• Journal of Korean Neurosurgical Society
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• v.60 no.4
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• pp.391-396
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• 2017

Objective : To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. Methods : Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. Results : GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. Conclusion : Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.

• Laboraroty Animal Research
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• v.33 no.3
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• pp.244-250
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• 2017

${\alpha}$-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined ${\alpha}$-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in ${\alpha}$-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased ${\alpha}$-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that ${\alpha}$-synuclein regulates neuronal survival, and low levels of ${\alpha}$-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in ${\alpha}$-synuclein and consequently causes serious brain damage.

• Journal of the Korean neurological association
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• v.36 no.4
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• pp.341-344
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• 2018

It is uncommon for Fabry's disease (FD) patient to present with an isolated ischemic stroke without other typical symptoms or signs of FD. A 48-year-old woman presented with recurrent limb weakness and her brain magnetic resonance imaging revealed multiple ischemic brain lesions. Ten years ago, the patient had been diagnosed with heterozygote FD by the genetic test, but she had not shown any typical symptoms or sign of FD so far. Isolated organ involvement could occur in heterozygote FD.

• YAKHAK HOEJI
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• v.32 no.5
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• pp.343-350
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• 1988

Recent hypothesis suggested that intracellular accumulation of calcium is a common denominator of ischemic celullar damage. Flunarizine, a calcium entry blocker, posses vasodilating properties in cerebral vascular beds and clinically used in circulatory disorders. The present study was designed to evaluate the effect of flunarizine on ischemic and hypoxic brain damage. An ischemic model was made by bilateral carotid artery ligation (BCAL) in Wistar strain rat. Hypoxic model was made by intravenous injection(i.v.) of KCN to rats and mice. In mice, flunarizine not only reduced the mortality of KCN, but also delayed the onset time of convulsion. The contents of ATP, creatine phosphate and glucose, cerebral energy metabolite, decreased 30 minutes after BCAL and KCN i, v, while that of lactate increased. But these variations were suppressed by flunarizine. Furthermore, increase in the dosage of flunarizne generally promoted the recovery of cerebral energy metabolites in hypoxic animals. The results suggest that flunarizine had a protective effect against ischemic and hypoxic brain damage due to its ameliorating action on the cerebral energy metabolism.

• Journal of Korean Neurosurgical Society
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• v.39 no.4
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• pp.300-302
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• 2006

"Stunning" represents prolonged contractile depression of any muscular component after alleviation of severe ischemia, as shown in reperfusion following acute myocardial ischemia or ischemic stroke. Clinically, it presents with no or delayed recovery past to thrombolytic therapy but its pathogenic mechanism is not fully uncovered yet. We describe a unique case of a 63-year-old woman, who was undertaken endovascular coiling for the aneurysms, deteriorated several hours later without known cause, and showed delayed clinical improvement over the next 3 days following thrombolysis. Immediate post-thrombolysis magnetic resonance imaging scan showed no apparent abnormality except for high signal intensity within the corresponding hemisphere. Reversible but delayed nature of " brain stunning" can be explained by these images and it seems to be caused by a certain type of reperfusion injury.

• Journal of Korean Neurosurgical Society
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• v.65 no.4
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• pp.603-608
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• 2022

Vertebral artery (VA) occlusion is frequently encountered, usually without acute ischemic injury of the brain. However, when it is accompanied by hypoplasia or stenosis of the opposite VA, brain ischemia may develop due to insufficient collateral supply. Both hemodynamic instability and embolic infarction can occur in VA occlusion, which may cause severe symptoms in a patient. Extracranial carotid-VA bypass should be considered for symptomatic VA occlusion patients, especially when the patient has repeated ischemic brain injuries. In this report, the cases of three extracranial carotid-VA bypass patients are introduced, along with a brief description of the surgical techniques. All three cases were treated with different bypass methods according to their disease location.

• Anatomy and Cell Biology
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• v.57 no.2
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• pp.155-162
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• 2024

Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca²⁺) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca²⁺ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca²⁺ and autophagic process in acute stage of ischemic stroke.

• Journal of Korean Neurosurgical Society
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• v.58 no.1
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• pp.22-29
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• 2015

Objective : Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are common neurologic problems that occur during childhood. However, there is insufficient evidence from experimental studies to conclude that pFS directly induces hippocampal injury. We studied cognitive function and histological changes in a rat model and investigated which among pFS, HIE, or a dual pathologic effect is most detrimental to the health of children. Methods : A rat model of HIE at postnatal day (PD) 7 and a pFS model at PD10 were used. Behavioral and cognitive functions were investigated by means of weekly open field tests from postnatal week (PW) 3 to PW7, and by daily testing with the Morris water maze test at PW8. Pathological changes in the hippocampus were observed in the control, pFS, HIE, and HIE+pFS groups at PW9. Results : The HIE priming group showed a seizure-prone state. The Morris water maze test revealed a decline in cognitive function in the HIE and HIE+pFS groups compared with the pFS and control groups. Additionally, the HIE and HIE+pFS groups showed significant hippocampal neuronal damage, astrogliosis, and volume loss, after maturation. The pFS alone induced minimal hippocampal neuronal damage without astrogliosis or volume loss. Conclusion : Our findings suggest that pFS alone causes no considerable memory or behavioral impairment, or cellular change. In contrast, HIE results in lasting memory impairment and neuronal damage, gliosis, and tissue loss. These findings may contribute to the understanding of the developing brain concerning conditions caused by HIE or pFS.

• Biomedical Science Letters
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• v.11 no.3
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• pp.355-363
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• 2005

This study aimed to investigate the cerebroprotective effect of vascular endothelial growth factor (VEGF) on permanent focal cerebral ischemia in Sprague-Dawley rats. Right middle cerebral artery (MCA) was occluded for 6 and 24 hours by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in regional cerebral blood flow (rCBF) by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. Brain edema was determined by measuring brain water content. In normal rats, rCBF was significantly increased by intravenous infusion of VEGF for 10 minutes. The VEGF-induced increase in rCBF was significantly inhibited by pretreatment with suramin, a heparin-binding growth factor inhibitor as well as $N^{\omega}-nitro-L-arginine$, a nitric oxide synthase inhibitor. In focal cerebral ischemic rats, the amplitude of decrease in rCBF during ischemic period was significantly less in VEGF-treated group, compared with that in vehicle-treated group. The cerebral infarct size was reduced by VEGF in a dose-dependent manner. The brain edema formation was dose-dependently reduced by VEGF in 24-hour MCA occlusion group but not in 6-hour MCA occlusion group. It is suggested that VEGF not only improves the rCBF during cerebral ischemic period but also reduces the brain edema formation, and thereby exert a protective effect on focal cerebral ischemia in rats.

• KIPS Transactions on Software and Data Engineering
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• v.5 no.2
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• pp.69-78
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• 2016

Ischemic stroke is a disease that the brain tissues cannot function by reducing blood flow due to thrombosis or embolisms. Due to the nature of the disease, it is most important to identify the status of cerebral vessel and the medical images are necessarily used for its diagnosis. Among many indicators, brain MRI is most widely utilized because experts can effectively obtain the semantic information such as cerebral anatomy aiding the diagnosis with it. However, in case of emergency diseases like ischemic stroke, even though a intelligent system is required for supporting the prompt diagnosis and treatment, the current systems have some difficulties to provide the information of medical images intuitively. In other words, as the current systems have managed the medical images based on the basic meta-data such as image name, ID and so on, they cannot consider semantic information inherent in medical images. Therefore, in this paper, to provide core information like cerebral anatomy contained in brain MRI, we suggest a template-driven medical images mapping method. The key idea of the method is defining the mapping characteristics between anatomic feature and representative images by using template images that can be representative of the whole brain MRI image set and revealing the semantic relations that only medical experts can check between images. With our method, it will be possible to manage the medical images based on semantic.