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Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes,(More)
Neuronal calcium-activated potassium channels of the BK type are activated by membrane depolarization and intracellular Ca(2+) ions. It has been suggested that these channels may play a key neuroprotective role during and after brain ischemia, but this hypothesis has so far not been tested by selective BK-channel manipulations in vivo. To elucidate the in(More)
OBJECTIVE Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Characterization of cytokine expression to the early damaged tissue might aid in further understanding of lesion development and contribute to definition of molecular targets for selective immunotherapy. Endothelial monocyte-activating polypeptide II (EMAPII) is(More)
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