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.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.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"]]

[["dc.bibliographiccitation.firstpage","867"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","SLEEP"],["dc.bibliographiccitation.lastpage","874"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Eggert, S."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Brunner, E."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:47:06Z"],["dc.date.available","2018-11-07T10:47:06Z"],["dc.date.issued","2004"],["dc.description.abstract","Study Objectives: The prostaglandin D system plays an important role in animal sleep. In humans, alterations in the prostaglandin D system have been found in diseases exhibiting sleep disturbances as a prominent symptom, such as trypanosoma infection, systemic mastocytosis, bacterial meningitis, major depression, or obstructive sleep apnea. Assessment of this system's activity in relation to human physiologic sleep was the target of the present study. Design: Serum concentrations of lipocalin-type prostaglandin D synthase (L-PGDS, former P-trace), and plasma levels of the pineal hormone melatonin were measured in 20 healthy humans (10 women, 10 men; aged: 23.3 +/- 2.39 years) at 4-hour intervals over a period of 5 days and nights, which included physiologic sleep, rapid eye movement sleep deprivation, and total sleep deprivation. In addition, the serum L-PGDS and plasma melatonin levels of 6 subjects were determined under conditions of bright white (10,000 lux) or dark red light (< 50 lux) in a crossover design during total sleep deprivation. Nocturnal blood sampling was performed by a through-the-wall tube system. L-PGDS was measured by an automated immunonephelometric assay, and melatonin was analyzed by direct radioimmunoassay. Results: Serum L-PGDS concentrations showed marked time-dependent changes with evening increases and the highest values at night (P < .0005). This nocturnal increase was suppressed during total sleep deprivation (P < .05), independent of external light conditions and melatonin secretion. Rapid eye movement sleep deprivation had no impact on circulating L-PGDS levels. Conclusions: The circadian L-PGDS pattern and its suppression by total sleep deprivation indicate an interaction of the prostaglandin D system and human sleep regulation. L-PGDS measurements may well provide new insights into physiologic and pathologic sleep regulation in humans."],["dc.identifier.isi","000223451400008"],["dc.identifier.pmid","15453544"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47897"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Academy Sleep Medicine"],["dc.relation.issn","0161-8105"],["dc.title","Prostaglandin D synthase (beta-trace) in healthy human sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","18"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Barchfeld, S."],["dc.contributor.author","Olgemoller, U."],["dc.contributor.author","Maier, K."],["dc.contributor.author","Lange, P."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:12:10Z"],["dc.date.available","2018-11-07T09:12:10Z"],["dc.date.issued","2000"],["dc.description.abstract","Apoptosis of dentate granular cells in the hippocampal formation during bacterial meningitis may be mediated by glutamate toxicity. For this reason, we studied the relationship between glutamine synthetase activity and regional neuronal apoptosis in rabbits with experimental pneumococcal meningitis. The duration of meningitis was 24 h, and the treatment was started 16 h after infection. Significant increases of glutamine synthetase protein concentration (P < 0.05) were found in the frontal cortex of rabbits with meningitis (n = 7) and rabbits with meningitis receiving ceftriaxone treatment (n = 12) as compared to the control animals (n = 14). No significant differences were seen in the hippocampal formation. The enzymatic activity of glutamine synthetase also was elevated in the frontal cortex (P < 0.05), but not in the hippocampal formation of rabbits with meningitis. After intravenous administration of L-methionine sulfoximine (specific inhibitor of glutamine synthetase) in rabbits with meningitis treated with ceftriaxone (n = 10), the concentration of neuron-specific enolase in CSF (P = 0.025) and the density of apoptotic neurons in the dentate gyrus quantified with the in-situ tailing reaction (P = 0.043) were higher than in meningitic animals receiving only ceftriaxone (n = 10). In conclusion, the inability of hippocampal glutamine synthetase to metabolize excess amounts of glutamate may contribute to neuronal apoptosis in the hippocampal formation during meningitis. GLIA 30:11-18, 2000. (C) 2000 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/(SICI)1098-1136(200003)30:1<11::AID-GLIA2>3.0.CO;2-E"],["dc.identifier.isi","000086084500002"],["dc.identifier.pmid","10696140"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26890"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","Inhibition of glutamine synthetase in rabbit pneumococcal meningitis is associated with neuronal apoptosis in the dentate gyrus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]