• Biomolecules & Therapeutics
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• v.8 no.2
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• pp.140-146
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• 2000

Recently, we reported that immunostimulation of primary rat cortical astrocyte caused stimulation of glucose deprivation induced apoptotic cell death. To enhance the understanding of the mechanism of the potentiated cell death of clucose-deprived astrocyte by immunostimulation, we investigated the effect of immunostimulation on the glucose deprivation induced cell death of rat C6 glioma cells. Co-treatment of C6 glioma cells with lipopolysaccharide (LPS, $1\;{\mu}\textrm{g}/ml$) and interferon ${\gamma}(IFN{\gamma},\;100U/ml)$ is serum free condition caused marked elevationo f nitric oxide production ($>50\;{\mu}M$). In this condition, glucose deprivation caused significant release of lactate dehdrogenase (LDH) from C6 glioma cells while control cells did not show LDH release. To investigate whether elevated level of nitric oxide is responsible for the enhanced LDH release in glucose-deprived condition, C6 glioma cells were treated with 3-morphorinosydnonimine (SIN-1) and it was observed that SIN-1 caused increase in LDH release from glucose-deprived C6 glioma cells. Treatment of C6 glioma cells with $25\;{\mu}M$ of pyrrolidinedithiocarbamate (PDTC) which inhibit Nuclear factor kB (NF-kB) activation, caused complete inhibition of nitric oxide production. Treatment of C6 glioma cells with NO synthase inhibitors, $N^{G}$-nitro-L-arginine (NNA) or L-$N{\omega}$-nitro-L-arginine methyl ester (L-NAME), caused inhibition of nitric oxide production and also glucose deprivation induced cell death of cytokine-stimulated C6 glioma cells. In addition, diaminohydroxypyrimidine (DAHP, 5 mM) which inhibits the synthesis of tetrahydrobiopterine (BH4), one of essential cofactors for iNOS activity, caused complete inhibition of NO production from immunostimulated C6 glioma cells. The results from the present study suggest that immunostimulation causes potentiation of glucose deprivation induced death of C6 glioma cells which is mediated at least in part by the increased production of nitric oxide. The vulnerability of immunostimulated C6 glioma cells to hypoglycemic insults may implicate that the elevated level of cytokines in various ischemic and neurodegenerative diseases may play a role in their pathogenesis.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.4
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• pp.397-405
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• 2019

Quantitative electroencephalography (QEEG) has been widely used in research and clinical fields. QEEG has been widely used to objectively document cerebral changes for the purpose of identifying the electrophysiological biomarkers across various clinical symptoms and for the stimulation of specific cortical regions associated with cognitive function. In electroencephalography (EEG), the difference in quantitative and qualitative analyses is discriminated not by its measurement methods and relevant clinical or research environments, but by its analysis methods. When performing a qualitative analysis, it is possible for a medical technologist or experienced researchers to read the EEG waveforms to exclude artifacts. However, the quantitative analysis is still based on mathematical modeling, and all EEG data are included for the analysis, leading the results to be affected by unexpected artifacts. In the hospital setting, the case that the medical technologists in charge of the EEG test perform academic research has been little reported, compared to other clinical physiological measurement-based research. This is because there are few laboratories specialized in clinical physiological research. In this respect, this study is expected to be utilized as a basic reference material for medical technologists, students, and academic researchers, all of whom would like to conduct a quantitative analysis.