Takuma Mabuchi

TL;DR: The panorama of acute microvessel responses to focal cerebral ischemia provide opportunities to understand interrelationships between neurons and their microvascular supply and changes that underlie a number of central nervous system neurodegenerative disorders.

TL;DR: The results suggest that CREB phosphorylation in neurons after ischemia and exposure to glutamate is induced by NMDA receptor-gated calcium influx and subsequent activation of CaMK II–IV and that CRE bosphorylation after metabolic stress might show a neuroprotective response through CRE-mediated gene induction.

TL;DR: The results suggest the importance of amoeboid microglia, macrophages, and their interleukin-1beta production in gradual expansion of cerebral infarction is suggested and resident oligodendrocytes may be resistant to ischemic insults, and oligod endocrine cells accumulated at the border of the infarctions may participate in tissue repair after cerebral infArction.

TL;DR: It is demonstrated that active proteases derived from ischemic tissue after middle cerebral artery occlusion (MCAO) and transferred to normal tissue can degrade vascular matrix.

TL;DR: The current study demonstrates the need for assessment of intracranial vasculature in each animal by measuring cortical microperfusion during temporary occlusion of both CCA, no matter whether cerebral ischemia is produced by bilateral CCA Occlusion or intraluminal suture occlusions in transgenic mice.