• IMMUNE NETWORK
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• v.3 no.4
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• pp.268-275
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• 2003

Background: Hemopoietic cells require the constant presence of growth factors for survival in vitro and in vivo. Caspases have been known as central executors of apoptotic cell death. We have, therefore, investigated the pathways that regulate caspase activity and apoptosis using the $CD34^+$ cell line, TF-1 which requires GM-CSF for survival. Methods: Apoptosis was measured by annexin V staining and mitochondrial membrane potential was measured by DiOC6 labelling. Intracellular pH was measured using pH sensitive fluorochrome, BCECF or SNARF-1, followed by flow cytometry analysis. Caspase activation was analyzed by PARP cleavage using anti-PARP antibody. Results: Removal of GM-CSF induceed PARP cleavage, a hallmark of caspase activity, concomitant with pHi acidification and a drop in mitochondrial potential. Treatment with ZVAD, a competitive inhibitor of caspases, partially rescued cell death without affecting pHi acidification and the reduction of mitochondrial potential, suggesting that both these events act upstream of caspases. Overexpression of Bcl-2 prevented cell death induced by GM-CSF deprivation as well as pHi acidification and the reduction in mitochondrial membrane potential. In parental cells maintained with GM-CSF, EIPA, a competitive inhibitor of $Na^+/H^+$ antiporter induced apoptosis, accompanied by a drastic reduction in mitochondrial potential. In contrast, EIPA induced apoptosis in Bcl-2 transfectants without causing mitochondrial membrane depolarization. Conclusion: Taken together, our results suggest that the regulation of $H^+$fluxes, either through a mitochondriondependent or independent pathway, is central to caspase activation and apoptosis.

• Herbal Formula Science
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• v.32 no.1
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• pp.29-37
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• 2024

Objectives : The purpose of this study was to examine the effects of insurance herbal medicines on colonic interstitial Cells of Cajal (ICC) in mice. Methods : Among the insurance herbal medicines, we chose Gamisoyo-san (GSS), Banhasasim-tang (BHSST) and Bojungikki-tang (BGIKT). We made the ICC culture in large intestine in mice and used the electrophysiological method to record pacemaker potentials. Also we used MTT assay to check cell viability and examined the ICC protein expression by western blot. Results : 1. GSS (1-10 mg/ml) induced the pacemaker potential depolarization and decreased frequency with concentration-dependent manners in colonic ICC. EC50 is 2.99 mg/ml. BHSST (1-10 mg/ml) induced the pacemaker potential depolarization and decreased frequency with concentration-dependent manners in colonic ICC. EC50 is 2.76 mg/ml. BGIKT (1-10 mg/ml) induced the pacemaker potential depolarization and decreased frequency with concentration-dependent manners in colonic ICC. EC50 is 4.49 mg/ml. 2. GSS, BHSST and BGIKT had no effects on cell viability in colonic ICC. 3. GSS and BGIKT increased the Anoctamin-1 (ANO1) protein expression and BHSST increased the transient receptor potential melastatin-subfamily member 7 (TRPM7) protein expression in colonic ICC. Conclusions : These results suggest that GSS, BHSST, and BGIKT have shown the potential to regulate gastrointestinal (GI) motility by regulating colonic ICC and may show the potential to treat colon-derived GI diseases such as irritable bowel syndrome (IBS).

• The Korea Journal of Herbology
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• v.28 no.6
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• Korean Journal of Materials Research
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• v.24 no.6
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• pp.326-337
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• 2014

The use of solar energy generation is steadily increasing, and photovoltaic modules are connected in series to generate higher voltage and power. However, solar panels are exposed to high-voltage stress (up to several hundreds of volts) between grounded module frames and the solar cells. Frequent high-voltage stress causes a power-drop in the modules, and this kind of degradation is called potential induced degradation (PID). Due to PID, a significant loss of power and performance has been reported in recent years. Many groups have suggested how to prevent or reduce PID, and have tried to determine the origin and mechanism of PID. Even so, the mechanism of PID is still unclear. This paper is focused on understanding the PID of crystalline-silicon solar cells and modules. A background for PID, as well as overviews of research on factors accelerating PID, mechanisms involving sodium ions, PID test methods, and possible solutions to the problem of PID, are covered in this paper.

• Journal of Korean Tunnelling and Underground Space Association
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• v.16 no.2
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• pp.261-267
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• 2014

Various types of external loads can be applied to the tunnel structure. In a shield tunnel, the vibration from the train may affect the behavior of the adjacent ground. In this study, the railway-induced vibration was estimated and applied to the shield tunnel through 3D numerical simulation. The effective stress analysis based on the finite difference method and Finn model was performed to investigate the potential of liquefaction below the tunnel. Furthermore, pore water pressure and displacement were monitored on a time domain; consequently, the liquefaction potential and dynamic response of the shield tunnel were analyzed. Consequently, it is confirmed that the generation of excess pore water pressure by train-induced vibrating load, however, the amount does not meaningfully affect the potential of liquefaction.

• Molecular & Cellular Toxicology
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• v.2 no.3
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• pp.193-201
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• 2006

Cephalexin, one of most widely prescribed cephalosporin, has been reported to cause acute renal failure as a side effect in human and experimental animals. Although numerous animal studies have been reported for the cephalosporin nephrotoxicity, the molecular and cellular nephrotoxic mechanisms of cephalexin are still unknown. This investigation evaluated the time-dependent gene expression profile of kidney in mouse during cephalexin induced nephrotoxicity. C57BL/6 female mice were administered either saline or 1,000 mg/kg cephalexin intraperitoneally. Mice were sacrificed at 3, 6, and 24 hr after administration. Blood biochemical and histopathological results indicated cephalexin induced nephrotoxicity. Microarray experiment carried out using Affymetrix $GeneChip^{(R)}$. There were 198 informative genes that were significantly expressed >5-fold versus control at 3, 6, and 24 hr (p<0.01), of which 156 and 42 were up-and down-regulated, respectively. Major classes of up-regulated genes at 3, 6 hr included those involved in MAPK/Jak-STAT signaling pathway and immune response such as cytokine-cytokine receptor interaction and complement and coagulation cascades. At 24 hr, up-regulated genes were mainly involved in regeneration/repair and immune response; down-regulated genes were generally associated with transporters and intermediary metabolism. Among the up-regulated genes at 24 hr, several potential biomarkers on nephrotoxicity such as Kim-1, Fga, Timp1, and Slc34a2 were clustered in a same category. In addition, Tnfrsf12a and Lcn2 which were consistently up-regulated (>5 fold) were also included as potential biomarkers. These results may provide clues for elucidating the mechanism of cephalexin induced nephrotoxicity and evaluating potential biomarkers to assess nephrotoxicity.

• JSTS:Journal of Semiconductor Technology and Science
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• v.5 no.3
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• pp.173-181
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• 2005

A new two dimensional (2-D) model for the potential distribution of fully depleted short-channel ion-implanted silicon MESFET's has been presented in this paper. The solution of the 2-D Poisson's equation has been considered as the superposition of the solutions of 1-D Poisson's equation in the lateral direction and the 2-D homogeneous Laplace equation with suitable boundary conditions. The minimum bottom potential at the interface of the depletion region due to the metal-semiconductor junction at the Schottky gate and depletion region due to the substrate-channel junction has been used to investigate the drain-induced barrier lowering (DIBL) and its effects on the threshold voltage of the device. Numerical results have been presented for the potential distribution and threshold voltage for different parameters such as the channel length, drain-source voltage, and implanted-dose and silicon film thickness.

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.537-541
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• 2020

Sphingosine-1-phosphate (S1P) and its receptors have been implicated in atopic dermatitis. S1P₂ was found to function as a proallergic receptor, while its antagonist JTE-013 was found to suppress allergic asthma in mice. Topical application of JTE-013 has not been investigated in an in vivo model of atopic dermatitis. Therefore, the therapeutic potential of JTE-013 topical application was evaluated by the use of a 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis mouse model. DNCB-induced inflammation and mast cell accumulation in skin tissues were significantly suppressed by topical JTE-013 treatment in BALB/c mice. DNCB-induced increase of lymph nodes sizes and elevated inflammatory cytokines (IL-4, IL-13, IL-17, and IFN-γ) in lymph nodes were also significantly reduced by the JTE-013 treatment. Elevated serum levels of IgE were significantly suppressed by the topical treatment of JTE-013. In summary, the topical treatment of JTE-013 S1P₂ antagonist suppressed DNCB-induced atopic dermatitis symptoms and immune responses. These results suggested JTE-013 as a potential therapeutic agent for atopic dermatitis.

• Advances in Traditional Medicine
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• v.6 no.4
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• pp.336-343
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• 2006

The present study was carried out to investigate the antidiabetic and antioxidant effect of methanolic extract of Berberis tinctoria leaves (MEBT), in streptozotocin induced diabetic rats. Oral administration of MEBT extract (150 mg/kg and 300 mg/kg) for a period of 14 days. Blood glucose levels, body weight food and liquid intake were measured on every $5^{th}$ day over a period of 14 days. In diabetic rats, MEBT at the dose of 150 mg/kg and 300 mg/kg body weight resulted in significant reduction in blood glucose levels. The study was further investigated to determine antioxidant and antihyperlipidemic potential of MEBT in streptozotocin (STZ) induced diabetic rats. These results suggest that the MEBT possess antidiabetic activity and is able to ameliorate biochemical damages in STZ induced diabetic rats and the results were found to be in a dose dependent manner.

• Biomolecules & Therapeutics
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• v.20 no.5
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.