• Applied Microscopy
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• v.24 no.2
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• pp.26-36
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• 1994

To investigate the effects of mercuric chloride ($HgCl_2$) on the differentiation in the cerebral neuron of chick embryo 7 days, the ultrastructural changes in nerve cells injected with a various doses of mercuric chloride were observed with transmission electron microscope. The enzyme activity of the some dehydrogenases, and adenosine triphophate (ATP) were also analyzed. The results obtained are as follows; The ultrastructural changes in 1.0mg-injected group, the nuclear envelope were irregular, and the RER, Golgi complexes and mitochondria were not well developed. In 2.0mg-injected group, the nuclear envelope were partly destroyed or detached, and mitochondria were decreased in number and their cristae were destroyed, too. The RER and Golgi complexes were less developed than those of the normal groups. In general, the activities of dehydrogenases were declined by increasing the dose of mercuric chloride. Lactate dehydrogenase (LDH) activity fatted to below 85% of the normal group in 1.0mg-injected group, and 69% in 2.0mg-injected group. Malate dehydrogenase (MDH) activity was decreased greatly to 76% in 2.0mg-injected group. Succinate dehydrogenase (SDH) activity fatted to 85% in 1.0mg-injected group, and 74% in 2.0mg-injected group. ATP content in 1.0mg-injected group was almost near to the normal level, but it was increased significantly in 2.0mg-injected group.

• The Journal of Korean Physical Therapy
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• v.24 no.4
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• pp.262-267
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• 2012

Purpose: This study was designed to analyze the differences in cerebral cortex activity of the elderly after extracting the movement related cortical potentials (MRCPs) from electroencephalogram (EEG) during a concentric and eccentric contraction of the elbow joint flexors, and entering them into the brain-mapping program to make the images. Methods: Right-dominant normal elderly people were divided into an eccentric contraction group and a concentric contraction group. Then, their MRCPs were measured using EEG and sEMG, during an eccentric and concentric contraction. Then, they were converted into images using the brain-mapping program. Results: Eccentric contraction group's $C_3$ and Cz showed statistically higher mean values of MRCP positive potential than the concentric contraction group. Conclusion: Researching a cerebral cortex activity, using MRCP, would provide basic data for clinical neuro-physiological researches on aging or neural plasticity of patients with a central nervous system injury.

• Advances in Traditional Medicine
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• v.8 no.4
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• pp.430-439
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• 2008

Chungpaesagan-tang (CPSGT) is most frequently used to treat ischemic brain injury in tradition Korean medicine. Clinically, cerebral ischemia is likely to be accompanied by preexisting or complicating disease. However, animal models used to examine the effects of herbal medicines on cerebral ischemia have not given this issue sufficient consideration. The present study was undertaken to determine the effects of CPSGT on focal cerebral ischemia in normal and SHR rats subjected to transient middle cerebral artery occlusion (MCAO). Animals were divided into four groups: Normal (Sprague-Dawley) rats subjected to MACO (the NC+MCAO group), normal rats subjected to MCAO and then administered CPSGT (NC + MCAO + CP), SHR rats subjected to MCAO (SHR + MCAO), and SHR rats subjected to MCAO and then administered CPSGT (SHR + MCAO + CP). MCAO was performed using the intraluminal method. CPSGT was administrated orally twice (1 and 4 h) after MCAO. All animals were sacrificed at 24 h postoperatively. Brain tissues were stained with hematoxylin & eosin, to examine the effect of CPSGT on ischemic brain tissues. In addition, changes in TNF-$\alpha$ expression in ischemic areas were examined by immunostaining. CPSGT was found to significantly reduce infarction areas in normal and SHR rats and infarction volumes in SHR rats. Similarly, CPGST markedly increased neuron numbers and sizes in all treated groups, except cell sizes in SHRs. Furthermore, CPSGT reduced TNF-$\alpha$ expression in MCAO administered SHR rats. The findings of the present study suggest that CPSGT effectively ameliorates neuron damage caused by MACO-induced cerebral ischemia, and that it has a significant neuroprotective effect after cerebral ischemia in SHR.

• Journal of Acupuncture Research
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• v.18 no.4
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• pp.116-124
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• 2001

Background and Objetive : The aim of this study was to investigate the effect of various electroacupuncture stimulation on NADPH-diaphorase in cerebral cortex, brain stem, cerebellum of spontaneously hypertensive rats. Materials and Methods : We evaluated the changes of NADPH-d-positive neurons using a histochemical method. The staining intensity of NADPH-d-positive neurons was assessed in a quantitative fashion using a microdensitometrical method based on optical density by means of an image analyzer. Results and Conculsion : The average optical density of NADPH-d-positive neurons of 100 Hz (bipolar square wave 0.2 ms duration and 100 Hz frequency) electroacupuncture treatment group significantly increased in most cortical areas comparison between the manual acupuncture and 2 Hz (bipolar square wave 0.2 ms duration and 2 Hz frequency) electroacupuncture groups. In the brain stem, the optical density of NADPH-d-positive neuron at only superficial gray layer of the superior colliculus area was same as cerebral cortex. We conclude that the morphological evidence for NADPH-d-positive neurons may be have regional change in cerebral cortex brain stem and cerebellum according to various electroacupuncture stimulations.

• Molecular & Cellular Toxicology
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• v.4 no.3
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• pp.218-223
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• 2008

Oxidative stress is believed to contribute to the neuronal damage induced by cerebral ischemia/reperfusion injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of hydroxyfullerene (a radical absorbing cage molecule) against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Wistar rats by four vessel- occlusion (4VO) for 10 min. Lipid peroxidation in brain tissues was determined by measuring the concentrations of thiobarbituric acid-reactive substances (TBARS). Furthermore, the apoptotic effects of ${H_2}{O_2}$ on PC12 cells were also investigated. Cell viabilities were measured using MTT [3-(4,5-dimethylthiazolyl-2)-2,-5-diphenyltetrazolium bromide] assays. Hydroxyfullerene, when administered to rats at 0.3-3 mg/kg i.p. at 0 and 90 minutes after 4-VO was found to significantly reduce CA1 neuron death by 72.4% on hippocampal CA1 neurons. Our findings suggest that hydroxyfullerene protects neurons from transient global cerebral injury in the rat hippocampus by reducing oxidative stress and lipid peroxidation levels, which contribute to apoptotic cell death.

• Journal of Genetic Medicine
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• v.18 no.2
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• pp.105-109
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• 2021

Tetrasomy 18p is a genetic syndrome caused by an isochromosome consisting of two copies of the short arm of chromosome 18. Clinically, pediatric cases of tetrasomy 18p manifest with global developmental delay, similar to most cases of chromosomal abnormality. In addition, it causes various symptoms including abnormal muscle tone. We report a case of an infant with global developmental delay and remarkable spasticity, the typical phenotype of bilateral spastic cerebral palsy. However, she had a subtle anomaly in her face, and brain magnetic resonance imaging (MRI) findings were inconsistent with her strong upper motor neuron signs. Upon genetic testing, she was determined to have an 18p isochromosome, confirming de novo non-mosaic tetrasomy 18p. Cerebral palsy is a neurological disorder that includes developmental delay caused by a non-progressive lesion in the developing brain. During diagnostic workup in patients with cerebral palsy, genetic testing should be considered when there are minor physical anomalies or equivocal MRI findings.

• Applied Microscopy
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• v.26 no.3
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• pp.253-266
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• 1996

To investigate the effects of mercuric chloride ($HgCl_2$) on the differentiation of the cerebral neuron of chick embryo 9 days, the ultrastructural changes in nerve cells injected with a various doses of mercuric chloride were observed with transmission electron microscope. The enzyme activity of the some dehydrogenases, cerebral proteins and adenosine triphosphate (ATP) were also analyzed. The results obtained are as follows: The ultrastructural changes in 0.5 and 1.0mg-injected groups were undetectable, but in 2.0mg-injected group, the nuclear envelops were very irregular and mitochondria, were swelled and destroyed partly. The number of polypeptide bands separated by SDS-PAGE in the normal group were 37 bands. According to the in creased dose of mercuric chloride, contends of the bands were increased in 7 bands. The activities of dehydrogenases were declined by increasing the dose of mercuric chloride. Lactate dehydrogenase (LDH) activity failed to 78% in 1.0mg-injected group and greatly to 68% in 2.0 mg-injected group. Malate dehydrogenase (MDH) activity failed to 81% in 2.0 mg-injected group. On the other hand, succinate dehydrogenase (SDH) activity decreased to 80% in 1.0 mg-injected group and greatly to 63% in 2.0 mg-injected group. ATP content in 1.0 mg-injected group was increased slightly and in 2.0 mg-injected group was increased greatly.

• Applied Microscopy
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• v.27 no.1
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• pp.87-100
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• 1997

To investigate the effects of mercuric chloride $(HgCl_2)$ on the differentiation of the cerebral neuron of chick embryo 10 days, the ultrastructural changes in nerve cells injected with a various doses of mercuric chloride were observed with transmission electron microscope. The enzyme activity of the some dehydrogenases, cerebral proteins and adenosine triphosphate (ATP) were also analyzed. The results obtained are as follows; The ultrastructural changes in 1.0 mg-injected group, the nuclear membranes were irregular, outer of mitochondria membrances dispressioned, their cristae were destroyed. In 2.0 mg-injected group, the nuclear envelops were destroyed and divided, were not observed organelle except of few ribosome, the RER and mitochondria. The number of polypeptide bands were separated by SDS-PAGE in the normal group were 38 bands. According to the in creased dose of mercuric chloride, contends of the bands were increased in 4 bands, but were decreased in 1 band. The activities of dehydrogenases were declined by increasing the dose of mercuric chloride. Lactate dehydrogenase (LDH) activity fatted to 61% in 2.0 mg-injected group. Malate dehydrogenase (MDH) activity fatted to 90% in 1.0 mg-injected group, greatly to 76% in 2.0 mg-injected group. Succinate dehydrogenase (SDH) activity decreased to 79% in 1.0 mg-injected group and greatly to 62% in 2.0 mg-injected group. ATP content in 1.0 mg-injected group was almost near to the normal level, but it was increased greatly in 2.0 mg-injected group.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.928-931
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• 2002

To elucidate the toxic effect of oxygen free radicals on cultured mouse cerebral neurons damaged by hydrogen peroxide(H₂O₂)-induced neurotoxicity, we examined the neurotoxicity induced by oxygen radicals by NR assay when cultured cerebral neurons were grown in the media containing various concentrations of H202 for 6 hours. In addition, neuroprotective effects of herb extracts such Rhizoma Gastrodiae(RG) on H202-induced neurotoxicity in cultured cerebral neurons were evaluated after cultured cerebral neurons were preincubated with various concentrations of herb extract, RG for 2 hours before 50uM H₂O₂ for 6 hours. H₂O₂ decreased remarkably cell viability in dose-and time-dependent manner in these cultures, and also herb exract, RG decreased LDH activity of cerebral neurons damaged by H₂O₂. From the above results, it is suggested that H₂O₂ was toxic in cultured cerebral neurons from mouse, and RG was effective in blocking the neurotoxicity induced by oxygen radicals in these cultures.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.101-104
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• 2003

It has been suggested that oxidative stress of reactive oxygen species(ROS) may play a key role in the pathogenesis of neuronal complications. The aim of this study was to examine the cytotoxic effect of hydrogen peroxide(H₂O₂) in the cultured mouse cerebral neurons and the protective effect of Schisandrae Fructus(SF) on ROS-induced neurotoxicity. Cytotoxic effect of H₂O₂ and neuroprotective effect of SF were determined by MTT assay. H₂O₂ decreased cell viability in dose-and time-dependent mannner, and SF decreased H₂O₂-induced neurotoxicity in these cultures. From above the results, H₂O₂ has toxic effect, and herb extract, SF is very effective against H₂O₂-induced neurotoxicity in cultured cerebral neurons of mouse.