Wagner, Stefan

[["dc.bibliographiccitation.artnumber","012009"],["dc.bibliographiccitation.seriesnr","25"],["dc.contributor.author","Sauer, Daniela"],["dc.contributor.author","Schülli-Maurer, Isabelle"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Scarciglia, Fabio"],["dc.contributor.author","Sperstad, Ragnhild"],["dc.contributor.author","Svendgård-Stokke, S."],["dc.contributor.author","Sørensen, Rolf"],["dc.contributor.author","Schellmann, Gerhard"],["dc.date.accessioned","2017-09-07T11:48:01Z"],["dc.date.available","2017-09-07T11:48:01Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1088/1755-1315/25/1/012009"],["dc.identifier.gro","3149443"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6117"],["dc.notes.intern","Sauer Crossref Import"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.publisher","IOP Publishing"],["dc.publisher.place","Bristol"],["dc.relation.conference","Soil Change Matters 2014"],["dc.relation.crisseries","IOP Conference Series. Earth and Environmental Science"],["dc.relation.eventend","2014-03-27"],["dc.relation.eventlocation","Bendigo, Victoria, Australia"],["dc.relation.eventstart","2014-03-24"],["dc.relation.ispartof","Soil Change Matters 2014"],["dc.relation.ispartofseries","IOP conference series: Earth and environmental science; 25"],["dc.title","Soil development over millennial timescales - a comparison of soil chronosequences of different climates and lithologies"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1134"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Kensah, George"],["dc.contributor.author","Lara, Angelica Roa"],["dc.contributor.author","Dahlmann, Julia"],["dc.contributor.author","Zweigerdt, Robert"],["dc.contributor.author","Schwanke, Kristin"],["dc.contributor.author","Hegermann, Jan"],["dc.contributor.author","Skvorc, David"],["dc.contributor.author","Gawol, Anke"],["dc.contributor.author","Azizian, Azadeh"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Krause, Andreas"],["dc.contributor.author","Draeger, Gerald"],["dc.contributor.author","Ochs, Matthias"],["dc.contributor.author","Haverich, Axel"],["dc.contributor.author","Gruh, Ina"],["dc.contributor.author","Martin, Ulrich"],["dc.date.accessioned","2018-11-07T09:26:20Z"],["dc.date.available","2018-11-07T09:26:20Z"],["dc.date.issued","2013"],["dc.description.abstract","We explored the use of highly purified murine and human pluripotent stem cell (PSC)-derived cardiomyocytes (CMs) to generate functional bioartificial cardiac tissue (BCT) and investigated the role of fibroblasts, ascorbic acid (AA), and mechanical stimuli on tissue formation, maturation, and functionality. Murine and human embryonic/induced PSC-derived CMs were genetically enriched to generate three-dimensional CM aggregates, termed cardiac bodies (CBs). Addressing the critical limitation of major CM loss after single-cell dissociation, non-dissociated CBs were used for BCT generation, which resulted in a structurally and functionally homogenous syncytium. Continuous in situ characterization of BCTs, for 21 days, revealed that three critical factors cooperatively improve BCT formation and function: both (i) addition of fibroblasts and (ii) ascorbic acid supplementation support extracellular matrix remodelling and CB fusion, and (iii) increasing static stretch supports sarcomere alignment and CM coupling. All factors together considerably enhanced the contractility of murine and human BCTs, leading to a so far unparalleled active tension of 4.4 mN/mm(2) in human BCTs using optimized conditions. Finally, advanced protocols were implemented for the generation of human PSC-derived cardiac tissue using a defined animal-free matrix composition. BCT with contractile forces comparable with native myocardium can be generated from enriched, PSC-derived CMs, based on a novel concept of tissue formation from non-dissociated cardiac cell aggregates. In combination with the successful generation of tissue using a defined animal-free matrix, this represents a major step towards clinical applicability of stem cell-based heart tissue for myocardial repair."],["dc.identifier.doi","10.1093/eurheartj/ehs349"],["dc.identifier.isi","000318077500012"],["dc.identifier.pmid","23103664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30278"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0195-668X"],["dc.title","Murine and human pluripotent stem cell-derived cardiac bodies form contractile myocardial tissue in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Human Gene Therapy"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Schwanke, Kristin"],["dc.contributor.author","Haase, Alexandra"],["dc.contributor.author","Olmer, Ruth"],["dc.contributor.author","Wunderlich, Stephanie"],["dc.contributor.author","Merkert, Sylvia"],["dc.contributor.author","Gruh, Ina"],["dc.contributor.author","Zweigerdt, Robert"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Martin, Ulrich"],["dc.date.accessioned","2018-11-07T11:22:43Z"],["dc.date.available","2018-11-07T11:22:43Z"],["dc.date.issued","2009"],["dc.format.extent","1459"],["dc.identifier.isi","000271441000317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56036"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc"],["dc.publisher.place","New rochelle"],["dc.relation.conference","Combined Meeting of the 17th European-Society-of-Gene-and-Cell-Therapy/16th German-Society-for-Gene-Therapy/4th German-Society-for-Stem-Cell-Research"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1043-0342"],["dc.title","Differentiation of human cord blood-derived induced pluripotent stem (iPS) cells into functional cardiomyocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3835"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.lastpage","3847"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Grandi, Eleonora"],["dc.contributor.author","Puglisi, Jose L."],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Severi, Stefano"],["dc.contributor.author","Bers, Donald M."],["dc.date.accessioned","2018-11-07T10:46:35Z"],["dc.date.available","2018-11-07T10:46:35Z"],["dc.date.issued","2007"],["dc.description.abstract","Ca-calmodulin- dependent protein kinase II ( CaMKII) was recently shown to alter Na+ channel gating and recapitulate a human Na+ channel genetic mutation that causes an unusual combined arrhythmogenic phenotype in patients: simultaneous long QT syndrome and Brugada syndrome. CaMKII is upregulated in heart failure where arrhythmias are common, and CaMKII inhibition can reduce arrhythmias. Thus, CaMKII- dependent channel modulation may contribute to acquired arrhythmic disease. We developed a Markovian Na+ channel model including CaMKII- dependent changes, and incorporated it into a comprehensive myocyte action potential ( AP) model with Na+ and Ca2+ transport. CaMKII shifts Na+ current (I-Na) availability to more negative voltage, enhances intermediate inactivation, and slows recovery from inactivation ( all loss- of- function effects), but also enhances late noninactivating I-Na ( gain of function). At slow heart rates, with long diastolic time for I-Na recovery, late I-Na is the predominant effect, leading to AP prolongation ( long QT syndrome). At fast heart rates, where recovery time is limited and APs are shorter, there is little effect on AP duration, but reduced availability decreases I-Na, AP upstroke velocity, and conduction ( Brugada syndrome). CaMKII also increases cardiac Ca2+ and K+ currents ( I-Ca and I-to), complicating CaMKII- dependent AP changes. Incorporating I-Ca and I-to effects individually prolongs and shortens AP duration. Combining I-Na, I-Ca, and I-to effects results in shortening of AP duration with CaMKII. With transmural heterogeneity of I-to and I-to downregulation in heart failure, CaMKII may accentuate dispersion of repolarization. This provides a useful initial framework to consider pathways by which CaMKII may contribute to arrhythmogenesis."],["dc.identifier.doi","10.1529/biophysj.107.114868"],["dc.identifier.isi","000250951900016"],["dc.identifier.pmid","17704163"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47779"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Soc"],["dc.relation.issn","0006-3495"],["dc.title","Simulation of Ca-calmodulin-dependent protein kinase II on rabbit ventricular myocyte ion currents and action potentials"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Wagemann, Olivia"],["dc.contributor.author","Lücht, Charlotte M."],["dc.contributor.author","Trum, Maximilian"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Tarnowski, Daniel"],["dc.contributor.author","Reinders, Jörg"],["dc.contributor.author","Perbellini, Filippo"],["dc.contributor.author","Terracciano, Cesare"],["dc.contributor.author","Schmid, Christof"],["dc.contributor.author","Schopka, Simon"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Zausig, York"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.12336"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69797"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Empagliflozin reduces Ca/calmodulin-dependent kinase II activity in isolated ventricular cardiomyocytes"],["dc.title.alternative","Empagliflozin reduces CaMKII activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","123"],["dc.bibliographiccitation.journal","JOURNAL OF NANO RESEARCH"],["dc.bibliographiccitation.lastpage","133"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Cizek, Jakub"],["dc.contributor.author","Melikhova, Oksana"],["dc.contributor.author","Vlcek, Marian"],["dc.contributor.author","Lukac, Frantisek"],["dc.contributor.author","Vlach, Martin"],["dc.contributor.author","Dobron, Patrik"],["dc.contributor.author","Prochazka, Ivan"],["dc.contributor.author","Anwand, Wolfgang"],["dc.contributor.author","Brauer, Gerhard"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Uchida, Helmut"],["dc.contributor.author","Gemma, Ryota"],["dc.contributor.author","Pundt, Astrid"],["dc.date.accessioned","2018-11-07T09:46:42Z"],["dc.date.available","2018-11-07T09:46:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Hydrogen interaction with defects and structural development of Pd films with various microstructures were investigated. Nanocrystalline, polycrystalline and epitaxial Pd films were prepared and electrochemically loaded with hydrogen. Structural changes of Pd films caused by absorbed hydrogen were studied by in-situ X-ray diffraction combined with acoustic emission and measurement of electromotorical force. Development of defects during hydrogen loading was investigated by positron annihilation spectroscopy. It was found that hydrogen firstly fills open volume defects existing already in the films and subsequently it occupies also interstitial sites in Pd lattice. Absorbed hydrogen causes volume expansion, which is strongly anisotropic in thin films. This introduces high stress into the films loaded with hydrogen. Acoustic emission measurements revealed that when hydrogen-induced stress achieves a certain critical level rearrangement of misfit dislocations takes place. The stress which grows with increasing hydrogen concentration can be further released by plastic deformation and also by detachment of the film from the substrate."],["dc.identifier.doi","10.4028/www.scientific.net/JNanoR.26.123"],["dc.identifier.isi","000330816600018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34943"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Trans Tech Publications Ltd"],["dc.relation.issn","1661-9897"],["dc.relation.issn","1662-5250"],["dc.title","Hydrogen Interaction with Defects in Nanocrystalline, Polycrystalline and Epitaxial Pd Films"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Rasenack, Eva C. L."],["dc.contributor.author","Ruff, Hanna"],["dc.contributor.author","Weber, Sarah L."],["dc.contributor.author","Schoendube, Friedrich A."],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Tenderich, Gero"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Belardinelli, Luiz"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:48:16Z"],["dc.date.available","2017-09-07T11:48:16Z"],["dc.date.issued","2008"],["dc.description.abstract","The goal of this study was to test the hypothesis that the novel anti-ischemic drug ratiolazine, which is known to inhibit late I-Na, could reduce intracellular [Na+](i) and diastolic [Ca2+](i) overload and improve diastolic function. Contractile dysfunction in human heart failure (HF) is associated with increased [Na+](i) and elevated diastolic [Ca2+](i). Increased Na influx through voltage-gated Na+ channels (late I-Na) has been suggested to contribute to elevated [Na+](i) in HF. In isometrically contracting ventricular muscle strips from end-stage failing human hearts, ranolazine (10 mu mol/L) did not exert negative inotropic effects on twitch force amplitude. However, ranolazine significantly reduced frequency-dependent increase in diastolic tension (i.e., diastolic dysfunction) by similar to 30% without significantly affecting sarcoplasmic reticulum (SR) Ca2+ loading. To investigate the mechanism of action of this beneficial effect of ranolazine on diastolic tension, Anemonia sulcata toxin II (ATX-II, 40 nmol/L) was used to increase intracellular Na+ loading in ventricular rabbit myocytes. ATX-II caused a significant rise in [Na+](i) typically seen in heart failure via increased late I-Na. In parallel, ATX-II significantly increased diastolic [Ca2+](i). In the presence of ranolazine the increases in late I-Na, as well as [Na+](i) and diastolic [Ca2+](i) were significantly blunted at all stimulation rates without significantly decreasing Ca2+ transient amplitudes or SR Ca2+ content. In summary, ranolazine reduced the frequency dependent increase in diastolic tension without having negative inotropic effects on contractility of muscles from end-stage failing human hearts. Moreover, in rabbit myocytes the increases in late I-Na, [Na+](i) and [Ca2+](i) caused by ATX-II, were significantly blunted by ranolazine. These results suggest that ratiolazine may be of therapeutic benefit in conditions of diastolic dysfunction due to elevated [Na+](i) and diastolic [Ca2+](i). (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yjmcc.2008.03.006"],["dc.identifier.gro","3143272"],["dc.identifier.isi","000257543800004"],["dc.identifier.pmid","18439620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/767"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.title","Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts - Role of late sodium current and intracellular ion accumulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1862"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Materialia"],["dc.bibliographiccitation.lastpage","1870"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Pundt, Astrid"],["dc.date.accessioned","2018-11-07T08:58:41Z"],["dc.date.available","2018-11-07T08:58:41Z"],["dc.date.issued","2011"],["dc.description.abstract","Palladium hydrogen thin films are used as a model system to investigate the impact of microstructure and mechanical stress release on the electrical resistivity of thin film metals and alloys that undergo structural phase transitions. The results are compared with bulk resistivity models. Nanocrystalline, multi-oriented and epitaxial films are investigated, yielding initial terminal resistivities rho(infinity)(0) = 152 - 200 Omega nm. The hydrogen-related resistivity changes of epitaxial films are shown to approach the predicted a-phase bulk increment Delta rho(H)/Delta c(H) = 451 Omega nm, while hydrogen trapping in nanocrystalline films strongly reduces the resistivity response. In the two-phase region, the resistivity is shown to be modified by the steric distribution and geometry of the hydride precipitates, yielding different proportions of serial and parallel conduction. Film delamination from the substrate strongly reduces the resistivity increment due to the Gorsky effect. (c) 2010 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [PU 131/7-2]"],["dc.identifier.doi","10.1016/j.actamat.2010.11.052"],["dc.identifier.isi","000287775400002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1359-6454"],["dc.title","Combined impact of microstructure and mechanical stress on the electrical resistivity of PdHc thin films"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","90"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Flenner, Frederik"],["dc.contributor.author","Friedrich, Felix W."],["dc.contributor.author","Ungeheuer, Nele"],["dc.contributor.author","Christ, Torsten"],["dc.contributor.author","Geertz, Birgit"],["dc.contributor.author","Reischmann, Silke"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Stathopoulou, Konstantina"],["dc.contributor.author","Soehren, Klaus-Dieter"],["dc.contributor.author","Weinberger, Florian"],["dc.contributor.author","Schwedhelm, Edzard"],["dc.contributor.author","Cuello, Friederike"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Carrier, Lucie"],["dc.date.accessioned","2018-11-07T10:21:19Z"],["dc.date.available","2018-11-07T10:21:19Z"],["dc.date.issued","2016"],["dc.description.abstract","Aims Hypertrophic cardiomyopathy (HCM) is often accompanied by increased myofilament Ca2+ sensitivity and diastolic dysfunction. Recent findings indicate increased late Na+ current density in human HCM cardiomyocytes. Since ranolazine has the potential to decrease myofilament Ca2+ sensitivity and late Na+ current, we investigated its effects in an Mybpc3-targeted knock-in (KI) mouse model of HCM. Methods and results Unloaded sarcomere shortening and Ca2+ transients were measured in KI and wild-type (WT) cardiomyocytes. Measurements were performed at baseline (1 Hz) and under increased workload (30 nM isoprenaline (ISO), 5 Hz) in the absence or presence of 10 mu M ranolazine. KI myocytes showed shorter diastolic sarcomere length at baseline, stronger inotropic response to ISO, and drastic drop of diastolic sarcomere length under increased workload. Ranolazine attenuated ISO responses in WT and KI cells and prevented workload-induced diastolic failure in KI. Late Na+ current density was diminished and insensitive to ranolazine in KI cardiomyocytes. Ca2+ sensitivity of skinned KI trabeculae was slightly decreased by ranolazine. Phosphorylation analysis of cAMP-dependent protein kinase A-target proteins and ISO concentration-response measurements on muscle strips indicated antagonism at beta-adrenoceptors with 10 mu M ranolazine shifting the ISO response by 0.6 log units. Six-month treatment with ranolazine (plasma level > 20 mu M) demonstrated a beta-blocking effect, but did not reverse cardiac hypertrophy or dysfunction in KI mice. Conclusion Ranolazine improved tolerance to high workload in mouse HCM cardiomyocytes, not by blocking late Na+ current, but by antagonizing beta-adrenergic stimulation and slightly desensitizing myofilaments to Ca2+. This effect did not translate in therapeutic efficacy in vivo."],["dc.identifier.doi","10.1093/cvr/cvv247"],["dc.identifier.isi","000368414600011"],["dc.identifier.pmid","26531128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42059"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1111"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1118"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Keyser, Andreas"],["dc.contributor.author","Rupprecht, Leopold"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Maier, Lars S"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:24:15Z"],["dc.date.available","2021-04-14T08:24:15Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/europace/euaa079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81221"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1532-2092"],["dc.relation.issn","1099-5129"],["dc.title","Dantrolene reduces CaMKIIδC-mediated atrial arrhythmias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]