Chan, Andrew S.

[["dc.bibliographiccitation.firstpage","1170"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","1173"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Decard, Bernhard F."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Grunwald, Thomas"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Stroet, Anke"],["dc.contributor.author","Niggemeier, Petra"],["dc.contributor.author","Schottstedt, Volkmar"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2018-11-07T09:02:57Z"],["dc.date.available","2018-11-07T09:02:57Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective Vitamin D deficiency and Epstein-Barr virus (EBV) infection may be associated with the development of multiple sclerosis (MS). We investigated serum 25-hydroxyvitamin D (25-OH-D) levels and anti-EBV immunoreactivity in 25 individuals before the first clinical manifestation of MS. Patients and methods 56 serum samples of 25 individuals who had donated blood prior to the first clinical MS manifestation (clinically isolated syndrome (CIS)) (four male subjects, 21 female subjects, mean age 31.5 years at time of pre-CIS blood sampling; mean age at disease onset 33.4 years) were available, covering an interval of 7.3 years-2 months (mean 31.5 months) before CIS. In 18 of 25 patients serum samples were also obtained after established diagnosis of MS. Longitudinal age- and gender-matched healthy blood donors (four male subjects, 21 female subjects, 39 samples, mean age 32.5 years) served as controls. Serum 25-OH-D was measured by isotope dilution-liquid chromatography-tandem mass spectrometry. 25-OH-D levels were deconvoluted using published seasonal coefficients from a German population. Immunoglobulin G (IgG) against Epstein-Barr virus nuclear antigen-1 (EBNA1) were assessed using commercially available ELISA. Results Low 25-OH-D levels were observed during the 24-month pre-CIS interval (47.8 (32.5-77.2) nmol/l, median (IQR); healthy controls: 81.6 (57.7-98.5), p=0.004, however, still higher than after established diagnosis (24.5 (13.7-47.7), p<0.0001 compared with controls). IgG against EBNA1 during the 36-month pre-CIS interval was increased (185.9 (91.2-460.0) IU/ml, median (IQR); healthy controls 63.7 (29.5-121.6), p=0.002). Conclusions Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years."],["dc.identifier.doi","10.1136/jnnp-2012-303068"],["dc.identifier.isi","000311097700012"],["dc.identifier.pmid","22888143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24794"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Low vitamin D and elevated immunoreactivity against Epsteine-Barr virus before first clinical manifestation of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e85"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology® neuroimmunology & neuroinflammation"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hoepner, Robert"],["dc.contributor.author","Faissner, Simon"],["dc.contributor.author","Klasing, Anja"],["dc.contributor.author","Schneider, Ruth"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Bellenberg, Barbara"],["dc.contributor.author","Lukas, Carsten"],["dc.contributor.author","Altmeyer, Peter"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2016-08-23T08:49:19Z"],["dc.date.accessioned","2021-10-27T13:20:42Z"],["dc.date.available","2016-08-23T08:49:19Z"],["dc.date.available","2021-10-27T13:20:42Z"],["dc.date.issued","2015-06-01"],["dc.description.abstract","not available"],["dc.identifier.doi","10.1212/NXI.0000000000000085"],["dc.identifier.fs","611967"],["dc.identifier.pmid","25798449"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13596"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91978"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2332-7812"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Progressive multifocal leukoencephalopathy during fumarate monotherapy of psoriasis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2517"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2530"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Cotte, S."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Huber, B."],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Starck, Michaela"],["dc.contributor.author","Koenig, N."],["dc.contributor.author","Tellez, N."],["dc.contributor.author","Doerr, J."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Koepsell, Hermann"],["dc.contributor.author","Pannek, H."],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, A."],["dc.date.accessioned","2018-11-07T11:24:34Z"],["dc.date.available","2018-11-07T11:24:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Escalation therapy with mitoxantrone (MX) in highly active multiple sclerosis is limited by partially dose-dependent side-effects. Predictors of therapeutic response may result in individualized risk stratification and MX dosing. ATP-binding cassette-transporters ABCB1 and ABCG2 represent multi-drug resistance mechanisms involved in active cellular MX efflux. Here, we investigated the role of ABC-gene single nucleotide polymorphisms (SNPs) for clinical MX response, corroborated by experimental in vitro and in vivo data. Frequencies of ABCB1 2677GT, 3435CT and five ABCG2-SNPs were analysed in 832 multiple sclerosis patients (Germany, Spain) and 264 healthy donors. Using a flow-cytometry-based in vitro assay, MX efflux in leukocytes from individuals with variant alleles in both ABC-genes (designated genotype ABCB1/ABCG2-L(ow), 22.2 of patients) was 37.7 lower than from individuals homozygous for common alleles (ABCB1/ABCG2-H(igh), P 0.05, 14.8 of patients), resulting in genotype-dependent MX accumulation and cell death. Addition of glucocorticosteroids (GCs) inhibited MX efflux in vitro. ABC-transporters were highly expressed in leukocyte subsets, glial and neuronal cells as well as myocardium, i.e. cells/tissues potentially affected by MX therapy. In vivo significance was further corroborated in experimental autoimmune encephalomyelitis in Abcg2(/) animals. Using a MX dose titrated to be ineffective in wild-type animals, disease course and histopathology in Abcg2(/) mice were strongly ameliorated. Retrospective clinical analysis in MX monotherapy patients (n 155) used expanded disability status scale, relapse rate and multiple sclerosis functional composite as major outcome parameters. The clinical response rate [overall 121 of 155 patients (78.1)] increased significantly with genotypes associated with decreasing ABCB1/ABCG2-function [ABCB1/ABCG2-H 15/24 (62.5) responders, ABCB1/ABCG2-I(ntermediate) 78/98 (79.6), ABCB1/ABCG2-L 28/33 (84.8), exact Cochran-Armitage test P 0.039]. The odds ratio for response was 1.9 (95 CI 1.03.5) with each increase in ABCB1/ABCG2 score (from ABCB1/ABCG2-H to I-, and I to L). In 36 patients with severe cardiac or haematological side effects no statistically relevant difference in genotype frequency was observed. However, one patient with biopsy proven cardiomyopathy only after 24 mg/m(2) MX exhibited a rare genotype with variant, partly homozygous alleles in 3 ABC-transporter genes. In conclusion, SNPs in ABC-transporter genes may serve as pharmacogenetic markers associated with clinical response to MX therapy in multiple sclerosis. Combined MX/GC-treatment warrants further investigation."],["dc.description.sponsorship","Merck Serono, Germany"],["dc.identifier.doi","10.1093/brain/awp164"],["dc.identifier.isi","000269963600021"],["dc.identifier.pmid","19605531"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56436"],["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","ABC-transporter gene-polymorphisms are potential pharmacogenetic markers for mitoxantrone response in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2803"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Current Pharmaceutical Design"],["dc.bibliographiccitation.lastpage","2807"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Chan, A."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.date.accessioned","2018-11-07T08:51:51Z"],["dc.date.available","2018-11-07T08:51:51Z"],["dc.date.issued","2011"],["dc.description.abstract","Owing to therapeutic progress, the role of ABC-transporters in infectious and autoimmune inflammatory CNS-diseases has recently gained considerable attention. In HIV-encephalitis and HIV-associated neurocognitive disorders, ABC-transporters are discussed to contribute to limited CNS-penetration and -retention of antiviral agents. In multiple sclerosis and its animal model experimental autoimmune encephalomyelitis, ABC-transporters may be involved in pathogenesis and treatment response alike. A prospective pharmacogenetic study is currently underway to examine the predictive role of genetic variations in ABC-transporters for treatment response and adverse events to mitoxantrone, a therapeutic agent used in aggressive MS. These approaches may aid in individualized treatment with this cytostatic anthracenedione, addressing its narrow therapeutic index with potentially fatal side effects. Finally, understanding regulation and function of ABC-transporters under inflammatory conditions may also optimize ABC-transporter-related treatment strategies in other neurological diseases (e. g. neurodegenerative, and neurovascular) where neuroinflammatory mechanisms have gained considerable attention as important contributors to pathogenesis."],["dc.identifier.isi","000299630800009"],["dc.identifier.pmid","21827405"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22032"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bentham Science Publ Ltd"],["dc.relation.issn","1381-6128"],["dc.title","ATP-Binding Cassette Transporters in Inflammatory Brain Disease"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","277"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","279"],["dc.bibliographiccitation.volume","278"],["dc.contributor.author","Grey (nee Cotte), Steffi"],["dc.contributor.author","Salmen (nee Stroet), Anke"],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Starck, Michaela"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Comabella, Manuel"],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Fleischer, Vinzenz"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2018-11-07T10:02:07Z"],["dc.date.available","2018-11-07T10:02:07Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Mitoxantrone is used on an off-label basis in primary progressive MS (PPMS).ABC-transporter-genotypes are associated with therapeutic response in relapsing/secondary progressive MS (RP/SPMS). Objective: To evaluate potential pharmacogenetic response markers for mitoxantrone in PPMS. Methods: 41 mitoxantrone-treated PPMS-patients, 155 mitoxantrone-treated RP/SPMS-patients and 43 PPMS-controls were retrospectively assessed for clinical therapy-response and in correlation with four single-nucleotide-polymorphisms in ABCB1- and ABCG2-genes. Results: 53.7% PPMS-patients were mitoxantrone-responders, in comparison to 78.1% of RP/SPMS-patients (p = 0.039). There was no association between genotype and treatment response. Conclusion: Our data discourages the use of mitoxantrone in PPMS regardless of pharmacogenetic response markers previously described in RP/SPMS. (C) 2014 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2014.11.017"],["dc.identifier.isi","000349269300035"],["dc.identifier.pmid","25468777"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38167"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Lack of efficacy of mitoxantrone in primary progressive Multiple Sclerosis irrespective of pharmacogenetic factors: A multi-center, retrospective analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1604"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1606"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","Chan, Andrew"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Linker, Ralf"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:57:12Z"],["dc.date.available","2018-11-07T10:57:12Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1007/s00415-007-0593-9"],["dc.identifier.isi","000251096000021"],["dc.identifier.pmid","17713826"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50186"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Rescue therapy with anti-CD20 treatment in neuroimmunologic breakthrough disease"],["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.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Cotte, S."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, A."],["dc.date.accessioned","2018-11-07T09:22:42Z"],["dc.date.available","2018-11-07T09:22:42Z"],["dc.date.issued","2006"],["dc.format.extent","S215"],["dc.identifier.isi","000241921400707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29413"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","22nd Congress of the European-Committee-for-the-Treatment-and-Resarch-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","ABC-transporter gene-polymorphisms as potential predictors of therapeutic efficacy of mitoxantrone in multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","NATURE CLINICAL PRACTICE NEUROLOGY"],["dc.bibliographiccitation.lastpage","73"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Chan, A."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:24:19Z"],["dc.date.available","2018-11-07T10:24:19Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1038/ncpneuro0120"],["dc.identifier.isi","000235533000005"],["dc.identifier.pmid","16932526"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42635"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1745-834X"],["dc.title","Can pathological patterns be used to guide individualized multiple sclerosis therapy?"],["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","430"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","438"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Schilling, S."],["dc.contributor.author","Linker, R. A."],["dc.contributor.author","König, F. B."],["dc.contributor.author","Koziolek, M."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Müller, G. A."],["dc.contributor.author","Paulus, W."],["dc.contributor.author","Gärtner, J."],["dc.contributor.author","Brück, W."],["dc.contributor.author","Chan, A."],["dc.contributor.author","Gold, R."],["dc.date.accessioned","2017-09-07T11:53:08Z"],["dc.date.available","2017-09-07T11:53:08Z"],["dc.date.issued","2006"],["dc.description.abstract","Patients with severe multiple sclerosis (MS) relapses which do not respond sufficiently to corticosteroids can undergo escalating immunotherapy with plasma exchange. We review the course of 14 apheresis cycles in 13 adult patients and three pediatric cases from our center between 2004 and 2005. Nine cases were due to optic neuritis, five had experienced clinically isolated syndromes, and two suffered from Devic's disease. Of the adult patients, 71% had good or very good outcome. The mean time point of improvement was after the third plasmapheresis session, and early initiation of plasma exchange therapy (within 1 month after begin of relapse) was associated with better outcome. In pediatric MS, two of three patients showed clear improvement. These data argue for a very good therapeutic effect of plasma exchange if performed early and with adequate indication."],["dc.identifier.doi","10.1007/s00115-005-2019-1"],["dc.identifier.gro","3143715"],["dc.identifier.isi","000237631700004"],["dc.identifier.pmid","16341736"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1260"],["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","0028-2804"],["dc.title","Plasma exchange therapy for steroid-unresponsive multiple sclerosis relapses. Clinical experience with 16 patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","293"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","302"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Blecharz, Kinga G."],["dc.contributor.author","Haghikia, Aiden"],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Drenckhahn, Detlev"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Roewer, Norbert"],["dc.contributor.author","Chan, Andrew"],["dc.contributor.author","Foerster, Carola Y."],["dc.date.accessioned","2018-11-07T08:45:36Z"],["dc.date.available","2018-11-07T08:45:36Z"],["dc.date.issued","2010"],["dc.description.abstract","Compromised blood-brain barrier integrity is a major hallmark of active multiple sclerosis (MS). Alterations in brain endothelial tight junction protein and gene expression occur early during neuroinflammation but there is little known about the underlying mechanisms. In this study, we analysed barrier compromising effects of sera from MS patients and barrier restoring effects of glucocorticoids on blood-brain barrier integrity in vitro. cEND murine brain microvascular endothelial cell monolayers were incubated with sera from patients in active phase of disease or in relapse. Data were compared with effects of the glucocorticoid dexamethasone alone or in combination with MS sera on barrier integrity. Tight junction protein levels and gene expression were evaluated concomitant with barrier integrity. We reveal down-regulation of claudin-5 and occludin protein and mRNA and an accompanying upregulation in expression of matrix metalloproteinase MMP-9 after incubation with serum from active disease and remission and also a minor reconstitution of barrier functions related to dexamethasone treatment. Moreover, we for the first time describe downregulation of claudin-5 and occludin protein after incubation of cEND cells with sera from patients in remission phase of MS. Our findings reveal direct and differential effects of MS sera on blood-brain barrier integrity."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SFB688-TPA5, SFB-TPA1 RG]"],["dc.identifier.doi","10.1177/1352458509358189"],["dc.identifier.isi","000275179200004"],["dc.identifier.pmid","20203147"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20482"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Glucocorticoid effects on endothelial barrier function in the murine brain endothelial cell line cEND incubated with sera from patients with multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]