• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.2
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• pp.328-332
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• 2008

The purpose of this study was to identify the protective effect of Codonopis pilosula extract on cell death induced by $H_2O_2$ in SK-N-MC neuroblastoma cells. We measured the antioxidant effect by DPPH radical scavenging analysis, BSA analyssis and examined the cell viability by crystal violet and cytochrome C, Bax, Bcl-2, p53, p21 by using Western blot analysis. Codonopis pilosula extract scavenged DPPH radical in a dose-dependent manner and shown direct free radical scavenging effect, suggested that Codonopis pilosula extract have antioxidant effect in vitro. Treatment of cells with hydrogen peroxide, a reactive oxygen species, was to induce cell death and pretreatment with Codonopis pilosula extract attenuated the occurrence of $H_2O_2-induced$ cell death. To elucidate the protective mechanisms of action of Codonopis pilosula extract, Western blot analyses for Bcl-2 and Bax expression and cytochrome c release were carried out. Pretreatment with Codonopis pilosula extract induced the expression of Bcl-2 and suppressed the release of cytochrome c and Bax into the cytosol, thereby arresting $H_2O_2-induced$ apoptotic cell death. Especially p21 and p53 were decreased prior to $H_2O_2$ treatment. These results suggest that Codonopis pilosula extract is associated with the cell cycle and anti-apoptotic cell death.

• Biomolecules & Therapeutics
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• v.9 no.4
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• pp.249-257
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• 2001

The effect of oxidative stress on the alterations of different antioxidant enzyme activities was investigated in human skin melanoma cell line (SK-MEL-2). Oxidative stress was induced by the exposure to hydrogen peroxide ($H_2O$$_2$). SK-MEL-2 cells were treated with antioxidants such as vitamin E and selenomethionine in combination with $H_2O$$_2$. SK-MEL-$_2$ cells were exposed to various concentrations of $H_2O$$_2$ and measured the time course of changes in cell viability and antioxidant enzyme activities for 24 hr. Oxidative stress was induced by the exposure to 2.5mM hydrogen peroxide ($H_2O$$_2$) resulted in declining significantly for 24 hr. GPX and CAT activities peaked at 3 hr and returned to control levels by 24 hr. On the contrary, SOD activity was inactive before 6 hr but recovered at 24 hr. In case vitamin E (Vit E) and selenomethionine (Se-Met) were used at nontoxic concentrations (25$\mu$M Vit E/500$\mu$M Se-Met) to oxidative stress was induced by the exposure to hydrogen peroxide ($H_2O$$_2$) led to a 3- and 5-fold increase on the viability comparing to control and caused an increase in GPX activity respectively.

• Journal of the Korean Ceramic Society
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• v.41 no.10 s.269
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• pp.756-765
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• 2004

We present extraction process and reaction mechanism of boric acid from one of calcium borate ores, colemanite by reaction with sulfuric acid. Colemanite has been fully decomposed under pH 5 with sufficiency amount of sulfuric acid, more than the amount stoichiometrically required. Calcium sulfate was separated out, leaving boron in the liquid phase after sulfuric acid addition. The extraction process of boric acid was affected by dissolution temperature and time, amount of sulfuric acid and ammonium sulfate, pH and a degree of concentration before recrystallization. The $SiO_2$ of the impurities which colemanite contains was insoluble so that it was separated out with calcium sulfate from liquid phase. The species of $CaO,\;Al_2O_3,\;Fe_2O_3,\;MgO$ were remained in a liquid phase after reaction with sulfuric acid. These impurities were separated out by addition of ammonia to the liquid phase, funhermore, boric acid was produced by process of pH adjustments and acidification, concentration, and recrystallization.

• Journal of the Korean Ceramic Society
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• v.31 no.12
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• pp.1437-1442
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• 1994

Self propagating synthesis and thermal explosion of combustion reactions were applied to Al/K2Cr2O7/Al2O3 system as the first stage for a production of magnesia-chromium refractory. Several factors related to products made by two combustion reactions were considered and properties of products were characterised. Two processes were required to preheat upto at least 80$0^{\circ}C$ for the thermal explosion and the self propagating synthesis. These processes were so violent and explosive that alumina as diluent was added to the system in order to absorb the reaction heat and reduce the reaction rate. The products consisted of crystal phases of KAl5O8, Cr2O3, Al2O3, K2CrO4, and K2Al2O4.3H2O. The amount of KAl5O8 and K2Al2O4.3H2O crystal phases of products were decreased with further addition of alumina.

• Journal of Dental Anesthesia and Pain Medicine
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• v.16 no.4
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• pp.263-271
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• 2016

Background: Bone injury is common in many clinical situations, such as surgery or trauma. During surgery, excessive reactive oxygen species (ROS) production decreases the quality and quantity of osteoblasts. Remifentanil decreases ROS production, reducing oxidative stress and the inflammatory response. We investigated remifentanil's protective effects against $H_2O_2$-induced oxidative stress in osteoblasts. Methods: To investigate the effect of remifentanil on human fetal osteoblast (hFOB) cells, the cells were incubated with 1 ng/ml of remifentanil for 2 h before exposure to $H_2O_2$. For induction of oxidative stress, hFOB cells were then treated with $200{\mu}M$ $H_2O_2$ for 2 h. To evaluate the effect on autophagy, a separate group of cells were incubated with 1 mM 3-methyladenine (3-MA) before treatment with remifentanil and $H_2O_2$. Cell viability and apoptotic cell death were determined via MTT assay and Hoechst staining, respectively. Mineralized matrix formation was visualized using alizarin red S staining. Western blot analysis was used to determine the expression levels of bone-related genes. Results: Cell viability and mineralized matrix formation increased on remifentanil pretreatment before exposure to $H_2O_2$-induced oxidative stress. As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and $TGF-{\beta}$). However, pretreatment with 3-MA before exposure to remifentanil and $H_2O_2$ inhibited remifentanil's protective effects on hFOB cells during oxidative stress. Conclusions: We showed that remifentanil prevents oxidative damage in hFOB cells via a mechanism that may be highly related to autophagy. Further clinical studies are required to investigate its potential as a therapeutic agent.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.77-84
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• 2006

Objectives : To evaluate the neuroprotective effects of modified Bo-Yang-Hwan-O-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in N2a neuroblastoma cells. Methods : To study the cytotoxic effect of BHT on N2a neuronal cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, N2a neuronal cells were induced oxidative damages by H2O2, and assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effects of BHT by tube test. Results : In MTT assay, $500{\mu}g/ml$ of BHT was not showed cytotoxic effect on N2a neuronal cells. BHT protected N2a neuronal cells from H2O2-induced cell death in a dose-dependent manner. BHT also protected N2a neuronal cells from H2O2-induced DNA fragmentation. BHT scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong anti-oxidant effects through the free radical scavenging and neuroprotective effects in neuronal cells.

• Journal of the Korean Chemical Society
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• v.66 no.5
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• pp.416-419
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• 2022

• 한국정보디스플레이학회:학술대회논문집
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• 2007.08b
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• pp.1273-1276
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• 2007

We provide a newly developed dry etching process for the fabrication of ZnO-based oxide TFTs. The etching characteristics of ZnO (active layer) and $Al_2O_3$ (gate insulator) thin films were systematically investigated when the etching gas mixtures and their mixing ratios were varied in the heliconplasma etching system.

• Korean Journal of Air-Conditioning and Refrigeration Engineering
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• v.10 no.6
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• pp.666-673
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• 1998

Solubilities (LiBr+$CaC1_2$) in water were measured at temperatures form 267.51 to 306.17K for $CaC1_2$ (LiBr+$CaC1_2$)=0.24 by mole. Experimental data were correlated with polynomial equations. Average absolute deviations between the measured and calculated values were 0.31% at concentration smaller than 60wt% and 0.41% at concentration larger than 60wt%, respectively. Vapor pressures were measured at temperatures from 296.75 to 436.75K and concentrations from 40 to 70wt%. Vapor pressure data were fitted to a Antoine-type equation and average absolute deviation was 2.98%. The P-T-X chart and H-T-X chart of $H_2O$/(LiBr+$CaC1_2$) system were constructed by using the correlation equations of solubility, vaper pressure, and heat capacity. The P-T-X chart indicates that $H_2O$/(LiBr+$CaC1_2$) system has potential as a possible working fluid for air-cooled absorption chillers.

• Journal of Life Science
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• v.24 no.6
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• pp.595-602
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• 2014

Styela Clava tunic (SCT) has found some applications in many areas of medical treatment including as an anti-inflammatory compound, a wound healing film, in guided bone regeneration, and as a food additive. The protective effect of SCT aqueous extract (AE-SCT) on cell death induced by $H_2O_2$ treatment was investigated by measuring the changes in cell viability in HepG2 cells after AE-SCT treatment. High concentrations of antioxidant compounds including flavonoids (3.3 mg/g) and phenolics (32.3 mg/g) were detected in AE-SCT but no significant cytotoxicity was observed in HepG2 cells treated with AE-SCT. The viability of HepG2 cells was also not changed by treatment with different concentrations of AE-SCT after $H_2O_2$ treatment. However, cell viability was significantly increased in cells treated with three different concentrations of AE-SCT before $H_2O_2$ treatment. The greatest increase in cell viability was observed in the group treated with $50{\mu}g/ml$ AE-SCT, when compared with vehicle-treated group. FACS and DAPI staining analysis indicated that the decrease in number of dead cells was dependent on the concentration of AE-SCT. Alterations in the Bax/Bcl-2 ratio after $H_2O_2$ treatment were significantly restored by treatment with different concentrations of AE-SCT. These results indicate that AE-SCT, which contains high levels of antioxidants, may protect cells against death induced by $H_2O_2$ treatment.