Scheidt, Uta

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T09:33:35Z"],["dc.date.available","2018-11-07T09:33:35Z"],["dc.date.issued","2014"],["dc.format.extent","129"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.346"],["dc.identifier.isi","000345192100336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31999"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Axonal damage and protection during early remyelination in multiple sclerosis and an animal model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","246"],["dc.contributor.author","Lescher, Juliane"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Redenbach, Laura"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Here we demonstrate that miRNA regulation in marmoset (Callithrix jacchus) and C57/BL6 mouse EAE lesions largely resembles miRNA regulation in active human MS lesions. Detailed quantitative PCR analyses of the most up- and downregulated miRNAs of active human MS lesions in dissected lesions from marmoset EAE brains and inflamed spinal cords of EAE mice revealed that the conserved and highly regulated miRNAs, miRNA-155, miRNA-142-3p, miRNA-146a, miRNA-146b and miRNA-21, turned out to be similarly upregulated in marmoset and mouse EAE lesions. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2012.02.012"],["dc.identifier.gro","3142535"],["dc.identifier.isi","000304026900004"],["dc.identifier.pmid","22445295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8897"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","MicroRNA regulation in experimental autoimmune encephalomyelitis in mice and marmosets resembles regulation in human multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","202"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, A."],["dc.date.accessioned","2018-11-07T10:08:48Z"],["dc.date.available","2018-11-07T10:08:48Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Biogen; Novartis; Genzyme; Teva"],["dc.identifier.isi","000383267201212"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39538"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","pH and K-V channel conductance are not central to damage of demyelinated axons in the cuprizone mouse model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e168"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Bachmann, Cornelius G."],["dc.contributor.author","Rolke, Roman"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Sommer, Martin"],["dc.contributor.author","Pavlakovic, Goran"],["dc.contributor.author","Happe, Svenja"],["dc.contributor.author","Treede, Rolf-Detlef"],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T08:57:30Z"],["dc.date.available","2018-11-07T08:57:30Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1093/brain/awq292"],["dc.identifier.isi","000289163300005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23412"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Reply: Sensory profile in primary restless legs syndrome and restless legs syndrome associated with small fibre neuropathy"],["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","1350"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1360"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T10:21:54Z"],["dc.date.available","2018-11-07T10:21:54Z"],["dc.date.issued","2017"],["dc.description.abstract","Remyelination is in the center of new therapies for the treatment of multiple sclerosis to resolve and improve disease symptoms and protect axons from further damage. Although remyelination is considered beneficial in the long term, it is not known, whether this is also the case early in lesion formation. Additionally, the precise timing of acute axonal damage and remyelination has not been assessed so far. To shed light onto the interrelation between axons and the myelin sheath during de-and remyelination, we employed cuprizone- and focal lysolecithin-induced demyelination and performed time course experiments assessing the evolution of early and late stage remyelination and axonal damage. We observed damaged axons with signs of remyelination after cuprizone diet cessation and lysolecithin injection. Similar observations were made in early multiple sclerosis lesions. To assess the correlation of remyelination and axonal damage in multiple sclerosis lesions, we took advantage of a cohort of patients with early and late stage remyelinated lesions and assessed the number of APP- and SMI32- positive damaged axons and the density of SMI31- positive and silver impregnated preserved axons. Early de-and remyelinating lesions did not differ with respect to axonal density and axonal damage, but we observed a lower axonal density in late stage demyelinated multiple sclerosis lesions than in remyelinated multiple sclerosis lesions. Our findings suggest that remyelination may not only be protective over a long period of time, but may play an important role in the immediate axonal recuperation after a demyelinating insult."],["dc.identifier.doi","10.1002/glia.23167"],["dc.identifier.isi","000403348100009"],["dc.identifier.pmid","28560740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Acutely damaged axons are remyelinated in multiple sclerosis and experimental models of demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]