Our first speaker is Dr. Kentaro Wada, who's going to be presenting subarachnoid hemorrhage in the rat brain. Thank you, Chairman. Good afternoon. I'm from Japan. Today I would like to talk about hospitalization of a neural NOSAT serine-1412 in the SH-RAT model. SH patients suffer from long-term cognitive impairment. Cognitive dysfunction is recognized as a poor outcome after SH. Many articles previously reported early brain injury after SH had an influence on damaged dented gyrus in the hippocampus. This slide shows AKT, Kanomochirin-Kinase, and PKA have been shown to be involved with NNOS activation. Especially, PKA is also related to NNOSAT serine-1412, so we also focus on activation of PKA. In this study, we investigated chronological and topographical changes in the hospitalization of NNOSAT and PKA at serine-1412 immediately after SH. Method. We made one hemorrhage injection SH-RAT model as shown in slide. Hippocampus and cortex sample were obtained at 1, 3, 6, 12, 24 hours at these time points. A crude fraction were made by using these phosphatase inhibitors. And NNOS fraction was made from crude fraction using ADP agarose gas. We did Western blot analysis using NNOS fraction with these antibodies. And also, we did immunohistochemistry with control sample and one hour after SH. Result. Western blot analysis revealed significant hospitalization of NNOSAT serine-1412 during 1 and 3 hours in hippocampus after SH. However, there is no significant cortex. Immunohistochemistry showed this hospitalization occurred in dented jars in hippocampus one hour after SH. Next, we injected the same dose serine instead of blood. The brain sample obtained from hippocampus one hour after injection. We did Western blot analysis using these antibodies. Injection of serine significantly hospitalized NNOSAT serine-1412 as like of injection of blood as compared with control. Next, we did Western blot analysis using crude fraction with these antibodies. And also, we did immunohistochemistry with control sample and one hour after SH. Result. Western blot analysis revealed significant hospitalization of PK at serine-197 during 1 and 3 hours in hippocampus after SH. Immunohistochemistry showed that this hospitalization also occurred in dented jars. Summary of results. Increase of hospitalization NNOSAT serine-1412 immediately occurred after SH in hippocampus. Why not in cortex? Hospitalization of NNOSAT serine-1412 and PK at serine-197 occurred in dented jars of hippocampus. Injection of serine also hospitalized NNOSAT serine-1412. Discussion. Clinical high ICP is complication immediately after SH. About two-thirds of patients suffer from cerebral ischemia at 1 to 3 days after SH. Whole brain ischemia induced the activation of PK in dented jars. Oscillation of NNOSAT serine-1412 increased production of NO. NO from NNOS is an inhibitory regular of neurogenesis in the dented jars. Significant decrease in neurogenesis occurred in the dented jars three days after SH in mice. SH increased ICP immediately after onset. Increased ICP induced cerebral ischemia. Activation of PK in dented jars. Oscillation of NO serine-1412 in dented jars. Overproduction of NO in dented jars might play a role in neural dysfunction after SH. I would like to summarize this slide in this study. And that's all I have to say. And thank you for your attention. Thank you.

subarachnoid hemorrhage

cognitive function

dentate gyrus

hippocampus

neural dysfunction