Capece, Vincenzo

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","7701"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","556"],["dc.contributor.author","Wendeln, Ann-Christin"],["dc.contributor.author","Degenhardt, Karoline"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Ulas, Thomas"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Wagner, Jessica"],["dc.contributor.author","Häsler, Lisa M."],["dc.contributor.author","Wild, Katleen"],["dc.contributor.author","Skodras, Angelos"],["dc.contributor.author","Blank, Thomas"],["dc.contributor.author","Staszewski, Ori"],["dc.contributor.author","Datta, Moumita"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Islam, Md. Rezaul"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Staufenbiel, Matthias"],["dc.contributor.author","Schultze, Joachim L."],["dc.contributor.author","Beyer, Marc"],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Jucker, Mathias"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Neher, Jonas J."],["dc.date.accessioned","2020-12-10T18:09:59Z"],["dc.date.available","2020-12-10T18:09:59Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41586-018-0023-4"],["dc.identifier.eissn","1476-4687"],["dc.identifier.issn","0028-0836"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73816"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Innate immune memory in the brain shapes neurological disease hallmarks"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Schütz, Anna-Lena"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Capece, Vincenzo"],["dc.date.accessioned","2018-04-11T16:20:54Z"],["dc.date.available","2018-04-11T16:20:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Although histone modifications and DNA methylation have been meticulously studied in the context of learning & memory formation, very few studies have demonstrated non-canonical histone variants as potential regulators of memory formation. Compared to canonical histones, these histone variants are expressed independently of DNA replication and are important for many physiological events as they confer altered chromatin structures, thereby regulating transcription. Recently, H2A.Z (variant of canonical histone, H2A) has been reported as a novel epigenetic regulator in memory formation (Zovkic et. al. 2014), which raised the question, whether differential binding of H2A.Z or its modification (e.g acetylation) across the whole genome could be a stable modulator for life-long memory acquisition and cognition. Here, we investigated genomic regions bound by H2A.Z and its acetylated variant (H2A.Zac) using chromatin immunoprecipitation followed by sequencing (ChIP-seq) in FACS-sorted neuronal and nonneuronal nuclei from hippocampal CA1 region. Initially, mRNA levels of H2afz (gene of H2A.Z) were assessed in CA1 region of aged (16 months old) and Alzheimer’s model mice (5XFAD) comparing them to young (3 months old) and wild type mice respectively. Furthermore, ChIP protocols for H2A.Z and H2A.Zac were optimized, as it has not been done before in this context. As a model of enhanced cognition, hippocampal CA1 regions from mice subjected to 4 months enriched environment (EE) were used for ChIP-seq against H2A.Z and H2A.Zac, comparing to home caged animals as controls. ChIP-seq analysis showed decreased binding of H2A.Z and its de-acetylation at specific promoter regions in CA1 neurons upon environmental enrichment. Promoters with decreased binding or decreased acetylation were found to be involved in genes functionally associated with neurogenesis, synaptic plasticity and several biosynthetic pathways. Further study is needed to prove their effect on transcription of those genes."],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13225"],["dc.language.iso","en"],["dc.notes.preprint","yes"],["dc.notes.status","final"],["dc.relation.eventend","4"],["dc.relation.eventlocation","Obergurgl, Austria"],["dc.relation.eventstart","28"],["dc.relation.iserratumof","yes"],["dc.title","Differential binding of non-canonical histone variant H2A.Z & its de-acetylation is evident in enhanced cognitive function"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Capece, V."],["dc.contributor.author","Lbik, D."],["dc.contributor.author","Mohamed, B."],["dc.contributor.author","Danner, Bernhard Christoph"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Fischer, A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2018-11-07T10:15:52Z"],["dc.date.available","2018-11-07T10:15:52Z"],["dc.date.issued","2016"],["dc.format.extent","S61"],["dc.identifier.isi","000375417500120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40903"],["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","Of mice and men - a direct comparison of signaling in pressure overload induced hypertrophy and failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3572"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","3584"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Haider, Rashi"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Navarro-Sala, Magdalena"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Schuetz, Anna-Lena"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Luehrmann, Reinhard"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:34Z"],["dc.date.available","2017-09-07T11:43:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Aging and increased amyloid burden are major risk factors for cognitive diseases such as Alzheimer's disease (AD). Effective therapies for these diseases are lacking. Here, we evaluated mouse models of age-associated memory impairment and amyloid deposition to study transcriptome and cell type-specific epigenome plasticity in the brain and peripheral organs. We determined that aging and amyloid pathology are associated with inflammation and impaired synaptic function in the hippocampal CA1 region as the result of epigenetic-dependent alterations in gene expression. In both amyloid and aging models, inflammation was associated with increased gene expression linked to a subset of transcription factors, while plasticity gene deregulation was differentially mediated. Amyloid pathology impaired histone acetylation and decreased expression of plasticity genes, while aging altered H4K12 acetylation-linked differential splicing at the intron-exon junction in neurons, but not nonneuronal cells. Furthermore, oral administration of the clinically approved histone deacetylase inhibitor vorinostat not only restored spatial memory, but also exerted antiinflammatory action and reinstated epigenetic balance and transcriptional homeostasis at the level of gene expression and exon usage. This study provides a systems-level investigation of transcriptome plasticity in the hippocampal CA1 region in aging and AD models and suggests that histone deacetylase inhibitors should be further explored as a cost-effective therapeutic strategy against age-associated cognitive decline."],["dc.identifier.doi","10.1172/JCI79942"],["dc.identifier.gro","3141833"],["dc.identifier.isi","000362303600031"],["dc.identifier.pmid","26280576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1579"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.title","HDAC inhibitor-dependent transcriptome and memory reinstatement in cognitive decline models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","538"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","548"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.date.accessioned","2018-01-09T14:45:29Z"],["dc.date.available","2018-01-09T14:45:29Z"],["dc.date.issued","2017-07-18"],["dc.description.abstract","Kmt2a and Kmt2b are H3K4 methyltransferases of the Set1/Trithorax class. We have recently shown the importance of Kmt2b for learning and memory. Here, we report that Kmt2a is also important in memory formation. We compare the decrease in H3K4 methylation and de-regulation of gene expression in hippocampal neurons of mice with knockdown of either Kmt2a or Kmt2b. Kmt2a and Kmt2b control largely distinct genomic regions and different molecular pathways linked to neuronal plasticity. Finally, we show that the decrease in H3K4 methylation resulting from Kmt2a knockdown partially recapitulates the pattern previously reported in CK-p25 mice, a model for neurodegeneration and memory impairment. Our findings point to the distinct functions of even closely related histone-modifying enzymes and provide essential insight for the development of more efficient and specific epigenetic therapies against brain diseases."],["dc.identifier.doi","10.1016/j.celrep.2017.06.072"],["dc.identifier.pmid","28723559"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11606"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","2211-1247"],["dc.title","KMT2A and KMT2B Mediate Memory Function by Affecting Distinct Genomic Regions"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","373"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","15"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:45:24Z"],["dc.date.available","2017-09-07T11:45:24Z"],["dc.date.issued","2014"],["dc.description.abstract","Aging is accompanied by gradually increasing impairment of cognitive abilities and constitutes the main risk factor of neurodegenerative conditions like Alzheimer's disease (AD). The underlying mechanisms are however not well understood. Here we analyze the hippocampal transcriptome of young adult mice and two groups of mice at advanced age using RNA sequencing. This approach enabled us to test differential expression of coding and non-coding transcripts, as well as differential splicing and RNA editing. We report a specific age-associated gene expression signature that is associated with major genetic risk factors for late-onset AD (LOAD). This signature is dominated by neuroinflammatory processes, specifically activation of the complement system at the level of increased gene expression, while de-regulation of neuronal plasticity appears to be mediated by compromised RNA splicing."],["dc.identifier.doi","10.3389/fncel.2014.00373"],["dc.identifier.gro","3142019"],["dc.identifier.isi","000345840200001"],["dc.identifier.pmid","25431548"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3645"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1662-5102"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","De-regulation of gene expression and alternative splicing affects distinct cellular pathways in the aging hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1239"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Translational psychiatry"],["dc.bibliographiccitation.lastpage","e1239"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Benito, E."],["dc.contributor.author","Ramachandran, B."],["dc.contributor.author","Schroeder, H."],["dc.contributor.author","Schmidt, G."],["dc.contributor.author","Urbanke, H."],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Capece, V."],["dc.contributor.author","Dean, C."],["dc.contributor.author","Fischer, A."],["dc.date.accessioned","2019-07-09T11:44:50Z"],["dc.date.available","2019-07-09T11:44:50Z"],["dc.date.issued","2017-09-26"],["dc.description.abstract","Histone acetylation is essential for memory formation and its deregulation contributes to the pathogenesis of Alzheimer's disease. Thus, targeting histone acetylation is discussed as a novel approach to treat dementia. The histone acetylation landscape is shaped by chromatin writer and eraser proteins, while readers link chromatin state to cellular function. Chromatin readers emerged novel drug targets in cancer research but little is known about the manipulation of readers in the adult brain. Here we tested the effect of JQ1-a small-molecule inhibitor of the chromatin readers BRD2, BRD3, BRD4 and BRDT-on brain function and show that JQ1 is able to enhance cognitive performance and long-term potentiation in wild-type animals and in a mouse model for Alzheimer's disease. Systemic administration of JQ1 elicited a hippocampal gene expression program that is associated with ion channel activity, transcription and DNA repair. Our findings suggest that JQ1 could be used as a therapy against dementia and should be further tested in the context of learning and memory."],["dc.identifier.doi","10.1038/tp.2017.202"],["dc.identifier.pmid","28949335"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14924"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59110"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/648898/EU//DEPICODE"],["dc.relation.issn","2158-3188"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","612"],["dc.title","The BET/BRD inhibitor JQ1 improves brain plasticity in WT and APP mice."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","546"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","554"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Pena-Centeno, Tonatiuh"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Zhou, Qihui"],["dc.contributor.author","Edbauer, Dieter"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2020-12-10T14:23:00Z"],["dc.date.available","2020-12-10T14:23:00Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.celrep.2018.03.059"],["dc.identifier.issn","2211-1247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71800"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","RNA-Dependent Intergenerational Inheritance of Enhanced Synaptic Plasticity after Environmental Enrichment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1912"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","1927"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Roenicke, Raik"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schuetz, Anna L."],["dc.contributor.author","Dyczkowski, Jerzy"],["dc.contributor.author","Martinez-Hernandez, Ana"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Dent, Sharon Y. R."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Reymann, Klaus G."],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:45:35Z"],["dc.date.available","2017-09-07T11:45:35Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuronal histone acetylation has been linked to memory consolidation, and targeting histone acetylation has emerged as a promising therapeutic strategy for neuropsychiatric diseases. However, the role of histone-modifying enzymes in the adult brain is still far from being understood. Here we use RNA sequencing to screen the levels of all known histone acetyltransferases (HATs) in the hippocampal CA1 region and find that K-acetyltransferase 2a (Kat2a)-a HAT that has not been studied for its role in memory function so far-shows highest expression. Mice that lack Kat2a show impaired hippocampal synaptic plasticity and long-term memory consolidation. We furthermore show that Kat2a regulates a highly interconnected hippocampal gene expression network linked to neuroactive receptor signaling via a mechanism that involves nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B). In conclusion, our data establish Kat2a as a novel and essential regulator of hippocampal memory consolidation."],["dc.identifier.doi","10.15252/embj.201487870"],["dc.identifier.gro","3142062"],["dc.identifier.isi","000341839500009"],["dc.identifier.pmid","25024434"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4123"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.title","K-Lysine acetyltransferase 2a regulates a hippocampal gene expression network linked to memory formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2205"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Bioinformatics"],["dc.bibliographiccitation.lastpage","2207"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Vizcaino, Julio C. Garcia"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Suberviola, Irantzu"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.date.accessioned","2017-09-07T11:43:44Z"],["dc.date.available","2017-09-07T11:43:44Z"],["dc.date.issued","2015"],["dc.description.abstract","Oasis is a web application that allows for the fast and flexible online analysis of small-RNA-seq (sRNA-seq) data. It was designed for the end user in the lab, providing an easy-to-use web frontend including video tutorials, demo data and best practice step-by-step guidelines on how to analyze sRNA-seq data. Oasis' exclusive selling points are a differential expression module that allows for the multivariate analysis of samples, a classification module for robust biomarker detection and an advanced programming interface that supports the batch submission of jobs. Both modules include the analysis of novel miRNAs, miRNA targets and functional analyses including GO and pathway enrichment. Oasis generates downloadable interactive web reports for easy visualization, exploration and analysis of data on a local system. Finally, Oasis' modular workflow enables for the rapid (re-) analysis of data."],["dc.identifier.doi","10.1093/bioinformatics/btv113"],["dc.identifier.gro","3141872"],["dc.identifier.isi","000357425800020"],["dc.identifier.pmid","25701573"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2012"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1460-2059"],["dc.relation.issn","1367-4803"],["dc.title","Oasis: online analysis of small RNA deep sequencing data"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]