Eschenhagen, Thomas

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Ultrasound in Medicine & Biology"],["dc.bibliographiccitation.lastpage","55"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Schineis, Nico"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Voigt, Jens-Uwe"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Flachskampf, Frank A."],["dc.contributor.author","Daniel, Werner G."],["dc.contributor.author","Nixdorff, Uwe"],["dc.date.accessioned","2017-09-07T11:48:49Z"],["dc.date.available","2017-09-07T11:48:49Z"],["dc.date.issued","2008"],["dc.description.abstract","Real-time myocardial contrast echocardiography (MCE) is a noninvasive perfusion imaging method, whereas technical and resolution problems impair its application in small animals. Hence, we investigated the feasibility of NICE in experimental cardiovascular set-ups involving healthy and infarcted myocardium in rats. Twenty-five male Wistar rats were examined under volatile anesthesia (2.5% isoflurane) with high-resolution conventional 2-D echocardiography (2DE) and real-time MICE (Sonos 7500 with 15MHz-transducer, Philips Medical Systems, Andover, MA, USA) in short-axis view. Contrast agent (SonoVue, Bracco, Milan, Italy) was infused as a bolus into a sublingual vein. Background-subtracted contrast signal intensity (SI) was measured off-line in six end-systolic segments and fitted to an exponential curve (gamma variate). Derived peak SI was subsequently calculated and compared with wall motion and common functional measured quantities (left ventricular end-diastolic diameter [LVEDD], area shortening [AS]). Recordings were performed before and 14 days after left anterior descending (LAD) ligature. Infarction induced anterior wall motion abnormalities (WMA) in all animals (16 akinetic, 9 hypokinetic), increased LVEDD (9.1 +/- 0.6 vs. 7.9 +/- 0.6 mm, p < 0.001), reduced AS (36.1 +/- 10.0 vs. 59.5 +/- 4.1%, p < 0.001) and reduced anterior segmental SI (0.4 +/- 0.4 dB akinetic / 1.7 +/- 1.7 dB hypokinetic vs. 15.8 +/- 10.9 dB preinfarct, p < 0.001 / p < 0.001). Segmental SI in normokinetic segments remained unchanged. Area at risk (perfusion defect) correlated well with WMA (r = 0.838). These data confirmed high-resolution real-time NICE as a rational tool for assessing myocardial perfusion of Wistar rats. It may therefore be a useful diagnostic tool for ill-vivo cardiovascular research in small animals."],["dc.identifier.doi","10.1016/j.ultrasmedbio.2007.06.027"],["dc.identifier.gro","3143391"],["dc.identifier.isi","000252038900007"],["dc.identifier.pmid","17854980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/899"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0301-5629"],["dc.title","Real-time myocardial contrast echocardiography for assessing perfusion and function in healthy and infarcted Wistar rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Nixdorff, U"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Budinsky, L."],["dc.contributor.author","Brune, K"],["dc.contributor.author","Michaelis, B."],["dc.contributor.author","Dhein, S."],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:53:08Z"],["dc.date.available","2017-09-07T11:53:08Z"],["dc.date.issued","2006"],["dc.description.abstract","The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/ diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts."],["dc.identifier.doi","10.1038/nm1394"],["dc.identifier.gro","3143714"],["dc.identifier.isi","000236581300035"],["dc.identifier.pmid","16582915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1259"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","283"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Coronary Artery Disease"],["dc.bibliographiccitation.lastpage","291"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Voigt, Jens-Uwe"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Schineis, Nico"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Flachskampf, Frank A."],["dc.contributor.author","Daniel, Werner G."],["dc.contributor.author","Nixdorff, Uwe"],["dc.date.accessioned","2017-09-07T11:49:28Z"],["dc.date.available","2017-09-07T11:49:28Z"],["dc.date.issued","2007"],["dc.description.abstract","Objective Transthoracic echocardiography has been employed to assess left ventricular dimensions and function in small animals. The aim of this study was to identify the limits of transthoracic echocardiography in a commonly used Wistar rat model by assessing intraobserver variability, interobserver variability, and day-to-day variability of examinations implying registrations and measurements. Methods Twenty male adult Wistar rats (body weight 496 52 g) were examined under volatile isoflurane anesthesia (heart rate 302 26 bpm) by transthoracic echocardiography (Sonos 7500; Philips) with a 15 MHz-transducer. For calculation of intraobserver variability, examinations were repeated by the same examiner and for interobserver variability, examinations were performed independently by two investigators. For day-to-day variability, examinations were repeated 14 days later. Left ventricular diameters and areas were analyzed in parasternal short axis and in a modified parasternal long axis. Fractional shortening, area shortening, ejection fraction, stroke volume, and cardiac output were calculated. Results Left ventricular end-diastolic diameter was 8.9 +/- 0.6 mm, fractional shortening 39.0 +/- 5.3%, area shortening 59.6 +/- 6.1%, ejection fraction 83.3 +/- 5.1%, stroke volume 0.24 +/- 0.06 ml, and cardiac output 72.9 +/- 20.6 ml/ min. Intraobserver variability of left ventricular end-diastolic diameter, fractional shortening, area shortening, and ejection fraction was less than 10%, increasing to 19% for stroke volume and cardiac output. Interobserver variability of left ventricular end-diastolic diameter, fractional shortening, area shortening, ejection fraction was less than 13%, increasing to 23% for stroke volume and 25% for cardiac output. Day-to-day variability of left ventricular end-diastolic diameter, area shortening, ejection fraction was less than 11% whereas for stroke volume it was 21% and for cardiac output it was 22%. F-ratio test comparing investigated variabilities did not reveal significant differences. Conclusions M-mode and two-dimensional echocardiography in large rats by clinically common high-end ultrasound systems can be assessed reliably. Parameters of global left ventricular performance like stroke volume and cardiac output could not be assessed with similar reliability."],["dc.identifier.doi","10.1097/MCA.0b013e3280d5a7e3"],["dc.identifier.gro","3143489"],["dc.identifier.isi","000247162700007"],["dc.identifier.pmid","17496492"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1008"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0954-6928"],["dc.title","Reproducibility of transthoracic echocardiography in small animals using clinical equipment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","419"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","429"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Doeker, Stephan"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Rogge, Christina"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:52:36Z"],["dc.date.available","2017-09-07T11:52:36Z"],["dc.date.issued","2006"],["dc.description.abstract","Cardiac muscle engineering aims at providing functional myocardium to repair diseased hearts and model cardiac development, physiology.. and disease in vitro. Several enabling technologies have been established over the past 10 years to create functional myocardium. Although none of the presently employed technologies yields a perfect match of natural heart muscle, it can be anticipated that human heart muscle equivalents will become available after fine tuning of currently established tissue engineering concepts. This review provides an update on the state of cardiac muscle engineering and its utilization in cardiac regeneration. We discuss the application of stem cells including the allocation of autologous cell material, transgenic technologies that may improve tissue structure as well as in vivo engraftment, and vascularization concepts. We also touch on legal and economic aspects that have to be considered before engineered myocardium may eventually be applied in patients and discuss who may be a potential recipient. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.cardiores.2006.03.023"],["dc.identifier.gro","3143648"],["dc.identifier.isi","000239883900007"],["dc.identifier.pmid","16697358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1185"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Heart muscle engineering: An update on cardiac muscle replacement therapy"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1639"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Biomaterials"],["dc.bibliographiccitation.lastpage","1647"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:43:53Z"],["dc.date.available","2017-09-07T11:43:53Z"],["dc.date.issued","2004"],["dc.description.abstract","Cardiac tissue engineering aims at providing contractile heart muscle constructs for replacement therapy in vivo. At present, most cardiac tissue engineering attempts utilize heart cells from embryonic chicken and neonatal rats and scaffold materials. Over the past years our group has developed a novel technique to engineer collagen/matrigel-based cardiac muscle constructs, which we termed engineered heart tissue (EHT). EHT display functional and morphological properties of differentiated heart muscle and call be constructed in different shape and size from collagen type I, extracellular matrix proteins (Matrigel(R)), and heart cells from neonatal rats and embryonic chicken. First implantation studies in syngeneic Fischer 344 rats provided evidence of EHT survival and integration in vivo. This review will focus oil our experience in tissue engineering of cardiac muscle. Mainly, EHT construction, matrix requirements, potential applications of different cell types including stem cells, and our first implantation experiences will be discussed. Despite many critical and unresolved questions, we believe that cardiac tissue engineering in general has an interesting perspective for the replacement of malfunctioning myocardium and reconstruction of congenital malformations. (C) 2003 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0142-9612(03)00521-0"],["dc.identifier.gro","3143998"],["dc.identifier.isi","000187916100018"],["dc.identifier.pmid","14697865"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1574"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","0142-9612"],["dc.title","Engineered heart tissue for regeneration of diseased hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","396"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","406"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Weinberger, Florian"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Peeck, Micha"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:48:07Z"],["dc.date.available","2017-09-07T11:48:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Phosphatase inhibitor-1 (I-1) is a conditional amplifier of beta-adrenergic signalling downstream of protein kinase A by inhibiting type-1 phosphatases only in its PKA-phosphorylated form. I-1 is downregulated in failing hearts and thus contributes to beta-adrenergic desensitization. It is unclear whether this should be viewed as a predominantly adverse or protective response. We generated transgenic mice with cardiac-specific I-1 overexpression (I-1-TG) and evaluated cardiac function and responses to catecholamines in mice with targeted disruption of the I-1 gene (I-1-KO). Both groups were compared with their wild-type (WT) littermates. I-1-TG developed cardiac hypertrophy and mild dysfunction which was accompanied by a substantial compensatory increase in PP1 abundance and activity, confounding cause-effect relationships. I-1-KO had normal heart structure with mildly reduced sensitivity, but unchanged maximal contractile responses to beta-adrenergic stimulation, both in vitro and in vivo. Notably, I-1-KO were partially protected from lethal catecholamine-induced arrhythmias and from hypertrophy and dilation induced by a 7 day infusion with the beta-adrenergic agonist isoprenaline. Moreover, I-1-KO exhibited a partially preserved acute beta-adrenergic response after chronic isoprenaline, which was completely absent in similarly treated WT. At the molecular level, I-1-KO showed lower steady-state phosphorylation of the cardiac ryanodine receptor/Ca(2+) release channel and the sarcoplasmic reticulum (SR) Ca(2+)-ATPase-regulating protein phospholamban. These alterations may lower the propensity for diastolic Ca(2+) release and Ca(2+) uptake and thus stabilize the SR and account for the protection. Taken together, loss of I-1 attenuates detrimental effects of catecholamines on the heart, suggesting I-1 downregulation in heart failure as a beneficial desensitization mechanism and I-1 inhibition as a potential novel strategy for heart failure treatment."],["dc.identifier.doi","10.1093/cvr/cvn208"],["dc.identifier.gro","3143199"],["dc.identifier.isi","000260973500012"],["dc.identifier.pmid","18689792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/687"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Phosphatase inhibitor-1-deficient mice are protected from catecholamine-induced arrhythmias and myocardial hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","I72"],["dc.bibliographiccitation.lastpage","I78"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Schneiderbanger, Karin"],["dc.contributor.author","Schubert, Pia"],["dc.contributor.author","Rosenkranz, Stephan"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:52:38Z"],["dc.date.available","2017-09-07T11:52:38Z"],["dc.date.issued","2006"],["dc.description.abstract","Background-Cardiac tissue engineering aims at providing heart muscle for cardiac regeneration. Here, we hypothesized that engineered heart tissue (EHT) can be improved by using mixed heart cell populations, culture in defined serum-free and Matrigel-free conditions, and fusion of single-unit EHTs to multi-unit heart muscle surrogates. Methods and Results-EHTs were constructed from native and cardiac myocyte enriched heart cell populations. The former demonstrated a superior contractile performance and developed vascular structures. Peptide growth factor-supplemented culture medium was developed to maintain contractile EHTs in a serum-free environment. Addition of triiodothyronine and insulin facilitated withdrawal of Matrigel from the EHT reconstitution mixture. Single-unit EHTs could be fused to form large multi-unit EHTs with variable geometries. Conclusions-Simulating a native heart cell environment in EHTs leads to improved function and formation of primitive capillaries. The latter may constitute a preformed vascular bed in vitro and facilitate engraftment in vivo. Serum- and Matrigel-free culture conditions are expected to reduce immunogenicity of EHT. Fusion of single-unit EHT allows production of large heart muscle constructs that may eventually serve as optimized tissue grafts in cardiac regeneration in vivo."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.105.001560"],["dc.identifier.gro","3143660"],["dc.identifier.isi","000238688200014"],["dc.identifier.pmid","16820649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1198"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Dallas, TX"],["dc.relation.ispartof","Circulation"],["dc.relation.issn","0009-7322"],["dc.title","Optimizing engineered heart tissue for therapeutic applications as surrogate heart muscle"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","12_suppl_1"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Nixdorff, Uwe"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Boy, Oliver"],["dc.contributor.author","Neuhuber, Winfried L."],["dc.contributor.author","Weyand, Michael"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2022-06-08T07:57:10Z"],["dc.date.available","2022-06-08T07:57:10Z"],["dc.date.issued","2002"],["dc.description.abstract","Background Cell grafting has emerged as a novel approach to treat heart diseases refractory to conventional therapy. We hypothesize that survival and functional and electrical integration of grafts may be improved by engineering cardiac tissue constructs in vitro before grafting. Methods and Results Engineered heart tissue (EHT) was reconstituted by mixing cardiac myocytes from neonatal Fischer 344 rats with liquid collagen type I, matrigel, and serum-containing culture medium. EHTs were designed in circular shape (inner/outer diameter: 8/10 mm; thickness: 1 mm) to fit around the circumference of hearts from syngenic rats. After 12 days in culture and before implantation on uninjured hearts, contractile function of EHT was measured under isometric conditions. Baseline twitch tension amounted to 0.34±0.03 mN (n=33) and was stimulated by Ca 2+ and isoprenaline to 200±12 and 185±10% of baseline values, respectively. Despite utilization of a syngenic model immunosuppression (mg/kg BW: azathioprine 2, cyclosporine A 5, methylprednisolone 2) was necessary for EHT survival in vivo. Echocardiography conducted 7, 14, and 28 days after implantation demonstrated no change in left ventricular function compared with pre-OP values (n=9). Fourteen days after implantation, EHTs were heavily vascularized and retained a well organized heart muscle structure as indicated by immunolabeling of actinin, connexin 43, and cadherins. Ultrastructural analysis demonstrated that implanted EHTs surpassed the degree of differentiation reached before implantation. Contractile function of EHT grafts was preserved in vivo. Conclusions EHTs can be employed for tissue grafting approaches and might serve as graft material to repair diseased myocardium."],["dc.identifier.doi","10.1161/01.cir.0000032876.55215.10"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110014"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Cardiac Grafting of Engineered Heart Tissue in Syngenic Rats"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]