Fischer, Marc

[["dc.bibliographiccitation.firstpage","1088"],["dc.bibliographiccitation.journal","Anesthesiology"],["dc.bibliographiccitation.lastpage","1100"],["dc.contributor.author","Spies, Claudia D."],["dc.contributor.author","von Dossow, Vera"],["dc.contributor.author","Eggers, Verena"],["dc.contributor.author","Jetschmann, Gesine"],["dc.contributor.author","El-Hilali, Ratiba"],["dc.contributor.author","Egert, Julia"],["dc.contributor.author","Fischer, Marc"],["dc.contributor.author","Schroder, Torsten"],["dc.contributor.author","Hoflich, Conny"],["dc.contributor.author","Sinha, Pranav"],["dc.contributor.author","Paschen, Christian"],["dc.contributor.author","Mirsalim, Parwis"],["dc.contributor.author","Brunsch, Ralf"],["dc.contributor.author","Hopf, Jürgen"],["dc.contributor.author","Marks, Christian"],["dc.contributor.author","Wernecke, Klaus-D."],["dc.contributor.author","Pragst, Fritz"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Müller, Christian"],["dc.contributor.author","Tonnesen, Hanne"],["dc.contributor.author","Oelkers, Wolfgang"],["dc.contributor.author","Rohde, Wolfgang"],["dc.contributor.author","Stein, Christoph"],["dc.contributor.author","Kox, Wolfgang J."],["dc.date.accessioned","2017-09-07T11:45:36Z"],["dc.date.available","2017-09-07T11:45:36Z"],["dc.date.issued","2004"],["dc.identifier.gro","3150400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7160"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0003-3022"],["dc.title","Altered cell-mediated immunity and increased postoperative infection rate in long-term alcoholic patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1016"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","1032"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Fischer, Marc"],["dc.contributor.author","Reuter, Julia"],["dc.contributor.author","Gerich, Florian J."],["dc.contributor.author","Hildebrandt, Belinda"],["dc.contributor.author","Haegele, Sonja"],["dc.contributor.author","Katschinski, Doerthe"],["dc.contributor.author","Mueller, Michael"],["dc.date.accessioned","2018-11-07T08:33:12Z"],["dc.date.available","2018-11-07T08:33:12Z"],["dc.date.issued","2009"],["dc.description.abstract","Fischer M, Reuter J, Gerich FJ, Hildebrandt B, Hagele S, Katschinski D, Muller M. Enhanced hypoxia susceptibility in hippocampal slices from a mouse model of Rett syndrome. J Neurophysiol 101: 1016-1032, 2009. First published December 10, 2008; doi: 10.1152/jn.91124.2008. Rett syndrome is a neurodevelopmental disorder caused by mutations in the X-chromosomal MECP2 gene encoding for the transcriptional regulator methyl CpG binding protein 2 (MeCP2). Rett patients suffer from episodic respiratory irregularities and reduced arterial oxygen levels. To elucidate whether such intermittent hypoxic episodes induce adaptation/preconditioning of the hypoxia-vulnerable hippocampal network, we analyzed its responses to severe hypoxia in adult Rett mice. The occurrence of hypoxia-induced spreading depression (HSD)-an experimental model for ischemic stroke-was hastened in Mecp2(-/y) males. The extracellular K+ rise during HSD was attenuated in Mecp2(-/y) males and the input resistance of CA1 pyramidal neurons decreased less before HSD onset. CA1 pyramidal neurons were smaller and more densely packed, but the cell swelling during HSD was unaffected. The intrinsic optical signal and the propagation of HSD were similar among the different genotypes. Basal synaptic function was intact, but Mecp2(-/y) males showed reduced paired-pulse facilitation and higher field potential/fiber volley ratios, but no increased seizure susceptibility. Synaptic failure during hypoxia was complete in all genotypes and the final degree of posthypoxic synaptic recovery indistinguishable. Cellular ATP content was normal in Mecp2(-/y) males, but their hematocrit was increased as was HIF-1 alpha expression throughout the brain. This is the first study showing that in Rett syndrome, the susceptibility of telencephalic neuronal networks to hypoxia is increased; the underlying molecular mechanisms apparently involve disturbed K+ channel function. Such an increase in hypoxia susceptibility may potentially contribute to the vulnerability of male Rett patients who are either not viable or severely disabled."],["dc.identifier.doi","10.1152/jn.91124.2008"],["dc.identifier.isi","000263120300047"],["dc.identifier.pmid","19073793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17518"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","0022-3077"],["dc.title","Enhanced Hypoxia Susceptibility in Hippocampal Slices From a Mouse Model of Rett Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","S2212041621001248"],["dc.bibliographiccitation.firstpage","101366"],["dc.bibliographiccitation.journal","Ecosystem Services"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Neyret, M."],["dc.contributor.author","Fischer, M."],["dc.contributor.author","Allan, E."],["dc.contributor.author","Hölzel, N."],["dc.contributor.author","Klaus, V.H."],["dc.contributor.author","Kleinebecker, T."],["dc.contributor.author","Krauss, J."],["dc.contributor.author","Le Provost, G."],["dc.contributor.author","Peter, S."],["dc.contributor.author","Schenk, N."],["dc.contributor.author","Manning, P."],["dc.date.accessioned","2021-12-01T09:24:10Z"],["dc.date.available","2021-12-01T09:24:10Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.ecoser.2021.101366"],["dc.identifier.pii","S2212041621001248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94869"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.issn","2212-0416"],["dc.title","Assessing the impact of grassland management on landscape multifunctionality"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","114"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Grosser, Emanuel"],["dc.contributor.author","Hirt, Ursula"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","Fischer, Marc"],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Vogelgesang, Steffen"],["dc.contributor.author","Manzke, Till U."],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:18:29Z"],["dc.date.available","2018-09-28T10:18:29Z"],["dc.date.issued","2012"],["dc.description.abstract","Rett syndrome is an X chromosome-linked neurodevelopmental disorder associated with cognitive impairment, motor dysfunction and breathing irregularities causing intermittent hypoxia. Evidence for impaired mitochondrial function is also accumulating. A subunit of complex III is among the potentially dys-regulated genes, the inner mitochondrial membrane is leaking protons, brain ATP levels seem reduced, and Rett patient blood samples confirm increased oxidative damage. We therefore screened for mitochondrial dysfunction and impaired redox balance. In hippocampal slices of a Rett mouse model (Mecp2(-/y)) we detected an increased FAD/NADH baseline-ratio indicating intensified oxidization. Cyanide-induced anoxia caused similar decreases in FAD/NADH ratio and mitochondrial membrane potential in both genotypes, but Mecp2(-/y) mitochondria seemed less polarized. Quantifying cytosolic redox balance with the genetically-encoded optical probe roGFP1 confirmed more oxidized baseline conditions, a more vulnerable redox-balance, and more intense responses of Mecp2(-/y) hippocampus to oxidative challenge and mitochondrial impairment. Trolox treatment improved the redox baseline of Mecp2(-/y) hippocampus and dampened its exaggerated responses to oxidative challenge. Microarray analysis of the hippocampal CA1 subfield did not detect alterations of key mitochondrial enzymes or scavenging systems. Yet, quantitative PCR confirmed a moderate upregulation of superoxide dismutase 1 in Mecp2(-/y) hippocampus, which might be a compensatory response to the increased oxidative burden. Since several receptors and ion-channels are redox-modulated, the mitochondrial and redox changes which already manifest in neonates could contribute to the hyperexcitability and diminished synaptic plasticity in MeCP2 deficiency. Therefore, targeting cellular redox balance might qualify as a potential pharmacotherapeutic approach to improve neuronal network function in Rett syndrome."],["dc.identifier.doi","10.1016/j.nbd.2012.06.007"],["dc.identifier.pmid","22750529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15855"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1095-953X"],["dc.title","Oxidative burden and mitochondrial dysfunction in a mouse model of Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]