Michel, Uwe

[["dc.bibliographiccitation.firstpage","278"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","EP Europace"],["dc.bibliographiccitation.lastpage","284"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Brugada, J."],["dc.contributor.author","Herse, B."],["dc.contributor.author","Sandsted, B."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Schubert, B. D."],["dc.contributor.author","Hahn, S. J."],["dc.date.accessioned","2018-11-07T08:34:18Z"],["dc.date.available","2018-11-07T08:34:18Z"],["dc.date.issued","2001"],["dc.description.abstract","Aims Improvements in the size and shape of implantable cardioverter defibrillators (ICDs) might be obtained by using one capacitor instead of the series connection of two capacitors traditionally used in ICDs. The aim of this study was to determine whether a biphasic waveform delivered from a single 336 muF capacitor had the same defibrillation efficacy as a standard biphasic waveform. Methods and Results Randomized. paired defibrillation threshold testing was acutely performed in 54 patients undergoing ICD implantation. A standard 140 muF 80% tilt biphasic waveform (two 280 muF capacitors connected in series) was compared with an experimental biphasic waveform delivered from a single 336 muF capacitor at either 60% tilt (33 patients) or 80% tilt (21 patients). All waveforms had a 60/40 phase1/phase2 duration ratio. Compared with the standard waveform, the 60% tilt experimental waveform had a lower delivered energy (6.7 +/- 2.8 vs 7.9 +/- 3.3 joules, P < 0.02), lower peak voltage (218 +/- 43 vs 333 +/- 68 V, P < 0.01), and a slightly longer pulse duration (13.4 +/- 1.4 vs 10.7 +/- 1.1 ms, P < 0-01). Conversely, the 80% tilt experimental waveform had a higher delivered energy (9.1 +/- 3.5 vs 6.3 +/- 2.4 joules, P < 0.01), a lower peak voltage (234 +/- 44 vs 302 +/- 51 V, P < 0.01) and a much longer pulse duration (25.7 +/- 2.5 vs 11.3 +/- 1 ms, P < 0.01). Conclusion Waveforms delivered from a large capacitance are feasible but require a lower tilt. This technique may allow smaller. thinner ICDs without jeopardizing defibrillation success. (C) 2001 The European Society of Cardiology."],["dc.identifier.doi","10.1053/eupc.2001.0184"],["dc.identifier.isi","000171580600005"],["dc.identifier.pmid","11678385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17781"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","1099-5129"],["dc.title","Clinical evaluation of defibrillation efficacy with a new single-capacitor biphasic waveform in patients undergoing implantation of an implantable cardioverter defibrillator"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","86"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-01-09T11:14:21Z"],["dc.date.available","2018-01-09T11:14:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Axonal degeneration is one of the initial steps in many traumatic and neurodegenerative central nervous system (CNS) disorders and thus a promising therapeutic target. A focal axonal lesion is followed by acute axonal degeneration (AAD) of both adjacent axon parts, before proximal and distal parts follow different degenerative fates at later time points. Blocking calcium influx by calcium channel inhibitors was previously shown to attenuate AAD after optic nerve crush (ONC). However, it remains unclear whether the attenuation of AAD also promotes consecutive axonal regeneration. Here, we used a rat ONC model to study the effects of calcium channel inhibitors on axonal degeneration, retinal ganglion cell (RGC) survival, and axonal regeneration, as well as the molecular mechanisms involved. Application of calcium channel inhibitors attenuated AAD after ONC and preserved axonal integrity as visualized by live imaging of optic nerve axons. Consecutively, this resulted in improved survival of RGCs and improved axonal regeneration at 28 days after ONC. We show further that calcium channel inhibition attenuated lesion-induced calpain activation in the proximity of the crush and inhibited the activation of the c-Jun N-terminal kinase pathway. Pro-survival signaling via Akt in the retina was also increased. Our data thus show that attenuation of AAD improves consecutive neuronal survival and axonal regeneration and that calcium channel inhibitors could be valuable tools for therapeutic interventions in traumatic and degenerative CNS disorders."],["dc.identifier.doi","10.1007/s12035-015-9676-2"],["dc.identifier.pmid","26732591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11580"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","Attenuation of Axonal Degeneration by Calcium Channel Inhibitors Improves Retinal Ganglion Cell Survival and Regeneration After Optic Nerve Crush"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1811"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bitow, F."],["dc.contributor.author","Haack, J."],["dc.contributor.author","D'Hedouville, Z."],["dc.contributor.author","Zhang, J-N"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Michel, U."],["dc.contributor.author","Oliveira, L. M. A."],["dc.contributor.author","Jovin, T. M."],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Tatenhorst, L."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:43:42Z"],["dc.date.available","2017-09-07T11:43:42Z"],["dc.date.issued","2015"],["dc.description.abstract","Many neuropathological and experimental studies suggest that the degeneration of dopaminergic terminals and axons precedes the demise of dopaminergic neurons in the substantia nigra, which finally results in the clinical symptoms of Parkinson disease (PD). The mechanisms underlying this early axonal degeneration are, however, still poorly understood. Here, we examined the effects of overexpression of human wildtype alpha-synuclein (alpha Syn-WT), a protein associated with PD, and its mutant variants alpha Syn-A30P and -A53T on neurite morphology and functional parameters in rat primary midbrain neurons (PMN). Moreover, axonal degeneration after overexpression of alpha Syn-WT and -A30P was analyzed by live imaging in the rat optic nerve in vivo. We found that overexpression of alpha Syn-WT and of its mutants A30P and A53T impaired neurite outgrowth of PMN and affected neurite branching assessed by Sholl analysis in a variant-dependent manner. Surprisingly, the number of primary neurites per neuron was increased in neurons transfected with alpha Syn. Axonal vesicle transport was examined by live imaging of PMN co-transfected with EGFP-labeled synaptophysin. Overexpression of all alpha Syn variants significantly decreased the number of motile vesicles and decelerated vesicle transport compared with control. Macroautophagic flux in PMN was enhanced by alpha Syn-WT and -A53T but not by alpha Syn-A30P. Correspondingly, colocalization of alpha Syn and the autophagy marker LC3 was reduced for alpha Syn-A30P compared with the other alpha Syn variants. The number of mitochondria colocalizing with LC3 as a marker for mitophagy did not differ among the groups. In the rat optic nerve, both alpha Syn-WT and -A30P accelerated kinetics of acute axonal degeneration following crush lesion as analyzed by in vivo live imaging. We conclude that alpha Syn overexpression impairs neurite outgrowth and augments axonal degeneration, whereas axonal vesicle transport and autophagy are severely altered."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1038/cddis.2015.169"],["dc.identifier.gro","3141868"],["dc.identifier.isi","000358788800011"],["dc.identifier.pmid","26158517"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1967"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Central nervous system; Molecular neuroscience; Parkinson's disease"],["dc.title","Alpha-Synuclein affects neurite morphology, autophagy, vesicle transport and axonal degeneration in CNS neurons"],["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","144"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Genomics"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Isbrandt, D."],["dc.contributor.author","Leicher, T."],["dc.contributor.author","Waldschutz, R."],["dc.contributor.author","Zhu, X."],["dc.contributor.author","Luhmann, U."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Sauter, K."],["dc.contributor.author","Pongs, Olaf"],["dc.date.accessioned","2018-11-07T09:10:46Z"],["dc.date.available","2018-11-07T09:10:46Z"],["dc.date.issued","2000"],["dc.description.abstract","The four known members of the KCND/Kv4 channel family encode voltage-gated potassium channels. Recent studies provide evidence that members of the Kv4 channel family are responsible for native, rapidly inactivating (A-type) currents described in heart (I-TO) and neurons (I-SA), In this study, we cloned the human KCND1 cDNA, localized the KCND1 gene to chromosome Xp11.23-p11.3, and determined the genomic structure and tissue-specific expression of the KCND1, KCND2, and KCND3 genes, respectively. The open reading frame of Kv4.1 is 1941 nucleotides long, predicting a protein of 647 amino acids. The deduced protein sequence of Kv4.1 shows an overall identity of 60% with Kv4.2 and Kv4.3L and corresponds to the common structure of voltage-gated potassium channels, KCND1-specific transcripts were detectable in human brain, heart, liver, kidney, thyroid gland, and pancreas, as revealed by Northern blot and RT-PCR experiments. The comparison of the expression patterns of the known Kv4 family members shows subtype specificity with significant overlaps, The KCND gene structures exhibit an evolutionarily conserved exon pattern with a large first exon containing the intracellular N-terminus and the putative membrane-spanning regions S1 to S5, as well as part of the pore region. The KCND3 gene contains an additional exon of 57 bp, which is not present in the other two KCND genes and gives rise to the C-terminal splice KCND3L variant with an insertion of 19 amino acids. (C) 2000 Academic Press."],["dc.identifier.doi","10.1006/geno.2000.6117"],["dc.identifier.isi","000086311000003"],["dc.identifier.pmid","10729221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26568"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc"],["dc.relation.issn","0888-7543"],["dc.title","Gene structures and expression profiles of three human KCND (Kv4) potassium channels mediating A-type currents I-TO and I-SA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3472"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","FEBS Journal"],["dc.bibliographiccitation.lastpage","3483"],["dc.bibliographiccitation.volume","278"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Michel, U."],["dc.date.accessioned","2017-09-07T11:43:25Z"],["dc.date.available","2017-09-07T11:43:25Z"],["dc.date.issued","2011"],["dc.description.abstract","Repressor element-1 silencing transcription factor (REST) is a transcriptional repressor of neuron-specific genes that binds to a conserved DNA element, the neuron restrictive silencer element (NRSE/RE1). Interestingly, increased REST activity is found in several neurological diseases like Huntington's disease and cerebral ischemia. Recently, it was shown that NRSE dsRNA, a double-stranded non-coding RNA can bind to REST during a defined period of neuronal differentiation, and thereby changes REST from a transcriptional repressor to an activator of neuron-specific genes. Here, we analyzed the effects of NRSE dsRNA expression in primary retinal ganglion cells. We found that NRSE dsRNA expression vectors significantly enhance neurite outgrowth even when axonal degeneration is induced by neurotrophin deprivation. Transfection of HEK cells with NRSE dsRNA-expressing vectors altered their morphology leading to the formation of thin processes and induced the expression of neurofilament-68. Surprisingly, control vectors containing REST-binding sites, but not expressing NRSE dsRNA, resulted in the same effects, also in the retinal ganglion cell model. Reporter assays and retention of REST in the cytoplasm with a labeled NRSE/RE1-containing plasmid incapable of entering the nucleus suggest that sequestration of REST in the cytoplasm is the reason for the observed effects. No evidence for a biological function of NRSE dsRNA could be found in these models. We conclude that sequestration of REST leads to enhanced neurite outgrowth in retinal ganglion cells and that an increased activity of REST, as it is found in several neurodegenerative diseases, can be effectively modulated by sequestration of REST with plasmids containing NRSE/RE1 sites."],["dc.identifier.doi","10.1111/j.1742-4658.2011.08269.x"],["dc.identifier.gro","3142674"],["dc.identifier.isi","000294810600024"],["dc.identifier.pmid","21790997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/104"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1742-464X"],["dc.title","Plasmids containing NRSE/RE1 sites enhance neurite outgrowth of retinal ganglion cells via sequestration of REST independent of NRSE dsRNA expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","685"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","697"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Balke, Dirk"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Vahsen, Björn F."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T14:14:28Z"],["dc.date.available","2020-12-10T14:14:28Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s12035-019-01744-0"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71353"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","AAV-Mediated Expression of Dominant-Negative ULK1 Increases Neuronal Survival and Enhances Motor Performance in the MPTP Mouse Model of Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","615"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Shock"],["dc.bibliographiccitation.lastpage","619"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Diesselberg, Catharina"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schuetze, Sandra"],["dc.date.accessioned","2018-11-07T09:03:01Z"],["dc.date.available","2018-11-07T09:03:01Z"],["dc.date.issued","2012"],["dc.description.abstract","Follistatin (FS) is the binding protein of activin A and inhibits its actions. The activin/FS system participates in the fine tuning of the immune response, and concentrations of activin A and FS are elevated in serum of patients with sepsis. Intraperitoneal injection of FS markedly reduced mortality after lipopolysaccharide-induced inflammation in a mouse model. Here, we investigated whether FS also influences the disease course in a mouse model of sepsis induced by intraperitoneal injection of Escherichia coli K1, a gram-negative bacterium frequently causing septic bacterial infections. Intraperitoneal injection of 10 mu g/mL FS 30 min before infection did not influence survival, weight, motor performance, or bacterial titers of the infected mice. Thus, we could not confirm the protective effect of FS observed during lipopolysaccharide-induced inflammation in our mouse model of E. coli sepsis. Although it is a promising therapeutic tool in chronic or acute inflammatory conditions not caused by virulent pathogens, FS does not seem to increase the resistance to bacterial infections."],["dc.identifier.doi","10.1097/SHK.0b013e3182748d96"],["dc.identifier.isi","000311338900007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24807"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1540-0514"],["dc.relation.issn","1073-2322"],["dc.title","FOLLISTATIN DOES NOT INFLUENCE THE COURSE OF ESCHERICHIA COLI K1 SEPSIS IN A MOUSE MODEL"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Dippel, N."],["dc.contributor.author","Liefner, M."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T11:04:29Z"],["dc.date.available","2018-11-07T11:04:29Z"],["dc.date.issued","2000"],["dc.format.extent","362"],["dc.identifier.isi","000088236602062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51852"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","0953-816X"],["dc.title","The role of matrix metalloproteinases and TNF-alpha during Wallerian degeneration in the mouse sciatic nerve"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","245"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","253"],["dc.bibliographiccitation.volume","341"],["dc.contributor.author","Malik, I."],["dc.contributor.author","Garrido, M."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kügler, S."],["dc.contributor.author","Michel, U."],["dc.date.accessioned","2017-09-07T11:53:12Z"],["dc.date.available","2017-09-07T11:53:12Z"],["dc.date.issued","2006"],["dc.description.abstract","RNAinterference (RNAi) has developed within a short time from an area of basic research occupied by a few experts to a widely used technical tool for reverse genetics, which is expected to have a broad utility not only in research, but also in medical and diagnostic applications. Despite its widespread use, the application of RNAi is often hampered because it difference of only a few nuclectides in the sequence of the target RNA can change the efficiency of a small interfering RNA (siRNA) from high to zero, and publicly available design tools for siRNAs are not yet perfect. We therefore developed and compared RNAi test systems based oil different promoters, reporters, and target sequences. Here, we show that fluorescence-based test systems have obvious disadvantages compared to luciferase-based test systems and that some combinations of promoter, reporter, and target sequences, although Currently in use, are not well suited for testing RNAi effects. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbrc.2005.12.173"],["dc.identifier.gro","3143725"],["dc.identifier.isi","000235313400036"],["dc.identifier.pmid","16423323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1271"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-291X"],["dc.title","Comparison of test systems for RNAinterference"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurodegenerative Diseases"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:44:02Z"],["dc.date.available","2017-09-07T11:44:02Z"],["dc.date.issued","2004"],["dc.description.abstract","Reverse genetics has been greatly advanced by the discovery of RNA interference (RNAi). This intracellular RNA-mediated gene silencing pathway is partially conserved from plants to mammals and offers a new powerful tool for the analysis of gene function. We give a brief overview of the discovery of RNAi, the underlying mechanisms and probable intrinsic roles of the pathway. Recent reports utilizing RNAi for gene silencing approaches in neuronal cells are reviewed and possible delivery techniques for small interfering RNA/double-stranded RNA are discussed. Copyright (C) 2004 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000076664"],["dc.identifier.gro","3144023"],["dc.identifier.isi","000208225900002"],["dc.identifier.pmid","16908968"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1602"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1660-2854"],["dc.title","The Long Processes of Short Interfering RNAs - RNA Interference and Its Implications in Neuronal Cells"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]