• Environmental and Resource Economics Review
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• 제23권4호
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• pp.689-718
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• 2014

This study analyzes the ripple effects on the national economy of the flood damage using a perfect foresight dynamic CGE model for 2010 as the base year in case that the flood damage reduces the capital of the relevant industrial sectors. The analysis is limited to the items of physical damage such as agricultural land, ships and public facilities, for which statistical data can be obtained. As flood damage scenarios we adopt the minimum, maximum and average value of flood damage's historical data over the period 1991~2010 for each item. The results show that the largest production decline happens to the industry of fishing and transport and the next largest to the agricultural and forestry industry. The GDP reduction in the base year turns out to be from 0.001 to 0.057 percent compared to the benchmark and 11 percent compared to the exogenous shock to capital stock. Dynamically, the GDP gradually decreases until the year of 2030, which shows the long-lasting impact on the national economy of flood damage via the chanel of the capital damage.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.111-115
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• 2005

Ultraviolet (UV) radiation to mammalian skin is known to alter cellular function via generation of Reactive Oxygen Species (ROS), DNA damage and DNA lesions, such as pyrimidine dimmers and photoproducts, which could lead to DNA mutation if they are not repaired. In this study, we have investigated the reduction of DNA damage and of apoptosis with a particular attention to genetic effect of paeoniflorin in Normal Human Epidermal Keratinocytes (NHEK). After UVB irradiation from $10\;to\;500mJ/cm^{2}$ to NHEK, Mean Tail Moments (MTM) were increased with UVB dose increase. The greatest amount of strand breaks was induced at $500mJ/cm^{2}$ of UVB. Even at the lowest dose of UVB ($10mJ/cm^{2}$), change in MTM was detected (P<0.0001). Pretreated cell with 0.1% paeoniflorin maximally reduced the level of DNA damage to about 21.3%, compared to untreated cell. In the lower concentrations less than 0.01% of paeoniflorin, MTM had a small increase but paeoniflorin still had reductive effects of DNA damage. We measured the apoptosis suppression of paeoniflorin with annexin V flous staining kit. As we observed under the fluorescence microscopy to detect apoptosis in the irradiated cell, the fluorescence intensity was clearly increased in the untreated cell, but decreased in treated cells with paeoniflorin. These results suggest that paeoniflorin reduces the alteration of cell membranes and prevents DNA damage. Therefore, the use of paeoniflorin as a free radical scavenger to reduce the harmful effects of UV lights such as chronic skin damage, wrinkling and skin cancer can be useful to prevent the formation of photooxidants that result in radical damage.

• Asian Pacific Journal of Cancer Prevention
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• 제15권17호
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• pp.7043-7048
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• 2014

Inhibition of heat shock protein 90 (Hsp90) leads to inappropriate processing of proteins involved in DNA damage repair pathways after DNA damage and may enhance tumor cell radio- and chemotherapy sensitivity. To investigate the potentiation of antitumor efficacy of lidamycin (LDM), an enediyne agent by the Hsp90 inhibitorgeldanamycin (GDM), and possible mechanisms, we have determined effects on ovarian cancer SKOV-3, hepatoma Bel-7402 and HepG2 cells by MTT assay, apoptosis assay, and cell cycle analysis. DNA damage was investigated with H2AX C-terminal phosphorylation (${\gamma}H2AX$) assays. We found that GDM synergistically sensitized SKOV-3 and Bel-7402 cells to the enediyne LDM, and this was accompanied by increased apoptosis. GDM pretreatment resulted in a greater LDM-induced DNA damage and reduced DNA repair as compared with LDM alone. However, in HepG2 cells GDM did not show significant sensitizing effects both in MTT assay and in DNA damage repair. Abrogation of LDM-induced $G_2/M$ arrest by GDM was found in SKOV-3 but not in HepG2 cells. Furthermore, the expression of ATM, related to DNA damage repair responses, was also decreased by GDM in SKOV-3 and Bel-7402 cells but not in HepG2 cells. These results demonstrate that Hsp90 inhibitors may potentiate the antitumor efficacy of LDM, possibly by reducing the repair of LDM-induced DNA damage.

• The Korea Journal of Herbology
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• 제23권4호
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• pp.31-38
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• 2008

Objectives: This study was performed to investigate the effects of water extract from Cynanchi Wilfordii Radix on prevention of hyperlipidemia and liver damage induced by alcohol. Methods: Except for the normal group, we fed rat on 25% alcohol for 55 days. And water extracts from Cynanchi Wilfordii Radix were administrated for the Cynanchi Wilfordii Radix group during the same period. We measured the serum components in rat's blood, body weight and weight of liver. Results: At first, we observed effects of Cynanchi Wilfordii Radix on prevention of hyperlipidemia induced by alcohol. Cynanchi Wilfordii Radix group showed significant decrease of total cholesterol and triglyceride in comparison with those of the control group. Cynanchi Wilfordii Radix group showed significant increase of HDL-cholesterol in comparison with those of the control group. Cynanchi Wilfordii Radix group showed significant increase of body weight in comparison with those of the control group in 4weeks and 8weeks. At second, we observed effects of Cynanchi Wilfordii Radix on prevention of liver damage induced by alcohol. Cynanchi Wilfordii Radix group showed significant decrease of GPT and ALP in comparison with those of the control group. Cynanchi Wilfordii Radix group showed significant increase of liver weight in comparison with those of the control group. Conclusions: Reviewing these experimental results, it appears that water extracts from Cynanchi Wilfordii Radix have pharmaceutical efficacy on prevention of hyperlipidemia and liver damage induced by alcohol. Therefore further additional study should be conducted to elucidate in depth the pharmaceutical efficacy of these.

• Biomolecules & Therapeutics
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• 제20권6호
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• pp.544-549
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• 2012

To examine the neuroprotective effects of ginsenoside R0, we investigated the effects of ginsenoside R0 in PC12 cells under an anoxic or oxidative environment with Edaravone as a control. PC12 neuroendocrine cells were used as a model target. Anoxic damage or oxidative damage in PC12 cells were induced by adding sodium dithionite or hydrogen peroxide respectively in cultured medium. Survival ratios of different groups were detected by an AlamarBlue assay. At the same time, the apoptosis of PC12 cells were determined with flow cytometry. The putative neuroprotective effects of ginsenoside R0 is thought to be exerted through enhancing the activity of antioxidant enzymes Superoxide dismutases (SOD). The activity of SOD and the level of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), were measured to evaluate the protective and therapeutic effects of ginsenoside R0. Ginsenoside R0 treated cells had a higher SOD activity, lower MDA level and lower ROS, and their survival ratio was higher with a lower apoptosis rate. It is suggested that ginsenoside R0 has a protective effect in the cultured PC12 cells, and the protection efficiency is higher than Edaravone. The protective mechanisms of these two are different. The prevent ability of ginsenoside R0 is higher than its repair ability in neuroprotection in vitro.

• Toxicological Research
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• 제29권1호
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• pp.43-52
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• 2013

Zearalenone (ZEN) is a non-steroidal estrogenic mycotoxin produced by several species of Fusarium that are found in cereals and agricultural products. ZEN has been implicated in mycotoxicosis in farm animals and in humans. The toxic effects of ZEN are well known, but the ability of an alkaline Comet assay to assess ZEN-induced oxidative DNA damage in Chang liver cells has not been established. The first aim of this study was to evaluate the Comet assay for the determination of cytotoxicity and extent of DNA damage induced by ZEN toxin, and the second aim was to investigate the ability of N-acetylcysteine amide (NACA) to protect cells from ZEN-induced toxicity. In the Comet assay, DNA damage was assessed by quantifying the tail extent moment (TEM; arbitrary unit) and tail length (TL; arbitrary unit), which are used as indicators of DNA strand breaks in SCGE. The cytotoxic effects of ZEN in Chang liver cells were mediated by inhibition of cell proliferation and induction of oxidative DNA damage. Increasing the concentration of ZEN increased the extent of DNA damage. The extent of DNA migration, and percentage of cells with tails were significantly increased in a concentration-dependent manner following treatment with ZEN toxin (p < 0.05). Treatment with a low concentration of ZEN toxin (25 ${\mu}M$) induced a relatively low level of DNA damage, compared to treatment of cells with a high concentration of ZEN toxin (250 ${\mu}M$). Oxidative DNA damage appeared to be a key determinant of ZEN-induced toxicity in Chang liver cells. Significant reductions in cytolethality and oxidative DNA damage were observed when cells were pretreated with NACA prior to exposure to any concentration of ZEN. Our data suggest that ZEN induces DNA damage in Chang liver cells, and that the antioxidant activity of NACA may contribute to the reduction of ZEN-induced DNA damage and cytotoxicity via elimination of oxidative stress.

• BMB Reports
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• 제51권8호
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• pp.400-405
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• 2018

Chronic stress induces neuronal cell death, which can cause nervous system disorders including Parkinson's disease and Alzheimer's disease. In this study, we evaluated the neuroprotective effects of Clematis terniflora extract (CTE) against corticosterone-induced apoptosis in rat pheochromocytoma (PC12) cells, and also investigated the underlying molecular mechanisms. At concentrations of 300 and $500{\mu}g/ml$, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by $200{\mu}M$ corticosterone. CTE decreased the expression levels of endoplasmic reticulum (ER) stress proteins GRP78, GADD153, and mitochondrial damage-related protein BAD, suggesting that it downregulates ER stress evoked by corticosterone. Furthermore, our results suggested that these protective effects were mediated by the upregulation of p-AKT and p-ERK1/2, which are involved in cell survival signaling. Collectively, our results indicate that CTE can lessen neural damage caused by chronic stress.

• Biomolecules & Therapeutics
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• 제21권3호
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• pp.210-215
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• 2013

Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to ${\gamma}$-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by ${\gamma}$-irradiation and thereby protected cells against ${\gamma}$-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting ${\gamma}$-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against ${\gamma}$-irradiation are mainly due to its inhibition of reactive oxygen species generation.

• The Korean Journal of Food & Health Convergence
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• 제5권6호
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• pp.1-4
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• 2019

Wernicke korsakoff syndrome is caused by thiamine deficiency in the body. Thiamine not available in the body, is a substance to be taken from outside with foods. There are some conditions that reduce the metabolism of thiamine taken from the body and cause a vital risk. The most important factor is alcoholism. Wernicke Korsakoff syndrome produces both neurological and vestibular symptoms. At the same time, the damage of these symptoms to the patient psychology cannot be ignored. The aim of this study is to investigate the damage and mechanism of the syndrome in the vestibular system. In this study, we investigated vestibular symptoms of Wernicke Korsakoff syndrome due to thiamine deficiency, differences of vestibular system according to individuals and mechanism of damage caused by syndrome in vestibular system. Thiamine deficiency is caused by Wernicke Karsokoff syndrome with some external factors. This syndrome shows the most important effects of alcoholism. It causes neurological, vestibular and psychological symptoms. In this context, we can say that thiamine deficiency is a disease that causes damage in the vestibular system due to nystagmus formation and imbalance. The most important detail in the treatment stage is the detailed evaluation of symptoms associated with each other.

• Nuclear Engineering and Technology
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• 제33권6호
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• pp.566-584
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• 2001

In this paper, the progressive deformation and the creep-fatigue damage for the conceptually designed reactor internals of KALIMER(Korea Advanced Liquid MEtal Reactor) are carried out by using the elastic analysis method in the RCC-MR code for normal operating conditions including the thermal load, seismic load (OBE) and dead weight. The maximum operating temperature of this reactor is 53$0^{\circ}C$ and the total service lifetime is 30 years. Thus, the time- dependent creep and stress-rupture effects become quite important in the structural design. The effects of the thermal induced membrane stress on the creep-fatigue damage are investigated with the risk of the elastic follow-up. To calculate the thermal stress, detailed thermal analyses considering conduction, convection and radiation heat transfer mechanisms are carried out with the ANSYS program. Using the results of the elastic analysis, the progressive deformation and creep-fatigue damages are calculated step by step using the RCC-MR in detail. This paper ill be a very useful guide for an actual application of the high temperature structural design of the nuclear power plant accounting for the time-dependent creep and stress-rupture effects.