Rebs, Sabine

[["dc.bibliographiccitation.firstpage","9"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Fomin, Andrey"],["dc.contributor.author","Luo, Xiaojing"],["dc.contributor.author","Li, Wener"],["dc.contributor.author","Fischer, Claudia"],["dc.contributor.author","Özcelik, Cemil"],["dc.contributor.author","Perrot, Andreas"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Vidal, Ramon Oliveira"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2018-04-23T11:49:17Z"],["dc.date.available","2018-04-23T11:49:17Z"],["dc.date.issued","2017"],["dc.description.abstract","The ability to generate patient-specific induced pluripotent stem cells (iPSCs) provides a unique opportunity for modeling heart disease in vitro. In this study, we generated iPSCs from a patient with dilated cardiomyopathy (DCM) caused by a missense mutation S635A in RNA-binding motif protein 20 (RBM20) and investigated the functionality and cell biology of cardiomyocytes (CMs) derived from patient-specific iPSCs (RBM20-iPSCs). The RBM20-iPSC-CMs showed abnormal distribution of sarcomeric α-actinin and defective calcium handling compared to control-iPSC-CMs, suggesting disorganized myofilament structure and altered calcium machinery in CMs of the RBM20 patient. Engineered heart muscles (EHMs) from RBM20-iPSC-CMs showed that not only active force generation was impaired in RBM20-EHMs but also passive stress of the tissue was decreased, suggesting a higher visco-elasticity of RBM20-EHMs. Furthermore, we observed a reduced titin (TTN) N2B-isoform expression in RBM20-iPSC-CMs by demonstrating a reduction of exon skipping in the PEVK region of TTN and an inhibition of TTN isoform switch. In contrast, in control-iPSC-CMs both TTN isoforms N2B and N2BA were expressed, indicating that the TTN isoform switch occurs already during early cardiogenesis. Using next generation RNA sequencing, we mapped transcriptome and splicing target profiles of RBM20-iPSC-CMs and identified different cardiac gene networks in response to the analyzed RBM20 mutation in cardiac-specific processes. These findings shed the first light on molecular mechanisms of RBM20-dependent pathological cardiac remodeling leading to DCM. Our data demonstrate that iPSC-CMs coupled with EHMs provide a powerful tool for evaluating disease-relevant functional defects and for a deeper mechanistic understanding of alternative splicing-related cardiac diseases."],["dc.identifier.doi","10.1016/j.yjmcc.2017.09.008"],["dc.identifier.gro","3142517"],["dc.identifier.pmid","28941705"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13672"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/191"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A08: Translationale und posttranslationale Kontrolle trunkierter Titinproteine in Kardiomyozyten von Patienten mit dilatativer Kardiomyopathie"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.issn","0022-2828"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Severe DCM phenotype of patient harboring RBM20 mutation S635A can be modeled by patient-specific induced pluripotent stem cell-derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","12230"],["dc.bibliographiccitation.firstpage","12230"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","23"],["dc.contributor.affiliation","Sedaghat-Hamedani, Farbod; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Rebs, Sabine; 4Department of Cardiology and Pneumology, Georg-August-University Göttingen, 37073 Göttingen, Germany"],["dc.contributor.affiliation","Kayvanpour, Elham; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Zhu, Chenchen; 7Department of Genetics, Stanford University, Stanford, CA 94305, USA"],["dc.contributor.affiliation","Amr, Ali; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Müller, Marion; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Haas, Jan; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Wu, Jingyan; 7Department of Genetics, Stanford University, Stanford, CA 94305, USA"],["dc.contributor.affiliation","Steinmetz, Lars M.; 2DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg and Mannheim, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Ehlermann, Philipp; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Streckfuss-Bömeke, Katrin; 4Department of Cardiology and Pneumology, Georg-August-University Göttingen, 37073 Göttingen, Germany"],["dc.contributor.affiliation","Frey, Norbert; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Meder, Benjamin; 1Institute for Cardiomyopathies Heidelberg (ICH), University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.author","Sedaghat-Hamedani, Farbod"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Kayvanpour, Elham"],["dc.contributor.author","Zhu, Chenchen"],["dc.contributor.author","Amr, Ali"],["dc.contributor.author","Müller, Marion"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Wu, Jingyan"],["dc.contributor.author","Steinmetz, Lars M."],["dc.contributor.author","Ehlermann, Philipp"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.editor","Chandra Janga, Sarath"],["dc.date.accessioned","2022-12-01T08:31:40Z"],["dc.date.available","2022-12-01T08:31:40Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:19Z"],["dc.description.abstract","Dilated cardiomyopathy (DCM) is a common cause of heart failure (HF) and is of familial origin in 20–40% of cases. Genetic testing by next-generation sequencing (NGS) has yielded a definite diagnosis in many cases; however, some remain elusive. In this study, we used a combination of NGS, human-induced pluripotent-stem-cell-derived cardiomyocytes (iPSC-CMs) and nanopore long-read sequencing to identify the causal variant in a multi-generational pedigree of DCM. A four-generation family with familial DCM was investigated. Next-generation sequencing (NGS) was performed on 22 family members. Skin biopsies from two affected family members were used to generate iPSCs, which were then differentiated into iPSC-CMs. Short-read RNA sequencing was used for the evaluation of the target gene expression, and long-read RNA nanopore sequencing was used to evaluate the relevance of the splice variants. The pedigree suggested a highly penetrant, autosomal dominant mode of inheritance. The phenotype of the family was suggestive of laminopathy, but previous genetic testing using both Sanger and panel sequencing only yielded conflicting evidence for LMNA p.R644C (rs142000963), which was not fully segregated. By re-sequencing four additional affected family members, further non-coding LMNA variants could be detected: rs149339264, rs199686967, rs201379016, and rs794728589. To explore the roles of these variants, iPSC-CMs were generated. RNA sequencing showed the LMNA expression levels to be significantly lower in the iPSC-CMs of the LMNA variant carriers. We demonstrated a dysregulated sarcomeric structure and altered calcium homeostasis in the iPSC-CMs of the LMNA variant carriers. Using targeted nanopore long-read sequencing, we revealed the biological significance of the variant c.356+1G>A, which generates a novel 5′ splice site in exon 1 of the cardiac isomer of LMNA, causing a nonsense mRNA product with almost complete RNA decay and haploinsufficiency. Using novel molecular analysis and nanopore technology, we demonstrated the pathogenesis of the rs794728589 (c.356+1G>A) splice variant in LMNA. This study highlights the importance of precise diagnostics in the clinical management and workup of cardiomyopathies."],["dc.identifier.doi","10.3390/ijms232012230"],["dc.identifier.pii","ijms232012230"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118233"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.publisher","MDPI"],["dc.relation.eissn","1422-0067"],["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","Genotype Complements the Phenotype: Identification of the Pathogenicity of an LMNA Splice Variant by Nanopore Long-Read Sequencing in a Large DCM Family"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12990"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Sedaghat-Hamedani, Farbod; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Rebs, Sabine; 3Clinic for Cardiology and Pneumology, Georg-August-University Göttingen, 37073 Göttingen, Germany; sabine.rebs@med.uni-goettingen.de (S.R.); katrin.streckfuss@med.uni-goettingen.de (K.S.-B.)"],["dc.contributor.affiliation","El-Battrawy, Ibrahim; 2DZHK (German Centre for Cardiovascular Research), Heidelberg-Mannheim, 17475 Greifswald, Germany; ibrahim.elbattrawy2006@gmail.com (I.E.-B.); xiaobo.zhou@medma.uni-heidelberg.de (X.Z.); Ibrahim.Akin@medma.uni-heidelberg.de (I.A.)"],["dc.contributor.affiliation","Chasan, Safak; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Krause, Tobias; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Haas, Jan; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Zhong, Rujia; 6Department of Medicine, University Medical Centre Mannheim (UMM), 68159 Mannheim, Germany; Rujia.Zhong@medma.uni-heidelberg.de (R.Z.); Zhenxing.Liao@medma.uni-heidelberg.de (Z.L.); Qiang.Xu@medma.uni-heidelberg.de (Q.X.)"],["dc.contributor.affiliation","Liao, Zhenxing; 6Department of Medicine, University Medical Centre Mannheim (UMM), 68159 Mannheim, Germany; Rujia.Zhong@medma.uni-heidelberg.de (R.Z.); Zhenxing.Liao@medma.uni-heidelberg.de (Z.L.); Qiang.Xu@medma.uni-heidelberg.de (Q.X.)"],["dc.contributor.affiliation","Xu, Qiang; 6Department of Medicine, University Medical Centre Mannheim (UMM), 68159 Mannheim, Germany; Rujia.Zhong@medma.uni-heidelberg.de (R.Z.); Zhenxing.Liao@medma.uni-heidelberg.de (Z.L.); Qiang.Xu@medma.uni-heidelberg.de (Q.X.)"],["dc.contributor.affiliation","Zhou, Xiaobo; 2DZHK (German Centre for Cardiovascular Research), Heidelberg-Mannheim, 17475 Greifswald, Germany; ibrahim.elbattrawy2006@gmail.com (I.E.-B.); xiaobo.zhou@medma.uni-heidelberg.de (X.Z.); Ibrahim.Akin@medma.uni-heidelberg.de (I.A.)"],["dc.contributor.affiliation","Akin, Ibrahim; 2DZHK (German Centre for Cardiovascular Research), Heidelberg-Mannheim, 17475 Greifswald, Germany; ibrahim.elbattrawy2006@gmail.com (I.E.-B.); xiaobo.zhou@medma.uni-heidelberg.de (X.Z.); Ibrahim.Akin@medma.uni-heidelberg.de (I.A.)"],["dc.contributor.affiliation","Zitron, Edgar; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Frey, Norbert; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.affiliation","Streckfuss-Bömeke, Katrin; 3Clinic for Cardiology and Pneumology, Georg-August-University Göttingen, 37073 Göttingen, Germany; sabine.rebs@med.uni-goettingen.de (S.R.); katrin.streckfuss@med.uni-goettingen.de (K.S.-B.)"],["dc.contributor.affiliation","Kayvanpour, Elham; 1Department of Medicine III, Institute for Cardiomyopathies Heidelberg (ICH), University of Heidelberg, 69120 Heidelberg, Germany; Farbod.Sedaghat-Hamedani@med.uni-heidelberg.de (F.S.-H.); Safak.Chasan@med.uni-heidelberg.de (S.C.); ttkrause@me.com (T.K.); jan.haas@med.uni-heidelberg.de (J.H.); edgar.zitron@med.uni-heidelberg.de (E.Z.); Norbert.Frey@med.uni-heidelberg.de (N.F.)"],["dc.contributor.author","Sedaghat-Hamedani, Farbod"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Chasan, Safak"],["dc.contributor.author","Krause, Tobias"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Kayvanpour, Elham"],["dc.contributor.author","Akin, Ibrahim"],["dc.contributor.author","Zitron, Edgar"],["dc.contributor.author","Frey, Norbert"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-02-01T10:31:49Z"],["dc.date.available","2022-02-01T10:31:49Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-03T23:21:13Z"],["dc.description.abstract","Introduction: Familial dilated cardiomyopathy (DCM) is clinically variable and has been associated with mutations in more than 50 genes. Rapid improvements in DNA sequencing have led to the identification of diverse rare variants with unknown significance (VUS), which underlines the importance of functional analyses. In this study, by investigating human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs), we evaluated the pathogenicity of the p.C335R sodium voltage-gated channel alpha subunit 5 (SCN5a) variant in a large family with familial DCM and conduction disease. Methods: A four-generation family with autosomal dominant familial DCM was investigated. Next-generation sequencing (NGS) was performed in all 16 family members. Clinical deep phenotyping, including endomyocardial biopsy, was performed. Skin biopsies from two patients and one healthy family member were used to generate human-induced pluripotent stem cells (iPSCs), which were then differentiated into cardiomyocytes. Patch-clamp analysis with Xenopus oocytes and iPSC-CMs were performed. Results: A SCN5a variant (c.1003T>C; p.C335R) could be detected in all family members with DCM or conduction disease. A novel truncating TTN variant (p.Ser24998LysfsTer28) could also be identified in two family members with DCM. Family members with the SCN5a variant (p.C335R) showed significantly longer PQ and QRS intervals and lower left ventricular ejection fractions (LV-EF). All four patients who received CRT-D were non-responders. Electrophysiological analysis with Xenopus oocytes showed a loss of function in SCN5a p.C335R. Na+ channel currents were also reduced in iPSC-CMs from DCM patients. Furthermore, iPSC-CM with compound heterozygosity (SCN5a p.C335R and TTNtv) showed significant dysregulation of sarcomere structures, which may be contributed to the severity of the disease and earlier onset of DCM. Conclusion: The SCN5a p.C335R variant is causing a loss of function of peak INa in patients with DCM and cardiac conduction disease. The co-existence of genetic variants in channels and structural genes (e.g., SCN5a p.C335R and TTNtv) increases the severity of the DCM phenotype."],["dc.description.abstract","Introduction: Familial dilated cardiomyopathy (DCM) is clinically variable and has been associated with mutations in more than 50 genes. Rapid improvements in DNA sequencing have led to the identification of diverse rare variants with unknown significance (VUS), which underlines the importance of functional analyses. In this study, by investigating human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs), we evaluated the pathogenicity of the p.C335R sodium voltage-gated channel alpha subunit 5 (SCN5a) variant in a large family with familial DCM and conduction disease. Methods: A four-generation family with autosomal dominant familial DCM was investigated. Next-generation sequencing (NGS) was performed in all 16 family members. Clinical deep phenotyping, including endomyocardial biopsy, was performed. Skin biopsies from two patients and one healthy family member were used to generate human-induced pluripotent stem cells (iPSCs), which were then differentiated into cardiomyocytes. Patch-clamp analysis with Xenopus oocytes and iPSC-CMs were performed. Results: A SCN5a variant (c.1003T>C; p.C335R) could be detected in all family members with DCM or conduction disease. A novel truncating TTN variant (p.Ser24998LysfsTer28) could also be identified in two family members with DCM. Family members with the SCN5a variant (p.C335R) showed significantly longer PQ and QRS intervals and lower left ventricular ejection fractions (LV-EF). All four patients who received CRT-D were non-responders. Electrophysiological analysis with Xenopus oocytes showed a loss of function in SCN5a p.C335R. Na+ channel currents were also reduced in iPSC-CMs from DCM patients. Furthermore, iPSC-CM with compound heterozygosity (SCN5a p.C335R and TTNtv) showed significant dysregulation of sarcomere structures, which may be contributed to the severity of the disease and earlier onset of DCM. Conclusion: The SCN5a p.C335R variant is causing a loss of function of peak INa in patients with DCM and cardiac conduction disease. The co-existence of genetic variants in channels and structural genes (e.g., SCN5a p.C335R and TTNtv) increases the severity of the DCM phenotype."],["dc.identifier.doi","10.3390/ijms222312990"],["dc.identifier.pii","ijms222312990"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98952"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.title","Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]