Zeisberg, Elisabeth M.

[["dc.bibliographiccitation.firstpage","264"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Pathology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","229"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T09:30:53Z"],["dc.date.accessioned","2019-02-19T16:44:38Z"],["dc.date.available","2018-11-07T09:30:53Z"],["dc.date.available","2019-02-19T16:44:38Z"],["dc.date.issued","2013"],["dc.description.abstract","The aberrant methylation of CpG island promoters of selected genes is the prominent epigenetic mechanism by which gene transcription can be effectively silenced. Aberrant hypermethylation of a few selected genes plays an important role in facilitating fibrotic fibroblast activation and in driving fibrogenesis. Here we review mechanisms of DNA methylation and demethylation and their implications for fibroblast activation and tissue fibrosis."],["dc.identifier.doi","10.1002/path.4120"],["dc.identifier.isi","000312542400013"],["dc.identifier.pmid","23097091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57601"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/78"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","0022-3417"],["dc.relation.issn","1096-9896"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","The role of promoter hypermethylation in fibroblast activation and fibrogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","16"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2019-07-09T11:41:46Z"],["dc.date.available","2019-07-09T11:41:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Based on extensive pre-clinical achievements over the past decades, it appears to be due time for a successful clinical translation in the renal fibrosis field—but what is the quickest road to get there? In light of the recent launch of the Precision Medicine Initiative and success of molecularly informed drugs in oncology, we here discuss what it may take to bring molecularly targeted anti-fibrotic to clinical use in chronic progressive kidney disease."],["dc.identifier.doi","10.1186/s13069-015-0033-x"],["dc.identifier.pmid","26330891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58506"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Precision renal medicine: a roadmap towards targeted kidney fibrosis therapies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","629"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Seminars in nephrology"],["dc.bibliographiccitation.lastpage","636"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Rath, Sandip K."],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2020-11-24T12:13:03Z"],["dc.date.available","2020-11-24T12:13:03Z"],["dc.date.issued","2018"],["dc.description.abstract","Cardiovascular disease and heart failure are the primary cause of morbidity and mortality in patients with chronic kidney disease. Because impairment of kidney function correlates with heart failure and cardiac fibrosis, a kidney-heart axis is suspected. Although our understanding of the underlying mechanisms still is evolving, the possibility that kidney-heart messengers could be intercepted offers ample reason to focus on this clinically highly relevant problem. Here, we review the current knowledge of how kidney injury causes heart failure and fibrosis."],["dc.identifier.doi","10.1016/j.semnephrol.2018.08.007"],["dc.identifier.pmid","30413256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69168"],["dc.language.iso","en"],["dc.relation.eissn","1558-4488"],["dc.relation.issn","0270-9295"],["dc.title","Causal Connections From Chronic Kidney Disease to Cardiac Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S18"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","S19"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Alnour, Fouzi"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:15:49Z"],["dc.date.available","2018-11-07T10:15:49Z"],["dc.date.issued","2016"],["dc.identifier.isi","000375417500031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40892"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","KIAA0182: a new gene relevant for cardiac development"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2687"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","2698"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2018-11-07T09:34:44Z"],["dc.date.available","2018-11-07T09:34:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Thrombospondin-1 (TSP1) is a multifunctional matricellular protein known to promote progression of chronic kidney disease. To gain insight into the underlying mechanisms through which TSP1 accelerates chronic kidney disease, we compared disease progression in Col4a3 knockout (K0) mice, which develop spontaneous kidney failure, with that of Col4a3;Tsp1 double-knockout (DK0) mice. Decline of excretory renal function was significantly delayed in the absence of TSP1. Although Col4a3;Tsp1 DK0 mice did progress toward end-stage renal failure, their kidneys exhibited distinct histopathological lesions, compared with creatinine level- matched Col4a3 K0 mice. Although kidneys of both Col4a3 K0 and Col4a3;Tsp1 DK0 mice exhibited a widened tubulointerstitium, predominant lesions in Col4a3 K0 kidneys were collagen deposition and fibroblast accumulation, whereas in Col4a3;Tsp1 DK0 kidney inflammation was predominant, with less collagen deposition. Altered disease progression correlated with impaired activation of transforming growth factor-beta 1 (TGF-beta 1) in vivo and in vitro in the absence of TSP1. In summary, our findings suggest that TSP1 contributes to progression of chronic kidney disease by catalyzing activation of latent TGF-beta 1, resulting in promotion of a fibroproliferative response over an inflammatory response. Furthermore, the findings suggest that fibro-proliferative and inflammatory lesions are independent entities, both of which contribute to decline of renal function."],["dc.identifier.doi","10.1016/j.ajpath.2014.06.014"],["dc.identifier.isi","000342276800010"],["dc.identifier.pmid","25111226"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32238"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/79"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1525-2191"],["dc.relation.issn","0002-9440"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Thrombospondin-1 Deficiency Causes a Shift from Fibroproliferative to Inflammatory Kidney Disease and Delays Onset of Renal Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3509"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.lastpage","15"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Wilhelmi, Tim"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Saito, Shoji"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2019-02-27T12:52:18Z"],["dc.date.available","2019-02-27T12:52:18Z"],["dc.date.issued","2018"],["dc.description.abstract","While suppression of specific genes through aberrant promoter methylation contributes to different diseases including organ fibrosis, gene-specific reactivation technology is not yet available for therapy. TET enzymes catalyze hydroxymethylation of methylated DNA, reactivating gene expression. We here report generation of a high-fidelity CRISPR/Cas9-based gene-specific dioxygenase by fusing an endonuclease deactivated high-fidelity Cas9 (dHFCas9) to TET3 catalytic domain (TET3CD), targeted to specific genes by guiding RNAs (sgRNA). We demonstrate use of this technology in four different anti-fibrotic genes in different cell types in vitro, among them RASAL1 and Klotho, both hypermethylated in kidney fibrosis. Furthermore, in vivo lentiviral delivery of the Rasal1-targeted fusion protein to interstitial cells and of the Klotho-targeted fusion protein to tubular epithelial cells each results in specific gene reactivation and attenuation of fibrosis, providing gene-specific demethylating technology in a disease model."],["dc.identifier.doi","10.1038/s41467-018-05766-5"],["dc.identifier.pmid","30158531"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57643"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/225"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | D03: ENPP3-vermittelter Phosphat-Metabolismus bei der Herzfibrose"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High-fidelity CRISPR/Cas9- based gene-specific hydroxymethylation rescues gene expression and attenuates renal fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Steinle, Ulrike"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Carstens, Julienne L."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2020-05-04T07:22:12Z"],["dc.date.available","2020-05-04T07:22:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Acute kidney injury (AKI) and progressive chronic kidney disease (CKD) are intrinsically tied syndromes. In this regard, the acutely injured kidney often does not achieve its full regenerative capacity and AKI directly transitions into progressive CKD associated with tubulointerstitial fibrosis. Underlying mechanisms of such AKI-to-CKD progression are still incompletely understood and specific therapeutic interventions are still elusive. Because epigenetic modifications play a role in maintaining tissue fibrosis, we used a murine model of ischemia-reperfusion injury to determine whether aberrant promoter methylation of RASAL1 contributes causally to the switch between physiological regeneration and tubulointerstitial fibrogenesis, a hallmark of AKI-to-CKD progression. It is known that the antihypertensive drug hydralazine has demethylating activity, and that its optimum demethylating activity occurs at concentrations below blood pressure-lowering doses. Administration of low-dose hydralazine effectively induced expression of hydroxylase TET3, which catalyzed RASAL1 hydroxymethylation and subsequent RASAL1 promoter demethylation. Hydralazine-induced CpG promoter demethylation subsequently attenuated renal fibrosis and preserved excretory renal function independent of its blood pressure-lowering effects. In comparison, RASAL1 demethylation and inhibition of tubulointerstitial fibrosis was not detected upon administration of the angiotensin-converting enzyme inhibitor Ramipril in this model. Thus, RASAL1 promoter methylation and subsequent transcriptional RASAL1 suppression plays a causal role in AKI-to-CKD progression."],["dc.identifier.doi","10.1016/j.kint.2016.07.042"],["dc.identifier.pmid","27692563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64543"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/307"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | D03: ENPP3-vermittelter Phosphat-Metabolismus bei der Herzfibrose"],["dc.relation.eissn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury-to-chronic kidney disease progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","225"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Differentiation"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Liu, Xiaopeng"],["dc.contributor.author","Qi, Jing"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Guan-Schmidt, Kaomei"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:07:27Z"],["dc.date.available","2018-11-07T10:07:27Z"],["dc.date.issued","2016"],["dc.description.abstract","Endothelial cells derived from human induced pluripotent stem cells (hiPSC-EC) are of significant value for research on human vascular development, in vitro disease models and drug screening. Here we report an alternative, highly efficient and cost-effective simple three step method (mesoderm induction, endothelial cell differentiation and endothelial cell expansion) to differentiate hiPSC directly into endothelial cells. We demonstrate that efficiency of described method to derive CD31 + and VE-Cadherin+ double positive cells is higher than 80% in 12 days. Most notably we established that hiPSC-EC differentiation efficacy depends on optimization of both mesoderm differentiation and endothelial cell differentiation steps. (C) 2016 International Society of Differentiation. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.diff.2016.05.004"],["dc.identifier.isi","000387936500010"],["dc.identifier.pmid","27266810"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39283"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1432-0436"],["dc.relation.issn","0301-4681"],["dc.title","Differentiation of functional endothelial cells from human induced pluripotent stem cells: A novel, highly efficient and cost effective method"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","24075"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nyamsuren, Gunsmaa"],["dc.contributor.author","Rapp, Gregor"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2022-01-11T14:06:04Z"],["dc.date.available","2022-01-11T14:06:04Z"],["dc.date.issued","2021"],["dc.description.abstract","Aryl hydrocarbon receptor nuclear translocator (ARNT) mediates anti-fibrotic activity in kidney and liver through induction of ALK3-receptor expression and subsequently increased Smad1/5/8 signaling. While expression of ARNT can be pharmacologically induced by sub-immunosuppressive doses of FK506 or by GPI1046, its anti-fibrotic activity is only realized when ARNT-ARNT homodimers form, as opposed to formation of ARNT-AHR or ARNT-HIF1α heterodimers. Mechanisms underlying ARNTs dimerization decision to specifically form ARNT–ARNT homodimers and possible cues to specifically induce ARNT homodimerization have been previously unknown. Here, we demonstrate that phosphorylation of the Ser77 residue is critical for ARNT–ARNT homodimer formation and stabilization. We further demonstrate that inhibition of PP2A phosphatase activity by LB100 enhances ARNT–ARNT homodimers both in vivo and in vitro (mouse tubular epithelial cells and human embryonic kidney cells). In murine models of kidney fibrosis, and also of liver fibrosis, combinations of FK506 or GPI1046 (to induce ARNT expression) with LB100 (to enhance ARNT homodimerization) elicit additive anti-fibrotic activities. Our study provides additional evidence for the anti-fibrotic activity of ARNT–ARNT homodimers and reveals Ser77 phosphorylation as a novel pharmacological target to realize the therapeutic potential of increased ARNT transactivation activity."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1038/s41598-021-03523-1"],["dc.identifier.pii","3523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97817"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2045-2322"],["dc.title","PP2A phosphatase inhibition is anti-fibrotic through Ser77 phosphorylation-mediated ARNT/ARNT homodimer formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2282"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","2287"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Potenta, Scott E."],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:15:44Z"],["dc.date.available","2020-11-24T12:15:44Z"],["dc.date.issued","2008-12"],["dc.description.abstract","Fibroblasts are key mediators of fibrosis in the kidney and other organs, but their origin during fibrosis is still not completely clear. Activated fibroblasts likely arise from resident quiescent fibroblasts via epithelial-to-mesenchymal transition and from the bone marrow. Here, we demonstrate that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT). We examined the contribution of EndMT to renal fibrosis in three mouse models of chronic kidney disease: (1) Unilateral ureteral obstructive nephropathy, (2) streptozotocin-induced diabetic nephropathy, and (3) a model of Alport renal disease. Approximately 30 to 50% of fibroblasts coexpressed the endothelial marker CD31 and markers of fibroblasts and myofibroblasts such as fibroblast specific protein-1 and alpha-smooth muscle actin. Endothelial lineage tracing using Tie2-Cre;R26R-stop-EYFP transgenic mice further confirmed the presence of EndMT-derived fibroblasts. Collectively, our results demonstrate that EndMT contributes to the accumulation of activated fibroblasts and myofibroblasts in kidney fibrosis and suggest that targeting EndMT might have therapeutic potential."],["dc.identifier.doi","10.1681/ASN.2008050513"],["dc.identifier.pmid","18987304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69201"],["dc.language.iso","en"],["dc.relation.eissn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.title","Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]