• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.30-38
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• 2005

Background : Arsenic trioxide ($As_2O_3$) has been used to treat acute promyelocytic leukemia, and it induces apoptosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal antiinflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with $As_2O_3$ and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. Material and Methods : The NCI-H157 cells were treated with $As_2O_3$, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide ($H_2O_2$) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. Results : The viability of the cells was decreased by a combination treatment of $As_2O_3$ and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased $H_2O_2$ generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial transmembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. Conclusion : Combination treatment with $As_2O_3$ and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction.

• Tuberculosis and Respiratory Diseases
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• v.40 no.1
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• pp.16-22
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• 1993

Background: The Microbicidal and cytotoxic activities of neutrophils are to a large extent dependent on a burst of oxidative metabolism which generates superoxide anion, hydrogen peroxide, and other reactive products of oxygen. The respiratory burst of PMN is initiated by intracellular calcium mobilization that follows immune or particular stimulation and is very sensitive to modulation by c-AMP or adenosine. Despite its antagonism against adenosine, earlier study has demonstrated potent theophylline inhibition of the PMN respiratory burst at variable ranges of blood concentrations of theophylline in the healthy normal volunteers and in the septic animals pretreated or early post-treated with aminophylline (AMPH) or pentoxifylline. However it is unclear whether theophylline inhibits the superoxide generation or not in the established human sepsis caused by acute pneumonia, as taking into consideration of the fact that full activation of neutrophils have occurred within minutes after the septic insult in the animal experiments. Methods: We measured the $O_2$ generation of peripheral arterial neutrophils obtained from 11 human septic subjects caused by acute pneumonia before and 1 hour after completion of continuous AMPH infusion. Patients were identified and studied within 48 hour of admission. All subjects were administered an intravenous loading and maintenance dose of AMPH. The generation of $O_2$ was measured at a discrete time point (60 min) by the reduction of ferricytochrome c.PMA (10 ${\mu}g/ml$) was used as a stimulating agent. PMNs were isolated at a concentration of $2{\times}10^6$ cells/ml. The arterial oxygen tension, blood pressure and heart rates were also checked to evaluate the systemic effects of AMPH in the acute pneumonia. Results: The mean serum concentration of AMPH at 60 minutes was $8.8{\pm}0.6{\mu}g/ml$. Sixty minutes after AMPH infusion the generatition of $O_2$ was decreased from $0.076{\pm}0.034$ to $0.013{\pm}0.004$(OD) (p<0.05) and from $0.177{\pm}0.044$ to $0.095{\pm}0.042$(OD) (p<0.01) in the resting and stimulated PMNs respectively. $PaO_2$ was not changed after AMPH infusion. Conclusion: AMPH may compromise host defense by significant inhibition of neutrophil release of superoxide anion and it had no effect on improving $PaO_2$ in the acute pneumonia.

• Journal of the Society of Disaster Information
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• v.9 no.4
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• pp.449-461
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• 2013

As the hydrofluoric acid leak in Gumi-si, Gyeongsangbuk-do or hydrochloric acid leak in Ulsan, Gyeongsangnam-do demonstrated, chemical related accidents are mostly caused by large amounts of volatile toxic substances leaking due to the damages of storage tank or pipe lines of transporter. Safety assessment is the most important concern because such toxic material accidents cause human and material damages to the environment and atmosphere of the surrounding area. Therefore, in this study, a hydrofluoric acid leaked from a storage tank was selected as the study example to simulate the leaked substance diffusing into the atmosphere and result analysis was performed through the numerical Analysis and diffusion simulation of ALOHA(Areal Location of Hazardous Atmospheres). the results of a qualitative evaluation of HAZOP (Hazard Operability)was looked at to find that the flange leak, operation delay due to leakage of the valve and the hose, and toxic gas leak were danger factors. Possibility of fire from temperature, pressure and corrosion, nitrogen supply overpressure and toxic leak from internal corrosion of tank or pipe joints were also found to be high. ALOHA resulting effects were a little different depending on the input data of Dense Gas Model, however, the wind direction and speed, rather than atmospheric stability, played bigger role. Higher wind speed affected the diffusion of contaminant. In term of the diffusion concentration, both liquid and gas leaks resulted in almost the same $LC_{50}$ and ALOHA AEGL-3(Acute Exposure Guidline Level) values. Each scenarios showed almost identical results in ALOHA model. Therefore, a buffer distance of toxic gas can be determined by comparing the numerical analysis and the diffusion concentration to the IDLH(Immediately Dangerous to Life and Health). Such study will help perform the risk assessment of toxic leak more efficiently and be utilized in establishing community emergency response system properly.

• Nuclear Engineering and Technology
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• v.39 no.5
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• pp.603-616
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• 2007

Roy Huddle, having invented the coated particle in Harwell 1957, stated in the early 1970s that we know now everything about particles and coatings and should be going over to deal with other problems. This was on the occasion of the Dragon fuel performance information meeting London 1973: How wrong a genius be! It took until 1978 that really good particles were made in Germany, then during the Japanese HTTR production in the 1990s and finally the Chinese 2000-2001 campaign for HTR-10. Here, we present a review of history and present status. Today, good fuel is measured by different standards from the seventies: where $9*10^{-4}$ initial free heavy metal fraction was typical for early AVR carbide fuel and $3*10^{-4}$ initial free heavy metal fraction was acceptable for oxide fuel in THTR, we insist on values more than an order of magnitude below this value today. Half a percent of particle failure at the end-of-irradiation, another ancient standard, is not even acceptable today, even for the most severe accidents. While legislation and licensing has not changed, one of the reasons we insist on these improvements is the preference for passive systems rather than active controls of earlier times. After renewed HTGR interest, we are reporting about the start of new or reactivated coated particle work in several parts of the world, considering the aspects of designs/ traditional and new materials, manufacturing technologies/ quality control quality assurance, irradiation and accident performance, modeling and performance predictions, and fuel cycle aspects and spent fuel treatment. In very general terms, the coated particle should be strong, reliable, retentive, and affordable. These properties have to be quantified and will be eventually optimized for a specific application system. Results obtained so far indicate that the same particle can be used for steam cycle applications with $700-750^{\circ}C$ helium coolant gas exit, for gas turbine applications at $850-900^{\circ}C$ and for process heat/hydrogen generation applications with $950^{\circ}C$ outlet temperatures. There is a clear set of standards for modem high quality fuel in terms of low levels of heavy metal contamination, manufacture-induced particle defects during fuel body and fuel element making, irradiation/accident induced particle failures and limits on fission product release from intact particles. While gas-cooled reactor design is still open-ended with blocks for the prismatic and spherical fuel elements for the pebble-bed design, there is near worldwide agreement on high quality fuel: a $500{\mu}m$ diameter $UO_2$ kernel of 10% enrichment is surrounded by a $100{\mu}m$ thick sacrificial buffer layer to be followed by a dense inner pyrocarbon layer, a high quality silicon carbide layer of $35{\mu}m$ thickness and theoretical density and another outer pyrocarbon layer. Good performance has been demonstrated both under operational and under accident conditions, i.e. to 10% FIMA and maximum $1600^{\circ}C$ afterwards. And it is the wide-ranging demonstration experience that makes this particle superior. Recommendations are made for further work: 1. Generation of data for presently manufactured materials, e.g. SiC strength and strength distribution, PyC creep and shrinkage and many more material data sets. 2. Renewed start of irradiation and accident testing of modem coated particle fuel. 3. Analysis of existing and newly created data with a view to demonstrate satisfactory performance at burnups beyond 10% FIMA and complete fission product retention even in accidents that go beyond $1600^{\circ}C$ for a short period of time. This work should proceed at both national and international level.

• Korean Journal of Food Science and Technology
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• v.46 no.3
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• pp.384-389
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• 2014

The objective of the present study was to investigate the chemical composition of anthocyanin-enriched extract of radiation-induced blackberry (Rubus fruticosus L.) mutant (${\gamma}$-B201) as well as the protective effect of ${\gamma}$-B201 against oxidative stress in vitro. The cytotoxicity, reactive oxygen species (ROS) scavenging capacity, and DNA damage were assessed by WST-1 assay, flow cytometry, and comet assay, respectively. Lactate dehydrogenase, superoxide dismutase, and catalase activities were determined by using a commercial kit. The in vitro results showed that ${\gamma}$-B201 increased the cell viability, reduction of lactate dehydrogenase release, and intracellular ROS scavenging capacity in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells. Furthermore, treatment with ${\gamma}$-B201 attenuated DNA damage in $H_2O_2$-treated HepG2 cells and treatment with ${\gamma}$-B201 restored the activity of superoxide dismutase and catalase in $H_2O_2$-treated HepG2 cells. In conclusion, the present study suggests that ${\gamma}$-B201 blackberry extract can exert a significant cytoprotective effect against $H_2O_2$-induced cell damage.

• Journal of Life Science
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• v.33 no.12
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• pp.1002-1014
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• 2023

The root of Cirsium japonicum var. maackii (Maxim.) has long been used in traditional medicine to prevent the onset and progression of various diseases and has been reported to exert a wide range of physiological effects, including antioxidant activity. However, research on its effects on hepatocytes remains scarce. This study used the human hepatocellular carcinoma HepG2 cell line to investigate the antioxidant activity of ethanol extract of C. japonicum root (EECJ) on hepatocytes. Hydrogen peroxide (H₂O₂) was used to mimic oxidative stress. The results showed that EECJ significantly reverted the decrease in cell viability and suppressed the release of lactate dehydrogenase in HepG2 cells treated with H₂O₂. Moreover, an analysis of changes in cell morphology, flow cytometry, and microtubule-associated protein light chain 3 (LC3) expression showed that EECJ significantly inhibited HepG2 cell autophagy induced by H₂O₂. Furthermore, it attenuated H₂O₂-induced apoptosis and cell cycle disruption by blocking intracellular reactive oxygen species and mitochondrial superoxide production, indicating strong antioxidant activity. EECJ also restored the decreased levels of intracellular glutathione (GSH) and enhanced the expression and activity of superoxide dismutase and GSH peroxidase in H₂O₂-treated HepG2 cells. Although an analysis of the components contained in EECJ and in vivo validation using animal models are needed, these findings indicate that EECJ is a promising candidate for the prevention and treatment of oxidative stress-induced liver cell damage.