Schnelle, Moritz Thomas

[["dc.bibliographiccitation.artnumber","149"],["dc.bibliographiccitation.journal","Journal of Translational Medicine"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Qasim, Mohamed"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2017-09-07T11:44:53Z"],["dc.date.available","2017-09-07T11:44:53Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Hemodynamic load leads to cardiac hypertrophy and heart failure. While afterload (pressure overload) induces concentric hypertrophy, elevation of preload (volume overload) yields eccentric hypertrophy and is associated with a better outcome. Here we analysed the proteomic pattern of mice subjected to short-term preload. Methods and Results: Female FVB/N mice were subjected to aortocaval shunt-induced volume overload that leads to an eccentric hypertrophy (left ventricular weight/tibia length +31 %) with sustained systolic heart function at 1 week after operation. Two-dimensional gel electrophoresis (2-DE) followed by mass spectrometric analysis showed alteration in the expression of 25 protein spots representing 21 different proteins. 64 % of these protein spots were up-regulated and 36 % of the protein spots were consistently down-regulated. Interestingly, alpha-1-antitrypsin was down-regulated, indicating higher elastin degradation and possibly contributing to the early dilatation. In addition to contractile and mitochondrial proteins, polymerase I and transcript release factor protein (PTRF) was also up-regulated, possibly contributing to the preload-induced signal transduction. Conclusions: Our findings reveal the proteomic changes of early-stage eccentric myocardial remodeling after volume overload. Induced expression of some of the respiratory chain enzymes suggests a metabolic shift towards an oxidative phosphorylation that might contribute to the favorable remodeling seen in early VO. Down-regulation of alpha-1-antitrypsin might contribute to extracellular matrix remodeling and left ventricular dilatation. We also identified PTRF as a potential signaling regulator of volume overload-induced cardiac hypertrophy."],["dc.identifier.doi","10.1186/s12967-016-0898-5"],["dc.identifier.gro","3141681"],["dc.identifier.isi","000377182700001"],["dc.identifier.pmid","27234427"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8784"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation [SFB1002]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1479-5876"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Proteomic analysis of short-term preload-induced eccentric cardiac hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","H422"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal of Physiology-Heart and Circulatory Physiology"],["dc.bibliographiccitation.lastpage","H431"],["dc.bibliographiccitation.volume","319"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Chong, Mei"],["dc.contributor.author","Zoccarato, Anna"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Sawyer, Greta Jane"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Ludwig, Christian"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-04-14T08:24:01Z"],["dc.date.available","2021-04-14T08:24:01Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1152/ajpheart.00219.2020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81138"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1522-1539"],["dc.relation.issn","0363-6135"],["dc.title","In vivo [U- 13 C]glucose labeling to assess heart metabolism in murine models of pressure and volume overload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","ejhf.2291"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.contributor.author","Kresoja, Karl‐Patrik"],["dc.contributor.author","Rommel, Karl‐Philipp"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Henger, Sylvia"],["dc.contributor.author","Besler, Christian"],["dc.contributor.author","Klöting, Nora"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Hoffmann, Anne"],["dc.contributor.author","Büttner, Petra"],["dc.contributor.author","Lurz, Philipp"],["dc.date.accessioned","2021-08-12T07:44:58Z"],["dc.date.available","2021-08-12T07:44:58Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ejhf.2291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88340"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Proteomics to improve phenotyping in obese patients with heart failure with preserved ejection fraction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","9889"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Buchholz, Eric"],["dc.contributor.author","Koszewa, Sabrina"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2019-08-06T11:25:13Z"],["dc.date.available","2019-08-06T11:25:13Z"],["dc.date.issued","2019"],["dc.description.abstract","Calcium/calmodulin-dependent protein kinase type II delta (CaMKIIδ), the predominant CaMKII isoform expressed in the heart, has been implicated in the progression of myocardial infarction- and pressure overload-induced pathological remodeling. However, the role of CaMKIIδ in volume overload (VO) has not been explored. We have previously reported an activation of CaMKII during transition to HF in long-term VO. Here, we address whether CaMKIIδ is critically involved in the mortality, myocardial remodeling, and heart failure (HF) progression in response to VO. CaMKIIδ knockout (δ-KO) and wild-type (WT) littermates were exposed to aortocaval shunt-induced VO, and the progression of adverse myocardial remodeling was assessed by serial echocardiography, histological and molecular analyses. The mortality rates during 10 weeks of VO were similar in δ-KO and WT mice. Both genotypes displayed comparable eccentric myocardial hypertrophy, altered left ventricle geometry, perturbed systolic and diastolic functions after shunt. Additionally, cardiomyocytes hypertrophy, augmented myocyte apoptosis, and up-regulation of hypertrophic genes were also not significantly different in δ-KO versus WT hearts after shunt. Therefore, CaMKIIδ signaling seems to be dispensable for the progression of VO-induced maladaptive cardiac remodeling. Accordingly, we hypothesize that CaMKIIδ-inhibition as a therapeutic approach might not be helpful in the context of VO-triggered HF."],["dc.identifier.doi","10.1038/s41598-019-46332-3"],["dc.identifier.pmid","31285482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62306"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/281"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","2045-2322"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genetic deletion of calcium/calmodulin-dependent protein kinase type II delta does not mitigate adverse myocardial remodeling in volume-overloaded hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e207"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Clinical Chemistry and Laboratory Medicine"],["dc.bibliographiccitation.lastpage","e210"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Eidizadeh, Abass"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Schnelle, Moritz"],["dc.date.accessioned","2020-12-10T18:42:19Z"],["dc.date.available","2020-12-10T18:42:19Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1515/cclm-2018-0916"],["dc.identifier.eissn","1437-4331"],["dc.identifier.issn","1434-6621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77889"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Differences in procalcitonin measurements between three BRAHMS-partnered immunoassays (Liaison, Elecsys and Architect)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33756"],["dc.bibliographiccitation.issue","44"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","33763"],["dc.bibliographiccitation.volume","285"],["dc.contributor.author","Vogel, Sabine"],["dc.contributor.author","Wottawa, Marieke"],["dc.contributor.author","Farhat, Katja"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Le-Huu, Sinja"],["dc.contributor.author","von Ahlen, Melanie"],["dc.contributor.author","Malz, Cordula R."],["dc.contributor.author","Camenisch, Gieri"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.date.accessioned","2018-11-07T08:37:53Z"],["dc.date.available","2018-11-07T08:37:53Z"],["dc.date.issued","2010"],["dc.description.abstract","Cells are responding to hypoxia via prolyl-4-hydroxylase domain (PHD) enzymes, which are responsible for oxygen-dependent hydroxylation of the hypoxia-inducible factor (HIF)-1 alpha subunit. To gain further insight into PHD function, we generated knockdown cell models for the PHD2 isoform, which is the main isoform regulating HIF-1 alpha hydroxylation and thus stability in normoxia. Induction of a PHD2 knockdown in tetracycline-inducible HeLa PHD2 knockdown cells resulted in increased F-actin formation as detected by phalloidin staining. A similar effect could be observed in the stably transfected PHD2 knockdown cell clones 1B6 and 3B7. F-actin is at least in part responsible for shaping cell morphology as well as regulating cell migration. Cell migration was impaired significantly as a consequence of PHD2 knockdown in a scratch assay. Mechanistically, PHD2 knockdown resulted in activation of the RhoA (Ras homolog gene family member A)/Rho-associated kinase pathway with subsequent phosphorylation of cofilin. Because cofilin phosphorylation impairs its actin-severing function, this may explain the F-actin phenotype, thereby providing a functional link between PHD2-dependent signaling and cell motility."],["dc.identifier.doi","10.1074/jbc.M110.132985"],["dc.identifier.isi","000283354000021"],["dc.identifier.pmid","20801873"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6193"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18648"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","0021-9258"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Prolyl Hydroxylase Domain (PHD) 2 Affects Cell Migration and F-actin Formation via RhoA/Rho-associated Kinase-dependent Cofilin Phosphorylation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2163"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","2177"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Zhang, Juqian"],["dc.contributor.author","Murdoch, Colin E."],["dc.contributor.author","Kossmann, Sabine"],["dc.contributor.author","Protti, Andrea"],["dc.contributor.author","Santos, Celio X.C."],["dc.contributor.author","Sawyer, Greta"],["dc.contributor.author","Zhang, Xiaohong"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-06-01T10:47:48Z"],["dc.date.available","2021-06-01T10:47:48Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.116.023877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85725"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Distinct Regulatory Effects of Myeloid Cell and Endothelial Cell NAPDH Oxidase 2 on Blood Pressure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2090"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","2091"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-06-01T10:47:49Z"],["dc.date.available","2021-06-01T10:47:49Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.117.030515"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85728"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Response by Sag et al to Letter Regarding Article, “Distinct Regulatory Effects of Myeloid Cell and Endothelial Cell NAPDH Oxidase 2 on Blood Pressure”"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102099"],["dc.bibliographiccitation.journal","Algal Research"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Abreu, Ilka N."],["dc.contributor.author","Aksmann, Anna"],["dc.contributor.author","Bajhaiya, Amit K."],["dc.contributor.author","Benlloch, Reyes"],["dc.contributor.author","Giordano, Mario"],["dc.contributor.author","Pokora, Wojciech"],["dc.contributor.author","Selstam, Eva"],["dc.contributor.author","Moritz, Thomas"],["dc.date.accessioned","2021-04-14T08:30:16Z"],["dc.date.available","2021-04-14T08:30:16Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.algal.2020.102099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83169"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","2211-9264"],["dc.title","Changes in lipid and carotenoid metabolism in Chlamydomonas reinhardtii during induction of CO2-concentrating mechanism: Cellular response to low CO2 stress"],["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"]]