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","762"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","770"],["dc.bibliographiccitation.volume","133"],["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","2018-11-07T08:45:14Z"],["dc.date.available","2018-11-07T08:45:14Z"],["dc.date.issued","2010"],["dc.description.abstract","This study aimed to assess thermal and mechanical perception and pain thresholds in primary idiopathic restless legs syndrome and secondary restless legs syndrome associated with small fibre neuropathy. Twenty-one patients (age: 53.4 +/- 8.4, n = 3, male) with primary restless legs syndrome and 13 patients (age: 63.0 +/- 8.2, n = 1, male) with secondary restless legs syndrome associated with small fibre neuropathy were compared with 20 healthy subjects (age: 58.0 +/- 7.0; n = 2, male). Differential diagnosis of secondary restless legs syndrome associated with small fibre neuropathy was based on clinical symptoms and confirmed with skin biopsies in all patients. A comprehensive quantitative sensory testing protocol encompassing thermal and mechanical detection and pain thresholds, as devised by the German Research Network on Neuropathic Pain, was performed on the clinically more affected foot between 2 pm and 1 am when restless legs syndrome symptoms were present in all patients. Patients with primary restless legs syndrome showed hyperalgesia to blunt pressure (P < 0.001), pinprick (P < 0.001) and vibratory hyperaesthesia (P < 0.001). Patients with secondary restless legs syndrome associated with small fibre neuropathy showed thermal hypoaesthesia to cold (A delta-fibre mediated) and warm (C-fibre mediated) (all P < 0.001) and hyperalgesia to pinprick (P < 0.001). Static mechanical hyperalgesia in primary and secondary restless legs syndrome is consistent with the concept of central disinhibition of nociceptive pathways, which might be induced by conditioning afferent input from damaged small fibre neurons in secondary restless legs syndrome."],["dc.identifier.doi","10.1093/brain/awq026"],["dc.identifier.isi","000276046000012"],["dc.identifier.pmid","20194142"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6232"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20388"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Thermal hypoaesthesia differentiates secondary restless legs syndrome associated with small fibre neuropathy from primary restless legs syndrome"],["dc.type","journal_article"],["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.artnumber","760"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Voigt, David; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, david-voigt@gmx.net"],["dc.contributor.affiliation","Scheidt, Uta; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, uscheidt@med.uni-goettingen.de"],["dc.contributor.affiliation","Derfuss, Tobias; \t\t \r\n\t\t Neurologic Clinic and Policlinic, University Hospital Basel, Basel 4031, Switzerland, tobias.derfuss@usb.ch"],["dc.contributor.affiliation","Brück, Wolfgang; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, wbrueck@med.uni-goettingen.de"],["dc.contributor.affiliation","Junker, Andreas; \t\t \r\n\t\t Institute of Neuropathology, University Hospital Essen, Hufelandstr. 55, Essen 45122, Germany, andreas.junker@uk-essen.de"],["dc.contributor.author","Voigt, David"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Derfuss, Tobias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T10:25:12Z"],["dc.date.available","2018-11-07T10:25:12Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-05T16:09:31Z"],["dc.description.abstract","Multiple sclerosis is a chronic inflammatory disease of the central nervous system, characterized by demyelination and axonal damage as well as neuronal degeneration. Since oxygen-derived free radicals are an important factor leading to tissue damage in inflammatory multiple sclerosis (MS) lesions, research on antioxidative systems is essential to identify endogenous factors which can possibly counteract oxidative damage. As an important scavenging enzyme family, peroxiredoxins (PRDXs) play a crucial role in preventing oxidative damage; however little is known about their expression and function in MS lesions. In the present study we examined the expression of PRDX2 in white matter lesions of MS patients with long-standing, chronic disease. PRDX2 expression was investigated by immunohistochemistry in the context of oxidative stress and inflammation (determined by microglia/macrophage and T cell infiltration) in ten MS autopsy cases as well as seven control autopsy cases. PRDX2 was found to be upregulated in white matter MS lesions mainly in astrocytes, and its expression level was positively correlated with the degree of inflammation and oxidative stress. Our data suggest that PRDX2 expression contributes to the resistance of astrocytes against oxidative damage."],["dc.identifier.doi","10.3390/ijms18040760"],["dc.identifier.isi","000402639400085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42804"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Expression of the Antioxidative Enzyme Peroxiredoxin 2 in Multiple Sclerosis Lesions in Relation to Inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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","641"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","652"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Wozniak, Jadwiga"],["dc.contributor.author","Voigt, David"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Antel, Jack"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:27:30Z"],["dc.date.available","2021-04-14T08:27:30Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Cortical demyelinated lesions are frequent and widespread in chronic multiple sclerosis (MS) patients, and may contribute to disease progression. Inflammation and related oxidative stress have been proposed as central mediators of cortical damage, yet meningeal and cortical inflammation is not specific to MS, but also occurs in other diseases. The first aim of this study was to test whether cortical demyelination was specific for demyelinating CNS diseases compared to other CNS disorders with prominent meningeal and cortical inflammation. The second aim was to assess whether oxidative tissue damage was associated with the extent of neuroaxonal damage. We studied a large cohort of patients diagnosed with demyelinating CNS diseases and non‐demyelinating diseases of autoimmune, infectious, neoplastic or metabolic origin affecting the meninges and the cortex. Included were patients with MS, acute disseminated encephalomyelitis (ADEM), neuromyelitis optica (NMO), viral and bacterial meningoencephalitis, progressive multifocal leukoencephalopathy (PML), subacute sclerosing panencephalitis (SSPE), carcinomatous and lymphomatous meningitis and metabolic disorders such as extrapontine myelinolysis, thus encompassing a wide range of adaptive and innate cytokine signatures. Using myelin protein immunohistochemistry, we found cortical demyelination in MS, ADEM, PML and extrapontine myelinolysis, whereby each condition showed a disease‐specific histopathological pattern. Remarkably, extensive ribbon‐like subpial demyelination was only observed in MS, thus providing an important pathogenetic and diagnostic cue. Cortical oxidative injury was detected in both demyelinating and non‐demyelinating CNS disorders. Our data demonstrate that meningeal and cortical inflammation alone accompanied by oxidative stress are not sufficient to generate the extensive subpial cortical demyelination found in MS, but require other MS‐specific factors."],["dc.description.sponsorship","National Multiple Sclerosis Society http://dx.doi.org/10.13039/100000890"],["dc.identifier.doi","10.1111/bpa.12813"],["dc.identifier.eissn","1750-3639"],["dc.identifier.issn","1015-6305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82309"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Extensive subpial cortical demyelination is specific to multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]