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천막상부 뇌졸중에서 소뇌의 혈역학 변화 -Dynamic Susceptibility Contrast MR 영상을 이용한-
한시령,김범수,곽태호,최영빈,김영인 대한임상신경생리학회 2002 Annals of Clinical Neurophysiology Vol.4 No.1
Background & Purpose : Dynamic susceptibility contrast MR imaging, one method of perfusion MRI, was developed to define cerebral hemodynamic status with good anatomical resolution. The authors investigated hemodynamic parameters using this imaging method, in an effort to identify hemodynamic changes on the remote crossed cerebellum of patients with a supratentorial infarct. Methods : Dynamic susceptibility contrast MR imaging was performed in 15 patients with only unilateral supratentorial infarcts. Imaging was obtained at the anatomic level of the cerebellum. rCBF, rCBV, MTT and TP were determined over both cerebellar hemispheres of interest. Results : The rCBF and rCBV values of the contralateral cerebellar hemisphere were significantly more decreased than those of the ipsilateral cerebellar hemisphere in 12 patients(p=0.028, 0.033). MTT and TP values of the contralateral and ipsilateral cerebellar hemispheres didn’t reveal any differences(p=0.130, 0.121). Conclusions : The results of this work suggest that the region which are remote from the ischemic brain lesion shows no changes of MTT or TP but show decrease of rCBF and rCBV, mean to diaschisis, it also demonstrates that perfusion MRI is an easily available method to evaluate the hemodynamic status of the brain.
한시령 대한뇌졸중학회 2000 Journal of stroke Vol.2 No.2
Leukocytoclastic vasculitis is a rare complication of warfarin use caused by immunoglobulin and complement deposition on the walls of small vessels in the skin. We report a patient with cerebral infarction who developed warfarin-induced leukocytoclastic vasculitis that involved the arm, breast, thigh and the buttock of the patient. Warfarin was replaced with a low molecular weight heparin and the symptoms disappeared immediately. Korean Journal of Stroke 2000;2(2): 218~220
한시령,Cheolsu Shin,Seongkyung Park,Seonyoung Rhyu,Jeongwook Park,김영인 연세대학교의과대학 2009 Yonsei medical journal Vol.50 No.2
Purpose: Lithium-pilocarpine induced status epilepticus (LPSE) causes selective and age-dependent neuronal death, although the mechanism of maturation-related injury has not yet been clarified. The activating transcription factor-2 (ATF-2) protein is essential for the normal development of mammalian brain and is activated by c-Jun N-terminal kinase (JNK). It induces the expression of the c-jun gene and modulates the function of the c-Jun protein, a mediator of neuronal death and survival. Therefore, we investigated the expression of c-Jun and ATF-2 protein in the immature and adult rat hippocampus to understand their roles in LPSE-induced neuronal death. Materials and Methods: Lithium chloride was administrated to P10 and adult rats followed by pilocarpine. Neuronal injury was assessed by silver and cresyl violet staining, performed 72 hours after status epilepticus. For evaluation of the expression of ATF-2 and c-Jun by immunohistochemical method and Western blot, animals were sacrificed at 0, 4, 24, and 72 hours after the initiation of seizure. Results: Neuronal injury and expression of c-Jun were maturation-dependently increased by LPSE, whereas ATF-2 immunoreactivity decreased in the mature brain. Since both c-Jun and ATF-2 are activated by JNK, and targets and competitors in the same signal transduction cascade, we could speculate that ATF-2 may compete with c-Jun for JNK phosphorylation. Conclusion: The results suggested a neuroprotective role of ATF-2 in this maturation-related evolution of neuronal cell death from status epilepticus. Purpose: Lithium-pilocarpine induced status epilepticus (LPSE) causes selective and age-dependent neuronal death, although the mechanism of maturation-related injury has not yet been clarified. The activating transcription factor-2 (ATF-2) protein is essential for the normal development of mammalian brain and is activated by c-Jun N-terminal kinase (JNK). It induces the expression of the c-jun gene and modulates the function of the c-Jun protein, a mediator of neuronal death and survival. Therefore, we investigated the expression of c-Jun and ATF-2 protein in the immature and adult rat hippocampus to understand their roles in LPSE-induced neuronal death. Materials and Methods: Lithium chloride was administrated to P10 and adult rats followed by pilocarpine. Neuronal injury was assessed by silver and cresyl violet staining, performed 72 hours after status epilepticus. For evaluation of the expression of ATF-2 and c-Jun by immunohistochemical method and Western blot, animals were sacrificed at 0, 4, 24, and 72 hours after the initiation of seizure. Results: Neuronal injury and expression of c-Jun were maturation-dependently increased by LPSE, whereas ATF-2 immunoreactivity decreased in the mature brain. Since both c-Jun and ATF-2 are activated by JNK, and targets and competitors in the same signal transduction cascade, we could speculate that ATF-2 may compete with c-Jun for JNK phosphorylation. Conclusion: The results suggested a neuroprotective role of ATF-2 in this maturation-related evolution of neuronal cell death from status epilepticus.