Differential activation of c-Fos in paraventricular nuclei of the hypothalamus and thalamus of the rat following myocardial infarction

조준휘,문중범,박찬우,옥택근,신명철,원무호 대한응급의학회 2016 대한응급의학회 학술대회초록집 Vol.2016 No.2

Ischemic Preconditioning Maintains Immunoreactivities of Glucokinase and Glucokinase Regulatory Protein in Neurons of the Gerbil Hippocampal CA1 Region Following Transient Cerebral Ischemia

조준휘,박찬우,옥택근,신명철,김기환,이준석 대한응급의학회 2015 대한응급의학회 학술대회초록집 Vol.2015 No.2

Glucokinase plays a key role in the control of blood glucose homeostasis. We investigated the effect of ischemic preconditioning on immunoreactivities of GK and its regulatory protein following 5 min of transient cerebral ischemia in gerbils. The gerbils were randomly assigned to 4 groups. IPC was induced by subjecting the gerbils to 2 min of ischemia followed by 1 day of recovery. In the ischemia-operated-group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post-ischemia; however, in the IPC+ischemiaoperated-group, neurons in the SP were well protected. In the immunohistochemical study, immunoreactivities of GK and GKRP in neurons of the SP were distinctively decreased in the CA1, not CA2/3, from 2 days post-ischemia, and hardly detected in the SP at 5 days post-ischemia. In the IPC+ischemia-operated-group, immunoreactivities of GK and GKRP in the SP of the CA1 were similar to those in the sham-group. Our findings show that IPC dramatically maintains immunoreactivities of GK and GKRP in neurons of the SP of the CA1 after ischemia-reperfusion and indicate that GK and GKRP may be necessary for neurons to survive against transient cerebral ischemia.

Ischemic Preconditioning Induces Neuroprotection cause by a Transient Global Ischemia via Maintaining the Expression of p63

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.

Effects of Long-term Exercise on Memory Recovery in the Aged Gerbil Hippocampus after Transient Cerebral Ischemia

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.

Hydroquinone Shows Neuroprotective Potential in Experimental Ischemic Stroke Model via Attenuation of Blood-brain Barrier Disruption

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.

Failure in neuroprotection of remote limb ischemic postconditioning in the hippocampus of a gerbil model of transient cerebral ischemia

조준휘,김기중,김가을,이두현,이정훈,원무호 대한응급의학회 2016 대한응급의학회 학술대회초록집 Vol.2016 No.2

Impact of Hyperthermia Before and During Ischemia-reperfusion on Neuronal Damage and Gliosis in the Gerbil Hippocampus Induced by Transient Cerebral Ischemia

조준휘,박찬우,옥택근,신명철,이두현,이정훈 대한응급의학회 2015 대한응급의학회 학술대회초록집 Vol.2015 No.2

Hyperthermia can exacerbate the brain damage produced by ischemia. In the present study, we investigated effects of hyperthermia before and during ischemia-reperfusion on neuronal damage and glial changes in the gerbil hippocampus following transient cerebral ischemia. The animals were randomly assigned to 4 groups: (1) sham-operated animals with normothermia (normothermia+sham group); (2) ischemia-operated animals with normothermia (normothermia +ischemia group); (3) sham-operated animals with hyperthermia (hyperthermia+sham group); and (4) ischemia-operated animals with hyperthermia (hyperthermia+ischemia group). In the normothermia+ischemia groups, a significant delayed neuronal death was observed in the SP of the hippocampal CA1 region 5 days after ischemia-reperfusion. In the hyperthermia+ischemia groups, neuronal death in the SP of the CA1 occurred at 1 day post-ischemia, and neuronal death was observed in the SP of the CA2/3 region at 2 days post-ischemia. In addition, we examined activations of astrocytes and microglia using immunohistochemistry for anti-glial fibrillary acidic protein and antiionized calcium-binding adapter molecule 1. We suggest that experimentally hyperthermic pre-condition before cerebral ischemic insult produces more extensive neuronal damage and glial activation in the ischemic hippocampus.

Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions

조준휘,김기환,이준석,박윤수,안웅찬,황병선 대한응급의학회 2016 대한응급의학회 학술대회초록집 Vol.2016 No.2

대량 폐동맥 혈전색전증으로 인한 심정지 환자의 심폐소생술 : 혈전용해제 사용 경험 2 예 The Use of t-PA in 2 Cases

조준휘,황성오,김성환,이강현,이진웅,이서영,박해상 대한응급의학회 2002 대한응급의학회지 Vol.13 No.1

The massive pulmonary thromboembolism is serious illness that can lead to death within an hour after its occurrence. The incidence of cardiac arrest caused by massive pulmonary thromboembolism has been known as about 7%. Invasive therapeutic modalities to treat massive pulmonary thromboembolism during cardiac arrest including thoracotomy or cardiopulmonary bypass have been shown little effect. administration of a thrombolytic agent is an alternative choice of treating massive pulmonary thromboembolism during cardiac arrest. This report describes our experience of cases with massive pulmonary thromboembolism that were treated with administration of a thrombolytic agent during CPR.

C-단백 결핍에 의한 응고항진으로 발생한 폐동맥 혈전색전증

조준휘,박찬우,조병렬,최대희,조성준,이성호,황성오,안희철,안무업,서정열,유기철 대한응급의학회 2003 대한응급의학회지 Vol.14 No.1

A pulmonary thromboembolism usually results from a serious complication of deep venous thrombosis (DVT). However, several prothrombotic genetic risk factors are known to predispose a patient to thrombotic events, with manifestation at a young age. Protein C and S deficiencies are known to increase the risk of venous thrombosis and pulmonary thromboembolism. We report a case of a young patient with protein C and S deficiencies suffering from a massive pulmonary thromboembolism.