Ahmad, Shakil

[["dc.bibliographiccitation.firstpage","179"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Heart Failure Reports"],["dc.bibliographiccitation.lastpage","186"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-01-30T13:29:01Z"],["dc.date.available","2019-01-30T13:29:01Z"],["dc.date.issued","2017"],["dc.description.abstract","Over the last years, evidence is accumulating that enhanced late sodium current (INaL) in cardiac pathologies has fundamental consequences for cellular electrophysiology. This review discusses the underlying mechanisms of INaL-induced arrhythmias and the significance of INaL-inhibition as a possible therapeutic approach."],["dc.identifier.doi","10.1007/s11897-017-0333-0"],["dc.identifier.pmid","28455610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57422"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1546-9549"],["dc.title","Inhibition of Late Sodium Current as an Innovative Antiarrhythmic Strategy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","687"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Nature Cell Biology"],["dc.bibliographiccitation.lastpage","699"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Gao, Xuefei"],["dc.contributor.author","Nowak-Imialek, Monika"],["dc.contributor.author","Chen, Xi"],["dc.contributor.author","Chen, Dongsheng"],["dc.contributor.author","Herrmann, Doris"],["dc.contributor.author","Ruan, Degong"],["dc.contributor.author","Chen, Andy Chun Hang"],["dc.contributor.author","Eckersley-Maslin, Melanie A."],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Lee, Yin Lau"],["dc.contributor.author","Liu, Pentao"],["dc.date.accessioned","2022-10-06T13:34:15Z"],["dc.date.available","2022-10-06T13:34:15Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41556-019-0333-2"],["dc.identifier.pii","333"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115866"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1476-4679"],["dc.relation.issn","1465-7392"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights.uri","http://www.springer.com/tdm"],["dc.title","Establishment of porcine and human expanded potential stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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","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","842"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","856"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Schultze, Frank"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:09:49Z"],["dc.date.available","2018-11-07T09:09:49Z"],["dc.date.issued","2012"],["dc.description.abstract","Liver is the central organ of iron metabolism. During acute-phase-response (APR), serum iron concentration rapidly decreases. The current study aimed to compare expression and localization of iron transport protein ferroportin-1 (Fpn-1) and of other iron import proteins after experimental tissue damage induced by injecting turpentine oil in the hind limbs of rats and mice. Serum and spleen iron concentration decreased with an increase in total liver, cytoplasmic and nuclear iron concentration. In liver, mRNA amount of Fpn-1, Fpn-1a, Fpn-1b, HFE, hemojuvelin (HJV) and hephaestin (heph) genes showed a rapid decrease. Hepcidin, divalent metal transporter-1 (DMT-1), transferrin (Tf) and Tf-receptor-1 (TfR1), TfR-2 (TfR2) gene expression was increased. Western blot analysis of liver tissue lysate confirmed the changes observed at mRNA level. In spleen, a rapid decrease in gene expression of Fpn-1, Fpn-1a, Fpn-1b, DMT-1, Tf, TfR1 and TfR2, and an increase in hepcidin was observed. Immunohistochemistry of DMT-1 and TfR2 were mainly detected in the nucleus of rat liver and spleen, whereas TfR1 was clearly localized in the plasma membrane. Fpn-1 was mostly found in the nuclei of liver cells, whereas in spleen, the protein was mainly detected in the cell membrane. Western blot analysis of liver fractions confirmed immunohistochemical results. In livers of wild-type mice, gene expression of Fpn-1, Fpn-1a and Fpn-1b was downregulated, whereas hepcidin gene expression was increased. In contrast, these changes were less pronounced in IL-6ko-mice. Cytokine (IL-6, IL-1 beta and TNF-alpha) treatment of rat hepatocytes showed a downregulation of Fpn-1, Fpn-1a and Fpn-1b, and upregulation of hepcidin gene expression. Moreover, western blot analysis of cell lysate of IL-6-treated hepatocytes detected, as expected, an increase of alpha 2-macroglobulin (positive acute-phase protein), whereas albumin (negative acute-phase protein) and Fpn-1 were downregulated. Our results demonstrate that liver behaves as a 'sponge' for iron under acute-phase conditions, and Fpn-1 behaves as a negative acute-phase protein in rat hepatocytes mainly, but not exclusively, because of the effect of IL-6. These changes could explain iron retention in the cytoplasm and in the nucleus of hepatocytes during APR. Laboratory Investigation (2012) 92, 842-856; doi:10.1038/labinvest.2012.52; published online 2 April 2012"],["dc.description.sponsorship","Deutsche Krebshilfe [108774]"],["dc.identifier.doi","10.1038/labinvest.2012.52"],["dc.identifier.isi","000304730600004"],["dc.identifier.pmid","22469696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26353"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","Ferroportin-1 is a 'nuclear'-negative acute-phase protein in rat liver: a comparison with other iron-transport proteins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S145"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","S146"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Naz, N."],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:26:10Z"],["dc.date.available","2018-11-07T09:26:10Z"],["dc.date.issued","2013"],["dc.identifier.isi","000322983000351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30239"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","International Liver Congress / 48th Annual Meeting of the European-Association-for-the-Study-of-the-Liver (EASL)"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","0168-8278"],["dc.title","FERROPORTIN 1 IS A \"NUCLEAR\" NEGATIVE ACUTE-PHASE PROTEIN IN RAT LIVER: A COMPARISON WITH OTHER IRON-TRANSPORT PROTEINS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","459"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Liver International"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Hielscher, Ruth"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T09:27:53Z"],["dc.date.available","2018-11-07T09:27:53Z"],["dc.date.issued","2013"],["dc.description.abstract","Background/Aim IL-6 IL-1 lipocalin2 (LCN2) liver irradiation oxidative stress TNF-a Lipocalin2 (LCN2) is an acute phase protein. The source of its increased serum level in oxidative stress conditions (ROS) remains still unknown. We prospectively evaluate the serum LCN2 increase after single dose liver irradiation along with hepatic LCN2 gene and protein expression. Methods A single dose of 25 Gray was administered percutaneously to the liver of randomly paired rats after a planning CT scan. Male Wistar rats were sacrificed 1, 3, 6, 12, 24 and 48h after irradiation along with sham-irradiated controls. ELISA, RT-PCR, Western blot and immunofluorescence staining was performed. Furthermore, hepatocytes, myofibroblasts and Kupffer cells were isolated from the liver of healthy rats and irradiated ex-vivo. Results After liver irradiation, LCN2 serum levels increased significantly up to 2.7g/ml within 6h and stayed elevated over 24h. LCN2 specific transcripts increased significantly up to 552 +/- 109-fold at 24h after liver irradiation, which was further confirmed at protein level. 2-macroglobulin and hemoxygenase-1 also showed an increase, but the magnitude was less as compared to LCN2. LCN2+ granulocytes were detected within 1h after irradiation around central and portal fields and remained high during the course of study. Ex-vivo irradiated hepatocytes (2.4 +/- 0.6-fold) showed a higher LCN2 gene expression as compared to myofibroblasts and Kupffer cells. IL-1 treatment further increased LCN2 gene expression in cultured hepatocytes. Conclusions Single dose liver irradiation induces a significant increase in LCN2 serum levels, comparable to the induction of acute phase proteins. We suggest LCN2 as marker for the early phase of radiation-induced tissue damage."],["dc.description.sponsorship","Deutsche Krebshilfe [108774]"],["dc.identifier.doi","10.1111/liv.12073"],["dc.identifier.isi","000314984200016"],["dc.identifier.pmid","23331620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30644"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1478-3223"],["dc.title","Serum Lipocalin2 is a potential biomarker of liver irradiation damage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Cameron, Silke"],["dc.date.accessioned","2018-11-07T09:10:23Z"],["dc.date.available","2018-11-07T09:10:23Z"],["dc.date.issued","2012"],["dc.identifier.isi","000318009801647"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26476"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0732-183X"],["dc.title","Serum lipocalin-2 as a potential biomarker of liver irradiation."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Hartmann, Nico"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Tirilomis, P."],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Pabel, Stefanie Corinna"],["dc.contributor.author","Stevens, E."],["dc.contributor.author","Frey, Norbert"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Sossalla, Samuel T."],["dc.date.accessioned","2018-11-07T10:15:51Z"],["dc.date.available","2018-11-07T10:15:51Z"],["dc.date.issued","2016"],["dc.format.extent","S20"],["dc.identifier.isi","000375417500034"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40899"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Role of sodium channel Nav1.8 for arrhythmogenesis in the human failing heart"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","35"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","46"],["dc.bibliographiccitation.volume","144"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Trum, Maximilian"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:25:53Z"],["dc.date.available","2021-04-14T08:25:53Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.yjmcc.2020.05.002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81759"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0022-2828"],["dc.title","Contribution of the neuronal sodium channel NaV1.8 to sodium- and calcium-dependent cellular proarrhythmia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]