• Journal of the Institute of Electronics Engineers of Korea SD
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• v.39 no.10
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• pp.25-34
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• 2002

In this paper, silicidation induced Schottky contact area was obtained using the current voltage(I-V) characteristics of shallow cobalt silicided p+-n and n+-p junctions. In reverse bias region, Poole-Frenkel barrier lowering influenced predominantly the reverse leakage current, masking thereby the effect of Schottky contact formation. However, Schottky contact was conclusively shown to be the root cause of the modified I-V behavior of n+-p junction in the forward bias region. The increase of leakage current in silicided n+-p diodes is consistent with the formation of Schottky contact via cobalt slicide penetrating into the p-substrate or near to the junction area and generating trap sites. The increase of reverse leakage current is proven to be attributed to the penetration of silicide into depletion region in case of the perimeter intensive n+-p junction. In case of the area intensive n+-p junction, the silicide penetrated near to the depletion region. There is no formation of Schottky contact in case of the p+-n junction where no increase in the leakage current is monitored. The Schottky contact amounting to less than 0.01% of the total junction was extracted by simultaneous characterization of forward and reverse characteristics of silicided n+-p diode.

• YAKHAK HOEJI
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• v.41 no.5
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• pp.629-637
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• 1997

Tumor necrosis factor-${alpha}$ (TNF) induced a cytotoxic response in ME-180 cervical carcinoma cells in vitro. This cytotoxic response was accompanied by a temporal series of mitogenic stimuli : increased c-fos, c-jun and jun-B expression. Depletion of protein kinase C (PKC) by exposure of ME-180 cells to 100ng/ml phorbol myristate acetate (PMA) for 24hours almost completely abolished TNF-mediated increase in these signals, indicating that a PKC-dependent pathway is involved in TNF-mediated increases in the expression of c-fos, c-jun and jun-B. Characteristics of TNF receptors after exposure to 100ng/ml PMA or 24hours were not altered, suggesting that diminished induction of these oncogenes by TNF after PMA treatment is not due to any changes at the receptor level. To examine whether a PKC-dependent pathway is involved in TNF-mediated cytotoxicity in ME-180 cells, cytotoxicity was measured after depletion of PKC. No apparent changes in cytototoxicity after PKC depletion suggest that a PKC-dependent pathway is not involved in TNF-mediated cytotoxicity. Furthermore, results from cytotoxicity tests after exposure to staurosporine (PKC inhibitor) did not show any changes in the TNF-mediated cytotoxicity, confirming that a PKC-dependent pathway is not involved in this process. These data indicate that 1) TNF induces expression of c-fos, c-jun and jun-B oncogenes via a PKC-dependent pathway and 2) PKC-dependent expression of these three oncogenes by TNF may not be involved in TNF-mediated cytotoxicity in ME-180 cells.

• Journal of Digital Convergence
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• v.14 no.3
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• pp.151-164
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• 2016

The purpose of this study was to evaluate the effects of self-efficacy that impacts on personal goal setting.. In addition, in the process of going to achieve the goal, this study was to evaluate the role of self-regulation resources. Specifically, this paper is divided into two groups of self-regulation resources, to analyze the relationship between self-efficacy and goal-setting theory. To achieve this goal, by manipulating the self-adjusting resources to target college students divided into two groups, this measured the performance of the self-efficacy and goal setting. In the test, the a mediated effect of goal setting between self-efficacy and performance was meaningful, and evidence of enhancing the self-regulatory resource by self-efficacy was found. As a result, this paper provides guideline that manages the performance by using the self-efficacy and self-regulatory resource.

• The Journal of Korean Obstetrics and Gynecology
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• v.23 no.4
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• pp.10-19
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• 2010

Methods: Intravenous administration of Platycodon grandiflorum was performed 2 days before tumor inoculation, then mice were killed 14 days after tumor inoculation, then number of tumor colonies were counted. Methanol extracts of Platycodon grandiflorum was added to colon26-M3.1 carcinoma cells, L5178Y-R lymphoma cells and Hela cells, and then cell growth was counted. To observe the immunomodulating effects of Platycodon grandiflorum, production of IL-6, IL-10, IL-12 and TNF-$\alpha$ were measured with ELISA assay and the cell growth of macrophage were also counted. Furthermore, antimetastatic experiment after depletion NK cells by injection of anti-asialo GM1 serum was also administered. Results: Intravenous administration of Platycodon grandiflorum significantly inhibited metastasis of colon26-M3.1 carcinoma cells. In an in vitro cytotoxicity analysis, Platycodon grandiflorum affected tumor cell growth above specific concentration. As compared with control, the production of IL-6, IL-10, IL-12 and TNF-$\alpha$ were incresed. And depletion NK cell completly abolished the inhibitory effect of metastasis. Conclusion: Platycodon grandiflorum appears to have considerable activity on immunomodulating effects and inhibit the metastasis of tumor. Further evaluation is needed for settling this.

• Journal of Nutrition and Health
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• v.18 no.3
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• pp.242-248
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• 1985

Weanling female Sprague Dawley rats were fed diets containing 22mg pyridoxine HCI/kg diet(control diet) and 1.2mg pyridoxine HCI/kg diet(deficient diet). One deficient group and one control group were fed their diets throughout the period of growth, gestation and lactation. After the pups were born and weaned, the deficient group was divided into two groups. Therefore, one(DC) switched to control diet and the other continued the same deficient diet until 10 week-old. Analysis of chemical composition of fatty acid in the total brain lipid was conducted in the pups of 5, 10, 15, 21, 35, 50 days of age. Arachidonic acid content was significantly decreased in the deficient group at 5 days compared to the control, but at almost all ages, there were no significant differences in fatty acid contens among all the groups. The fatty acid compositions of the brain phospholipids were determined on pups at 1, 14, 21, 35, 70 days of age. The content of $C_{20}\;_{4}$ in the brain phosphatidylcholine birth and contents of $C_{22}\;_{4}$ and $C_{22}\;_{5}$ at birtd, and $C_{22}\;_{5}$ and $C_{22}\;_{6}$ at 14 days in the phosphatidylethanolamine were depressed in the deficient group. These changes were not consistent with ages. Therefore, it may reflect that the major part of the changes occuring in the pyridoxine depleted rats depends, not so much on the pyridoxine depletion itself, as on the age or development of the rats.

• Nutrition Research and Practice
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• v.9 no.6
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• pp.592-598
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• 2015

BACKGROUND/OBJECTIVES: Increased mass of adipose tissue in obese persons is caused by excessive adipogenesis, which is elaborately controlled by an array of transcription factors. Inhibition of adipogenesis by diverse plant-derived substances has been explored. The aim of the current study was to examine the effects of the aqueous methanol extract of laver (Porphyra yezoensis) on adipogenesis and apoptosis in 3T3-L1 adipocytes and to investigate the mechanism underlying the effect of the laver extract. MATERIALS/METHODS: 3T3-L1 cells were treated with various concentrations of laver extract in differentiation medium. Lipid accumulation, expression of adipogenic proteins, including CCAAT enhancer-binding protein ${\alpha}$, peroxisome proliferator-activated receptor ${\gamma}$, fatty acid binding protein 4, and fatty acid synthase, cell viability, apoptosis, and the total content and the ratio of reduced to oxidized forms of glutathione (GSH/GSSG) were analyzed. RESULTS: Treatment with laver extract resulted in a significant decrease in lipid accumulation in 3T3-L1 adipocytes, which showed correlation with a reduction in expression of adipogenic proteins. Treatment with laver extract also resulted in a decrease in the viability of preadipocytes and an increase in the apoptosis of mature adipocytes. Treatment with laver extract led to exacerbated depletion of cellular glutathione and abolished the transient increase in GSH/GSSG ratio during adipogenesis in 3T3-L1 adipocytes. CONCLUSION: Results of our study demonstrated that treatment with the laver extract caused inhibition of adipogenesis, a decrease in proliferation of preadipocytes, and an increase in the apoptosis of mature adipocytes. It appears that these effects were caused by increasing oxidative stress, as demonstrated by the depletion and oxidation of the cellular glutathione pool in the extract-treated adipocytes. Our results suggest that a prooxidant role of laver extract is associated with its antiadipogenic and proapoptotic effects.

• BMB Reports
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• v.34 no.6
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• pp.544-550
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• 2001

In pre-transplant total-body irradiation (TBI), the lung is a critical dose-limiting organ. Also, the possible role of oxidative stress was suggested in the development of TBI-induced lung damage. This study explores the association between TBI-induced oxidative stress and the induction of lung pathogenesis by investigating TBI-induced oxidative stress in the lungs of male C57BL/6 mice after a single dose of 10 Gy TBI. We showed significant increases of reactive oxygen species (ROS) formation and lipid peroxidation, and also a depletion and oxidation of glutathione after TBI. There is evidence that pretreatment with 1,10-phenanthroline (o-phen) significantly reduces oxidative stress in the lung. This indicates that the TBI-induced ROS generation involves a metal-catalyzed Fenton-type reaction. A pretreatment of buthionine sulfoximine (BSO) augmented the glutathione depletion and oxidation, but had no effect on the ROS formation and lipid peroxidation up to 6 h after TBI. Histopathological features that are consistent with pneumonitis were observed in the BSO pretreated-mice 1 week after irradiation. The results suggest that TBI-induced oxidative stress in the lung involves a generation of ROS through a Fenton-type reaction. Also, glutathione plays an important inhibitory role in the radiation-induced lung pathogenesis by participating in the self-amplifying cascade subsequent to the ROS generation by irradiation.

• Journal of Nutrition and Health
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• v.32 no.3
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• pp.213-220
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• 1999

The purpose of this study was to determine the dose effects of taurine supplementation and effects of taurine depletion in diabetic rats. Sprague-Dawley male rats were fed the purified diets and supplemented with 1, 2 or 3% taurine in drinking water for 7 weeks(E1, E2 and E3, respectively). To induce taurine depletion, rats were treated with 5% $\beta$-alanine in drinkeng water (EA). Diabetes was induced by streptozotocin injection(50mg/kg B.W) after 3 weeks. Taurine-depleted diabetic rats(EA)had significantly lower body weight compared to those of nondiabetic(CO), nontaurine-supplemented diabetic(E0) and taurine-supplemented diabetic rats(E1, E2 and E3). E0 had significantly higher food intake compared to that of CO and EA. E1, E2 and E3, however, had significantly lower food intake compared to that of E0, and E3 had significantly lower food intake compared to that of E1 and E2. E0 had significantly higher water intake compare to that of CO and EA. EI had significantly lower water intake compared to that of E0. Blood glucose concentration of E0 was significantly increased compared to that of CO and EA. E2 and E3 had significantly lower blood glucose concentration compared to E0 and E1. Also there was a dose effect in blood glucose concentration between E2 and E3. The total cholesterol and LDL-cholesterol concentrations of EA were significantly increased compared to those of other groups. Therefore, it may be suggested that taurine supplementation is necessary for diabetes in order to prevent diabetic complications such as cardiac vascular diseases.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.12
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• pp.1752-1757
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• 2001

The present study was conducted to assess the dietary effect of T-2 toxin on the antioxidant systems of the liver in growing quail and to comparatively evaluate the protective properties of two different mycotoxin-adsorbent additives, Mycosorb and zeolite, in preventing inhibition of the antioxidant system. Four groups of 4 day old quail were formed with 20 birds in each group. The birds were maintained on the floor for the course of the study. The three treatment diets consisted of the basal diet with T-2 toxin added in the form of Fusarium sporotrichioides culture (8.1 mg/kg feed), T-2 toxin (8.1 mg/kg) plus zeolite (30 g/kg feed), and T-2 toxin (8.1 mg/kg) plus Mycosorb (1 g/kg feed). After 30 days of feeding (34 days old) all birds were sacrificed and liver samples for biochemical analyses were collected from five quail in each of the four groups. Antioxidant concentrations were evaluated by HPLC-based methods. Inclusion of T-2 toxin in the quail diet was associated with a significant (p<0.05) decrease in concentrations of all forms of antioxidants studied, including ${\alpha}$- and ${\gamma}$-tocopherols, ascorbic acid, retinol and retinyl esters. At the same time, liver susceptibility to lipid peroxidation significantly (p<0.05) increased. Inclusion of zeolite in the quail diet at the level of 3% was ineffective in preventing antioxidant depletion in the liver by mycotoxicosis. In contrast, Mycosorb in the diet at a 0.1% level was able to significantly inhibit liver antioxidant depletion and as a result decreased lipid peroxidation in the liver. Concentrations of all forms of antioxidants studied were significantly higher in the livers of the quails fed the basal and T-2 toxin/Mycosorb combination in comparison to birds fed the basal with T-2 toxin alone.

• Korean Journal of Metals and Materials
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• v.48 no.8
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• pp.691-698
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• 2010

A study has been carried out to evaluate the interaction behavior between a lanthanide element and clad material in order to analyze the effect of the lanthanide element on the fuel cladding chemical interaction (FCCI). A diffusion couple test between Misch metal (70Ce-30La) and ferritic-martensitic steel (Gr.92) was performed at $660^{\circ}C$, followed by a microstructural analysis of the coupled sample. The results showed that Ce in the Misch metal, rather than La, reacted with the ferritic-martensitic steel (FMS) to form an interaction layer that penetrated the clad thickness. Fe diffused outside the clad interface to form an $Fe_2Ce$ compound, leaving a depletion of Fe caused by excess diffusion as well as by the formation of Cr-rich precipitation inside the interaction layer. The rate of growth followed the cubic rate law, which indicated that Fe depletion was caused by the diffusion of Fe and that the associated Cr-rich phase formation controlled the whole diffusion process.