Mansouri, Ahmed

[["dc.bibliographiccitation.firstpage","3948"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3957"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Shamsi, Farnaz"],["dc.contributor.author","Parlato, Rosanna"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:31:14Z"],["dc.date.available","2018-11-07T09:31:14Z"],["dc.date.issued","2014"],["dc.description.abstract","The putative induction of adult -cell regeneration represents a promising approach for the treatment of type 1 diabetes. Toward this ultimate goal, it is essential to develop an inducible model mimicking the long-lasting disease progression. In the current study, we have established a novel -cell ablation mouse model, in which the -cell mass progressively declines, as seen in type 1 diabetes. The model is based on the -cell specific genetic ablation of the transcription initiation factor 1A, TIF-IA, essential for RNA Polymerase I activity (TIF-IA(/)). Using this approach, we induced a slow apoptotic response that eventually leads to a protracted -cell death. In this model, we observed -cell regeneration that resulted in a complete recovery of the -cell mass and normoglycemia. In addition, we showed that adaptive proliferation of remaining -cells is the prominent mechanism acting to compensate for the massive -cell loss in young but also aged mice. Interestingly, at any age, we also detected -like cells expressing the glucagon hormone, suggesting a transition between - and -cell identities or vice versa. Taken together, the TIF-IA(/) mouse model can be used to investigate the potential therapeutic approaches for type 1 diabetes targeting -cell regeneration."],["dc.identifier.doi","10.4161/15384101.2014.952176"],["dc.identifier.isi","000348329600024"],["dc.identifier.pmid","25558832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31496"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.title","A genetic mouse model for progressive ablation and regeneration of insulin producing beta-cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3243"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3244"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Al-Hasani, Keith"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Faurite, Biljana"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:18:37Z"],["dc.date.available","2018-11-07T09:18:37Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.4161/cc.26357"],["dc.identifier.isi","000327381100004"],["dc.identifier.pmid","24036539"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28443"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Induction of multiple cycles of pancreatic beta-cell replacement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Al-Hasani, Keith"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Leuckx, Gunter"],["dc.contributor.author","Lacas-Gervais, Sandra"],["dc.contributor.author","Ambrosetti, Damien"],["dc.contributor.author","Benizri, Emmanuel"],["dc.contributor.author","Hecksher-Sorensen, Jacob"],["dc.contributor.author","Gounon, Pierre"],["dc.contributor.author","Ferrer, Jorge"],["dc.contributor.author","Gradwohl, Gerard"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:22:22Z"],["dc.date.available","2018-11-07T09:22:22Z"],["dc.date.issued","2013"],["dc.description.abstract","It was recently demonstrated that embryonic glucagon-producing cells in the pancreas can regenerate and convert into insulin-producing beta-like cells through the constitutive/ectopic expression of the Pax4 gene. However, whether alpha cells in adult mice display the same plasticity is unknown. Similarly, the mechanisms underlying such reprogramming remain unclear. We now demonstrate that the misexpression of Pax4 in glucagon(+) cells age-independently induces their conversion into beta-like cells and their glucagon shortage-mediated replacement, resulting in islet hypertrophy and in an unexpected islet neogenesis. Combining several lineage-tracing approaches, we show that, upon Pax4-mediated alpha-to-beta-like cell conversion, pancreatic duct-lining precursor cells are continuously mobilized, re-express the developmental gene Ngn3, and successively adopt a glucagon+ and a beta-like cell identity through a mechanism involving the reawakening of the epithelial-to-mesenchymal transition. Importantly, these processes can repeatedly regenerate the whole beta cell mass and thereby reverse several rounds of toxin-induced diabetes, providing perspectives to design therapeutic regenerative strategies."],["dc.identifier.doi","10.1016/j.devcel.2013.05.018"],["dc.identifier.isi","000322087400009"],["dc.identifier.pmid","23810513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29326"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1534-5807"],["dc.title","Adult Duct-Lining Cells Can Reprogram into beta-like Cells Able to Counter Repeated Cycles of Toxin-Induced Diabetes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","838"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Seminars in Cell and Developmental Biology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T08:38:58Z"],["dc.date.available","2018-11-07T08:38:58Z"],["dc.date.issued","2010"],["dc.description.abstract","The pancreas is composed of two main compartments consisting of endocrine and exocrine tissues. The majority of the organ is exocrine and responsible for the synthesis of digestive enzymes and for their transport via an intricate ductal system into the duodenum. The endocrine tissue represents less than 2% of the organ and is organized into functional units called islets of Langerhans, comprising alpha-, beta-, delta-, epsilon- and PP-cells, producing the hormones glucagon, insulin, somatostatin, ghrelin and pancreatic polypeptide (PP), respectively. Insulin-producing beta- cells play a central role in the control of the glucose homeostasis. Accordingly, absolute or relative deficiency in beta-cells may ultimately lead to type 1 and/or type 2 diabetes, respectively. One major goal of diabetes research is therefore to understand the molecular mechanisms controlling the development of beta-cells during pancreas morphogenesis, but also those underlying the regeneration of adult injured pancreas, and assess their significance for future cell-based therapy. In this review, we will therefore present new insights into beta-cell development with focus on beta-cell regeneration. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.semcdb.2010.07.007"],["dc.identifier.isi","000283598400010"],["dc.identifier.pmid","20688184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18878"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1084-9521"],["dc.title","Pancreatic beta-cells: From generation to regeneration"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1003934"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Ravaud, Christophe"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Leuckx, Gunter"],["dc.contributor.author","Lacas-Gervais, Sandra"],["dc.contributor.author","Burel-Vandenbos, Fanny"],["dc.contributor.author","Ambrosetti, Damien"],["dc.contributor.author","Hecksher-Sorensen, Jacob"],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:18:47Z"],["dc.date.available","2018-11-07T09:18:47Z"],["dc.date.issued","2013"],["dc.description.abstract","Recently, it was demonstrated that pancreatic new-born glucagon-producing cells can regenerate and convert into insulinproducing beta-like cells through the ectopic expression of a single gene, Pax4. Here, combining conditional loss-of-function and lineage tracing approaches, we show that the selective inhibition of the Arx gene in alpha-cells is sufficient to promote the conversion of adult alpha-cells into beta-like cells at any age. Interestingly, this conversion induces the continuous mobilization of duct-lining precursor cells to adopt an endocrine cell fate, the glucagon(+) cells thereby generated being subsequently converted into beta-like cells upon Arx inhibition. Of interest, through the generation and analysis of Arx and Pax4 conditional double-mutants, we provide evidence that Pax4 is dispensable for these regeneration processes, indicating that Arx represents the main trigger of alpha-cell-mediated beta-like cell neogenesis. Importantly, the loss of Arx in alpha-cells is sufficient to regenerate a functional beta-cell mass and thereby reverse diabetes following toxin-induced beta-cell depletion. Our data therefore suggest that strategies aiming at inhibiting the expression of Arx, or its molecular targets/co-factors, may pave new avenues for the treatment of diabetes."],["dc.identifier.doi","10.1371/journal.pgen.1003934"],["dc.identifier.isi","000330367200085"],["dc.identifier.pmid","24204325"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9441"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28484"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Inactivation of Arx in Pancreatic alpha-Cells Triggers Their Neogenesis and Conversion into Functional beta-Like Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0201536"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Vergoni, Bastien"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Druelle, Noémie"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Hadzic, Biljana"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Napolitano, Tiziana"],["dc.contributor.author","Navarro Sanz, Sergi"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.editor","Rooman, Ilse"],["dc.date.accessioned","2020-12-10T18:42:07Z"],["dc.date.available","2020-12-10T18:42:07Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1371/journal.pone.0201536"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77817"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Neurog3 misexpression unravels mouse pancreatic ductal cell plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3450"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3451"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:22:28Z"],["dc.date.available","2018-11-07T11:22:28Z"],["dc.date.issued","2009"],["dc.description.sponsorship","NIDDK NIH HHS [U19 DK 072495-01]"],["dc.identifier.doi","10.4161/cc.8.21.9791"],["dc.identifier.isi","000272218600009"],["dc.identifier.pmid","19838059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55998"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","Turning on the beta-cell identity in the pancreas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4299"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","4311"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Druelle, Noémie"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Shabro, Aidin"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Mondin, Magali"],["dc.contributor.author","Rekima, Samah"],["dc.contributor.author","Napolitano, Tiziana"],["dc.contributor.author","Silvano, Serena"],["dc.contributor.author","Navarro-Sanz, Sergi"],["dc.contributor.author","Hadzic, Biljana"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Rassoulzadegan, Minoo"],["dc.contributor.author","Schmid, Herbert A."],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2020-12-10T18:15:35Z"],["dc.date.available","2020-12-10T18:15:35Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1083/jcb.201704044"],["dc.identifier.eissn","1540-8140"],["dc.identifier.issn","0021-9525"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74895"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ectopic expression of Pax4 in pancreatic δ cells results in β-like cell neogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","248"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","World journal of stem cells"],["dc.bibliographiccitation.lastpage","255"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Liao, Mei-Chih"],["dc.contributor.author","Diaconu, Mihaela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Timaeus, Charles"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2019-07-09T11:42:00Z"],["dc.date.available","2019-07-09T11:42:00Z"],["dc.date.issued","2014-04-26"],["dc.description.abstract","AIM: To find a safe source for dopaminergic neurons, we generated neural progenitor cell lines from human embryonic stem cells. METHODS: The human embryonic stem (hES) cell line H9 was used to generate human neural progenitor (HNP) cell lines. The resulting HNP cell lines were differentiated into dopaminergic neurons and analyzed by quantitative real-time polymerase chain reaction and immunofluorescence for the expression of neuronal differentiation markers, including beta-III tubulin (TUJ1) and tyrosine hydroxylase (TH). To assess the risk of teratoma or other tumor formation, HNP cell lines and mouse neuronal progenitor (MNP) cell lines were injected subcutaneously into immunodeficient SCID/beige mice. RESULTS: We developed a fairly simple and fast protocol to obtain HNP cell lines from hES cells. These cell lines, which can be stored in liquid nitrogen for several years, have the potential to differentiate in vitro into dopaminergic neurons. Following day 30 of differentiation culture, the majority of the cells analyzed expressed the neuronal marker TUJ1 and a high proportion of these cells were positive for TH, indicating differentiation into dopaminergic neurons. In contrast to H9 ES cells, the HNP cell lines did not form tumors in immunodeficient SCID/beige mice within 6 mo after subcutaneous injection. Similarly, no tumors developed after injection of MNP cells. Notably, mouse ES cells or neuronal cells directly differentiated from mouse ES cells formed teratomas in more than 90% of the recipients. CONCLUSION: Our findings indicate that neural progenitor cell lines can differentiate into dopaminergic neurons and bear no risk of generating teratomas or other tumors in immunodeficient mice."],["dc.identifier.doi","10.4252/wjsc.v6.i2.248"],["dc.identifier.fs","604380"],["dc.identifier.pmid","24772251"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12652"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58563"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1948-0210"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Embryonic stem cell-derived neural progenitors as non-tumorigenic source for dopaminergic neurons."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","52"],["dc.bibliographiccitation.journal","BMC Developmental Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Kordowich, Simon"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Serup, Palle"],["dc.date.accessioned","2018-11-07T08:53:03Z"],["dc.date.available","2018-11-07T08:53:03Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: Nkx2.2 and Arx represent key transcription factors implicated in the specification of islet cell subtypes during pancreas development. Mice deficient for Arx do not develop any alpha-cells whereas beta- and delta-cells are found in considerably higher numbers. In Nkx2.2 mutant animals, alpha- and beta-cell development is severely impaired whereas a ghrelin-expressing cell population is found augmented. Notably, Arx transcription is clearly enhanced in Nkx2.2-deficient pancreata. Hence in order to precise the functional link between both factors we performed a comparative analysis of Nkx2.2/Arx single- and double-mutants but also of Pax6-deficient animals. Results: We show that most of the ghrelin(+) cells emerging in pancreata of Nkx2.2- and Pax6-deficient mice, express the alpha-cell specifier Arx, but also additional beta-cell related genes. In Nkx2.2-deficient mice, Arx directly co-localizes with iAPP, PC1/3 and Pdx1 suggesting an Nkx2.2-dependent control of Arx in committed beta-cells. The combined loss of Nkx2.2 and Arx likewise results in the formation of a hyperplastic ghrelin(+) cell population at the expense of mature alpha- and beta-cells. Surprisingly, such Nkx2.2(-/-)Arx(-) ghrelin(+) cells also express the somatostatin hormone. Conclusions: Our data indicate that Nkx2.2 acts by reinforcing the transcriptional networks initiated by Pax4 and Arx in early committed beta- and alpha-cell, respectively. Our analysis also suggests that one of the coupled functions of Nkx2.2 and Pax4 is to counteract Arx gene activity in early committed beta-cells."],["dc.identifier.doi","10.1186/1471-213X-11-52"],["dc.identifier.isi","000295264200001"],["dc.identifier.pmid","21880149"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6945"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22316"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-213X"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Arx and Nkx2.2 compound deficiency redirects pancreatic alpha- and beta-cell differentiation to a somatostatin/ghrelin co-expressing cell lineage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]