• 대한한의학회지
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• 제21권4호
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• pp.9-15
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• 2000

Objective : The aim of this study was to investigate the neuroprotection effect of estrogen on brain atrophy following cerebral infarction. Method : All animals in this study were classified into 4 groups; ovariectomy group (OVXgroup), cerebral infarction group (INF group), combination ovariectomy and cerebral infarction group (OVX + INF group), and naturally intact group for control data (NOR group). Cerebral infarction was made by Chen's method with some modification. Ovariectomy was performed by Wayforth's method. Experimental data for each group was collected at 15 days, month, 3 months, and 6 months after starting observation. Serum $17{\beta}-estradiol(E2)$ was determined by radioimmunoassay. Brain volume was measured and calculated with image analysis. Each brain was sliced at intervals of 2mm in chamber after 30 min of freezing in refregerater. Cerebral volume was obtained by sum of volume of each slice level, which was mean $area{\;}{\times}{\;}2mm$. Results : Cerebral ischemia was found to decrease the serum concentration of $17{\beta}-{\;}estradiol(E2)$ and to inhibit the physiologically conpensatary function of the ovariectomized rats. Also we found that deprivation of estrogen have resulted in more severe cerebral atrophy followed by cerebral infarction. Conclusion : It is suggested that estrogen has a neuroprotection effect on cerebral atrophy following cerebral infarction.

• 대한한의학회지
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• 제18권2호
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• pp.316-325
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• 1997

In a 36-month period, 23 selected Patients with Acute Cerebral Infarction were studied utilizing Computerized Tomography, Barthel Index in an attempt to correlate Brain Computerized Tomography findings with 1week, 4weeks rehabilitation and evaluate the influences of the size and location of the lesion. The study suggested that the size of the lesion had impact on 4 weeks rehabilitation. There was significant different between the patients with Middle Cerebral Artery Pial Territory Infarction(I.P.B.M.C.A.) lesion and the patients with Lacunar Infarction(L.I.), Striatocapsular Infarction(S.C.I.), Internal Watershed Infarction(I.W.I.) lesion, but there was no significant difference between the patients with L.I. lesion and the patients with S.C.I. lesion and the patients with I.W.I. lesion. The size and location of the lesion should be considered together in predicting the functional outcomes of Acute Cerebral Infarction.

• 대한핵의학회지
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• 제33권3호
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• pp.337-340
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• 1999

Thallium-201 brain SPECT is utilized in the diagnosis of brain tumor especially in cases where CT or MRI findings alone cannot differentiate malignant lesion from benign. Recently we came across two cases of positive T1-201 brain SPECT in clinically suspected brain tumor patients that turned out to be hemorrhagic cerebral infarction instead on biopsy. The findings in these cases demonstrate that thallium-201 accumulation may occur by the breakdown of the blood-brain barrier and phagocytic cell infiltration in the liquefaction stage of infarction.

• 대한한방내과학회지
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• 제30권4호
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• pp.674-684
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• 2009

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

• Journal of Chest Surgery
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• 제18권4호
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• pp.746-752
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• 1985

A retrospective clinical observation was made of 40 patients with postoperative cerebral dysfunction among 2634 patients who underwent open-heart operations in Severance Hospital. Yonsei University between 1962, the year the first successful open heart operation was done, and June 1985. Suspected causes of brain damage were reviewed. Brain CT findings were evaluated in 24 patients. There were 15 cerebral infarcts, 4 intracerebral bleedings, 3 ischemic brain damages, 1 infarction with intracerebral hemorrhage and 1 diffuse cortical atrophy from unknown cause. The most frequent site of cerebral infarction was the middle cerebral artery area with no predilection on the right of left.

• Journal of Korean Biological Nursing Science
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• 제10권1호
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• pp.1-10
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• 2008

Purpose: The purpose of this study was to investigate the cerebral infarction size, antioxidant enzyme activities and lipid peroxidation changes after 6 weeks of dietary soybean protein intake in a rat focal brain ischemia model. Method: Weaning Sprague-Dawley rats were fed with either modified AIN-93G diet containing casein 20% (control), 20% soybean protein isolate-based diet (S20), or 40% of soybean protein isolate-based diet (S40) for 6 weeks. The animals were subject to right middle cerebral artery occlusion for 2 hr. After 24 hr of recirculation, the rats were sacrificed. Antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and thiobarbituric acid reactive substance (TBARS) level in the right brain were also measured. Result: There were no significant differences in the right cortical infarction volume, TBARS level, SOD and CAT activities among the three groups whereas the GPx activities of the S20 group were significantly higher than those of the control group (p=.02). Conclusion: Our results suggest that 20% of soybean protein may have a modulating effect on GPx and possibly have some protective effect against oxidative stress although it may enough to decrease cerebral infarction volume in rat focal brain ischemia model.

• 대한한의학회지
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• 제27권2호
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• pp.70-85
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• 2006

Objectives; This study examined the neuroprotective effect of Hyulbuchookautang (血府逐瘀湯, HBCAT)against neural damage following focal cerebral infarction. Methods : Sprague-Dawley Rats were induced with focal cerebral infarction by temporal middle cerebral artery occlusion (MCAO). The rats were divided into 2 groups. We treated extract of HBCAT to one group after operation (sample group), and the other group wasn't treated after operation (control group). We observed neurological scores and TIC-stained infarct area, total infarct volume in brain sections and Bax-positive neurons, HSP70- positive neurons in brain regions. Results : HBCAT treatment at 3 days after MCAO reduced neurological scores induced by MCAO. HBCAT treatment at 5 days after MCAO reduced TTC-stained infarct area in brain sections induced by MCAO. HBCAT treatment at 5 days after MCAO reduced total infarct volume in brain sections induced by MCAO. HBCAT treatment after MCAO reduced Bax-positive neurons in cortex infarct core and cortex infarct penumbra and caudo-putamen of brain regions induced by MCAO. HBCAT treatment after MCAO reduced HSP70- positive neurons in cortex infarct penumbra of brain regions induced by MCAO. Conclusions : These results suggest that HBCAT has a neuroprotective effect against focal cerebral ischemia.

• 대한핵의학회지
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• 제34권5호
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• pp.433-435
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• 2000

A 6000-year-old male with carcinoma of the prostate and cerebral infarction underwent a Tc-99m MDP bone scintigraphy for the evaluation of skeletal metastases. Bone scintigraphy (Fig. 1) showed multiple areas of increased uptake of Tc-99m MDP in the skull, spine, and ribs representing skeletal metastases. Two different patterns of uptake occurred in the skull region (Fig. 1A-C); one represents bony metastasis and the ether represents cerebral infarction. The shape, size, location, intensity, and border of the increased uptake differed between the two lesions. An oval-shaped pattern with smaller size, greater intensity and more sharply defined border in the frontal region was consistent with bony metastasis. A rectangular-shaped pattern with larger size, lesser intensity and relatively indistinct border in the temporo-parieto-occipital region was consistent with cerebral infarction. Increased uptake of bone-seeking radiotracers in cerebral infarction has been reported previously.$^{1-4)}$ A suggested mechanism by which bone-seeking radiotracers accumulate in the necrotizing cerebral tissue is an alteration of the blood-brain barrier induced during cerebral infarction, which results in entry of the radiotracers into the extracellular space of the brain.$^{4)}$ Brain CT (Fig. 2) performed 7 days before and one month after the bone scintigraphy revealed lesions on the right temporo-parieto-occipital region consistent with acute hemorrhagic and chronic cerebral infarction, respectively.

• Journal of Acupuncture Research
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• 제36권3호
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• pp.140-146
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• 2019

Background: This study investigated the effects of Vipera lebetina turanica snake venom (SV) on cerebral infarction induced by middle cerebral artery occlusion in mice. Methods: Following cerebral infarction, SV was injected intravenously or added to BV2 cell culture. Tissue injury was detected using triphenyltetrazolium chloride (TTC) staining, neurological deficit score, NO, ROS, and GSH/GSSG assays, qPCR, Western blot, and cell viability. Results: Cerebral infarction caused by middle cerebral artery occlusion as observed by TTC staining, showed SV inhibited cell death, reducing the number of brain cells injured due to infarction. SV treatment for cerebral infarction showed a significant decrease in abnormal behavior, as determined by the neurological deficit score. The oxidation and inflammation of the cells that had cerebral infarction caused by middle cerebral artery occlusion (NO assay, ROS, GSH/GSSG assay, and qPCR), showed significant protection by SV. Western blot of brain infarction cells showed the expression of iNOS, COX-2, p-IkB-${\alpha}$, P38, p-JNK, p-ERK to be lower in the SV group. In addition, the expression of IkB increased. BV2 cells were viable when treated with SV at $20{\mu}g/mL$ or less. Western blot of BV2 cells, treated with 0.625, 1.5, $2.5{\mu}g/mL$ of SV, showed a significant decrease in the expression of p-IkB-${\alpha}$, p-JNK, iNOS, and COX-2 on BV2 cells induced by LPS. Conclusion: SV showed anti-inflammatory and anti-oxidant effects against cerebral infarction and inflammation.

• Journal of Korean Neurosurgical Society
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• 제50권3호
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• pp.256-259
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• 2011

We report a rare case of Williams syndrome accompanying moyamoya disease in whom postoperative global cerebral infarction occurred unpredictably. Williams syndrome is an uncommon hereditary disorder associated with the connective tissue abnormalities and cardiovascular disease. To our knowledge, our case report is the second case of Williams syndrome accompanying moyamoya disease. A 9-year-old boy was presented with right hemiparesis after second operation for coarctation of aorta. He was diagnosed as having Williams syndrome at the age of 1 year. Brain MRI showed left cerebral cortical infarction, and angiography showed severe stenosis of bilateral internal carotid arteries and moyamoya vessels. To reduce the risk of furthermore cerebral infarction, we performed indirect anastomosis successfully. Postoperatively, the patient recovered well, but at postoperative third day, without any unusual predictive abnormal findings the patient's pupils were suddenly dilated. Brain CT showed the global cerebral infarction. Despite of vigorous treatment, the patient was not recovered and fell in brain death one week later. We suggest that in this kind of labile patient with Williams syndrome accompanying moyamoya disease, postoperative sedation should be done with more thorough strict patient monitoring than usual moyamoya patients. Also, we should decide the revascularization surgery more cautiously than usual moyamoya disease. The possibility of unpredictable postoperative ischemic complication should be kept in mind.