Ramadori, Giuliano

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

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

[["dc.bibliographiccitation.firstpage","546"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Liver International"],["dc.bibliographiccitation.lastpage","557"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Aprigliano, Isabella"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T11:16:44Z"],["dc.date.available","2018-11-07T11:16:44Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Statins are shown to have cholesterol-independent properties such as anti-inflammation and immunomodulation. Activated hepatic stellate cells (HSCs) acquire the capacity to synthesize matrix proteins in damaged liver. We tested the hypothesis that atorvastatin may be capable of inducing apoptosis in HSCs. Methods: Primary cultures of rat HSCs were exposed to atorvastatin, mevalonic acid and U0126. Quantification of living, apoptotic and necrotic HSCs was performed by flow cytometry and laser-scan microscopy. Cell-cycle analysis was performed by flow cytometry. Pro- and anti-apoptotic factors were investigated by Western blot and electrophoresis mobility shift assay. Protease activity of caspases was calculated using a colorimetric kit. Results: Atorvastatin leads to a G2-arrest and induces apoptosis in activated HSCs. Atorvastatin-mediated apoptosis could be blocked by co-administration of mevalonic acid and U0126. No effects of atorvastatin on gene expression of CD95, CD95L, NF-kappa B, p53 and p21WAF1 could be observed. Atorvastatin-induced apoptosis in activated HSCs is related to an increased protease activity of caspase-9 and -3. Gene expression of the major proteins of the bcl-system shows that truncated Bid is involved in apoptosis mediated by atorvastatin. By blocking the extracellular signal-regulated protein kinase (ERK1/2) activation by adding U0126, we could prevent the apoptosis induced by atorvastatin. By Western blot we could not detect any change in the activation of c-jun N-terminal kinase (JNK). Conclusions: Atorvastatin induces apoptosis in activated HSCs acting through an ERK-dependent cleavage of Bid and a highly increased protease activity of caspase-9 and -3. JNK is not involved in atorvastatin-mediated apoptosis in HSCs."],["dc.identifier.doi","10.1111/j.1478-3231.2008.01682.x"],["dc.identifier.isi","000253980300018"],["dc.identifier.pmid","18339080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54661"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","1478-3223"],["dc.title","Atorvastatin induces apoptosis by a caspase-9-dependent pathway: an in vitro study on activated rat hepatic stellate cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","910"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Liver International"],["dc.bibliographiccitation.lastpage","921"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Qesaraku, Blendi"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T08:28:20Z"],["dc.date.available","2018-11-07T08:28:20Z"],["dc.date.issued","2009"],["dc.description.abstract","Tumour necrosis factor alpha (TNF-alpha) may exhibit antitumoral activity and can influence the reaction of both tumour and normal tissue to radiation. To test the effect of TNF-alpha and/or irradiation on hepatocellular (HepG2, Hep3B, Sk-Hep1, HuH7) and cholangiocellular (Sk-chA1, Mz-chA1) tumour cell lines. Colony formation, apoptosis analysis and trypan blue exclusion were used to assess cell viability. Doses of radiation (2-25 Gy) and TNF-alpha (100-50 000 U) as well as their respective sequencing were varied (24 and 12 h before and 6 h after). The expression of TNF-alpha and TNF receptors 1/2 was determined using real-time polymerase chain reaction and I kappa B alpha protein expression was detected by Western blot. Sole irradiation induced a reduction in colony formation in all cell lines and sole TNF-alpha in HepG2 and Sk-chA1 cells only. No difference in apoptosis induction after TNF-alpha or irradiation was observed. Cellular death induced by the combination of TNF-alpha and radiation was not superior to the use of any of the two agents alone. All cell lines revealed that radiation induced upregulation of TNF-alpha whereas the extent of TNF receptor-specific transcription did not change. Furthermore, radiation-induced changes in I kappa B alpha expression were not detectable. Our data suggest that both TNF-alpha and radiation may be treatment options for hepatocellular and cholangiocellular carcinomas. Because TNF-alpha and radiation do not interact in terms of radiosensitization, anti-TNF-alpha treatment may have the potential to protect against hepatocellular injury after abdominal irradiation. However, further in vivo studies are needed to confirm that anti-TNF-alpha treatment does not compromise tumour control and actually attenuates radiation-induced liver injury."],["dc.identifier.doi","10.1111/j.1478-3231.2009.01980.x"],["dc.identifier.isi","000266715400018"],["dc.identifier.pmid","19226333"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16397"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","1478-3223"],["dc.title","Effect of tumour necrosis factor-alpha and irradiation alone or in combination on the viability of hepatocellular and biliary adenocarcinoma cell lines in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","85"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Tello, Khodr"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T08:33:19Z"],["dc.date.available","2018-11-07T08:33:19Z"],["dc.date.issued","2009"],["dc.description.abstract","This study aimed to reveal the pathophysiological signalling responsible for radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis. I kappa B was upregulated in irradiated hepatocytes. Administration of I kappa B antisense oligonucleotides prior to irradiation inhibited occurrence of apoptosis after TNF-alpha administration. Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by I kappa B antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation. Herein, upregulation of FLIP may play a crucial role. Cleavage of bid, upregulation of bax, downregulation of bcl-2 and release of cytochrome c after TNF-alpha-administration depend on radiation-induced upregulation of I kappa B, thus demonstrating an apoptosis permitting effect of I kappa B."],["dc.description.sponsorship","Deutsche Krebshilfe [106760]"],["dc.identifier.doi","10.1007/s00411-008-0200-1"],["dc.identifier.isi","000262316300009"],["dc.identifier.pmid","18956207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17548"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-2099"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Irradiation leads to sensitization of hepatocytes to TNF-alpha-mediated apoptosis by upregulation of I kappa B expression"],["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.issue","4"],["dc.bibliographiccitation.journal","Hepatology"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz"],["dc.contributor.author","Ghayor, Ahmad"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Rove-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","2018-11-07T11:10:33Z"],["dc.date.available","2018-11-07T11:10:33Z"],["dc.date.issued","2008"],["dc.format.extent","999A"],["dc.identifier.isi","000259757402229"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53230"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Inc"],["dc.publisher.place","Hoboken"],["dc.relation.conference","59th Annual Meeting of the American-Association-for-the-Study-of-Liver-Diseases"],["dc.relation.eventlocation","San Francisco, CA"],["dc.relation.issn","0270-9139"],["dc.title","EFFECT OF IRRADIATION ON GENE EXPRESSION OF RAT LIVER ADHESION MOLECULES: IN VIVO AND IN VITRO STUDIES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]