Nau, Roland

[["dc.bibliographiccitation.firstpage","231"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","AKTUELLE NEUROLOGIE"],["dc.bibliographiccitation.lastpage","240"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:48:13Z"],["dc.date.available","2018-11-07T10:48:13Z"],["dc.date.issued","2004"],["dc.description.abstract","Usually, purulent meningitis is an acute bacterial disease. For more than fifty years, antibiotic chemotherapy is widely available. However, the course of bacterial meningitis remains lethal in more than 20% of affected adult patients. Survivors often suffer from neurological and neuropsychological sequelae. The following article provides an overview of the current therapeutical concepts for community acquired bacterial meningitis in adults. For the treatment of purulent meningitis in Germany, we recommend ampicillin and a third-generation cephalosporin as initial antibiotic therapy. A recent study demonstrated a reduction of mortality and neurological sequelae with adjuvant dexamethasone therapy."],["dc.identifier.doi","10.1055/s-2003-814936"],["dc.identifier.isi","000222195200004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48137"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0302-4350"],["dc.title","Therapy of bacterial meningitis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","108"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Schutze, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:38:56Z"],["dc.date.available","2018-11-07T09:38:56Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Palmitoylethanolamide (PEA), an endogenous lipid and a congener of anandamide, possesses a wide range of effects related to metabolic and cellular homeostasis including anti-inflammatory and neuroprotective properties. Methods: In vitro, we studied the ability of macrophages to phagocytose Escherichia coli K1 after stimulation with increasing doses of PEA. In vivo, wild-type mice were treated with PEA intraperitoneally 12 hours and 30 minutes before infection. Meningoencephalitis or sepsis was induced by intracerebral or intraperitoneal infection with E. coli K1. Results: Stimulation of macrophages with PEA for 30 minutes increased the phagocytosis of E. coli K1 without inducing the release of TNF alpha or CXCL1. Intracellular killing of E. coli K1 was higher in PEA-stimulated than in unstimulated peritoneal macrophages and microglial cells. Pre-treatment with PEA significantly increased survival of mice challenged intracerebrally or intraperitoneally with E. coli K1. This effect was associated with a decreased production of CXCL1, IL-1 beta and IL-6 in homogenates of spleen and cerebellum in mice treated with PEA. Conclusions: Our observations suggest that these protective effects of PEA in mice can increase the resistance to bacterial infections without the hazard of collateral damage by excessive stimulation of phagocytes."],["dc.identifier.doi","10.1186/1742-2094-11-108"],["dc.identifier.isi","000338670800001"],["dc.identifier.pmid","24927796"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10430"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33166"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Palmitoylethanolamide stimulates phagocytosis of Escherichia coli K1 by macrophages and increases the resistance of mice against infections"],["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","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.artnumber","64"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Jaiswal, Manoj Kumar"],["dc.contributor.author","Zech, Wolf-Dieter"],["dc.contributor.author","Goos, Miriam"],["dc.contributor.author","Leutbecher, Christine"],["dc.contributor.author","Ferri, Alberto"],["dc.contributor.author","Zippelius, Annette"],["dc.contributor.author","Carri, Maria Teresa"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Keller, Bernhard U."],["dc.date.accessioned","2018-11-07T08:28:40Z"],["dc.date.available","2018-11-07T08:28:40Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons (MN) in the brain stem and spinal cord. Intracellular disruptions of cytosolic and mitochondrial calcium have been associated with selective MN degeneration, but the underlying mechanisms are not well understood. The present evidence supports a hypothesis that mitochondria are a target of mutant SOD1-mediated toxicity in familial amyotrophic lateral sclerosis (fALS) and intracellular alterations of cytosolic and mitochondrial calcium might aggravate the course of this neurodegenerative disease. In this study, we used a fluorescence charged cool device (CCD) imaging system to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells in an established cellular model of ALS. Results: To gain insights into the molecular mechanisms of SOD1(G93A) associated motor neuron disease, we simultaneously monitored cytosolic and mitochondrial calcium concentrations in individual cells. Voltage - dependent cytosolic Ca(2+) elevations and mitochondria - controlled calcium release mechanisms were monitored after loading cells with fluorescent dyes fura-2 and rhod-2. Interestingly, comparable voltage-dependent cytosolic Ca(2+) elevations in WT (SH-SY5Y(WT)) and G93A (SH-SY5Y(G93A)) expressing cells were observed. In contrast, mitochondrial intracellular Ca(2+) release responses evoked by bath application of the mitochondrial toxin FCCP were significantly smaller in G93A expressing cells, suggesting impaired calcium stores. Pharmacological experiments further supported the concept that the presence of G93A severely disrupts mitochondrial Ca(2+) regulation. Conclusion: In this study, by fluorescence measurement of cytosolic calcium and using simultaneous [Ca(2+)]i and [Ca(2+)](mito) measurements, we are able to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells an established cellular model of ALS. The primary goals of this paper are (1) method development, and (2) screening for deficits in mutant cells on the single cell level. On the technological level, our method promises to serve as a valuable tool to identify mitochondrial and Ca(2+)-related defects during G93A-mediated MN degeneration. In addition, our experiments support a model where a specialized interplay between cytosolic calcium profiles and mitochondrial mechanisms contribute to the selective degeneration of neurons in ALS."],["dc.identifier.doi","10.1186/1471-2202-10-64"],["dc.identifier.isi","000268695200001"],["dc.identifier.pmid","19545440"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5754"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16476"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1471-2202"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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","126"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Fronek, Kathrin"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Lange, Peter"],["dc.date.accessioned","2018-11-07T08:51:09Z"],["dc.date.available","2018-11-07T08:51:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Background/Aims: Determination of marker proteins of neuronal degeneration in cerebrospinal fluid (CSF) is of increasing importance. However, preanalytical problems may compromise the results. Methods: We studied the influence of the transport tube material and shaking at room temperature on the CSF concentrations of beta-amyloid and tau protein determined by enzyme immunoassays. Results: The materials of the transport tube moderately influenced the CSF concentrations of beta-amyloid and tau protein. Polyethylene and polypropylene tubes were well suited, but glass, polycarbonate and polystyrene tubes caused a decrease in the CSF beta-amyloid and tau protein concentrations. The strongest impact, however, was caused by bacterial contamination of samples. Contamination with high concentrations of Pseudomonas aeruginosa and related species rendered beta-amyloid undetectable and strongly diminished tau protein concentrations. The effects of several Gram-positive bacteria were less pronounced. Addition of 0.1% sodium azide prior to bacterial contamination increased the interval at which CSF could be kept at room temperature without a substantial reduction of the beta-amyloid or tau protein concentration. Conclusion: Polyethylene or polypropylene tubes are suitable transport vessels for CSF samples. Bacterial contamination during sampling and portioning must be avoided. Addition of sodium azide may be an option when transport of the sample is delayed. Copyright (C) 2011 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000330912"],["dc.identifier.fs","580959"],["dc.identifier.isi","000295875400006"],["dc.identifier.pmid","21952521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21862"],["dc.language.iso","en"],["dc.notes","This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively."],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/8159"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Amyloid beta-Peptides"],["dc.subject.mesh","Cerebrospinal Fluid"],["dc.subject.mesh","Cerebrospinal Fluid Proteins"],["dc.subject.mesh","Dementia"],["dc.subject.mesh","Enzyme-Linked Immunosorbent Assay"],["dc.subject.mesh","Equipment Design"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Pseudomonas aeruginosa"],["dc.subject.mesh","Quality Control"],["dc.subject.mesh","Specimen Handling"],["dc.subject.mesh","Stenotrophomonas maltophilia"],["dc.subject.mesh","tau Proteins"],["dc.title","Bacterial Contamination and the Transport Vial Material Affect Cerebrospinal Fluid Concentrations of beta-Amyloid and Tau Protein as Determined by Enzyme Immunoassay"],["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","865"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","871"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:46:16Z"],["dc.date.available","2018-11-07T08:46:16Z"],["dc.date.issued","2010"],["dc.description.abstract","Toll-like receptors (TLRs) are crucial pattern recognition receptors in innate immunity that are expressed in microglia, the resident macrophages of the brain. TLR2, -4, and -9 are important in the responses against Streptococcus pneumoniae, the most common agent causing bacterial meningitis beyond the neonatal period. Murine microglial cultures were stimulated with agonists for TLR1/2 (Pam3CSK4), TLR4 (lipopolysaccharide), and TLR9 (CpG oligodeoxynucleotide) for 24 h and then exposed to either the encapsulated D39 (serotype 2) or the nonencapsulated R6 strain of S. pneumoniae. After stimulation, the levels of interleukin-6 and CCL5 (RANTES [regulated upon activation normal T-cell expressed and secreted]) were increased, confirming microglial activation. The TLR1/2, -4, and -9 agonist-stimulated microglia ingested significantly more bacteria than unstimulated cells (P < 0.05). The presence of cytochalasin D, an inhibitor of actin polymerizaton, blocked >90% of phagocytosis. Along with an increased phagocytic activity, the intracellular bacterial killing was also increased in TLR-stimulated cells compared to unstimulated cells. Together, our data suggest that microglial stimulation by these TLRs may increase the resistance of the brain against pneumococcal infections."],["dc.identifier.doi","10.1128/IAI.01110-09"],["dc.identifier.isi","000273855600033"],["dc.identifier.pmid","19933834"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Toll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and Encapsulated Streptococcus pneumoniae by Murine Microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","445"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Diagnostic Microbiology and Infectious Disease"],["dc.bibliographiccitation.lastpage","452"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Lodise, Thomas P., Jr."],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Kinzig, Martina"],["dc.contributor.author","Jones, Ronald N."],["dc.contributor.author","Drusano, G. L."],["dc.contributor.author","Soergel, Fritz"],["dc.date.accessioned","2018-11-07T10:59:52Z"],["dc.date.available","2018-11-07T10:59:52Z"],["dc.date.issued","2007"],["dc.description.abstract","Although the disposition of ceftriaxone and cefepime in the cerebrospinal fluid (CSF) has been described, the ability of these agents to achieve critical pharmacodynamic targets against Streptococcus pneumoniae in CSF has not been reported. Plasma and CSF pharmacokinetic data were obtained from hospital patients with external ventricular drains and receiving ceftriaxone or cefepime. Concentration-time profiles in plasma and CSF were modeled using a 3-compartment model with 0-order infusion and 1 st-order elimination and transfer. The model parameters were identified with population pharmacokinetic analysis (Big Non-Parametric Adaptive Grid with adaptive gamma). A Monte Carlo Simulation (9999 subjects) estimated the probability of target attainment (PTA) for total drug CSF concentrations at 50% and 100% T > MIC for ceftriaxone 2G IV Q 12H and cefepime 2G IV Q8H. The S. pneumoniae bloodstream infection isolates from the SENTRY Antimicrobial Surveillance Program (USA) provided the distribution of contemporary (2003-2004) MICs. Post-Bayesian measures of bias and precision, observed-predicted plots, and R 2 values were highly acceptable for both drugs. The probabilities of achieving 50% and 100% T > MIC in the CSF for ceftriaxone were 76% and 65%, respectively. For cefepime, the PTA at 50% and 100% T > MIC in the CSF were 91.8% and 82%, respectively. The CSF pharmacodynamics against S. pneumoniae for cefepime were superior to that of ceftriaxone. The implications of these findings need to be reexamined in the clinical setting. (c) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.diagmicrobio.2007.03.015"],["dc.identifier.isi","000248937500011"],["dc.identifier.pmid","17512154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50794"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1879-0070"],["dc.relation.issn","0732-8893"],["dc.title","Comparison of the probability of target attainment between ceftriaxone and cefepime in the cerebrospinal fluid and serum against Streptococcus pneumoniae"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","30"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Schmidt, H"],["dc.contributor.author","Tlustochowska, A."],["dc.contributor.author","Stuertz, K."],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Kuhnt, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2021-06-01T10:50:09Z"],["dc.date.available","2021-06-01T10:50:09Z"],["dc.date.issued","2001"],["dc.description.abstract","Hippocampal slices of newborn rats were exposed to either heat-inactivated Streptococcus pneumoniae R6 (hiR6) equivalent to 10(6) and 10(8) CFU/ml, lipoteichoic acid (LTA) (0.3 mug/ml and 30 mug/ml), peptidoglycans (PG) (0.3, 30, 50 and 100 mug/ml), pneumococcal DNA (pDNA) (0.3 and 30 mug/ml) or medium only (control). Cell injury was examined by Nissl staining, Annexin V and NeuN immunohistochemistry, and quantified by propidium iodide (PI) uptake and by determining neuron-specific enolase (NSE) concentration in the culture medium. Necrotic and apoptotic cell damage occurred in all treatment groups. Overall damage (Nissl and PI staining) was most prominent after hiR6 (10(8) CFU/ml), followed by LTA (30 mug/ml), pDNA (30 mug/ml), and not detectable after PG (30 mug/ml) exposure. PG (100 mug/ml) induced severe damage. Apoptotic cells were most frequent after exposure to LTA and hiR6. Damage in the neuronal cell layers (NeuN, NSE) was most severe after treatment with hiR6 (10(8) CFU/ml), followed by PG (100 mug/ml), pDNA (30 mug/ml), and LTA (30 mug/ml). (C) 2001 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0165-5728(00)00402-1"],["dc.identifier.isi","000166575000004"],["dc.identifier.pmid","11137574"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86547"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Organotypic hippocampal cultures A model of brain tissue damage in 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","2"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Harms, Kristian"],["dc.contributor.author","Falkenburger, Bjoern H."],["dc.contributor.author","Weis, Joachim"],["dc.contributor.author","Sellhaus, Bernd"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Reich, Arno"],["dc.date.accessioned","2018-11-07T09:46:12Z"],["dc.date.available","2018-11-07T09:46:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Fas-apoptotic inhibitory molecule 2 (Faim2) is a neuron-specific membrane protein and a member of the evolutionary conserved lifeguard apoptosis regulatory gene family. Its neuroprotective effect in acute neurological diseases has been demonstrated in an in vivo model of focal cerebral ischemia. Here we show that Faim2 is physiologically expressed in the human brain with a changing pattern in cases of infectious meningoencephalitis.In Faim2-deficient mice, there was increased caspase-associated hippocampal apoptotic cell death and an increased extracellular signal-regulated kinase pattern during acute bacterial meningitis induced by subarachnoid infection with Streptococcus pneumoniae type 3 strain. However, after rescuing the animals by antibiotic treatment, Faim2 deficiency led to increased hippocampal neurogenesis at 7 weeks after infection. This was associated with improved performance of Faim2-deficient mice compared to wild-type littermates in the Morris water maze, a paradigm for hippocampal spatial learning and memory. Thus, Faim2 deficiency aggravated degenerative processes in the acute phase but induced regenerative processes in the repair phase of a mouse model of pneumococcal meningitis. Hence, time-dependent modulation of neuroplasticity by Faim2 may offer a new therapeutic approach for reducing hippocampal neuronal cell death and improving cognitive deficits after bacterial meningitis."],["dc.identifier.doi","10.1097/NEN.0000000000000020"],["dc.identifier.isi","000335647400001"],["dc.identifier.pmid","24335530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34817"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Modulation of Hippocampal Neuroplasticity by Fas/CD95 Regulatory Protein 2 (Faim2) in the Course of Bacterial Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]