• Journal of Neurocritical Care
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• v.11 no.2
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• pp.129-133
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• 2018

Background: A few cases of moyamoya syndrome associated with thyrotoxicosis have been reported. However, studies on the association of hyperthyroidism with moyamoya syndrome are insufficient. Case Report: Here we report a case of hyperthyroidism associated with moyamoya syndrome in a 41-year-old woman with aphasia and right side weakness. Brain imaging revealed acute cerebral infarction of left middle cerebral artery territory and occlusion of bilateral distal internal carotid arteries. Conclusion: Antithyroid medication stabilized the patient's neurologic deterioration, suggesting that thyrotoxicosis could aggravate acute cerebral infarction caused by moyamoya syndrome.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.303.1-303.1
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• 2002

Recent studies have suggested that the cerebral ischemia induced the neuronal cell death by mediating multiple mechanisms with necrosis and/or apoptosis. The present study examined neuroprotective mechanism of aloesin against transient focal cerebral ischemia. Aloesin. main component of aloe possesses various biological activates such as wound healing. anti-gastric ulcer. and chemopreventive activity. Transient focal cerebral ischemia was induced by 120 min MCAO. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.305.1-305.1
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• 2002

The temporal profiles of the changes of dopaminergic cell and microglial activation induced by transient cerebral ischemia was investigated in the substantia nigral region which lay outside ischemic areas of rat brain after middle cerebral artery occlusion (MCAO). Transient cerebral ischemia was induced by intraluminal occlusion of the right middle cerebral artery for 2 hand reperfusion was continued for 1, 2. 3. 7. 10. 14. 30, 60. and 120 days. Activated microglial cells were visualized with immunohistochmistry using OX-43 antibody. (omitted)

• Annals of Clinical Neurophysiology
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• v.24 no.1
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• pp.30-34
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• 2022

In cases of hyponatremia induced by brain damage, it is important to distinguish between the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) and cerebral salt wasting syndrome. A ventriculoperitoneal (VP) shunt is the standard treatment for hydrocephalus, and external lumbar drainage (ELD) is an option to evaluate the effect of a VP shunt. However, ELD has potential complications, such as subarachnoid hemorrhage, meningitis, and rarely hyponatremia. Therefore, we report a case of a patient with cerebral salt-wasting syndrome resulting from ELD to treat normal-pressure hydrocephalus during the rehabilitation of acute ischemic stroke.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.3
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• pp.774-782
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• 2004

The water extract of Dancheonhwan (DCH) has been used to treat ischemic brain and heart damage in oriental medicine. However, little is known about the mechanism by which the water extract of DCH rescues cells from ischemic damage. Therefore, this study was designed to investigate the protective mechanisms of DCH on the H₂O₂-induced toxicity in H9c2 cardiomyoblast cells. Treatment of H₂O₂ markedly decreased the viability of H9c2 cardiomyoblast in a dose-dependent and time-dependent manner. The nature of H₂O₂-induced toxicity of H9c2 cells resulted from apoptotic death confirmed with genomic DNA fragmentation. DCH increased the viability of H₂O₂-treated H9c2 cells by about 23%, and partially suppressed the genomic DNA fragmentation and PARP cleavage. H₂O₂ also activated caspase-3 protease and -9 protease, but not both caspase-6 protease and -8 protease. H₂O₂ induced the mitochondria dysfunction, including mitochondria membrane permeability transition (MPT) and cytosolic release of cytochrome c from mitochondria, which was prevented in part by pretreatment of DCH. N-acetylcystein (NAC), a free-radical scavenger, alone increased the viability of H₂O₂-treated H9c2 cells in a dose-dependent manner. Furthermore, the combination of NAC with DCH significantly increased the viability of the H₂O₂-treated H9c2 cells in a dose-dependent manner. These data indicate that DCH has the protective effect on ROS-induced apoptosis of cadiomyoblast H9c2 cells.

• Physical Therapy Rehabilitation Science
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• v.2 no.2
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• pp.87-91
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• 2013

Objective: The present study was aimed at determining the effect of physical training on glutamate transporter activity in a middle cerebral artery occlusion (MCAO)-induced ischemia injury rat model. Design: Randomized controlled trial. Methods: In this study, we randomly divided them into three groups. Group I included non-occlusion sham controls (n=10), Group II included non-physical training after MCAO (n=10), and Group III included rats that were subjected to physical training after MCAO (n=10). Rats in the physical training group underwent treadmill training, which began at 24 h after MCAO and continued for 14 consecutive days. The training intensity was gradually increased from 5 m/min on the first day to 12 m/min on day 3, and it was maintained until day 14. Focal cerebral ischemia was examined in adult male Sprague-Dawley rats by using the MCAO model. We determined the functional outcomes for each rat on days 1, 7, and 14. Glutamate transporter-1 (GLT-1) activity in the cortex of rats from all three groups was examined at the end of the experiment. Results: Out result show that MCAO rats exhibited severe neurological deficits on the 1 day, and there was no statistically significant in each groups. We observed that the functional outcomes were improved at days 7 and 14 after middle cerebral artery occlusion, and GLT-1 activity was increased in the physical training group (p<0.05). Conclusions: These results indicated that physical training after focal cerebral ischemia exerts neuroprotective effects against ischemic brain injury by improving motor performance and increasing the levels of GLT-1 activity.

• The Journal of Korea Assosiation for Disability and Oral Health
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• v.8 no.1
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• pp.22-25
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• 2012

Hypoxic ischemic encephalopathy(HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply and associated in most cases with oxygen deprivation in the neonate due to birth asphyxia. Children with HIE develop problems such as cerebral palsy, mental retardation, learning difficulties, and other disabilities. We hereby report the case of treating a child patient with HIE whose chief complaint of severe lingual ulceration. A 12-month-old boy referred to our hospital to treat ulcers of ventral surface of tongue. He has been suffering from lingual ulceration due to persistent tongue thrusting. He has bitten his own tongue involuntary. The ulceration was apparently seemed to be not healed because of the constant irritation by lower incisors. So we designed tongue protector to prevent lingual ulcers. The appliance was proved to be effective to reduce tongue trauma by lower incisors and periodic follow-up is needed.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.19
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• pp.8251-8257
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• 2014

Apoptosis is one of main types of neural cell death and is reversible and is a major target of therapeutic interventions. However, detailed apoptotic cascades still need to be recognized. In present study, we determined the promotion of HIF-$1{\alpha}$ and survivin in brain samples of a mouse model of hypoxic-ischemia and in neuroblastoma SH-SY5Y cells post hypoxia treatment. Then gain-of-function and loss-of-function strategies were adopted to manipulate the HIF-$1{\alpha}$ in SH-SY5Y cells, and hypoxia-induced survivin upregulation and cell apoptosis were determined. Results demonstrated that the HIF-$1{\alpha}$ and survivin were significantly promoted in a mouse model of hypoxic-ischemia or in SH-SY5Y cells post hypoxia in vitro. Manually upregulated HIF-$1{\alpha}$ could promote the hypoxia-induced survivin upregulation and improve the hypoxia-induced SH-SY5Y cell apoptosis. On the other hand, the HIF-$1{\alpha}$ knockdown by RNAi reduced the hypoxia-induced survivin upregulation and cell apoptosis. Therefore, the present study confirmed the protective role of HIF-$1{\alpha}$ and survivin in the hypoxia-induced SH-SY5Y cell apoptosis, and the survivin upregulation by hypoxia is HIF-$1{\alpha}$-dependent. Promotion of HIF-$1{\alpha}$ and survivin might be a valuable stragegy for therapeutic intervention for hypoxic-ischemic encephalopathy.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.673-679
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• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.

• Journal of Korean Neurosurgical Society
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• v.59 no.6
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• pp.544-550
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• 2016

Objective : Cerebral endothelial cells have unique biological features and are fascinating candidate cells for stroke therapy. Methods : In order to understand the molecular mechanisms of human cerebral endothelial cell (hCMEC/D3) transplantation in a rat stroke model, we performed proteomic analysis using 2-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Protein expression was confirmed by quantitative real-time PCR and Western blot. Results : Several protein spots were identified by gel electrophoresis in the sham, cerebral ischemia (CI), and CI with hCMEC/D3 treatment cerebral ischemia with cell transplantation (CT) groups, and we identified 14 differentially expressed proteins in the CT group. Proteins involved in mitochondrial dysfunction (paraplegin matrix AAA peptidase subunit, SPG7), neuroinflammation (peroxiredoxin 6, PRDX6), and neuronal death (zinc finger protein 90, ZFP90) were markedly reduced in the CT group compared with the CI group. The expression of chloride intracellular channel 4 proteins involved in post-ischemic vasculogenesis was significantly decreased in the CI group but comparable to sham in the CT group. Conclusion : These results contribute to our understanding of the early phase processes that follow cerebral endothelial cell treatment in CI. Moreover, some of the identified proteins may present promising new targets for stroke therapy.