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Report on the 4'th scientific meeting of the “Verein zur F?rderung des Wissenschaftlichen Nachwuchses in der Neurologie” (NEUROWIND e.V.) held in Motzen, Germany, Nov. 2’nd – Nov. 4’th, 2012

DOI: 10.1186/2040-7378-4-22

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Abstract:

Mathias Gelderblom from the group of Tim Magnus, Hamburg, reported on the role of the IL-17 axis in a murine model of ischemic stroke. He nicely showed that gamma delta T cell derived IL-17, TNF-α, and CXCL1 are important mediators of neutrophil invasion and tissue damage after an ischemic insult.Next, Arthur Liesz from the group of Roland Veltkamp, Heidelberg, gave a talk on clonal expansion of T cells after experimental stroke. Via CDR3 spectratyping, he showed monoclonal and oligoclonal TCR expansion patterns especially in the brain at later time points after ischemia.Katarzyna Winek from the group of Andreas Meisel, Berlin, presented preliminary findings on the link between gut microbiota and cerebral ischemia and vice versa. By using deep sequencing of the gut microbiome, different surgery conditions for ischemia induction and gut decontamination, it might become possible to unveil an influence of the microbiome on brain infarction in the future.Sweena Chaudhari from Alma Zernecke`s laboratory in Munich focused on the role of the transcription factor HIF-1α in dendritic cells (DC). An increased atherosclerotic plaque growth was observed in a DC specific conditional HIF-1α knockout mouse on a high fat diet. This phenotype is associated with increased IL-12 expression in DC and higher Th1 activation, which is controlled via STAT3.Golo Kronenberg (group of Matthias Endres, Berlin) employed transient middle cerebral artery occlusion (tMCAO) in combination with the Porsolt forced swim test and citalopram treatment to analyze post-stroke depression in mice. This model allows for probing monoaminergic transmitter mediated effects after cerebral ischemia, both on a behavioral and neurochemical level.Christoph Harms from Berlin focused on the role of small ubiquitin-like modifiers (SUMO) in neuroprotection during stroke. He reported that in an oxygen glucose deprivation cell culture model, the formation of SUMO2/3 conjugates is part of the cellular stressresponse. This

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