Malik, Ihtzaz Ahmed

[["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.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","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","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","1569"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Gene Therapy"],["dc.bibliographiccitation.lastpage","1578"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Shevtsova, Z."],["dc.contributor.author","Malik, I."],["dc.contributor.author","Garrido, M."],["dc.contributor.author","Schoell, U."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kügler, S"],["dc.date.accessioned","2017-09-07T11:52:27Z"],["dc.date.available","2017-09-07T11:52:27Z"],["dc.date.issued","2006"],["dc.description.abstract","To elucidate effective and long-lasting neuroprotective strategies, we analysed a combination of mitochondrial protection and neurotrophic support in two well-defined animal models of neurodegeneration, traumatic lesion of optic nerve and complete 6-hydroxydopamine (6-OHDA) lesion of nigrostriatal pathway. Neuroprotection by BclX(L), Glial cell line-derived neurotrophic factor (GDNF) or BclX(L) plus GDNF co-expression were studied at 2 weeks and at 6-8 weeks after lesions. In both lesion paradigms, the efficacy of this combination approach significantly differed depending on post-lesion time. We show that BclX(L) expression is more important for neuronal survival in the early phase after lesions, whereas GDNF-mediated neuroprotection becomes more prominent in the advanced state of neurodegeneration. BclX(L) expression was not sufficient to finally inhibit degeneration of deafferentiated central nervous system neurons. Long-lasting GDNF-mediated neuroprotection depended on BclX(L) co-expression in the traumatic lesion paradigm, but was independent of BclX(L) in the 6-OHDA lesion model. The results demonstrate that neuroprotection studies in animal models of neurodegenerative diseases should generally be performed over extended periods of time in order to reveal the actual potency of a therapeutic approach."],["dc.identifier.doi","10.1038/sj.gt.3302822"],["dc.identifier.gro","3143599"],["dc.identifier.isi","000241818000003"],["dc.identifier.pmid","16838029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1131"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0969-7128"],["dc.title","Potentiation of in vivo neuroprotection by BclX(L) and GDNF co-expression depends on post-lesion time in deafferentiated CNS neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","297"],["dc.bibliographiccitation.lastpage","346"],["dc.contributor.author","Kloeser, L."],["dc.contributor.author","Kües, Ursula"],["dc.contributor.author","Schöpper, C."],["dc.contributor.author","Hosseinkhani, H."],["dc.contributor.author","Schütze, S."],["dc.contributor.author","Dantz, S."],["dc.contributor.author","Malik, I."],["dc.contributor.author","Vos, H."],["dc.contributor.author","Bartholme, M."],["dc.contributor.author","Müller, C."],["dc.contributor.author","Polle, Andrea"],["dc.contributor.author","Kharazipour, Alireza"],["dc.contributor.editor","Kües, Ursula"],["dc.date.accessioned","2017-09-07T11:49:55Z"],["dc.date.available","2017-09-07T11:49:55Z"],["dc.date.issued","2007"],["dc.identifier.gro","3149760"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6457"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.publisher","Georg-August-Universität Göttingen"],["dc.publisher.place","Göttingen"],["dc.relation.isbn","978-3-940344-11-3"],["dc.relation.ispartof","Wood Production, Wood Technology, and Biotechnological Impacts"],["dc.title","Boards and Conventional Adhesives"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Naz, N."],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:59:20Z"],["dc.date.available","2018-11-07T08:59:20Z"],["dc.date.issued","2011"],["dc.format.extent","368A"],["dc.identifier.isi","000291285001219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23867"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","100th Annual Meeting of the United States and Canadian-Academy-of-Pathology"],["dc.relation.eventlocation","San Antonio, TX"],["dc.relation.issn","0023-6837"],["dc.title","Comparison of Changes in the Gene Expression of Transferrin Receptor-1 and Other Iron Regulatory Proteins in the Rat Liver and Brain during Acute-Phase-Response"],["dc.type","conference_abstract"],["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"]]

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","233"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Wojcik, Marta"],["dc.contributor.author","Ramadori, Pierluigi"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Martius, Gesa"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Schultze, Frank Christian"],["dc.date.accessioned","2018-11-07T09:14:07Z"],["dc.date.available","2018-11-07T09:14:07Z"],["dc.date.issued","2012"],["dc.description.abstract","It has been suggested that cyclooxygenase-2 (COX-2)-mediated prostaglandin synthesis is associated with liver inflammation and carcinogenesis. The aim of this study is to identify the cellular source of COX-2 expression in different stages, from acute liver injury through liver fibrosis to cholangiocarcinoma (CC). We induced in rats acute and \"chronic\" liver injury (thioacetamide (TAA) or carbon tetrachloride (CCl(4))) and CC development (TAA) and assessed COX-2 gene expression in normal and damaged liver tissue by RT-PCR of total RNA. The cellular localization of COX-2 protein in liver tissue was analyzed by immunohistochemistry as well as in isolated rat liver cells by Western blotting. The findings were compared with those obtained in human cirrhotic liver tissue. The specificity of the antibodies was tested by 2-DE Western blot and mass spectrometric identification of the positive protein spots. RT-PCR analysis of total RNA revealed an increase of hepatic COX-2 gene expression in acutely as well as \"chronically\" damaged liver. COX-2-protein was detected in those ED1(+)/ED2(+) cells located in the non-damaged tissue (resident tissue macrophages). In addition COX-2 positivity in inflammatory mononuclear phagocytes (ED1(+)/ED2(-)), which were also present within the tumoral tissue was detected. COX-2 protein was clearly detectable in isolated Kupffer cells as well as (at lower level) in isolated \"inflammatory\" macrophages. Similar results were obtained in human cirrhotic liver. COX-2 protein is constitutively detectable in liver tissue macrophages. Inflammatory mononuclear phagocytes contribute to the increase of COX-2 gene expression in acute and chronic liver damage induced by different toxins and in the CC microenvironment."],["dc.description.sponsorship","Ministry of Science and Higher Education, Poland [N N308 3169 33]"],["dc.identifier.doi","10.1007/s00418-011-0889-9"],["dc.identifier.isi","000299371500008"],["dc.identifier.pmid","22131058"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8811"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27328"],["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","Immunodetection of cyclooxygenase-2 (COX-2) is restricted to tissue macrophages in normal rat liver and to recruited mononuclear phagocytes in liver injury and cholangiocarcinoma"],["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","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Forst und Holz"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Hawighorst, Peter"],["dc.contributor.author","Müller, Günter S."],["dc.contributor.author","Navarro-González, Monica"],["dc.contributor.author","Malik, Ithzaz"],["dc.contributor.author","Kües, Ursula"],["dc.contributor.author","Polle, Andrea"],["dc.date.accessioned","2017-09-07T11:49:42Z"],["dc.date.available","2017-09-07T11:49:42Z"],["dc.date.issued","2010"],["dc.identifier.gro","3149757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6452"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.title","Wissensbasierte Produktion und Dauerhaftigkeit von innovativen Holzwerkstoffen aus Buchen- und Küstentannenholz"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]