Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","2325"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Cancer"],["dc.bibliographiccitation.lastpage","2333"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Joensuu, Heikki"],["dc.contributor.author","Eriksson, Mikael"],["dc.contributor.author","Hall, Kirsten Sundby"],["dc.contributor.author","Hartmann, Joerg Thomas"],["dc.contributor.author","Pink, Daniel"],["dc.contributor.author","Schuette, Jochen"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Hohenberger, Peter"],["dc.contributor.author","Duyster, Justus"],["dc.contributor.author","Al-Batran, Salah-Eddin"],["dc.contributor.author","Schlemmer, Marcus"],["dc.contributor.author","Bauer, Sebastian"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Sarlomo-Rikala, Maarit"],["dc.contributor.author","Nilsson, Bengt"],["dc.contributor.author","Sihto, Harri"],["dc.contributor.author","Ballman, Karla V."],["dc.contributor.author","Leinonen, Mika"],["dc.contributor.author","DeMatteo, Ronald P."],["dc.contributor.author","Reichardt, Peter"],["dc.date.accessioned","2018-11-07T09:37:08Z"],["dc.date.available","2018-11-07T09:37:08Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: Little is known about the factors that predict for gastrointestinal stromal tumor (GIST) recurrence in patients treated with adjuvant imatinib. METHODS: Risk factors for GIST recurrence were identified, and 2 risk stratification scores were developed using the database of the Scandinavian Sarcoma Group (SSG) XVIII trial, where 358 patients with high-risk GIST with no overt metastases were randomly assigned to adjuvant imatinib 400 mg/day either for 12 or 36 months after surgery. The findings were validated in the imatinib arm of the American College of Surgeons Oncology Group Z9001 trial, where 359 patients with GIST were randomized to receive imatinib and 354 were to receive placebo for 12 months. RESULTS: Five factors (high tumor mitotic count, nongastric location, large size, rupture, and adjuvant imatinib for 12 months) were independently associated with unfavorable recurrence-free survival (RFS) in a multivariable analysis in the SSGXVIII cohort. A risk score based on these 5 factors had a concordance index with GIST recurrence of 78.9%. When a simpler score consisting of the 2 strongest predictive factors (mitotic count and tumor site) was devised, the groups with the lowest, intermediate high, and the highest risk had 5-year RFS of 76.7%, 47.5%, and 8.4%, respectively. Both scores were strongly associated with RFS in the validation cohort (P<.001 for each comparison). CONCLUSIONS: The scores generated were effective in stratifying the risk of GIST recurrence in patient populations treated with adjuvant imatinib. Patients with nongastric GIST with a high mitotic count are at a particularly high risk for recurrence. (C) 2014 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made."],["dc.identifier.doi","10.1002/cncr.28669"],["dc.identifier.isi","000340241500015"],["dc.identifier.pmid","24737415"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32770"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0142"],["dc.relation.issn","0008-543X"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Risk Factors for Gastrointestinal Stromal Tumor Recurrence in Patients Treated With Adjuvant Imatinib"],["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","2374"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","2382"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Attar, Bashar M."],["dc.contributor.author","Moore, Christopher M."],["dc.contributor.author","George, Magdalena"],["dc.contributor.author","Ion-Nedelcu, Nicolae"],["dc.contributor.author","Turbay, Rafael"],["dc.contributor.author","Zachariah, Annamma"],["dc.contributor.author","Ramadori, Guiliano"],["dc.contributor.author","Fareed, Jawed"],["dc.contributor.author","van Thiel, David H."],["dc.date.accessioned","2018-11-07T09:42:39Z"],["dc.date.available","2018-11-07T09:42:39Z"],["dc.date.issued","2014"],["dc.description.abstract","AIM: To quantitate the simultaneous serum and ascitic fluid levels of procalcitonin and inflammatory markers in cirrhotics with and without ascites. METHODS: A total of 88 consecutive severe cirrhotic patients seen in a large city hospital liver clinic were studied and divided into two groups, those with and without ascites. Group 1 consisted of 41 cirrhotic patients with massive ascites, as demonstrated by necessity for therapeutic large-volume paracentesis. Group 2 consisted of 47 cirrhotic patients without any clinically documented ascites to include either a recent abdominal computed tomography scan or ultrasound study. Serum and ascitic fluid levels of an array of inflammatory markers, including procalcitonin, were measured and compared to each other and a normal plasma panel (NPP). RESULTS: The values for inflammatory markers assayed in the serum of Groups 1 and 2, and ascitic fluid of the Group 1. The plasma levels of the inflammatory cytokines interleukin (IL)-2, IL-4, IL-6, IL-8, interferon gamma (IFN gamma) and epidermal growth factor (EGF) were all significantly greater in the serum of Group 1 as compared to that of the serum obtained from the Group 2 subjects (all P < 0.05). There were significantly greater serum levels of IL-6, IL-8, IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, vascular endothelial growth factor and EGF when comparing Group 2 to the NPP. There was no significant difference for IL-1A, IL-1B, IL-2, IL-4 and IFN gamma levels between these two groups. Serum procalcitonin levels were increased in cirrhotics with ascites compared to cirrhotics without ascites, but serum levels were similar to ascites levels within the ascites group. Furthermore, many of these cytokines, but not procalcitonin, demonstrate an ascites-to-serum gradient. Serum procalcitonin does not demonstrate any significant difference segregated by liver etiology in the ascites group; but ascitic fluid procalcitonin is elevated significantly in cardiac cirrhosis/miscellaneous subgroup compared to the hepatitis C virus and alcoholic cirrhosis subgroups. CONCLUSION: Procalcitonin in the ascitic fluid, but not in the serum, differentiates between cirrhotic subgroup reflecting the dynamic interplay of ascites, bacterial translocation and the peri-peritoneal cytokine. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved."],["dc.identifier.doi","10.3748/wjg.v20.i9.2374"],["dc.identifier.isi","000332692300025"],["dc.identifier.pmid","24605035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34005"],["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","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Procalcitonin, and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites"],["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","279"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","291"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Triebel, Jakob"],["dc.contributor.author","Posselt, Jessica"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:13:12Z"],["dc.date.available","2018-11-07T09:13:12Z"],["dc.date.issued","2012"],["dc.description.abstract","MCRs are known to be expressed predominantly in the brain where they mediate metabolic and anti-inflammatory functions. Leptin plays an important role in appetite and energy regulation via signaling through melanocortin receptors (MCRs) in the brain. As serum levels of MCR ligands are elevated in a clinical situation [acute-phase response (APR)] to tissue damage, where the liver is responsible for the metabolic changes, we studied hepatic gene expression of MCRs in a model of muscle tissue damage induced by turpentine oil (TO) injection in rats. A significant increase in gene expression of all five MCRs (MC4R was the highest) in liver at the RNA and protein level was detected after TO injection. A similar pattern of increase was also found in the brain. Immunohistology showed MC4R in the cytoplasm, but also in the nucleus of parenchymal and non-parenchymal liver cells, whereas MC3R-positivity was mainly cytoplasmic. A time-dependent migration of MC4R protein from the cytoplasm into the nucleus was observed during APR, in parallel with an increase in alpha-MSH and leptin serum levels. An increase of MC4R was detected at the protein level in wild-type mice, while such an increase was not observed in IL-6ko mice during APR. Moreover, treatment of isolated liver cells with melanocortin agonists (alpha-MSH and THIQ) inhibited the endotoxin-induced upregulation of the acute-phase cytokine (IL-6, IL1 beta and TNF-alpha) gene expression in Kupffer cells and of chemokine gene expression in hepatocytes. MCRs are expressed not only in the brain, but also in liver cells and their gene expression in liver and brain tissue is upregulated during APR. Due to the presence of specific ligands in the serum, they may mediate metabolic changes and exert a protective effect on liver cells."],["dc.identifier.doi","10.1007/s00418-011-0899-7"],["dc.identifier.isi","000300326100002"],["dc.identifier.pmid","22183812"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27120"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Melanocortin receptors in rat liver cells: change of gene expression and intracellular localization during acute-phase response"],["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.artnumber","285"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Alwahsh, Salamah; \t\t \r\n\t\t Clinic for Gastroenterology and Endocrinology, University Medical Center, Georg-August-University Goettingen, Goettingen D-37075, Germany, salwahsh@exseed.ed.ac.uk\t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, salwahsh@exseed.ed.ac.uk"],["dc.contributor.affiliation","Dwyer, Benjamin; \t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, bdwyer@exseed.ed.ac.uk"],["dc.contributor.affiliation","Forbes, Shareen; \t\t \r\n\t\t Endocrinology Unit, University/BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK, Shareen.Forbes@ed.ac.uk"],["dc.contributor.affiliation","Van Thiel, David; \t\t \r\n\t\t Advanced Liver and Gastrointestinal Disease Center, Chicago, IL 60611, USA, dvanthiel@dr.com"],["dc.contributor.affiliation","Starkey Lewis, Philip; \t\t \r\n\t\t MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK, pstarkey@exseed.ed.ac.uk"],["dc.contributor.affiliation","Ramadori, Giuliano; \t\t \r\n\t\t Clinic for Gastroenterology and Endocrinology, University Medical Center, Georg-August-University Goettingen, Goettingen D-37075, Germany, gramado@med.uni-goettingen.de"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Dwyer, Benjamin J."],["dc.contributor.author","Forbes, Shareen"],["dc.contributor.author","van Thiel, David H."],["dc.contributor.author","Lewis, Philip J. Starkey"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:27:50Z"],["dc.date.available","2018-11-07T10:27:50Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-06T10:50:57Z"],["dc.description.abstract","The role of the liver and the endocrine pancreas in development of hyperinsulinemia in different types of obesity remains unclear. Sedentary rats (160 g) were fed a low-fat-diet (LFD, chow 13% kcal fat), high-fat-diet (HFD, 35% fat), or HFD+ 30% ethanol+ 30% fructose (HF-EFr, 22% fat). Overnight-fasted rats were culled after one, four or eight weeks. Pancreatic and hepatic mRNAs were isolated for subsequent RT-PCR analysis. After eight weeks, body weights increased three-fold in the LFD group, 2.8-fold in the HFD group, and 2.4-fold in the HF-EFr (p < 0.01). HF-EFr-fed rats had the greatest liver weights and consumed less food during Weeks 4-8 (p < 0.05). Hepatic-triglyceride content increased progressively in all groups. At Week 8, HOMA-IR values, fasting serum glucose, C-peptide, and triglycerides levels were significantly increased in LFD-fed rats compared to that at earlier time points. The greatest plasma levels of glucose, triglycerides and leptin were observed in the HF-EFr at Week 8. Gene expression of pancreatic-insulin was significantly greater in the HFD and HF-EFr groups versus the LFD. Nevertheless, insulin: C-peptide ratios and HOMA-IR values were substantially higher in HF-EFr. Hepatic gene-expression of insulin-receptor-substrate-1/2 was downregulated in the HF-EFr. The expression of phospho-ERK-1/2 and inflammatory-mediators were greatest in the HF-EFr-fed rats. Chronic intake of both LFD and HFD induced obesity, MetS, and intrahepatic-fat accumulation. The hyperinsulinemia is the strongest in rats with the lowest body weights, but having the highest liver weights. This accompanies the strongest increase of pancreatic insulin production and the maximal decrease of hepatic insulin signaling, which is possibly secondary to hepatic fat deposition, inflammation and other factors."],["dc.description.sponsorship","German Research Foundation (DFG); Gottingen University"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3390/ijms18020285"],["dc.identifier.isi","000395457700054"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43306"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Insulin Production and Resistance in Different Models of Diet-Induced Obesity and Metabolic Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Journal of Cellular and Molecular Medicine"],["dc.bibliographiccitation.lastpage","9"],["dc.contributor.author","Malik, Gesa"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2019-07-09T11:50:04Z"],["dc.date.available","2019-07-09T11:50:04Z"],["dc.date.issued","2019"],["dc.description.abstract","The mechanisms of radiation-induced liver damage are poorly understood. We investigated if tumour necrosis factor (TNF)-α acts synergistically with irradiation, and how its activity is influenced by platelet endothelial cell adhesion molecule-1 (PECAM-1). We studied murine models of selective single-dose (25 Gy) liver irradiation with and without TNF-α application (2 μg/mouse; i.p.). In serum of wild-type (wt)-mice, irradiation induced a mild increase in hepatic damage marker aspartate aminotransferase (AST) in comparison to sham-irradiated controls. AST levels further increased in mice treated with both irradiation and TNF-α. Accordingly, elevated numbers of leucocytes and increased expression of the macrophage marker CD68 were observed in the liver of these mice. In parallel to hepatic damage, a consecutive decrease in expression of hepatic PECAM-1 was found in mice that received radiation or TNF-α treatment alone. The combination of radiation and TNF-α induced an additional significant decline of PECAM-1. Furthermore, increased expression of hepatic lipocalin-2 (LCN-2), a hepatoprotective protein, was detected at mRNA and protein levels after irradiation or TNF-α treatment alone and the combination of both. Signal transducer and activator of transcription-3 (STAT-3) seems to be involved in the signalling cascade. To study the involvement of PECAM-1 in hepatic damage more deeply, the liver of both wt- and PECAM-1-knock-out-mice were selectively irradiated (25 Gy). Thereby, ko-mice showed higher liver damage as revealed by elevated AST levels, but also increased hepatoprotective LCN-2 expression. Our studies show that TNF-α has a pivotal role in radiation-induced hepatic damage. It acts in concert with irradiation and its activity is modulated by PECAM-1, which mediates pro- and anti-inflammatory signalling."],["dc.identifier.doi","10.1111/jcmm.14224"],["dc.identifier.pmid","30761739"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15851"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59695"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1582-4934"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","PECAM-1 modulates liver damage induced by synergistic effects of TNF-α and irradiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","470"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Malik, Ihtzaz Ahmed; 1Department of Geriatrics, University Medical Center Goettingen, Waldweg 33, D-37073 Goettingen, Germany"],["dc.contributor.affiliation","Ramadori, Giuliano; 2Center of Internal Medicine, University Medical Center Goettingen, Robert-Koch Str. 38, D-37075 Goettingen, Germany; giulianoramadori@gmail.com"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2022-04-01T10:02:04Z"],["dc.date.available","2022-04-01T10:02:04Z"],["dc.date.issued","2022"],["dc.date.updated","2022-04-08T07:27:40Z"],["dc.description.abstract","A mild to moderate increase in acute-phase proteins (APPs) and a decrease in serum albumin levels are detected in hospitalized COVID-19 patients. A similar trend is also observed for acute-phase cytokines (APC), mainly IL6, besides chemokines (e.g., CXCL8 and CCL2). However, the source of the chemokines in these patients at different stages of disease remains to be elucidated. We investigated hepatic gene expression of CXC- and CC-chemokines in a model of a localized extrahepatic aseptic abscess and in a model of septicemia produced by the intramuscular injection of turpentine oil (TO) into each hindlimb or lipopolysaccharide (LPS) intraperitoneally (i.p.) in rats and mice (wild-type (WT) and IL6-KO). Together with a striking increase in the serum IL6 level, strong serum CXCL2 and CXCL8 concentrations were detected. Correspondingly, rapid (2 h) upregulation of CXCL1, CXCL2, CXCL5, and CXCL8 was observed in rat liver after intramuscular TO injection. The induction of the gene expression of CXCL1 and CXCL8 was the fastest and strongest. The hepatic CXC-chemokines behaved like positive APPs that depend on IL6 production by activated macrophages recruited to extrahepatic damaged tissue. Chemokine upregulation was greatly reduced in IL6-KO mice. However, IL6 was dispensable in the LPS–APR model, as massive induction of hepatic chemokines studied was measured in IL6-KO mice."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/biology11030470"],["dc.identifier.pii","biology11030470"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105816"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2079-7737"],["dc.rights","CC BY 4.0"],["dc.title","Interleukin-6-Production Is Responsible for Induction of Hepatic Synthesis of Several Chemokines as Acute-Phase Mediators in Two Animal Models: Possible Significance for Interpretation of Laboratory Changes in Severely Ill Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International journal of surgery case reports"],["dc.bibliographiccitation.lastpage","6"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Alekseev, Denis"],["dc.contributor.author","Goralczyk, Armin"],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Obed, Aiman"],["dc.date.accessioned","2019-07-09T11:40:00Z"],["dc.date.available","2019-07-09T11:40:00Z"],["dc.date.issued","2012"],["dc.description.abstract","BACKGROUND: Primary hepatic carcinoid tumors (PHCT) are rare entities; they are even rarer than extrahepatic neuroendocrine gastrointestinal tumors with only about 95 cases reported in the literature. An extrahepatic primary tumor must be excluded to confirm the diagnosis of PHCT. CASE PRESENTATION: We report a case of a 42-year-old male patient with a primary hepatic neuroendocrine carcinoma, who successfully underwent living donor liver transplantation from his 70 years old mother with 10 years follow-up. Both donor and recipient are still alive and in the good health. CONCLUSION: Living liver donation from elderly donors for the patients with irresectable neuroendocrine liver malignancies can be as safe as deceased donation or liver donation from young donors (age < 50). Living donation from elderly donors might significantly expand the donor pool for patients with liver neuroendocrine tumors (NET) and potentially reduce waiting list mortality. Especially young patients with irresectable NET can benefit from this option. However, case-control studies are needed to verify the advantage of living liver transplantation (LDLT) for the patients with irresectable liver NET and to define selection criteria for these patients."],["dc.identifier.doi","10.1016/j.ijscr.2011.08.016"],["dc.identifier.fs","585944"],["dc.identifier.pmid","22288038"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58075"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2210-2612"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Ten years survival with excellent outcome after living donor liver transplantation from 70 years old donor for primary hepatic neuroendocrine carcinoma: Case report."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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.firstpage","253"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","262"],["dc.bibliographiccitation.volume","215"],["dc.contributor.author","Haller, Florian"],["dc.contributor.author","Loebke, Christian"],["dc.contributor.author","Ruschhaupt, M."],["dc.contributor.author","Cameron, S."],["dc.contributor.author","Schulten, H-J"],["dc.contributor.author","Schwager, Stefanie"],["dc.contributor.author","von Heydebreck, Anja"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Langer, C."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Sueltmann, Holger"],["dc.contributor.author","Poustka, Annemarie"],["dc.contributor.author","Korf, Ulrike"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.date.accessioned","2018-11-07T11:13:38Z"],["dc.date.available","2018-11-07T11:13:38Z"],["dc.date.issued","2008"],["dc.description.abstract","Loss of chromosome 9p is a reliable predictor of malignant behaviour in gastrointestinal stromal tumours (GISTS). p16(INK4A) located at 9p21 inhibits the CDK4/6/cyclin D complex from phosphorylating RB. Phosphorylation of RB through CDK4/6/cyclin D in early G(1) phase frees the transcription factor E2F1 from RB and enables mRNA transcription of genes essential for G(1)/S phase transition. This study aims to determine the impact of 9p loss on mRNA and protein expression of p16(INK4A) and further key cell cycle regulators in the different phases of the cell cycle. Sixty primary GISTS previously characterized for 9p loss by comparative genomic hybridization were analysed for mRNA expression of p16(INK4A), p15(INK4B), CDK4, CDK6, cyclin D, p 21(CIP1)p27(KIP1), CDK2, cyclin E, cyclin B, RB and E2F1, using quantitative RT-PCR. The protein expression of CDK6, CDK2, p2(CIP1), p27(KIP1) and phosphorylated RB (S807/S811) was evaluated using protein arrays as a novel and highly sensitive platform for profiling of protein abundance and protein phosphorylation. In parallel, the nuclear percentages of immunohistochemical staining for p16(INK4A), cyclin D, E2F1 and RB were quantified on a tissue microarray. GISTS with 9p loss had significantly higher proliferation rates, higher metastatic behaviour and shorter disease-free survival. On the molecular level, GISTS with 9p loss had a significantly reduced mRNA as well as nuclear protein expression of p16(INK4A). RB was significantly more phosphorylated in these tumours, together with increased mRNA expression and nuclear staining for E2F1 Furthermore, GISTS with 9p loss had up-regulation of the late G(1)/S phase promoters CDK2 and cyclin E. We conclude that loss of 9p accompanied by early G(1) phase inhibitor p16(INK4A) down-regulation in GISTS facilitates phosphorylation of RB, enabling F2F1-dependent transcription of genes essential for late G(1)/S phase transition. This study provides a possible basis for the accelerated proliferation and particularly malignant behaviour in GISTS with 9p loss. Copyright (C) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.2352"],["dc.identifier.isi","000257332500006"],["dc.identifier.pmid","18438954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53943"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1096-9896"],["dc.relation.issn","0022-3417"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Loss of 9p leads to p16(INK4A) down-regulation and enables RB/E2F1-dependent cell cycle promotion in gastrointestinal stromal tumours (GISTs)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7347"],["dc.bibliographiccitation.issue","41"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","7358"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Naz, Naila"],["dc.date.accessioned","2019-07-09T11:44:36Z"],["dc.date.available","2019-07-09T11:44:36Z"],["dc.date.issued","2017"],["dc.description.abstract","AIM To studied iron metabolism in liver, spleen, and serum after acute liver-damage, in relation to surrogate markers for liver-damage and repair. METHODS Rats received intraperitoneal injection of the hepatotoxin thioacetamide (TAA), and were sacrificed regularly between 1 and 96 h thereafter. Serum levels of transaminases and iron were measured using conventional laboratory assays. Liver tissue was used for conventional histology, immunohistology, and iron staining. The expression of acute-phase cytokines, ferritin light chain (FTL), and ferritin heavy chain (FTH) was investigated in the liver by qRT-PCR. Western blotting was used to investigate FTL and FTH in liver tissue and serum. Liver and spleen tissue was also used to determine iron concentrations. RESULTS After a short initial decrease, iron serum concentrations increased in parallel with serum transaminase (aspartate aminotransferase and alanine aminotransferase) levels, which reached a maximum at 48 h, and decreased thereafter. Similarly, after 48 h a significant increase in FTL, and after 72h in FTH was detected in serum. While earliest morphological signs of inflammation in liver were visible after 6 h, increased expression of the two acute-phase cytokines IFN-γ (1h) and IL-1β (3h) was detectable earlier, with maximum values after 12-24 h. Iron concentrations in liver tissue increased steadily between 1 h and 48 h, and remained high at 96 h. In contrast, spleen iron concentrations remained unchanged until 48 h, and increased mildly thereafter (96 h). Although tissue iron staining was negative, hepatic FTL and FTH protein levels were strongly elevated. Our results reveal effects on hepatic iron concentrations after direct liver injury by TAA. The increase of liver iron concentrations may be due to the uptake of a significant proportion of the metal by healthy hepatocytes, and only to a minor extent by macrophages, as spleen iron concentrations do not increase in parallel. The temporary increase of iron, FTH and transaminases in serum is obviously due to their release by damaged hepatocytes. CONCLUSION Increased liver iron levels may be the consequence of hepatocyte damage. Iron released into serum by damaged hepatocytes is obviously transported back and stored via ferritins."],["dc.identifier.doi","10.3748/wjg.v23.i41.7347"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14835"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59046"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2219-2840"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Reabsorption of iron into acutely damaged rat liver: A role for ferritins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]