Bunkowski, Stephanie

[["dc.bibliographiccitation.firstpage","1877"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1883"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schulz, Daniela"],["dc.contributor.author","Kellert, Benedikt"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T08:29:27Z"],["dc.date.available","2018-11-07T08:29:27Z"],["dc.date.issued","2009"],["dc.description.abstract","An increase in adult neurogenesis was observed after exposure to enriched environment (EE) and during reconvalescence from experimental pneumococcal meningitis. This study investigated neurogenesis and spatial learning performance 5 weeks after bacterial meningitis and exposure to EE. C57BL/6 mice were infected by intracerebral injection of Streptococcus pneumoniae and treated with ceftriaxone for 5 days. Forty-eight hours after infection, one group (n = 22) was exposed to EE and the other group (n = 23) housed under standard conditions. Another set of mice was kept under either enriched (n = 16) or standard (n = 15) conditions without bacterial meningitis. Five weeks later, the Morris water maze was performed, and neurogenesis was evaluated by means of immunohistochemistry. Mice housed in EE without prior bacterial infection displayed both increased neurogenesis and improved water maze performance in comparison with uninfected control animals. Bacterial meningitis stimulated neurogenesis in the granular cell layer of the dentate gyrus: with standard housing conditions, we observed a higher density of BrdU-immunolabeled and TUC-4-expressing cells 5 weeks after induction of bacterial meningitis than in the noninfected control group. EE did not further increase progenitor cell proliferation and neuronal differentiation in the subgranular cell layer of the dentate gyrus after bacterial meningitis in comparison with infected mice housed under standard conditions. Moreover, the Morris water maze showed no significant differences between survivors of meningitis exposed to EE and animals kept in standard housing. In summary, exposure to EE after pneumococcal meningitis did not further increase meningitis-induced neurogenesis or improve spatial learning. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung [1161/06//A70/06]"],["dc.identifier.doi","10.1002/jnr.22010"],["dc.identifier.isi","000265462800015"],["dc.identifier.pmid","19170185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16657"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Enriched Environment Fails To Increase Meningitis-Induced Neurogenesis and Spatial Memory in a Mouse Model of Pneumococcal Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","809"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","816"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Michel, W."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schneider, O."],["dc.contributor.author","Shintani, Y."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Stringaris, A. K."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:33:22Z"],["dc.date.available","2018-11-07T10:33:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: Follistatin (FS) is the specific binding protein of activin and expression of both factors is regulated by inflammatory agents. Therefore. FS concentrations were determined in cerebrospinal fluid (CSF) of patients with bacterial and viral meningitis or multiple sclerosis (MS), as well as in the CSF of patients without meningial inflammation or autoimmune diseases. Furthermore, a mouse pneumococcal meningitis model was used to localise the cellular sources of FS in brains of normal and meningitic mice. Methods: FS concentrations in CSF were determined by ELISA; FS in mice was localised by in situ hybridisation and immunohistochemistry. Results: FS concentrations were greater than or equal to0.4 mug/l in 22 of 66 CSF samples of meningitis patients versus 2 of 27 CSF samples from patients with multiple sclerosis (P < 0.05) and 2 of 41 CSF specimen from patients without neuroinflammatory diseases (P < 0.01). In the CSF of patients with meningitis, the concentration of FS was correlated with total protein (P < 0.005) and lactate concentrations (P < 0.05), but not with leukocyte counts, interval between onset of disease and CSF analysis, or clinical outcome. The CSF-to-serum ratios of FS and albumin also correlated significantly (P < 0.0005). in some patients with meningitis the CSF-to-serum ratios suggested that the elevated FS in CSF did not originate from serum alone. FS was localised in mice brains to neurones of the hippocampus, dentate gyrus, neocortex, and to the choroid plexus. Analyses of brains and other organs from uninfected and infected animals sacrificed 6-36 h after infection did not reveal any obvious differences in the distribution and intensity of FS mRNA and protein expression. Conclusions: The concentration of FS in humans is elevated during meningitis. In some patients the increase is caused by a release of FS from brain into CSF. Data from the mouse meningitis model suggest that increased CSF concentrations of FS in meningitis appear not to be accompanied by an elevated number of cells containing FS mRNA or protein in the brain."],["dc.identifier.isi","000166654700013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44594"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bioscientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Follistatin (FS) in human cerebrospinal fluid and regulation of FS expression in a mouse model of meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","509"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","511"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:51:11Z"],["dc.date.available","2018-11-07T10:51:11Z"],["dc.date.issued","2004"],["dc.description.abstract","The contribution of axonal injury to CNS damage in bacterial meningitis was studied by histology and immunohistochemistry for amyloid-beta precursor protein in humans and experimental rabbits. Axonal injury in the white matter caused predominantly but not exclusively by ischemia was detected in all autopsy cases (n = 5) and in 11 of 15 brains of rabbits 18 to 24 hours after intracisternal infection with Streptococcus pneumoniae. This suggests a substantial contribution of axonal pathology to neurologic sequelae after bacterial meningitis."],["dc.identifier.isi","000189238800038"],["dc.identifier.pmid","14872046"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48830"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Axonal injury, a neglected cause of CNS damage in bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1450"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1460"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Böttcher, Tobias"],["dc.contributor.author","Ren, Hao"],["dc.contributor.author","Goiny, Michel"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Lykkesfeldt, Jens"],["dc.contributor.author","Kuhnt, Ulrich"],["dc.contributor.author","Lotz, Miriam"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Werner, Carola"],["dc.contributor.author","Schau, Ingmar"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Christen, Stephan"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T10:43:30Z"],["dc.date.available","2018-11-07T10:43:30Z"],["dc.date.issued","2004"],["dc.description.abstract","In animal models of Streptococcus pneumoniae meningitis, rifampin is neuroprotective in comparison to ceftriaxone. So far it is not clear whether this can be generalized for other protein synthesis-inhibiting antimicrobial agents. We examined the effects of the bactericidal protein synthesis-inhibiting clindamycin (n = 12) on the release of proinflammatory bacterial components, the formation of neurotoxic compounds and neuronal injury compared with the standard therapy with ceftriaxone (n = 12) in a rabbit model of pneumococcal meningitis. Analysis of the CSF and histological evaluation were combined with microdialysis from the hippocampal formation and the neocortex. Compared with ceftriaxone, clindamycin reduced the release of lipoteichoic acids from the bacteria (p = 0.004) into the CSF and the CSF leucocyte count (p = 0.011). This led to lower extracellular concentrations of hydroxyl radicals (p = 0.034) and glutamate (p = 0.016) in the hippocampal formation and a subsequent reduction of extracellular glycerol levels (p = 0.018) and neuronal apoptosis in the dentate gyrus (p = 0.008). The present data document beneficial effects of clindamycin compared with ceftriaxone on various parameters linked with the pathophysiology of pneumococcal meningitis and development of neuronal injury. This study suggests neuroprotection to be a group effect of bactericidal protein synthesis-inhibiting antimicrobial agents compared with the standard therapy with beta-lactam antibiotics in meningitis."],["dc.description.sponsorship","NINDS NIH HHS [R01 NS33997]"],["dc.identifier.doi","10.1111/j.1471-4159.2004.02837.x"],["dc.identifier.isi","000226115900020"],["dc.identifier.pmid","15584921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47067"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0022-3042"],["dc.title","Clindamycin is neuroprotective in experimental Streptococcus pneumoniae meningitis compared with ceftriaxone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","104"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","475"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Stuertz, K."],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Fischer, F. R."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:43:14Z"],["dc.date.available","2018-11-07T08:43:14Z"],["dc.date.issued","2010"],["dc.description.abstract","The rabbit model provides an important experimental setting for the evaluation of antibiotic agents against pneumococcal meningitis. One of the primary targets of this model is the study of neuronal and glial cell damage in bacterial meningitis. The aim of this investigation was to evaluate whether a significant increase of S100B in the cerebrospinal fluid (CSF) as an indicator of white matter damage could be observed in this meningitis model. Seven rabbits were infected intracisternally with S. pneumoniae, and CSF S100B concentrations were examined serially before infection, at 12h, 14h, 17h, 20h, and at 24h after infection. The course of CSF S100B increase and its relation to other parameters of brain tissue destruction and CSF inflammation were measured. Axonal damage was visualized by amyloid precursor protein (APP) immunostaining and demyelination by Luxol Fast Blue/Periodic Acid Schiff (LFB-PAS) stain. In each animal, we observed a distinct rise in S100B concentration in the CSF due to pneumococcal meningitis. We conclude that the CSF concentration of the glial S100B protein can be used as an additional parameter for future interventional studies focusing on glial cell damage in the rabbit model of bacterial meningitis. (C) 2010 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2010.03.059"],["dc.identifier.isi","000279785000010"],["dc.identifier.pmid","20347934"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19911"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","S100B in the cerebrospinal fluid-A marker for glial damage in the rabbit model of pneumococcal meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","238"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","O'Connor, A. E."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Phillips, David J."],["dc.date.accessioned","2018-11-07T10:38:01Z"],["dc.date.available","2018-11-07T10:38:01Z"],["dc.date.issued","2003"],["dc.description.abstract","Activin, a member of the transforming growth factor superfamily, is upregulated in a number of inflammatory episodes such as septicemia and rheumatoid arthritis. In the CNS, activin has been predominantly assessed in terms of a neuroprotective role. In this report we characterized the activin response in the CNS in a rabbit model of meningitis. In normal animals, cerebrospinal fluid (CSF) activin levels were higher than those in serum, indicating an intracranial secretion of this cytokine. Following intracisternal inoculation with Streptococcus pneumoniae , activin in CSF was unchanged for the first 12 h and then rose progressively; levels were increased approximately 15-fold within 24 h. Activin levels were correlated positively with CSF protein content and with the number of apoptotic neurons in the dentate gyrus. No apparent correlation was observed between CSF activin concentrations and bacterial titer, lactate concentrations or leukocyte density. Using immunohistochemistry, activin staining was localized to epithelial cells of the choroid plexus, cortical neurons and the CA3 region of the hippocampus, with similar staining intensities in both normal and meningitic brains. However, in meningitic brains there was also strong staining in activated microglia and infiltrating macrophages. Taken together, these results demonstrate that activin forms part of the CNS response to immune challenge and may be an important mediator to modulate inflammatory processes in the brain."],["dc.identifier.doi","10.1046/j.1471-4159.2003.01834.x"],["dc.identifier.isi","000183526200025"],["dc.identifier.pmid","12807443"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45708"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0022-3042"],["dc.title","Increased activin levels in cerebrospinal fluid of rabbits with bacterial meningitis are associated with activation of microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Hahn, M."],["dc.contributor.author","Siemer, A."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:48:42Z"],["dc.date.available","2018-11-07T10:48:42Z"],["dc.date.issued","2004"],["dc.description.abstract","Tumor necrosis factor-alpha (TNF-alpha) is critically involved in inflammation and may participate in hippocampal injury in bacterial meningitis. In a mouse model of ceftriaxone-treated pneumococcal meningitis, spatial memory and motor performance of TNF-alpha-deficient (n = 57) and control mice (n = 55) were investigated. After infection, therapy was initiated with ceftriaxone (100 mg/kg twice daily for 5 days). Sixty-three percent TNF-alpha-deficient mice and 40% control animals died within 6 days (Fisher's exact test: P = 0.02). TNF-alpha-deficient mice surviving pneumococcal meningitis took substantially longer to reach the hidden platform than controls, and the distance of swim tracks was longer (P = 0.02). The swim speed in both groups was similar (P = 0.59). The proliferation of dentate granule cells was lower in TNF-alpha-deficient than in wild-type mice (P = 0.03). In pneumococcal meningitis, TNF-alpha deficiency caused increased mortality and stronger deficits in spatial memory possibly due to impaired neurogenesis. (C) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.nbd.2004.01.013"],["dc.identifier.isi","000221365300015"],["dc.identifier.pmid","15207270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48257"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0969-9961"],["dc.title","Increased mortality and spatial memory deficits in TNF-alpha-deficient mice in ceftriaxone-treated experimental pneumococcal meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","441"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","446"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Bering, J."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Kuhnt, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:36:58Z"],["dc.date.available","2018-11-07T10:36:58Z"],["dc.date.issued","2003"],["dc.description.abstract","Neuronal damage in the hippocampal formation is a common feature in animal models of bacterial meningitis and human disease. In mouse and rabbit models of Streptococcus pneumoniae meningitis, proliferation of neural progenitor cells quantified by bromodeoxyuridine (BrdU) incorporation was enhanced in the subgranular layer of the dentate gyrus. In mice, the density of BrdU-labeled cells was maximal on Day 2 after infection. Approximately 60% of the cells labeled by BrdU between Days 7 and 10 after infection that remained present 28 days later had migrated into deeper layers of the dentate gyrus and differentiated into neurons, as evidenced by immunohistochemical staining for TUC-4, MAP-2 and beta-tubulin. This suggests that endogenous repair mechanisms may limit consequences of neuronal destruction after meningitis. (C) 2003 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jnr.10682"],["dc.identifier.isi","000184521000002"],["dc.identifier.pmid","12898528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45450"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0360-4012"],["dc.title","Increased neurogenesis after experimental Streptococcus pneumoniae meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","497"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","503"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Ruehlmann, Malte"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T11:10:21Z"],["dc.date.available","2018-11-07T11:10:21Z"],["dc.date.issued","2008"],["dc.description.abstract","Glucocorticoids are prenatally administered to promote the maturation of the lungs. They, however, can affect neuronal proliferation and differentiation. In newborn marmoset monkeys, intrauterine hyperexposure to dexamethasone (DEX) resulted in a significantly decreased proliferation rate in the hippocampal dentate gyrus without affecting neuronal differentiation. In this study, marmoset monkeys received 5 mg/kg body weight DEX either during early (days 42-48) or late (days 90-96) pregnancy. The volume of the dentate granule cell layer as well as the proliferation and neuronal differentiation in the dentate gyrus of their 2-year-old offspring were investigated. The density of proliferating cells (Ki-67), apoptotic cells (in situ tailing) and cells differentiating to neurons (double cortin, TUC-4 and calretinin) were determined immunohistochemically. Analysis of the dentate granule cell layer volume showed no significant differences between early or late DEX-exposed marmosets and untreated control animals. Similarly, proliferation and neuronal differentiation in DEX-treated animals was not significantly different in comparison with controls. In summary, the decreased proliferation rate observed in newborn marmosets after intrauterine exposure to DEX was no longer detectable in their 2-year-old siblings suggesting no long-lasting effect of prenatal hyperexposure to DEX on neuronal proliferation and differentiation in the dentate gyrus of marmoset monkeys."],["dc.description.sponsorship","European Commission [QLRT-2001-02758 (EUPEAH)]"],["dc.identifier.doi","10.1111/j.1750-3639.2008.00149.x"],["dc.identifier.isi","000259146700004"],["dc.identifier.pmid","18422980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53194"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1015-6305"],["dc.title","No long-term effect two years after intrauterine exposure to dexamethasone on dentate gyrus volume, neuronal proliferation and differentiation in common marmoset monkeys"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical Neuropathology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Seitz, R.-C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:34:09Z"],["dc.date.available","2018-11-07T08:34:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Aims: We aimed at quantifying acute axonal injury ill victims of bacterial meningitis. Methods: The brains of 26 autopsies with bacterial meningitis and of 10 control cases were Studied by histology and quantitative immunohistochemistry for amyloid-beta precursor protein (APP). Results: Mild to severe axonal injury in the white matter was present in 25 of 26 victims of meningitis. The area of axonal damage ranged from 0.0% to 1.38% (median 0.08%. mean = 0.36%) of the total area Studied in each individual case. In 4 of 10 and sex-matched control brains small areas also stained For APP (p = 0.0007). Axonal injury in meningitis was most prominent in the basal ganglia and polls, followed by the hippocampal formation. neocortex and the cervical spinal cord. The cerebellum was least affected. Conclusion: Axonal injury is a frequent complication or bacterial meningitis probably contributing to long-term sequelae in survivours."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.isi","000262976000005"],["dc.identifier.pmid","19216218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17751"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dustri-verlag Dr Karl Feistle"],["dc.relation.issn","0722-5091"],["dc.title","Evidence for frequent focal and diffuse acute axonal injury in human bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]