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- 저자 : 조준휘 (검색결과 173 건)
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조준휘,박찬우,옥택근,박윤수,김기중 대한응급의학회 2015 대한응급의학회 학술대회초록집 Vol.2015 No.2
P63 is a transcription factor of p53 gene family, which are involved in development, differentiation and cell response to stress; however, their roles in ischemic preconditioning in the brain are not clear. In the present study, we investigated the effect of IPC on p63 immunoreactivity caused by transient cerebral ischemia, which was induced by 5 min of transient ischemia, in gerbils, and IPC was induced by subjecting the gerbils to 2 min of ischemia followed by 1 day of recovery. The animals were randomly assigned to 4 groups (sham-operated-group, ischemia-operated-group, IPC plus (+)-sham- operated-group and IPC+ischemia-operated-group). The number of viable neurons in the stratum pyramidale of the hippocampal CA1 region was significantly increased by IPC+ischemia-operated-group compared with that in the ischemia-operatedgroup 5 days after ischemic insult. We found that strong p63 immunoreactivity was detected in the CA1 pyramidal neurons in the sham-operated-group, and the immunoreactivity was decreased with time after ischemia-reperfusion. Our present findings showed that IPC dramatically protected the reduction of p63 immunoreactivity in the pyramidal neurons of the CA1 region after ischemia-reperfusion, and this result suggests that the expression of p63 may be necessary for the neurons to survive after transient cerebral ischemia.
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조준휘,박찬우,옥택근,신명철,김가을,이두현 대한응급의학회 2015 대한응급의학회 학술대회초록집 Vol.2015 No.2
Introduction: Therapeutic exercise is an integral component of rehabilitation of patients with stroke. We investigated effects of long-term exercise on neuronal death and memory recovery in the aged gerbil hippocampus after transient cerebral ischemia. Material & Methods: The gerbils were divided into four groups : 1) Sham, 2) 4 weeks sedentary group following ischemia, 3) 1 week treadmill group following ischemia and 4) 4 weeks treadmill group following ischemia. Treadmill exercise was stared at 5 days after ischemia/reperfusion (I/R) and lasted for 1 or 4 weeks, and the animals were sacrificed 31 days after ischemia. Results: In this study, 4 weeks of treadmill exercise facilitated memory recovery despite neuronal damage in the CA1 region after I/R. On the other hand, the long-term treadmill exercise alleviated the increased gliosis in the CA1 region, and increased the myelin repairing and microvessels in the CA1 region and DG, and enhanced the ischemia-induced cell proliferation, neuroblast differentiation, neuronal maturation of the newly generated cells, and BDNF expression in the ischemic DG of the aged gerbil. Conclusion: These results suggest that, in the aged gerbil, long-term treadmill exercise after ischemic stroke could restore the impaired short-term memory function through the cumulative effects of multiple neurorestorative processes.
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조준휘,박찬우,옥택근,신명철,김기중,김가을 대한응급의학회 2015 대한응급의학회 학술대회초록집 Vol.2015 No.2
Introduction: Hydroquinone (HQ), a major benzene metabolite, occurs naturally in various plants and food, and is also manufactured for commercial use. Although many studies have demonstrated the various biological effects of HQ, the neuroprotective effects of HQ following ischemic stroke have not been investigated. Material & Methods: Therefore, in this study, we first examined that the neuroprotective effects of HQ against ischemic damage in a focal cerebral ischemia rat model. Results: It was proven that pre- and post-treatment with 100 mg/kg of HQ protects from ischemiainduced cerebral damage, which was confirmed by evaluation of neurological deficit, PET (Positronemission tomography) and TTC (2, 3, 5-triphenyltetrazoliumchloride) staining. In addition, pre- and post-treatment with 100 mg/kg of HQ significantly attenuated ischemia-induced Evans blue dye extravasation, and significantly increased the immunoreactivities and protein levels of SMI-71 and glucose transporter-1 (GLUT-1), which were well-known as useful makers of endothelial cell, in ischemic cortex compared to vehicle-treated-group. Conclusion: Briefly, these results indicate that pre- and post-treatment with HQ can protect from ischemic damage induced by transient focal cerebral ischemia, and the neuroprotective effects of HQ may be closely associated with the prevention of BBB disruption via increasing of SMI-71 and GLUT-1 expressions.
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조준휘,문중범,박찬우,옥택근,신명철,김가을,박윤수,원무호 대한응급의학회 2020 대한응급의학회 학술대회초록집 Vol.2020 No.2
Introduction We investigated neuroprotective effect of post-risperidone (RIS) treatment against transient ischemic injury and its mechanisms in the gerbil brain. Material & Method Transient ischemia (TI) was induced in the telencephalon by bilateral common carotid artery occlusion (BCCAO) for 5 min under normothermic condition (37 ± 0.2ºC). Post-treatment of RIS induced hypothermia until 12 h after TI in the TI-induced animals under uncontrolled body temperature (UBT) compared to that under controlled body temperature (CBT) (about 37ºC). Result Neuroprotective effect was statistically significant when we used 5 and 10 mg/kg doses (P < 0.05, respectively). In the RIS-treated TI group, many CA1 pyramidal neurons of the hippocampus survived under UBT compared to those under CBT. In this group under UBT, post-treatment with RIS to TI-induced animals markedly attenuated the activation of glial cells, increases of oxidative stress markers (dihydroethidium, 8-OHdG and 4-HNE), and a decrease of superoxide dismutase 2 in their CA1 pyramidal neurons. Conclusion Our findings indicate that RIS-induced hypothermia can effectively protect neuronal cell death from TI injury through attenuation of glial activation and maintenance of antioxidants, showing that 5-HT2A receptor is involved in RIS-induced hypothermia.
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