Hasenfuß, Gerd P.

[["dc.bibliographiccitation.artnumber","P4479"],["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","suppl_1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Iyer, L. M."],["dc.contributor.author","Noack, C."],["dc.contributor.author","Nagarajan, S."],["dc.contributor.author","Woelfer, M."],["dc.contributor.author","Schoger, E."],["dc.contributor.author","Pang, S. T."],["dc.contributor.author","Kari, V."],["dc.contributor.author","Zafeiriou, M. P."],["dc.contributor.author","Toischer, K."],["dc.contributor.author","Hasenfuss, G."],["dc.contributor.author","Johnsen, S. A."],["dc.contributor.author","Zelarayan, L. C."],["dc.date.accessioned","2019-02-19T13:47:43Z"],["dc.date.available","2019-02-19T13:47:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/eurheartj/ehx504.P4479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57586"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/177"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.issn","0195-668X"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","B-catenin/TCF7L2 signaling orchestrates initiation of pathological hypertrophic cardiac remodeling by inducing chromatin modifications"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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","1363"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","1369"],["dc.bibliographiccitation.volume","586"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Kochhaeuser, Simon"],["dc.contributor.author","Phuc Nguyen Van, Phuc Nguyen Van"],["dc.contributor.author","Leineweber, Kirsten"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Koegler, Harald"],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Proteins are folded in the endoplasmic reticulum (ER). ER stress initially leads to compensatory upregulation of ER chaperones and later to apoptosis, but the contribution of biomechanical load vs. neurohumoral stress to myocardial ER stress is unknown. We show that the ER chaperones Grp78 and calreticulin (CRT) are upregulated by afterload, but not by preload in vitro and in vivo. Angiotensin II upregulated ER chaperones in unloaded muscle strips, but the angiotensin receptor-1 antagonist irbesartan did not significantly blunt the induction of ER chaperones by afterload. In monocrotaline-treated rats, Grp78 and CRT were upregulated in the afterloaded right ventricle, but not in the only neurohumorally stressed left ventricle. These findings suggest that afterload but not preload induces myocardial ER stress, largely independent of angiotensin II signaling. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved."],["dc.identifier.doi","10.1016/j.febslet.2012.03.055"],["dc.identifier.gro","3142537"],["dc.identifier.isi","000303434200018"],["dc.identifier.pmid","22504142"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8899"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0014-5793"],["dc.title","Mechanical load-dependent cardiac ER stress in vitro and in vivo: Effects of preload and afterload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","S1"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Zelarayan, Laura"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Regitz‐Zagrosek, Vera"],["dc.date.accessioned","2021-12-08T12:27:38Z"],["dc.date.available","2021-12-08T12:27:38Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1096/fasebj.29.1_supplement.966.1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95409"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","In C57Bl/6N Female Mice 17β‐Estradiol Leads to Cardiac Mass and Function Loss via a β‐Catenin Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","528"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Aims The calcineurin and nuclear factor of activated T cells (NFAT) pathway can mediate pro-hypertrophic signalling in the heart. Recently, it has been shown that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) phosphorylates NFAT, which limits calcineurin/NFAT signal transduction in T cells and hypertrophy in cultured cardiomyocytes. The hypothesis tested in this study was that DYRK1A prevents calcineurin/NFAT-mediated cardiac hypertrophy in vivo. Methods and results In cultured rat cardiomyocytes, adenovirus-mediated overexpression of DYRK1A antagonized calcineurin-mediated nuclear NFAT translocation and the phenylephrine-induced hypertrophic growth response. To test the ability of DYRK1A to reduce hypertrophic cardiac growth in vivo, we created tetracycline-repressible Dyrk1a transgenic mice to avoid the cardiac developmental defects associated with embryonic DYRK1A expression. However, in the mouse model, histological determination of myocyte diameter, heart weight/body weight ratio, and echocardiographic measurements revealed that myocardial expression of DYRK1A failed to reduce hypertrophy induced via aortic banding or co-expression of calcineurin. This discrepancy is explained, at least in part, by insufficient long-term inhibition of NFAT and the activation of DYRK1A-resistant maladaptive genes in vivo. Conclusion Isolated augmentation of DYRK1A can be compensated for in vivo, and this may significantly limit anti-hypertrophic interventions aimed at enhancing DYRK1A activity."],["dc.identifier.doi","10.1093/cvr/cvr023"],["dc.identifier.gro","3142722"],["dc.identifier.isi","000290820200018"],["dc.identifier.pmid","21273244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/157"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","744"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T08:52:46Z"],["dc.date.available","2018-11-07T08:52:46Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1093/cvr/cvr193"],["dc.identifier.isi","000294069300024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22252"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Letter concerning: 'Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo': reply"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Open Journal of Bioresources"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Beuthner, Bo E. C."],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Derks, Mareike"],["dc.contributor.author","Franke, Thomas"],["dc.contributor.author","Seelke, Sandra"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Nußbeck, Sara Y."],["dc.date.accessioned","2020-06-16T13:21:23Z"],["dc.date.available","2020-06-16T13:21:23Z"],["dc.date.issued","2020"],["dc.description.abstract","The bioresource (>265 patients with >27,600 biospecimens until December 2019; recruitment ongoing) on severe aortic stenosis is of vital importance to improve the still incomplete understanding of its etiology as well as its transition to heart failure. The bioresource contains various biospecimens, standardised clinical and imaging data sets including transthoracic echocardiography, computed tomography and magnetic resonance imaging of the heart. Biospecimen sampling follows the SOP-driven collection scheme of the German Center for Cardiovascular Research (DZHK) for venous blood and urine [1]. In addition, left-ventricular endomyocardial biopsies, rectal swabs and skin biopsies (for subsequent generation of induced pluripotent stem cells) are collected. Data management includes the use of a professional biospecimen management system as well as a Picture Archiving and Communication System (PACS) for imaging data. A Good Clinical Practice (GCP)-conform software for the management of clinical data and a trusted third party for the management of patient identifying data and pseudonyms are in place. Given these conditions, there is a high reuse-potential for biospecimens and data."],["dc.identifier.doi","10.5334/ojb.65"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66366"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/340"],["dc.language.iso","en"],["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 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.issn","2056-5542"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nußbeck"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 3.0"],["dc.title","Interdisciplinary Research on Aortic Valve Stenosis: A Longitudinal Collection of Biospecimens and Clinical Data of Patients Undergoing Transcatheter Aortic Valve Replacement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Comelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:09:54Z"],["dc.date.available","2018-11-07T11:09:54Z"],["dc.date.issued","2008"],["dc.format.extent","S394"],["dc.identifier.isi","000262104500562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53103"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A is a NFAT Kinase Mediating Negative Feedback on Calcineurin/NFAT Signaling."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.date.accessioned","2018-11-07T09:57:25Z"],["dc.date.available","2018-11-07T09:57:25Z"],["dc.date.issued","2015"],["dc.format.extent","247"],["dc.identifier.isi","000366200402401"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37151"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Loss of cardiac mass and function induced by 17beta-oestradiol via a beta-catenin mechanism in C57Bl/6N female mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3970"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Evertz, Ruben"],["dc.contributor.author","Hub, Sebastian"],["dc.contributor.author","Backhaus, Sören J."],["dc.contributor.author","Lange, Torben"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Kowallick, Johannes T."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.editor","Santarpino, Giuseppe"],["dc.date.accessioned","2021-10-01T09:58:14Z"],["dc.date.available","2021-10-01T09:58:14Z"],["dc.date.issued","2021"],["dc.description.abstract","Aortic valve calcification (AVC) in aortic stenosis patients has diagnostic and prognostic implications. Little is known about the interchangeability of AVC obtained from different multidetector computed tomography (MDCT) software solutions. Contrast-enhanced MDCT data sets of 50 randomly selected aortic stenosis patients were analysed using three different software vendors (3Mensio, CVI42, Syngo.Via). A subset of 10 patients were analysed twice for the estimation of intra-observer variability. Intra- and inter-observer variability were determined using the ICC reliability method, Bland-Altman analysis and coefficients of variation. No differences were revealed between the software solutions in the AVC calculations (3Mensio 941 ± 623, Syngo.Via 948 mm3 ± 655, CVI42 941 ± 637; p = 0.455). The best inter-vendor agreement was found between the CVI42 and the Syngo.Via (ICC 0.997 (CI 0.995–0.998)), followed by the 3Mensio and the CVI42 (ICC 0.996 (CI 0.922–0.998)), and the 3Mensio and the Syngo.Via (ICC 0.992 (CI 0.986–0.995)). There was excellent intra- (3Mensio: ICC 0.999 (0.995–1.000); CVI42: ICC 1.000 (0.999–1.000); Syngo.Via: ICC 0.998 (0.993–1.000)) and inter-observer variability (3Mensio: ICC 1.000 (0.999–1.000); CVI42: ICC 1.000 (1.000–1.000); Syngo.Via: ICC 0.996 (0.985–0.999)) for all software types. Contrast-enhanced MDCT-derived AVC scores are interchangeable between and reproducible within different commercially available software solutions. This is important since sufficient reproducibility, interchangeability and valid results represent prerequisites for accurate TAVR planning and its widespread clinical use."],["dc.description.abstract","Aortic valve calcification (AVC) in aortic stenosis patients has diagnostic and prognostic implications. Little is known about the interchangeability of AVC obtained from different multidetector computed tomography (MDCT) software solutions. Contrast-enhanced MDCT data sets of 50 randomly selected aortic stenosis patients were analysed using three different software vendors (3Mensio, CVI42, Syngo.Via). A subset of 10 patients were analysed twice for the estimation of intra-observer variability. Intra- and inter-observer variability were determined using the ICC reliability method, Bland-Altman analysis and coefficients of variation. No differences were revealed between the software solutions in the AVC calculations (3Mensio 941 ± 623, Syngo.Via 948 mm3 ± 655, CVI42 941 ± 637; p = 0.455). The best inter-vendor agreement was found between the CVI42 and the Syngo.Via (ICC 0.997 (CI 0.995–0.998)), followed by the 3Mensio and the CVI42 (ICC 0.996 (CI 0.922–0.998)), and the 3Mensio and the Syngo.Via (ICC 0.992 (CI 0.986–0.995)). There was excellent intra- (3Mensio: ICC 0.999 (0.995–1.000); CVI42: ICC 1.000 (0.999–1.000); Syngo.Via: ICC 0.998 (0.993–1.000)) and inter-observer variability (3Mensio: ICC 1.000 (0.999–1.000); CVI42: ICC 1.000 (1.000–1.000); Syngo.Via: ICC 0.996 (0.985–0.999)) for all software types. Contrast-enhanced MDCT-derived AVC scores are interchangeable between and reproducible within different commercially available software solutions. This is important since sufficient reproducibility, interchangeability and valid results represent prerequisites for accurate TAVR planning and its widespread clinical use."],["dc.identifier.doi","10.3390/jcm10173970"],["dc.identifier.pii","jcm10173970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90018"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.title","Head-to-Head Comparison of Different Software Solutions for AVC Quantification Using Contrast-Enhanced MDCT"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]