectin, ICAM-1, PECAM-1, VCAM-1, Madcam-1 (mucosal addressin cell adhesion molecule-1), beta(2)-integrin, and E-cadherin were downregulated. However, incubation of irradiated hepatocytes with either tumor necrosis factor-(TNF-)alpha, interleukin-(IL-)1 beta, or IL-6 plus TNF-alpha led to an upregulation of P-setectin, ICAM-1 and VCAM-1. Conclusion: The findings suggest that liver irradiation modulates gene expression of the main adhesion molecules in vivo and in cytokine-activated hepatocytes, with the exception of PECAM-1. This may be one reason for the Lack of inflammation in the irradiated rat liver."],["dc.identifier.doi","10.1007/s00066-009-1964-1"],["dc.identifier.isi","000268224900007"],["dc.identifier.pmid","19714308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16456"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.relation.issn","0179-7158"],["dc.title","Effect of Irradiation on Gene Expression of Rat Liver Adhesion Molecules 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","1252"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","1260"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Ahmad, Ghayyor"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Malik, Ihtzaz"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Merli, Manuela"],["dc.contributor.author","Riggio, Oliviero"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:22:56Z"],["dc.date.available","2018-11-07T11:22:56Z"],["dc.date.issued","2009"],["dc.description.abstract","The liver and the spleen are the organs in which cellular material and aged erythrocytes are eliminated from the blood. Within the liver, Kupffer cells (KCs) are mainly responsible for this task, as such KCs have a pivotal role in iron metabolism. The aim of this study is to investigate the changes of hepatic gene expression in two models of KC phagocytosis. Gadolinium chloride (GD) or zymosan was injected intraperitoneally into rats and to endotoxin-resistant mice (C3H/HeJ). The animals were killed at different time points and their livers were immediately frozen in liquid nitrogen for RNA isolation and immunohistological studies. RNA was analyzed by real-time PCR and northern blot. Sera were used to measure transaminases, hepcidin and iron levels. The expression of iron metabolism genes, hepcidin, hemojuvelin (Hjv), ferroportin-1 (Fpn-1) and of the inflammatory cytokines IL-6, IL-1 beta, TNF-alpha and IFN-gamma was determined. Although phagocytosed material was detected in ED-1- and C1q-positive cells, no inflammatory cells were identified within the liver parenchyma. Serum levels of hepcidin, iron and transaminases did not differ from those of control animals. Both GD and zymosan induced an upregulation of hepcidin-gene expression in rat liver as early as 3 h, reaching a maximum 6 h after treatment. Hjv- and Fpn-1-gene expression was downregulated at the same time. IL-6 was by far the most induced acute-phase-cytokine in GD- and zymosan-treated livers, although IL-1 beta and TNF-alpha were also strongly upregulated by zymosan and to a lesser extent by GD. Similar results were obtained in the C3H/HeJ mouse strain excluding the possible role of contaminating endotoxin. This study shows that phagocytosis upregulates hepcidin-gene expression and downregulates Hjv- and Fpn-1-gene expression within the liver. These changes in iron-regulating-gene expression may be mediated by the locally produced acute-phase-cytokines. Laboratory Investigation (2009) 89, 1252-1260; doi: 10.1038/labinvest.2009.92; published online 31 August 2009"],["dc.description.sponsorship","'Deutsche Forschungsgemeinschaft' [SFB 402 TP C6, C7, D3, GRK 335]"],["dc.identifier.doi","10.1038/labinvest.2009.92"],["dc.identifier.isi","000271248200006"],["dc.identifier.pmid","19721414"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56084"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","Phagocytosis of gadolinium chloride or zymosan induces simultaneous upregulation of hepcidin- and downregulation of hemojuvelin- and Fpn-1-gene expression in murine liver"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.journal","JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY"],["dc.bibliographiccitation.lastpage","117"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Dudas, Jozsef"],["dc.date.accessioned","2018-11-07T11:13:38Z"],["dc.date.available","2018-11-07T11:13:38Z"],["dc.date.issued","2008"],["dc.description.abstract","The liver is the largest organ of the body. It is located between the portal and the general circulation, between the organs of the gastrointestinal tract and the heart. The main function of the liver is to take up nutrients, to store them, and to provide nutrients to the other organs. At the same time has the liver to take up potentially damaging substances like bacterial products or drugs delivered by the portal blood or microorganisms, which reach the circulation. The liver is not only an important power and sewage treatment plant of the body. In fact, the liver is probably the best example for a cheap recycling system. Both parenchymal and nonparenchymal liver cells participate in the clearance activities. The function of the liver as clearance organ, however, harbors the danger that the substances that should be degraded and/or eliminated lead to tissue damage. Thus, effective defense mechanisms are necessary. Among the nonparenchymal cells Kupffer cells, sinusoidal endothelial cells, and natural killer (NK) lymphocytes exert cellular defense functions for the whole body but also for the liver itself. Furthermore, each cell type of the liver, including the hepatocytes, possesses its own defense apparatus."],["dc.identifier.isi","000259923400006"],["dc.identifier.pmid","18802219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53944"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Polish Physiological Soc"],["dc.publisher.place","Grzegorzecka"],["dc.relation.conference","24th Congress of the Polish-Physiological-Society"],["dc.relation.eventlocation","Lublin, POLAND"],["dc.relation.issn","0867-5910"],["dc.title","PHYSIOLOGY AND PATHOPHYSIOLOGY OF LIVER INFLAMMATION, DAMAGE AND REPAIR"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1801"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","1815"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:44:15Z"],["dc.date.available","2018-11-07T08:44:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Liver damage is a serious clinical complication of gamma-irradiation. We therefore exposed rats to single-dose gamma-irradiation (25 Gy) that was focused on the liver. Three to six hours after irradiation, an increased number of neutrophils (but not mononuclear phagocytes) was observed by immunohistochemistry to be attached to portal vessels between and around the portal (myo)fibroblasts (smooth muscle actin and Thy-1(+) cells). MCP-1/CCL2 staining was also detected in the portal vessel walls, including some cells of the portal area. CC-chemokine (MCP-1/CCL2 and MCP-3/CCL7) and CXC-chemokine (KC/CXCL1, MIP-2/CXCL2, and LIX/CXCL5) gene expression was significantly induced in total RNA from irradiated livers. In laser capture microdissected samples, an early (1 to 3 hours) up-regulation of CCL2, CXCL1, CXCL8, and CXCR2 gene expression was detected in the portal area but not in the parenchyma; with the exception of CXCL1 gene expression. In addition, treatment with an antibody against MCP-1/CCL2 before irradiation led to an increase in gene expression of interferon-gamma and IP-10/CXCL10 in liver tissue without influencing the recruitment of granulocytes. Indeed, the CCL2, CXCL1, CXCL2, and CXCL5 genes were strongly expressed and further up-regulated in liver (myo)fibroblasts after irradiation (8 Gy). Taken together, these results suggest that gamma-irradiation of the liver induces a transient accumulation of granulocytes within the portal area and that (myo)fibroblasts of the portal vessels may be one of the major sources of the chemokines involved in neutrophil recruitment. Moreover, inhibition of more than one chemokine (eg, CXCL1 and CXCL8) may be necessary to reduce leukocytes recruitment. (Am J Pathol 2010, 176:1801-1815; DOI. 10.2353/ajpath.2010.090505)"],["dc.description.sponsorship","Deutsche Krebshilfe [108774]; Bundesamt fur Strahlenschutz [StSch4546]"],["dc.identifier.doi","10.2353/ajpath.2010.090505"],["dc.identifier.isi","000276471500027"],["dc.identifier.pmid","20185578"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20155"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Single-Dose Gamma-Irradiation Induces Up-Regulation of Chemokine Gene Expression and Recruitment of Granulocytes into the Portal Area but Not into Other Regions of Rat Hepatic Tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]