Cyganek, Lukas

[["dc.bibliographiccitation.firstpage","1137"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1148"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Fan, Xuehui"],["dc.contributor.author","Yang, Zhen"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Yuecel, Goekhan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Yingrui"],["dc.contributor.author","Wendel, Angela"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Borggrefe, Martin"],["dc.date.accessioned","2021-10-01T09:57:54Z"],["dc.date.available","2021-10-01T09:57:54Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Aims This study aimed to investigate possible roles and underlying mechanisms of alpha-adrenoceptor coupled signalling for the pathogenesis of Takotsubo syndrome (TTS). Methods and results Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were treated with a toxic concentration of epinephrine (Epi, 0.5 mM for 1 h) to mimic the setting of TTS. Patch-clamp technique, polymerase chain reaction (PCR) and Fluorescence-activated cell sorting (FACS) were employed for the study. High concentration Epi suppressed the depolarization velocity, prolonged duration of action potentials and induced arrhythmic events in hiPSC-CMs. The Epi effects were attenuated by an alpha-adrenoceptor blocker (phentolamine), suggesting involvement of alpha-adrenoceptor signalling in arrhythmogenesis related to QT interval prolongation in the setting of TTS. An alpha 1-adrenoceptor agonist (phenylephrine) but not an alpha 2-adrenoceptor agonist (clonidine) mimicked Epi effects. Epi enhanced ROS production, which could be attenuated by the alpha- adrenoceptor blocker. Treatment of cells with H2O2 (100 µM) mimicked the effects of Epi on action potentials and a reactive oxygen species (ROS)-blocker (N-acetyl-I-cysteine, 1 mM) prevented the Epi effects, indicating that the ROS signalling is involved in the alpha-adrenoceptor actions. Nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidases were involved in alpha 1-adrenoceptor signalling. A protein kinase C (PKC) blocker suppressed the effects of Epi, phenylephrine and ROS as well, implying that PKC participated in alpha 1-adrenoceptor signalling and acted as a downstream factor of ROS. The abnormal action potentials resulted from alpha 1-adrenoceptor activation-induced dysfunctions of ion channels including the voltage-dependent Na+ and L-type Ca2+ channels. Conclusions Alpha 1-adrenoceptor signalling plays important roles for arrhythmogenesis of TTS. Alpha-adrenoceptor blockers might be clinically helpful for treating arrhythmias in patients with TTS."],["dc.identifier.doi","10.1093/europace/euab008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/89942"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","1532-2092"],["dc.relation.issn","1099-5129"],["dc.title","Alpha 1-adrenoceptor signalling contributes to toxic effects of catecholamine on electrical properties in cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Stem Cells International"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","2018"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:37:41Z"],["dc.date.available","2020-12-10T18:37:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1155/2018/6067096"],["dc.identifier.pmid","29535773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77065"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/325"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ion Channel Expression and Characterization in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1140"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","1146"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Besler, Johanna"],["dc.contributor.author","Ansari, Uzair"],["dc.contributor.author","Liebe, Volker"],["dc.contributor.author","Schimpf, Rainer"],["dc.contributor.author","Tülümen, Erol"],["dc.contributor.author","Rudic, Boris"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Odening, Katja"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Wolpert, Christian"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T14:10:22Z"],["dc.date.available","2020-12-10T14:10:22Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00392-019-01449-3"],["dc.identifier.eissn","1861-0692"],["dc.identifier.issn","1861-0684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70740"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Long-term follow-up of implantable cardioverter-defibrillators in Short QT syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1410"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1421"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Albers, Sebastian"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Kleinsorge, Mandy"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Rudic, Boris"],["dc.contributor.author","Müller, Jonas"],["dc.contributor.author","Dinkel, Hendrik"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Diecke, Sebastian"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:19:09Z"],["dc.date.available","2020-12-10T18:19:09Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1093/europace/euz122"],["dc.identifier.pmid","31106349"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75142"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/328"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","A cellular model of Brugada syndrome with SCN10A variants using human-induced pluripotent stem cell-derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cardiovascular Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Yang, Zhen"],["dc.contributor.author","Li, Yingrui"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Yuecel, Goekhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2022-04-01T10:01:10Z"],["dc.date.available","2022-04-01T10:01:10Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Previous studies suggested involvement of non-ß-adrenoceptors in the pathogenesis of Takotsubo cardiomyopathy (TTC). This study was designed to explore possible roles and underlying mechanisms of dopamine D1/D5 receptor coupled signaling in arrhythmogenesis of TTC. Methods Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were challenged by toxic concentration of epinephrine (Epi, 0.5 mM for 1 h) for mimicking the catecholamine excess in setting of TTC. Specific receptor blockers and activators were used to unveil roles of D1/D5 receptors. Patch clamp, qPCR, and FACS analyses were performed in the study. Results High concentration Epi and two dopamine D1/D5 receptor agonists [(±)-SKF 38393 and fenoldopam] reduced the depolarization velocity and prolonged the duration of action potentials (APs) and caused arrhythmic events in iPSC-CMs, suggesting involvement of dopamine D1/D5 receptor signaling in arrhythmogenesis associated with QT interval prolongation in the setting of TTC. (±)-SKF 38393 and fenoldopam enhanced the reactive oxygen species (ROS)-production. H 2 O 2 (100 μM) recapitulated the effects of (±)-SKF 38393 and fenoldopam on APs and a ROS-blocker N -acetylcysteine (NAC, 1 mM) abolished the effects, suggesting that the ROS-signaling is involved in the dopamine D1/D5 receptor actions. A NADPH oxidases blocker and a PKA- or PKC-blocker suppressed the effects of the dopamine receptor agonist, implying that PKA, NADPH oxidases and PKC participated in dopamine D1/D5 receptor signaling. The abnormal APs resulted from dopamine D1/D5 receptor activation-induced dysfunctions of ion channels including the Na + and L-type Ca 2+ and I Kr channels. Conclusions Dopamine D1/D5 receptor signaling plays important roles for arrhythmogenesis of TTC. Dopamine D1/D5 receptor signaling in cardiomyocytes might be a potential target for treating arrhythmias in patients with TTC."],["dc.identifier.doi","10.3389/fcvm.2021.777463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105614"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2297-055X"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Dopamine D1/D5 Receptor Signaling Is Involved in Arrhythmogenesis in the Setting of Takotsubo Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","486"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Lomada, Santosh K."],["dc.contributor.author","Chatterjee, Anupriya"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:47:12Z"],["dc.date.available","2020-12-10T18:47:12Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/jcm9020486"],["dc.identifier.eissn","2077-0383"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78680"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Nucleoside Diphosphate Kinase B Contributes to Arrhythmogenesis in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes from a Patient with Arrhythmogenic Right Ventricular Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","195"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","202"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Schünemann, Jan-Dierk"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Patocskai, Bence"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Nowak, Daniel"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2018-04-23T11:49:14Z"],["dc.date.available","2018-04-23T11:49:14Z"],["dc.date.issued","2018"],["dc.description.abstract","Background and purpose Previous studies revealed that Takotsubo cardiomyopathy (TTC), a transient disorder of ventricular dysfunction affecting predominantly postmenopausal women, is associated with acquired long QT syndrome and arrhythmias, but the exact pathophysiologic mechanism is unknown. Our aim is to investigate the electrophysiological mechanism for QT-prolongation in TTC-patients by using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Methods hiPSC-CMs, which were generated from human skin fibroblasts of three healthy donors, were treated by estradiol (10 μM for one week) and a toxic concentration of isoprenaline (Iso, 1 mM for 2 h). Patch clamp techniques, qPCR and fluorescence-activated cell sorting (FACS) were employed for the study. Key results Iso enhanced late INa and suppressed Ito and thus prolonged the action potential duration (APD), suggesting possible reasons for arrhythmias in TTC. Iso elevated the production of reactive oxygen species (ROS). N-acetylcystein (1 mM), a ROS-blocker, abolished the effects of Iso on late INa and Ito. H2O2 (100 μM) mimicked Iso effects on late INa and Ito. These data indicate that the effects of Iso were mediated by ROS. Metoprolol (1 mM), a beta-blocker, prevented the effects of Iso on late INa and APD, confirming the adrenoceptor-dependent effects of Iso. Estradiol treatment prevented the APD-prolongation, attenuated the enhancement of INa, diminished the reduction of Ito, suppressed ROS-production induced by Iso and reduced the expression levels of adrenoceptors, suggesting protective effects of estragon against toxic effects of catecholamine. Conclusions Estradiol has protective effects against catecholamine excess and hence reduction in estrogen level may increase the risk of acquired long QT syndrome in TTC."],["dc.identifier.doi","10.1016/j.ijcard.2017.11.007"],["dc.identifier.gro","3142511"],["dc.identifier.pmid","29407091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13665"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/324"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0167-5273"],["dc.title","Estradiol protection against toxic effects of catecholamine on electrical properties in human-induced pluripotent stem cell derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","f46"],["dc.bibliographiccitation.issue","FI1"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","f56"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tombers, Christoph"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:19:08Z"],["dc.date.available","2020-12-10T18:19:08Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1093/europace/euy042"],["dc.identifier.pmid","29566126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75139"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/271"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Electrical dysfunctions in human-induced pluripotent stem cell-derived cardiomyocytes from a patient with an arrhythmogenic right ventricular cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cardiovascular Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Zhang, Feng"],["dc.contributor.author","Yang, Zhen"],["dc.contributor.author","Li, Yingrui"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Burgermeister, Elke"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Borggrefe, Martin"],["dc.date.accessioned","2022-04-01T10:01:06Z"],["dc.date.available","2022-04-01T10:01:06Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Cardiac dysfunction including arrhythmias appear frequently in patients with cancers, which are expected to be caused mainly by cardiotoxic effects of chemotherapy. Experimental studies investigating the effects of cancer cell secretion without chemotherapy on ion channel function in human cardiomyocytes are still lacking. Methods The human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) generated from three healthy donors were treated with gastrointestinal (GI) cancer (AGS and SW480 cells) medium for 48 h. The qPCR, patch-clamp, western blotting, immunostaining, dot blotting, bisulfite sequence, and overexpression of the ten-eleven translocation (TET) enzyme were performed for the study. Results After treated with cancer cell secretion, the maximum depolarization velocity and the action potential amplitude were reduced, the action potential duration prolonged, peak Na + current, and the transient outward current were decreased, late Na + and the slowly activating delayed rectifier K + current were increased. Changes of mRNA and protein level of respective channels were detected along with altered DNA methylation level in CpG island in the promoter regions of ion channel genes and increased protein levels of DNA methyltransferases. Phosphoinositide 3-kinase (PI3K) inhibitor attenuated and transforming growth factor-β (TGF-β) mimicked the effects of cancer cell secretion. Conclusions GI cancer cell secretion could induce ion channel dysfunction, which may contribute to occurrence of arrhythmias in cancer patients. The ion channel dysfunction could result from DNA methylation of ion channel genes via activation of TGF-β/PI3K signaling. This study may provide new insights into pathogenesis of arrhythmia in cancer patients."],["dc.identifier.doi","10.3389/fcvm.2022.839104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105603"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2297-055X"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Regulation of Ion Channel Function in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes by Cancer Cell Secretion Through DNA Methylation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","651"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","El‐Battrawy, Ibrahim"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Akin, Ibrahim"],["dc.contributor.author","Zhou, Xiao‐Bo"],["dc.date.accessioned","2022-03-01T11:45:24Z"],["dc.date.available","2022-03-01T11:45:24Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/cpt.1449"],["dc.identifier.pmid","30947366"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103314"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/270"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1532-6535"],["dc.relation.issn","0009-9236"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","Drug Testing in Human‐Induced Pluripotent Stem Cell–Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]