Fischer, Andreas

[["dc.bibliographiccitation.firstpage","3086"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Jarausch, Johannes; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Neuenroth, Lisa; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Andag, Reiner; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Leha, Andreas; 3Department of Medical Statistics, University Medical Center Goettingen, Humboldtallee 32, 37073 Goettingen, Germany"],["dc.contributor.affiliation","Fischer, Andreas; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Asif, Abdul R.; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Lenz, Christof; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Eidizadeh, Abass; 1Department of Clinical Chemistry and Interdisciplinary UMG Laboratory, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany"],["dc.contributor.author","Jarausch, Johannes"],["dc.contributor.author","Neuenroth, Lisa"],["dc.contributor.author","Andag, Reiner"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Fischer, Andreas"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Eidizadeh, Abass"],["dc.contributor.editor","Zhou, Changcheng"],["dc.contributor.editor","Chen, Hong"],["dc.date.accessioned","2022-11-01T10:17:24Z"],["dc.date.available","2022-11-01T10:17:24Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:33Z"],["dc.description.abstract","Atherosclerosis is an important risk factor in the development of cardiovascular diseases. In addition to increased plasma lipid concentrations, irregular/oscillatory shear stress and inflammatory processes trigger atherosclerosis. Inhibitors of the transcription modulatory bromo- and extra-terminal domain (BET) protein family (BETi) could offer a possible therapeutic approach due to their epigenetic mechanism and anti-inflammatory properties. In this study, the influence of laminar shear stress, inflammation and BETi treatment on human endothelial cells was investigated using global protein expression profiling by ion mobility separation-enhanced data independent acquisition mass spectrometry (IMS-DIA-MS). For this purpose, primary human umbilical cord derived vascular endothelial cells were treated with TNFα to mimic inflammation and exposed to laminar shear stress in the presence or absence of the BRD4 inhibitor JQ1. IMS-DIA-MS detected over 4037 proteins expressed in endothelial cells. Inflammation, shear stress and BETi led to pronounced changes in protein expression patterns with JQ1 having the greatest effect. To our knowledge, this is the first proteomics study on primary endothelial cells, which provides an extensive database for the effects of shear stress, inflammation and BETi on the endothelial proteome."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/cells11193086"],["dc.identifier.pii","cells11193086"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116800"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-605"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","CC BY 4.0"],["dc.title","Influence of Shear Stress, Inflammation and BRD4 Inhibition on Human Endothelial Cells: A Holistic Proteomic Approach"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2239"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Viruses"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Dierks, Sascha; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Thiele, Karin; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Bohne, Wolfgang; 2Interdisciplinary UMG Laboratory, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Lugert, Raimond; 2Interdisciplinary UMG Laboratory, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Weig, Michael; 2Interdisciplinary UMG Laboratory, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Groß, Uwe; 2Interdisciplinary UMG Laboratory, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","von Ahsen, Nicolas; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Schanz, Julie; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Fischer, Andreas; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.affiliation","Schnelle, Moritz; 1Department of Clinical Chemistry, University Medical Center Göttingen, 37075 Göttingen, Germany"],["dc.contributor.author","Dierks, Sascha"],["dc.contributor.author","Thiele, Karin"],["dc.contributor.author","Bohne, Wolfgang"],["dc.contributor.author","Lugert, Raimond"],["dc.contributor.author","Weig, Michael"],["dc.contributor.author","Groß, Uwe"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Schanz, Julie"],["dc.contributor.author","Fischer, Andreas"],["dc.contributor.author","Schnelle, Moritz"],["dc.date.accessioned","2022-12-01T08:31:48Z"],["dc.date.available","2022-12-01T08:31:48Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:11:59Z"],["dc.description.abstract","In SARS-CoV-2 diagnostics, cycle threshold (Ct) values from qRT-PCRs semi-quantitatively estimate a patient’s viral load. However, relevant analytical differences between qRT-PCR assays are often neglected. This study was designed (i) to identify such differences between five commonly used assays and (ii) to demonstrate a straightforward strategy to harmonize them. QRT-PCRs for SARS-CoV-2 were carried out in 85 oropharyngeal swab samples using three fully automated (Alinity m, cobas®6800 and GeneXpert) and two semi-automated (genesig® and RIDA®GENE) assays. Qualitative results (positive/negative) showed excellent comparability between the fully automated assays, but not between the Alinity m and semi-automated methods. Ct values significantly varied between all the methods, with the median values ranging from 22.76 (Alinity m) to 30.89 (RIDA®GENE) and 31.50 (genesig®), indicating the lowest sensitivity for semi-automated methods. Passing–Bablok analysis further revealed systemic biases. Assay-specific viral load concentration calculations—based on generated individual standard curves—resulted in much better comparability between the assays. Applying these calculations, significant differences were no longer detectable. This study highlights relevant analytical differences between SARS-CoV-2 qRT-PCR assays, leading to divergent decisions about the mandatory isolation of infected individuals. Secondly, we propose a strategy to harmonize qRT-PCR assays to achieve better comparability. Our findings are of particular interest for laboratories utilizing different assays."],["dc.description.sponsorship","VolkswagenStiftung"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/v14102239"],["dc.identifier.pii","v14102239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118269"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1999-4915"],["dc.rights","CC BY 4.0"],["dc.title","Comparison and Harmonization of Different Semi-Automated and Automated qRT-PCR Assays in the Assessment of SARS-CoV-2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","unpublished"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7453"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Molecules"],["dc.bibliographiccitation.volume","27"],["dc.contributor.affiliation","Shahid, Sidra; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Pantakani, Marlena; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Binder, Lutz; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Fischer, Andreas; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Pantakani, Krishna; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Asif, Abdul R.; 1Institute for Clinical Chemistry, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.author","Shahid, Sidra"],["dc.contributor.author","Pantakani, Marlena"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Fischer, Andreas"],["dc.contributor.author","Pantakani, Krishna"],["dc.contributor.author","Asif, Abdul R."],["dc.date.accessioned","2022-12-07T15:55:02Z"],["dc.date.available","2022-12-07T15:55:02Z"],["dc.date.issued","2022-11-02"],["dc.date.updated","2022-12-07T14:41:11Z"],["dc.description.abstract","NF-κB signaling is a key regulator of inflammation and atherosclerosis. NF-κB cooperates with bromodomain-containing protein 4 (BRD4), a transcriptional and epigenetic regulator, in endothelial inflammation. This study aimed to investigate whether BRD4 inhibition would prevent the proinflammatory response towards TNF-α in endothelial cells. We used TNF-α treatment of human umbilical cord-derived vascular endothelial cells to create an in vitro inflammatory model system. Two small molecule inhibitors of BRD4—namely, RVX208 (Apabetalone), which is in clinical trials for the treatment of atherosclerosis, and JQ1—were used to analyze the effect of BRD4 inhibition on endothelial inflammation and barrier integrity. BRD4 inhibition reduced the expression of proinflammatory markers such as SELE, VCAM-I, and IL6 in endothelial cells and prevented TNF-α-induced endothelial tight junction hyperpermeability. Endothelial inflammation was associated with increased expression of the heparin-binding growth factor midkine. BRD4 inhibition reduced midkine expression and normalized endothelial permeability upon TNF-α treatment. In conclusion, we identified that TNF-α increased midkine expression and compromised tight junction integrity in endothelial cells, which was preventable by pharmacological BRD4 inhibition."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG)"],["dc.description.sponsorship","Volkswagen Stiftung"],["dc.description.sponsorship","Göttingen University"],["dc.identifier.doi","10.3390/molecules27217453"],["dc.identifier.pii","molecules27217453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118485"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1420-3049"],["dc.rights","CC BY 4.0"],["dc.title","Small Molecule BRD4 Inhibitors Apabetalone and JQ1 Rescues Endothelial Cells Dysfunction, Protects Monolayer Integrity and Reduces Midkine Expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]