Müller, Michael

[["dc.bibliographiccitation.firstpage","2915"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","2930"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Kobe, Fritz"],["dc.contributor.author","Guseva, Daria"],["dc.contributor.author","Jensen, Thomas P."],["dc.contributor.author","Wirth, Alexander"],["dc.contributor.author","Renner, Ute"],["dc.contributor.author","Hess, Dietmar"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Zhang, Weiqi"],["dc.contributor.author","Zhang, Mingyue"],["dc.contributor.author","Braun, Katharina"],["dc.contributor.author","Westerholz, Sören"],["dc.contributor.author","Herzog, Andreas"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Rusakov, Dmitri A."],["dc.contributor.author","Ponimaskin, Evgeni"],["dc.date.accessioned","2017-09-07T11:46:22Z"],["dc.date.available","2017-09-07T11:46:22Z"],["dc.date.issued","2012"],["dc.description.abstract","The common neurotransmitter serotonin controls different aspects of early neuronal differentiation, although the underlying mechanisms are poorly understood. Here we report that activation of the serotonin 5-HT7 receptor promotes synaptogenesis and enhances synaptic activity in hippocampal neurons at early postnatal stages. An analysis of Gα12-deficient mice reveals a critical role of G12-protein for 5-HT7 receptor-mediated effects in neurons. In organotypic preparations from the hippocampus of juvenile mice, stimulation of 5-HT7R/G12 signaling potentiates formation of dendritic spines, increases neuronal excitability, and modulates synaptic plasticity. In contrast, in older neuronal preparations, morphogenetic and synaptogenic effects of 5-HT7/G12 signaling are abolished. Moreover, inhibition of 5-HT7 receptor had no effect on synaptic plasticity in hippocampus of adult animals. Expression analysis reveals that the production of 5-HT7 and Gα12-proteins in the hippocampus undergoes strong regulation with a pronounced transient increase during early postnatal stages. Thus, regulated expression of 5-HT7 receptor and Gα12-protein may represent a molecular mechanism by which serotonin specifically modulates formation of initial neuronal networks during early postnatal development."],["dc.identifier.doi","10.1523/JNEUROSCI.2765-11.2012"],["dc.identifier.gro","3150488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7258"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.title","5-HT₇R/G₁₂ signaling regulates neuronal morphology and function in an age-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1089"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.lastpage","1109"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Steiner, Eric"],["dc.contributor.author","Vordermark, Dirk"],["dc.contributor.author","Uleer, Christoph"],["dc.contributor.author","Bock, Nina"],["dc.contributor.author","Paradies, Kerstin"],["dc.contributor.author","Ortmann, Olaf"],["dc.contributor.author","Aretz, Stefan"],["dc.contributor.author","Mallmann, Peter"],["dc.contributor.author","Kurzeder, Christian"],["dc.contributor.author","Hagen, Volker"],["dc.contributor.author","van Oorschot, Birgitt"],["dc.contributor.author","Höcht, Stefan"],["dc.contributor.author","Feyer, Petra"],["dc.contributor.author","Egerer, Gerlinde"],["dc.contributor.author","Friedrich, Michael"],["dc.contributor.author","Cremer, Wolfgang"],["dc.contributor.author","Prott, Franz-Josef"],["dc.contributor.author","Horn, Lars-Christian"],["dc.contributor.author","Prömpeler, Heinrich"],["dc.contributor.author","Langrehr, Jan"],["dc.contributor.author","Leinung, Steffen"],["dc.contributor.author","Beckmann, Matthias"],["dc.contributor.author","Kimmig, Rainer"],["dc.contributor.author","Letsch, Anne"],["dc.contributor.author","Reinhardt, Michael"],["dc.contributor.author","Alt-Epping, Bernd"],["dc.contributor.author","Kiesel, Ludwig"],["dc.contributor.author","Menke, Jan"],["dc.contributor.author","Gebhardt, Marion"],["dc.contributor.author","Steinke-Lange, Verena"],["dc.contributor.author","Rahner, Nils"],["dc.contributor.author","Lichtenegger, Werner"],["dc.contributor.author","Zeimet, Alain"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Weis, Joachim"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Henscher, Ulla"],["dc.contributor.author","Schmutzler, Rita"],["dc.contributor.author","Meindl, Alfons"],["dc.contributor.author","Hilpert, Felix"],["dc.contributor.author","Panke, Joan"],["dc.contributor.author","Strnad, Vratislav"],["dc.contributor.author","Niehues, Christiane"],["dc.contributor.author","Dauelsberg, Timm"],["dc.contributor.author","Niehoff, Peter"],["dc.contributor.author","Mayr, Doris"],["dc.contributor.author","Grab, Dieter"],["dc.contributor.author","Kreißl, Michael"],["dc.contributor.author","Witteler, Ralf"],["dc.contributor.author","Schorsch, Annemarie"],["dc.contributor.author","Mustea, Alexander"],["dc.contributor.author","Petru, Edgar"],["dc.contributor.author","Hübner, Jutta"],["dc.contributor.author","Rose, Anne"],["dc.contributor.author","Wight, Edward"],["dc.contributor.author","Tholen, Reina"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Fleisch, Markus"],["dc.contributor.author","Juhasz-Boess, Ingolf"],["dc.contributor.author","Lax, Sigurd"],["dc.contributor.author","Runnebaum, Ingo"],["dc.contributor.author","Tempfer, Clemens"],["dc.contributor.author","Nothacker, Monika"],["dc.contributor.author","Blödt, Susanne"],["dc.contributor.author","Follmann, Markus"],["dc.contributor.author","Langer, Thomas"],["dc.contributor.author","Raatz, Heike"],["dc.contributor.author","Wesselmann, Simone"],["dc.contributor.author","Erdogan, Saskia"],["dc.date.accessioned","2020-12-10T18:12:05Z"],["dc.date.available","2020-12-10T18:12:05Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1055/a-0715-2964"],["dc.identifier.eissn","1438-8804"],["dc.identifier.issn","0016-5751"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74238"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interdisciplinary Diagnosis, Therapy and Follow-up of Patients with Endometrial Cancer. Guideline (S3-Level, AWMF Registry Number 032/034-OL, April 2018) – Part 2 with Recommendations on the Therapy and Follow-up of Endometrial Cancer, Palliative Care, Psycho-oncological/Psychosocial Care/Rehabilitation/Patient Information and Healthcare Facilities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","959"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biochemical Society Transactions"],["dc.bibliographiccitation.lastpage","964"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Can, Karolina"],["dc.date.accessioned","2018-09-28T10:11:26Z"],["dc.date.available","2018-09-28T10:11:26Z"],["dc.date.issued","2014"],["dc.description.abstract","RTT (Rett syndrome) is a severe progressive neurodevelopmental disorder with a monogenetic cause, but complex and multifaceted clinical appearance. Compelling evidence suggests that mitochondrial alterations and aberrant redox homoeostasis result in oxidative challenge. Yet, compared with other severe neuropathologies, RTT is not associated with marked neurodegeneration, but rather a chemical imbalance and miscommunication of neuronal elements. Different pharmacotherapies mediate partial improvement of conditions in RTT, and also antioxidants or compounds improving mitochondrial function may be of potential merit. In the present paper, we summarize findings from patients and transgenic mice that point towards the nature of RTT as a mitochondrial disease. Also, open questions are addressed that require clarification to fully understand and successfully target the associated cellular redox imbalance."],["dc.identifier.doi","10.1042/BST20140071"],["dc.identifier.pmid","25109986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15853"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1470-8752"],["dc.title","Aberrant redox homoeostasis and mitochondrial dysfunction in Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","108666"],["dc.bibliographiccitation.journal","Archives of Biochemistry and Biophysics"],["dc.bibliographiccitation.volume","696"],["dc.contributor.author","Adebayo, Olusegun L."],["dc.contributor.author","Dewenter, Ina"],["dc.contributor.author","Rinne, Lena"],["dc.contributor.author","Golubiani, Gocha"],["dc.contributor.author","Solomonia, Revaz"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2021-04-14T08:30:22Z"],["dc.date.available","2021-04-14T08:30:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.abb.2020.108666"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83211"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0003-9861"],["dc.title","Intensified mitochondrial hydrogen peroxide release occurs in all brain regions, affects male as well as female Rett mice, and constitutes a life-long burden"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3067"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","3079"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Kron, Miriam"],["dc.contributor.author","Zimmermann, Jasper L."],["dc.contributor.author","Dutschmann, Mathias"],["dc.contributor.author","Funke, Frank"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:28:17Z"],["dc.date.available","2018-09-28T10:28:17Z"],["dc.date.issued","2011"],["dc.description.abstract","Rett syndrome (RTT) patients suffer from respiratory arrhythmias with frequent apneas causing intermittent hypoxia. In a RTT mouse model (methyl-CpG-binding protein 2-deficient mice; Mecp2(-/y)) we recently discovered an enhanced hippocampal susceptibility to hypoxia and hypoxia-induced spreading depression (HSD). In the present study we investigated whether this also applies to infant Mecp2(-/y) brain stem, which could become life-threatening due to failure of cardiorespiratory control. HSD most reliably occurred in the nucleus of the solitary tract (NTS) and the spinal trigeminal nucleus (Sp5). HSD susceptibility of the Mecp2(-/y) NTS and Sp5 was increased on 8 mM K(+)-mediated conditioning. 5-HT(1A) receptor stimulation with 8-hydroxy-2-(di-propylamino)tetralin (8-OH-DPAT) postponed HSD by up to 40%, mediating genotype-independent protection. The deleterious impact of HSD on in vitro respiration became obvious in rhythmically active slices, where HSD propagation into the pre-Bötzinger complex (pre-BötC) immediately arrested the respiratory rhythm. Compared with wild-type, the Mecp2(-/y) pre-BötC was invaded less frequently by HSD, but if so, HSD occurred earlier. On reoxygenation, in vitro rhythms reappeared with increased frequency, which was less pronounced in Mecp2(-/y) slices. 8-OH-DPAT increased respiratory frequency but failed to postpone HSD in the pre-BötC. Repetitive hypoxia facilitated posthypoxic recovery only if HSD occurred. In 57% of Mecp2(-/y) slices, however, HSD spared the pre-BötC. Although this occasionally promoted residual hypoxic respiratory activity (\"gasping\"), it also prolonged the posthypoxic recovery, and thus the absence of central inspiratory drive, which in vivo would lengthen respiratory arrest. In view of the breathing disorders in RTTs, the increased hypoxia susceptibility of MeCP2-deficient brain stem potentially contributes to life-threatening disturbances of cardiorespiratory control."],["dc.identifier.doi","10.1152/jn.00822.2010"],["dc.identifier.pmid","21471397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15858"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1522-1598"],["dc.title","Altered responses of MeCP2-deficient mouse brain stem to severe hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","no"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","ChemInform"],["dc.bibliographiccitation.lastpage","no"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Schuetzenmeister, Nina"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Reinscheid, Uwe M."],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Leonov, Andrei"],["dc.date.accessioned","2021-12-08T12:30:12Z"],["dc.date.available","2021-12-08T12:30:12Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1002/chin.201420217"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/96357"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.issn","0931-7597"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","ChemInform Abstract: Trapped in Misbelief for Almost 40 Years: Selective Synthesis of the Four Stereoisomers of Mefloquine."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2615"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","ChemBioChem"],["dc.bibliographiccitation.lastpage","2619"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Roth, Sebastian"],["dc.contributor.author","Stockinger, Peter"],["dc.contributor.author","Steff, Jakob"],["dc.contributor.author","Steimle, Simon"],["dc.contributor.author","Sautner, Viktor"],["dc.contributor.author","Tittmann, Kai"],["dc.contributor.author","Pleiss, Jürgen"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2021-04-14T08:24:57Z"],["dc.date.available","2021-04-14T08:24:57Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/cbic.202000233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81475"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1439-7633"],["dc.relation.issn","1439-4227"],["dc.title","Crossing the Border: From Keto‐ to Imine Reduction in Short‐Chain Dehydrogenases/Reductases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4S_Part_12"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Pillot, Thierry"],["dc.contributor.author","Papot‐Couturier, Sophie"],["dc.contributor.author","Lefebvre, Thomas"],["dc.contributor.author","Sprenger, Frederick"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2021-12-08T12:27:20Z"],["dc.date.available","2021-12-08T12:27:20Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.jalz.2013.05.1030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95320"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","P2–381: Tg4–42: A new mouse model of Alzheimer's disease—N‐truncated beta‐amyloid 4–42 affects memory decline and synaptic plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1843"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","1852"],["dc.bibliographiccitation.volume","95"],["dc.contributor.author","Neusch, Clemens"],["dc.contributor.author","Papadopoulos, Nestoras"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Maletzki, Iris"],["dc.contributor.author","Winter, S M"],["dc.contributor.author","Hirrlinger, J"],["dc.contributor.author","Handschuh, M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Hülsmann, Swen"],["dc.date.accessioned","2017-09-07T11:53:20Z"],["dc.date.available","2017-09-07T11:53:20Z"],["dc.date.issued","2006"],["dc.description.abstract","Ongoing rhythmic neuronal activity in the ventral respiratory group (VRG) of the brain stem results in periodic changes of extracellular K+. To estimate the involvement of the weakly inwardly rectifying K+ channel Kir4.1 (KCNJ10) in extracellular K+ clearance, we examined its functional expression in astrocytes of the respiratory network. Kir4.1 was expressed in astroglial cells of the VRG, predominantly in fine astrocytic processes surrounding capillaries and in close proximity to VRG neurons. Kir4.1 expression was up-regulated during early postnatal development. The physiological role of astrocytic Kir4.1 was studied using mice with a null mutation in the Kir4.1 channel gene that were interbred with transgenic mice expressing the enhanced green fluorescent protein in their astrocytes. The membrane potential was depolarized in astrocytes of Kir4.1(-/-) mice, and Ba2+-sensitive inward K+ currents were diminished. Brain slices from Kir4.1(-/-) mice, containing the pre-Botzinger complex, which generates a respiratory rhythm, did not show any obvious differences in rhythmic bursting activity compared with wild-type controls, indicating that the lack of Kir4.1 channels alone does not impair respiratory network activity. Extracellular K+ measurements revealed that Kir4.1 channels contribute to extracellular K+ regulation. Kir4.1 channels reduce baseline K+ levels, and they compensate for the K+ undershoot. Our data indicate that Kir4.1 channels 1) are expressed in perineuronal processes of astrocytes, 2) constitute the major part of the astrocytic Kir conductance, and 3) contribute to regulation of extracellular K+ in the respiratory network."],["dc.identifier.doi","10.1152/jn.00996.2005"],["dc.identifier.gro","3143730"],["dc.identifier.isi","000235477900049"],["dc.identifier.pmid","16306174"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1276"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0022-3077"],["dc.title","Lack of the Kir4.1 channel subunit abolishes K+ buffering properties of astrocytes in the ventral respiratory group: Impact on extracellular K+ regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.journal","Free Radical Biology & Medicine"],["dc.bibliographiccitation.lastpage","241"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Weller, Jonathan"],["dc.contributor.author","Kizina, Kathrin M."],["dc.contributor.author","Can, Karolina"],["dc.contributor.author","Bao, Guobin"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T09:56:42Z"],["dc.date.available","2018-09-28T09:56:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Reactive oxygen species mediate cellular signaling and neuropathologies. Hence, there is tremendous interest in monitoring (sub)cellular redox conditions. We evaluated the genetically engineered redox sensor HyPer in mouse hippocampal cell cultures. Two days after lipofection, neurons and glia showed sufficient expression levels, and H2O2 reversibly and dose-dependently increased the fluorescence ratio of cytosolic HyPer. Yet, repeated H2O2 treatment caused progressively declining responses, and with millimolar doses an apparent recovery started while H2O2 was still present. Although HyPer should be H2O2 specific, it seemingly responded also to other oxidants and altered cell-endogenous superoxide production. Control experiments with the SypHer pH sensor confirmed that the HyPer ratio responds to pH changes, decreasing with acidosis and increasing during alkalosis. Anoxia/reoxygenation evoked biphasic HyPer responses reporting apparent reduction/oxidation; replacing Cl(-) exerted only negligible effects. Mitochondria-targeted HyPer readily responded to H2O2-albeit less intensely than cytosolic HyPer. With ratiometric two-photon excitation, H2O2 increased the cytosolic HyPer ratio. Time-correlated fluorescence-lifetime imaging microscopy (FLIM) revealed a monoexponential decay of HyPer fluorescence, and H2O2 decreased fluorescence lifetimes. Dithiothreitol failed to further reduce HyPer or to induce reasonable FLIM and two-photon responses. By enabling dynamic recordings, HyPer is superior to synthetic redox-sensitive dyes. Its feasibility for two-photon excitation also enables studies in more complex preparations. Based on FLIM, quantitative analyses might be possible independent of switching excitation wavelengths. Yet, because of its pronounced pH sensitivity, adaptation to repeated oxidation, and insensitivity to reducing stimuli, HyPer responses have to be interpreted carefully. For reliable data, side-by-side pH monitoring with SypHer is essential."],["dc.identifier.doi","10.1016/j.freeradbiomed.2014.07.045"],["dc.identifier.pmid","25179473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15849"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1873-4596"],["dc.title","Response properties of the genetically encoded optical H2O2 sensor HyPer"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]