Tumani, Hayrettin

[["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","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","713"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.lastpage","718"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Herrendorf, Gregor"],["dc.contributor.author","Mogge, Sebastian"],["dc.contributor.author","Steinhoff, Bernhard J."],["dc.date.accessioned","2017-09-07T11:44:34Z"],["dc.date.available","2017-09-07T11:44:34Z"],["dc.date.issued","1999"],["dc.description.abstract","Summary: Purpose: To investigate and compare the temporal profile of serial levels of neuron-specific enolase (NSE) and prolactin in serum from patients after single epileptic seizures.Methods: Measurement of NSE and prolactin by sensitive immunoassays in 21 patients with complex partial seizure (CPSs; n = 11) and secondarily generalized tonic-clonic seizures (SGTCSs; n = 10) during continuous video-EEG monitoring at four different time points (1, 3, 6, and 24 h after ictal event). Statistical analysis was performed by using a repeated-measures analysis of variance (ANOVA) model.Results: Mean ± SD values for NSE levels (ng/ml) were 12.5 ± 4.4 (1 h), 10.8 ± 3.8 (3 h), 11.1 ± 4.9 (6 h), and 8.2 ± 1.9 (24 h). The corresponding prolactin levels (mU/L) were 1,311 ± 1,034, 232 ± 158, 237 ± 175, and 251 ± 98. There was a significant decrease of NSE and prolactin levels over time (p < 0.001). The pair-wise comparison of NSE levels showed significant differences between the time points 1 vs. 24 h (p < 0.001), 3 vs. 24 h (p = 0.007), and 6 vs. 24 h (p = 0.009). In contrast, serum prolactin levels showed a significant difference between 1 vs. 3 h (p < 0.001) only. Most of the NSE levels remained normal after CPSs and SGTCSs. At 1 h after the seizure, only 33% of the subjects had increased NSE, whereas abnormal prolactin levels occurred with a sensitivity of 80%.Conclusions: In contrast to prolactin, serum NSE is not a sensitive marker of individual seizures. Only some individuals showed an increase of NSE beyond the prolactin-sensitive time frame after a single seizure, and mean NSE levels were not significantly increased compared with those of normal controls."],["dc.identifier.doi","10.1111/j.1528-1157.1999.tb00768.x"],["dc.identifier.gro","3151700"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8519"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0013-9580"],["dc.title","Kinetics of Serum Neuron-Specific Enolase and Prolactin in Patients After Single Epileptic Seizures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e7624"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lee, D. H."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:52:40Z"],["dc.date.available","2019-07-09T11:52:40Z"],["dc.date.issued","2009-10-28"],["dc.description.abstract","The identification of new biomarkers is of high interest for the prediction of the disease course and also for the identification of pathomechanisms in multiple sclerosis (MS). To specify markers of the chronic disease phase, we performed proteome profiling during the later phase of myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE, day 35 after immunization) as a model disease mimicking many aspects of secondary progressive MS. In comparison to healthy controls, high resolution 2 dimensional gel electrophoresis revealed a number of regulated proteins, among them glial fibrilary acidic protein (GFAP). Phase specific up-regulation of GFAP in chronic EAE was confirmed by western blotting and immunohistochemistry. Protein levels of GFAP were also increased in the cerebrospinal fluid of MS patients with specificity for the secondary progressive disease phase. In a next step, proteome profiling of an EAE model with enhanced degenerative mechanisms revealed regulation of alpha-internexin, syntaxin binding protein 1, annexin V and glutamate decarboxylase in the ciliary neurotrophic factor (CNTF) knockout mouse. The identification of these proteins implicate an increased apoptosis and enhanced axonal disintegration and correlate well the described pattern of tissue injury in CNTF -/- mice which involve oligodendrocyte (OL) apoptosis and axonal injury.In summary, our findings underscore the value of proteome analyses as screening method for stage specific biomarkers and for the identification of new culprits for tissue damage in chronic autoimmune demyelination."],["dc.format.extent","9"],["dc.identifier.doi","10.1371/journal.pone.0007624"],["dc.identifier.fs","544326"],["dc.identifier.pmid","19865482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5819"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Axons"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Encephalomyelitis, Autoimmune, Experimental"],["dc.subject.mesh","Gene Expression Profiling"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Multiple Sclerosis"],["dc.subject.mesh","Oligodendroglia"],["dc.subject.mesh","Proteome"],["dc.subject.mesh","Proteomics"],["dc.subject.mesh","Time Factors"],["dc.title","Proteome profiling in murine models of multiple sclerosis: identification of stage specific markers and culprits for tissue damage."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e48783"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Parnetti, Lucilla"],["dc.contributor.author","Soininen, Hilkka"],["dc.contributor.author","Herukka, Sanna-Kaisa"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Tawfik, Saskia"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Kulaksiz, Hasan"],["dc.contributor.author","Lenter, Martin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Ferger, Boris"],["dc.contributor.author","Hengerer, Bastian"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:53:59Z"],["dc.date.available","2019-07-09T11:53:59Z"],["dc.date.issued","2012-11-08"],["dc.description.abstract","The prevalence of Parkinson’s disease (PD) increases with age. Up to 50% of PD show cognitive decline in terms of a mild cognitive impairment already in early stages that predict the development of dementia, which can occur in up to 80% of PD patients over the long term, called Parkinson’s disease dementia (PDD). So far, diagnosis of PD/PDD is made according to clinical and neuropsychological examinations while laboratory data is only used for exclusion of other diseases. The aim of this study was the identification of possible biomarkers in cerebrospinal fluid (CSF) of PD, PDD and controls (CON) which predict the development of dementia in PD. For this, a proteomic approach optimized for CSF was performed using 18 clinically well characterized patients in a first step with subsequent validation using 84 patients. Here, we detected differentially sialylated isoforms of Serpin A1 as marker for differentiation of PD versus PDD in CSF. Performing 2Dimmunoblots, all PDD patients could be identified correctly (sensitivity 100%). Ten out of 24 PD patients showed Serpin A1 isoforms in a similar pattern like PDD, indicating a specificity of 58% for the test-procedure. In control samples, no additional isoform was detected. On the basis of these results, we conclude that differentially sialylated products of Serpin A1 are an interesting biomarker to indicate the development of a dementia during the course of PD."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0048783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60545"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Differential Sialylation of Serpin A1 in the Early Diagnosis of Parkinson’s Disease Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","629"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","640"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Boström, Gustaf"],["dc.contributor.author","Freyhult, Eva"],["dc.contributor.author","Virhammar, Johan"],["dc.contributor.author","Alcolea, Daniel"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Brundin, Rose-Marie"],["dc.contributor.author","Kilander, Lena"],["dc.contributor.author","Löwenmark, Malin"],["dc.contributor.author","Ingelsson, Martin"],["dc.date.accessioned","2021-08-12T07:45:42Z"],["dc.date.available","2021-08-12T07:45:42Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Neuroinflammatory processes are common in neurodegenerative diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but current knowledge is limited as to whether cerebrospinal fluid (CSF) levels of neuroinflammatory proteins are altered in these diseases. Objective: To identify and characterize neuroinflammatory signatures in CSF from patients with AD, mild cognitive impairment (MCI), and FTD. Methods: We used proximity extension assay and ANOVA to measure and compare levels of 92 inflammatory proteins in CSF from 42 patients with AD, 29 with MCI due to AD (MCI/AD), 22 with stable MCI, 42 with FTD, and 49 control subjects, correcting for age, gender, collection unit, and multiple testing. Results: Levels of matrix metalloproteinase-10 (MMP-10) were increased in AD, MCI/AD, and FTD compared with controls (AD: fold change [FC] = 1.32, 95% confidence interval [CI] 1.14–1.53, q = 0.018; MCI/AD: FC = 1.53, 95% CI 1.20–1.94, q = 0.045; and FTD: FC = 1.42, 95% CI 1.10–1.83, q = 0.020). MMP-10 and eleven additional proteins were increased in MCI/AD, compared with MCI (q < 0.05). In FTD, 36 proteins were decreased, while none was decreased in AD or MCI/AD, compared with controls (q < 0.05). Conclusion: In this cross-sectional multi-center study, we found distinct patterns of CSF inflammatory marker levels in FTD and in both early and established AD, suggesting differing neuroinflammatory processes in the two disorders."],["dc.description.abstract","Background: Neuroinflammatory processes are common in neurodegenerative diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but current knowledge is limited as to whether cerebrospinal fluid (CSF) levels of neuroinflammatory proteins are altered in these diseases. Objective: To identify and characterize neuroinflammatory signatures in CSF from patients with AD, mild cognitive impairment (MCI), and FTD. Methods: We used proximity extension assay and ANOVA to measure and compare levels of 92 inflammatory proteins in CSF from 42 patients with AD, 29 with MCI due to AD (MCI/AD), 22 with stable MCI, 42 with FTD, and 49 control subjects, correcting for age, gender, collection unit, and multiple testing. Results: Levels of matrix metalloproteinase-10 (MMP-10) were increased in AD, MCI/AD, and FTD compared with controls (AD: fold change [FC] = 1.32, 95% confidence interval [CI] 1.14–1.53, q = 0.018; MCI/AD: FC = 1.53, 95% CI 1.20–1.94, q = 0.045; and FTD: FC = 1.42, 95% CI 1.10–1.83, q = 0.020). MMP-10 and eleven additional proteins were increased in MCI/AD, compared with MCI (q < 0.05). In FTD, 36 proteins were decreased, while none was decreased in AD or MCI/AD, compared with controls (q < 0.05). Conclusion: In this cross-sectional multi-center study, we found distinct patterns of CSF inflammatory marker levels in FTD and in both early and established AD, suggesting differing neuroinflammatory processes in the two disorders."],["dc.identifier.doi","10.3233/JAD-201565"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88530"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Different Inflammatory Signatures in Alzheimer’s Disease and Frontotemporal Dementia Cerebrospinal Fluid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","229"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","242"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Suessmuth, Sigurd D."],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Wick, M."],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Lewinger, Juan Pablo"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Tumani, Hayrettin"],["dc.date.accessioned","2018-11-07T09:28:33Z"],["dc.date.available","2018-11-07T09:28:33Z"],["dc.date.issued","2013"],["dc.description.abstract","Cerebrospinal fluid (CSF) analysis is of utmost importance to establish an early diagnosis of central nervous system (CNS) infections and to start appropriate therapy. The CSF white cell count, lactate concentration and total protein levels are usually available very quickly even from non-specialized laboratories and the combination of these parameters often provides sufficient information for decision-making in emergency cases. It is, however, not always possible to identify the underlying infective agent despite further CSF analyses, such as bacterial and fungal staining, evaluation of the blood-CSF barrier function, intrathecal immunoglobulin synthesis and oligoclonal IgG bands. Therefore, close communication between the laboratory and the clinician is an important prerequisite to specify additional pathogen-related diagnostic measures for successful confirmation of the diagnosis."],["dc.identifier.doi","10.1007/s00115-012-3701-8"],["dc.identifier.isi","000314897400015"],["dc.identifier.pmid","23371378"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30806"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Current cerebrospinal fluid diagnostics for pathogen-related diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","17565"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.lastpage","17588"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Abdelhak, Ahmed"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Tumani, Hayrettin"],["dc.date.accessioned","2018-11-07T09:53:26Z"],["dc.date.available","2018-11-07T09:53:26Z"],["dc.date.issued","2015"],["dc.description.abstract","Many neurodegenerative disorders share a common pathophysiological pathway involving axonal degeneration despite different etiological triggers. Analysis of cytoskeletal markers such as neurofilaments, protein tau and tubulin in cerebrospinal fluid (CSF) may be a useful approach to detect the process of axonal damage and its severity during disease course. In this article, we review the published literature regarding brain-specific CSF markers for cytoskeletal damage in primary progressive multiple sclerosis and amyotrophic lateral sclerosis in order to evaluate their utility as a biomarker for disease progression in conjunction with imaging and histological markers which might also be useful in other neurodegenerative diseases associated with affection of the upper motor neurons. A long-term benefit of such an approach could be facilitating early diagnostic and prognostic tools and assessment of treatment efficacy of disease modifying drugs."],["dc.description.sponsorship","BMBF-funded competence network multiple sclerosis (KKNMS)"],["dc.identifier.doi","10.3390/ijms160817565"],["dc.identifier.isi","000366826100046"],["dc.identifier.pmid","26263977"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12759"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36329"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mdpi Ag"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Brain-Specific Cytoskeletal Damage Markers in Cerebrospinal Fluid: Is There a Common Pattern between Amyotrophic Lateral Sclerosis and Primary Progressive Multiple Sclerosis?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2499"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","2504"],["dc.bibliographiccitation.volume","263"],["dc.contributor.author","Huss, Andre M."],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Borisow, Nadja"],["dc.contributor.author","Harrer, Andrea"],["dc.contributor.author","Brecht, Isabel"],["dc.contributor.author","Balint, Bettina"],["dc.contributor.author","Stich, Oliver"],["dc.contributor.author","Schlegel, Sabine"],["dc.contributor.author","Retzlaff, Nele"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Roesler, Romy"],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Yildiz, Oezlem"],["dc.contributor.author","Voss, Elke"],["dc.contributor.author","Muche, Rainer"],["dc.contributor.author","Rauer, Sebastian"],["dc.contributor.author","Bergh, Florian Then"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Kraus, Joerg"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Buttmann, Mathias"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Tumani, Hayrettin"],["dc.date.accessioned","2018-11-07T10:05:23Z"],["dc.date.available","2018-11-07T10:05:23Z"],["dc.date.issued","2016"],["dc.description.abstract","The majority of patients presenting with a first clinical symptom suggestive of multiple sclerosis (MS) do not fulfill the MRI criteria for dissemination in space and time according to the 2010 revision of the McDonald diagnostic criteria for MS and are thus classified as clinically isolated syndrome (CIS). To re-evaluate the utility of cerebrospinal fluid (CSF) analysis in the context of the revised McDonald criteria from 2010, we conducted a retrospective multicenter study aimed at determining the prevalence and predictive value of oligoclonal IgG bands (OCBs) in patients with CIS. Patients were recruited from ten specialized MS centers in Germany and Austria. We collected data from 406 patients; at disease onset, 44/406 (11 %) fulfilled the McDonald 2010 criteria for MS. Intrathecal IgG OCBs were detected in 310/362 (86 %) of CIS patients. Those patients were twice as likely to convert to MS according to McDonald 2010 criteria as OCB-negative individuals (hazard ratio = 2.1, p = 0.0014) and in a shorter time period of 25 months (95 % CI 21-34) compared to 47 months in OCB-negative individuals (95 % CI 36-85). In patients without brain lesions at first attack and presence of intrathecal OCBs (30/44), conversion rate to MS was 60 % (18/30), whereas it was only 21 % (3/14) in those without OCBs. Our data confirm that in patients with CIS the risk of conversion to MS substantially increases if OCBs are present at onset. CSF analysis definitely helps to evaluate the prognosis in patients who do not have MS according to the revised McDonald criteria."],["dc.identifier.doi","10.1007/s00415-016-8302-1"],["dc.identifier.isi","000388625500020"],["dc.identifier.pmid","27730374"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14162"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38882"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1432-1459"],["dc.relation.issn","0340-5354"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Importance of cerebrospinal fluid analysis in the era of McDonald 2010 criteria: a German-Austrian retrospective multicenter study in patients with a clinically isolated syndrome"],["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.artnumber","73"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Mogge, Sebastian"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Pfahlberg, A."],["dc.contributor.author","Steinhoff, B."],["dc.date.accessioned","2017-11-21T10:16:56Z"],["dc.date.available","2017-11-21T10:16:56Z"],["dc.date.issued","1998"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10129"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Changing levels of S100 protein in serum after epileptic seizures"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]