Tumani, Hayrettin

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Clinica Chimica Acta"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","292"],["dc.contributor.author","Smirnov, Alexander V."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Henne, Sergej"],["dc.contributor.author","Barchfeld, Sandra"],["dc.contributor.author","Olgemöller, Ulrike"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Mäder, Michael"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:45:22Z"],["dc.date.available","2017-09-07T11:45:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Glutamine synthetase (GS) activity is higher in the neocortex but not in the hippocampal formation of rabbit brain during Streptococcus pneumoniae meningitis compared to the respective brain region of uninfected control animals. One-dimensional polyacrylamide gel electrophoresis (1D-SDS-PAGE) revealed an apparent molecular mass (Mr) of 44 000 Dalton (Da) for GS from rabbit brain. After two-dimensional gel electrophoresis (2D-PAGE), followed by Coomassie-blue staining, GS separated into three distinct spots (S1, S2, S3). One additional spot (S4) occurred on the immunoblot. All four GS spots exhibited the same Mr (44 000 Da), but differed in their isoelectric points. Densitometric evaluation of the two-dimensional maps revealed a strong increase of optical density (OD) of S3 in the frontal cortex of infected animals. The calculated OD ratio S3/S2 in the frontal cortex from rabbits with meningitis was 1.75±0.68 (mean±standard deviation). Compared to controls (0.85±0.39), this value was significantly increased (p=0.0006). In the hippocampal formation, the ratio S3/S2 was nearly unchanged during meningitis. It is suggested that the ratio S3/S2 may indicate a neuroprotective feature of rabbit brain during meningitis since neuronal apoptosis occurs only in the dentate gyrus and not in the frontal cortex."],["dc.identifier.doi","10.1016/s0009-8981(99)00180-1"],["dc.identifier.gro","3151752"],["dc.identifier.pmid","10686272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8576"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0009-8981"],["dc.title","Glutamine synthetase in experimental meningitis: increased ratio of the subunits 3 and 2 may indicate enhanced activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ELECTROPHORESIS"],["dc.bibliographiccitation.lastpage","362"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Haußmann, Ute"],["dc.contributor.author","Klafki, Hans"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:42Z"],["dc.date.available","2017-09-07T11:44:42Z"],["dc.date.issued","2014"],["dc.description.abstract","The detection of oligoclonal bands (OCBs) in cerebrospinal fluid is an indicator of intrathecal synthesis of immunoglobulins which is a neurochemical sign of chronic inflammatory brain diseases. Intrathecally synthesized IgGs are typically observed in patients with multiple sclerosis. The current standard protocol for the detection of OCBs is IEF on agarose or polyacrylamide gels followed by immunoblotting or silver staining. These methods are time consuming, show substantial interlaboratory variation and cannot be used in a high throughput-approach. We have developed a new nanoscale method for the detection of OCBs based on automated capillary IEF followed by immunological detection. Evidence for intrathecal IgG synthesis was found in all tested patients (n = 27) with multiple sclerosis, even in two subjects who did not have oligoclonal bands according to standard methods. The test specificity was at 97.5% (n = 19). Our findings indicate that the novel OCB-CIEF-immunoassay is suitable for the rapid and highly sensitive detection of OCBs in clinical samples. Furthermore, the method allows for a higher sample throughput than the current standard methods."],["dc.identifier.doi","10.1002/elps.201400339"],["dc.identifier.gro","3151730"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8550"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0173-0835"],["dc.title","Capillary isoelectric focusing immunoassay as a new nanoscale approach for the detection of oligoclonal bands"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e33"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology® neuroimmunology & neuroinflammation"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Thomas, Katja"],["dc.contributor.author","Dietze, Kristin"],["dc.contributor.author","Wehner, Rebekka"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Schultheiß, Thorsten"],["dc.contributor.author","Günther, Claudia"],["dc.contributor.author","Schäkel, Knut"],["dc.contributor.author","Reichmann, Heinz"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Schmitz, Marc"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.date.accessioned","2015-10-20T13:57:53Z"],["dc.date.accessioned","2021-10-27T13:20:20Z"],["dc.date.available","2015-10-20T13:57:53Z"],["dc.date.available","2021-10-27T13:20:20Z"],["dc.date.issued","2014-10-01"],["dc.description.abstract","OBJECTIVE: To examine the potential role of 6-sulfo LacNAc(+) (slan) dendritic cells (DCs) displaying pronounced proinflammatory properties in the pathogenesis of multiple sclerosis (MS). METHODS: We determined the presence of slanDCs in demyelinated brain lesions and CSF samples of patients with MS. In addition, we explored the impact of methylprednisolone, interferon-β, glatiramer acetate, or natalizumab on the frequency of blood-circulating slanDCs in patients with MS. We also evaluated whether interferon-β modulates important proinflammatory capabilities of slanDCs. RESULTS: SlanDCs accumulate in highly inflammatory brain lesions and are present in the majority of CSF samples of patients with MS. Short-term methylprednisolone administration reduces the percentage of slanDCs in blood of patients with MS and the proportion of tumor necrosis factor-α- or CD150-expressing slanDCs. Long-term interferon-β treatment decreases the percentage of blood-circulating slanDCs in contrast to glatiramer acetate or natalizumab. Furthermore, interferon-β inhibits the secretion of proinflammatory cytokines by slanDCs and their capacity to promote proliferation and differentiation of T cells. CONCLUSION: Accumulation of slanDCs in highly inflammatory brain lesions and their presence in CSF indicate that slanDCs may play an important role in the immunopathogenesis of MS. The reduction of blood-circulating slanDCs and the inhibition of their proinflammatory properties by methylprednisolone and interferon-β may contribute to the therapeutic efficiency of these drugs in patients with MS."],["dc.identifier.doi","10.1212/NXI.0000000000000033"],["dc.identifier.fs","611429"],["dc.identifier.pmid","25340085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91957"],["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","Accumulation and therapeutic modulation of 6-sulfo LacNAc(+) dendritic cells in multiple sclerosis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","158"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Respiratory Journal"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Hagedohm, J."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Laier-Groeneveld, G."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:20:54Z"],["dc.date.available","2018-11-07T10:20:54Z"],["dc.date.issued","2002"],["dc.description.abstract","Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy. Therefore, in 10 patients with mild SAS (age 50.8+/-9.9 yrs, respiratory disturbance index (RDI) 18+/-3.6, lowest arterial oxygen saturation (min Sa,O-2) 80.5+/-4.06%) and nine patients with severe SAS (age 50.3+/-11.5 yes, RDI 75.4+/-21.7, min Sa,O-2 56.56+/-14.58%), serum concentrations of neuron-specific enolase (NSE), S-100beta protein, and beta-trace were measured just before and after sleep using commercially available assays. Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS. Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100beta, neuron-specific enolase and beta-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome."],["dc.identifier.doi","10.1183/09031936.02.00862001"],["dc.identifier.isi","000177188600026"],["dc.identifier.pmid","12166564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","European Respiratory Soc Journals Ltd"],["dc.relation.issn","0903-1936"],["dc.title","Biochemical markers of cerebrovascular injury in sleep apnoea syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","822"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","826"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Millonig, A."],["dc.contributor.author","Dressel, Alexander"],["dc.contributor.author","Bahner, D."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Bogumil, T."],["dc.contributor.author","Elitok, E."],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Weber, F."],["dc.contributor.author","Gneiss, C."],["dc.contributor.author","Deisenhammer, Florian"],["dc.date.accessioned","2018-11-07T11:12:24Z"],["dc.date.available","2018-11-07T11:12:24Z"],["dc.date.issued","2008"],["dc.description.abstract","Background and purpose: Interferon beta (IFN beta) preparations have some effect on the progressive phase of multiple sclerosis ( MS). This limited effect might be partially because of a certain number of IFN beta non-responders. Myxovirus resistance protein A (MxA)-a marker of IFN beta bioactivity - was correlated with the clinical response during an uncontrolled trial, investigating the safety of IFN beta-1 beta in primary progressive (PPMS) patients. Methods: Twenty PPMS were treated with IFN beta-1 beta (s.c.) for 1 year. Blood samples were taken before and 1, 2, 3, 6, 9, 12, and 15 months after treatment initiation and MxA protein levels were measured. Patients were clinically evaluated by EDSS and the more sensitive Incapacity Status Scale (ISS) and stratified in a stable and a progressing group. Results: Using ISS criteria, 11 patients remained stable and nine patients progressed during treatment. The mean area under the curve of log MxA levels during treatment were significantly higher in stable than in progressing patients (10.87 vs. 5.99; P = 0.002). Conclusion: A good biological response to IFNb might be associated with a better clinical effect of this drug and could be helpful in future clinical studies for early identification of treatment responders."],["dc.identifier.doi","10.1111/j.1468-1331.2008.02190.x"],["dc.identifier.isi","000257715400022"],["dc.identifier.pmid","18549400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53656"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1351-5101"],["dc.title","MxA protein - an interferon beta biomarker in primary progressive multiple sclerosis patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e10079"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Sdzuj, Martin"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T08:44:10Z"],["dc.date.available","2018-11-07T08:44:10Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: The discrimination of bacterial meningitis (BM) versus viral meningitis (VM) shapes up as a problem, when laboratory data are not equivocal, in particular, when Gram stain is negative. Methodology/Principal Findings: With the aim to determine reliable marker for bacterial or viral meningitis, we subjected cerebrospinal fluid (CSF) to a quantitative proteomic screening. By using a recently established 2D-DIGE protocol which was adapted to the individual CSF flow, we compared a small set of patients with proven BM and VM. Thereby, we identified six potential biomarkers out of which Prostaglandin-H2 D-isomerase was already described in BM, showing proof of concept. In the subsequent validation phase on a more comprehensive collective of 80 patients, we could validate that in BM high levels of glial fibrillary acidic protein (GFAP) and low levels of soluble amyloid precursor protein alpha/beta (sAPP alpha/beta) are present as possible binding partner of Fibulin-1. Conclusions/Significance: We conclude that our CSF flow-adapted 2D-DIGE protocol is valid especially in comparing samples with high differences in total protein and suppose that GFAP and sAPP alpha/beta have a high potential as additional diagnostic markers for differentiation of BM from VM. In the clinical setting, this might lead to an improved early diagnosis and to an individual therapy."],["dc.identifier.doi","10.1371/journal.pone.0010079"],["dc.identifier.isi","000276482000014"],["dc.identifier.pmid","20386697"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20140"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A Proteomic Approach for the Diagnosis of Bacterial Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1498"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1501"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Dressel, Alexander"],["dc.contributor.author","Meier, K."],["dc.contributor.author","Bogumil, T."],["dc.contributor.author","Deisenhammer, Florian"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Weber, F."],["dc.date.accessioned","2018-11-07T10:43:31Z"],["dc.date.available","2018-11-07T10:43:31Z"],["dc.date.issued","2004"],["dc.description.abstract","We conducted an open-labeled clinical trial of interferon beta-1b (IFNB) treatment in 20 patients with primary progressive multiple sclerosis (PPMS) and longitudinally monitored autoantibodies against double-stranded DNA (dsDNA), thyroid peroxidase (TPO),myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), synapsin and S-100B. Before treatment, one patient had elevated TPO antibodies, four patients had elevated antibodies against S-100B, two patients against MOG or synapsin and one patient against MBP. In two patients we observed a continuous increase of dsDNA or TPO antibodies above the normal range. This rise paralleled IFNB treatment. In addition, 11 of 20 patients developed neutralizing antibodies against IFNB. There was no increase of autoantibodies directed against central nervous system antigens. Like patients with relapsing remitting or secondary progressive multiple sclerosis, PPMS patients may be at risk of an autoimmune response during IFNB treatment."],["dc.identifier.doi","10.1007/s00415-004-0580-3"],["dc.identifier.isi","000226302000010"],["dc.identifier.pmid","15645350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47070"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Autoantibody synthesis in primary progressive multiple sclerosis patients treated with interferon beta-1b"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","205"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","289"],["dc.contributor.author","Dabbert, D."],["dc.contributor.author","Rosner, S."],["dc.contributor.author","Kramer, M."],["dc.contributor.author","Scholl, U."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Mader, M."],["dc.contributor.author","Weber, F."],["dc.date.accessioned","2018-11-07T10:33:43Z"],["dc.date.available","2018-11-07T10:33:43Z"],["dc.date.issued","2000"],["dc.description.abstract","Glatiramer acetate (GA), represents an established treatment of relapsing/remitting multiple sclerosis (MS). The mechanisms responsible for the effect of GA are not fully understood. We generated GA-, myelin basic protein (MBP)- and purified protein derivative (PPD)-specific T cell lines from three MS patients and one healthy donor. The GA-specific lines were CD3(+), CD4(+), CD8(-) and produced tumor-necrosis-factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-4 (IL-4), interleukin-6 (IL-6) and interleukin-10 (IL-10) after stimulation with GA in the presence of irradiated peripheral blood mononuclear cells. MBP-specific T cell lines showed an identical phenotype and secreted TNF-alpha, IFN-gamma, IL-4, IL-10, but not IL-6. Co-culture experiments demonstrated, that GA-specific T cell lines have the capability to suppress the proliferation of MBP-specific T cell lines. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(00)01289-1"],["dc.identifier.isi","000088629600013"],["dc.identifier.pmid","10961665"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44680"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Glatiramer acetate (copolymer-1)-specific, human T cell lines: cytokine profile and suppression of T cell lines reactive against myelin basic protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","639"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neurology, Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","647"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Stellmann, Jan-Patrick"],["dc.contributor.author","Krumbholz, Markus"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Gahlen, Anna"],["dc.contributor.author","Borisow, Nadja"],["dc.contributor.author","Fischer, Katrin"],["dc.contributor.author","Hellwig, Kerstin"],["dc.contributor.author","Pache, Florence"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Havla, Joachim"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Geis, Christian"],["dc.contributor.author","Kleinschnitz, Christoph"],["dc.contributor.author","Berthele, Achim"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Angstwurm, Klemens"],["dc.contributor.author","Young, Kim Lea"],["dc.contributor.author","Schuster, Simon"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Mayer, Christoph"],["dc.contributor.author","Zeltner, Lena"],["dc.contributor.author","Ziemann, Ulf"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Marziniak, Martin"],["dc.contributor.author","Then Bergh, Florian"],["dc.contributor.author","Hofstadt-van Oy, Ulrich"],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Zettl, Uwe"],["dc.contributor.author","Faiss, Jürgen"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Kleiter, Ingo"],["dc.date.accessioned","2020-12-10T18:37:16Z"],["dc.date.available","2020-12-10T18:37:16Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1136/jnnp-2017-315603"],["dc.identifier.eissn","1468-330X"],["dc.identifier.issn","0022-3050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76897"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Immunotherapies in neuromyelitis optica spectrum disorder: efficacy and predictors of response"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1224"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1228"],["dc.bibliographiccitation.volume","250"],["dc.contributor.author","Yushchenko, M."],["dc.contributor.author","Mader, M."],["dc.contributor.author","Elitok, E."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Dressel, Alexander"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Bogumil, T."],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Weber, F."],["dc.date.accessioned","2018-11-07T10:35:52Z"],["dc.date.available","2018-11-07T10:35:52Z"],["dc.date.issued","2003"],["dc.description.abstract","Recent reports have shown that matrix-metalloproteinases (MMPs) facilitate T-cell migration into the CNS and play a role in disruption of the blood-brain-barrier and myelin breakdown. An increase of MMP-9 serum levels predicts disease activity in relapsing remitting multiple sclerosis (RRMS). Interferon-beta (IFN-beta), which is an established treatment for RRMS, inhibits T-cell migration in vitro in parallel with the downregulation of MMP expression. Only limited data are available for primary progressive multiple sclerosis (PPMS) which differs in demographic and immunological aspects as well as in MRI criteria from RRMS. In this study, 19 patients with laboratory-supported definite PPMS were treated with 8 x 10(6) IU IFN-beta1b (Betaferon(R)) subcutaneously every other day. Serum was collected before treatment and on months 1, 2, 3,6 and 9 during treatment. Levels of MMP-9 and of its natural inhibitor known as tissue-inhibitor of matrix-metalloproteinase-1 (TIMP-1) were quantified by ELISA. In addition MMP-2 serum levels were determined by zymography. 19 healthy volunteers served as controls. Before treatment serum levels of MMP-9 were elevated in patients with PPMS compared with controls, whereas there was no difference in TIMP-1 serum levels. During treatment with IFN-beta1b the concentration of MMP-9 in the serum of 18 out of 19 PPMS patients decreased, whereas serum levels of MMP-2 and TIMP-1 remained nearly unaffected. Our results demonstrate that the MMP-9 to TIMP-1 ratio in patients with PPMS is elevated in comparison with healthy controls. The suppression of MMP-9 by IFN-beta1b indicates that this drug is immunomodulatory active in PPMS patients. Further studies are necessary to test if IFN-beta exerts a beneficial effect in PPMS."],["dc.identifier.doi","10.1007/s00415-003-0191-4"],["dc.identifier.isi","000186231900015"],["dc.identifier.pmid","14586607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45190"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Interferon-beta-1b decreased matrix metalloproteinase-9 serum levels in primary progressive multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]