• Nuclear Engineering and Technology
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• v.50 no.2
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• pp.313-317
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• 2018

Licenses for the storage of spent nuclear fuel (SNF) and vitrified highly active waste in casks under dry conditions are limited to 40 years and have to be renewed for prolonged storage periods. If such a license renewal has to be expected since as in accordance with the new site selection procedure a final repository for spent fuel in Germany will not be available before the year 2050. For transport and possible unloading and loading in new casks for final storage, the integrity and the maintenance of the geometry of the cask's inventory is essential because the SNF rod cladding and the cladding of the vitrified highly active waste are stipulated as a barrier in the storage concept. For SNF, the cladding integrity is ensured currently by limiting the hoop stress and hoop strain as well as the maximum temperature to certain values for a 40-year storage period. For a prolonged storage period, other cladding degradation mechanisms such as inner and outer oxide layer formation, hydrogen pick up, irradiation damages in cladding material crystal structure, helium production from alpha decay, and long-term fission gas release may become leading effects driving degradation mechanisms that have to be discussed.

• Journal of agriculture & life science
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• v.46 no.2
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• pp.115-127
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• 2012

Antioxidant and neuronal cell protective effects of aqueous extract from lotus (Nelumbo nucifera) leaf tea (LLTE) were investigated. The 2,2'-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) radical scavenging effect, ferric reducing antioxidant power, and malondialdehyde inhibition of LLTE were increased in a dose dependent manner. Intracellular reactive oxygen species accumulation resulting from hydrogen peroxide ($H_2O_2$) treatment was significantly reduced when LLTE were present in the media compared to PC12 cells treated with $H_2O_2$ only. In neuronal cell viability assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT), LLTE showed protective effect against $H_2O_2$-induced neurotoxicity. In addition, lactate dehydrogenase release into medium was also inhibited by LLTE (7.13-43.89%). Total phenolics of LLTE were 33.16 mg/g and a quercetin was identified as major phenolics (105.93 mg/100g). Therefore, above these data suggest that LLTE including quercetin may be useful in the natural antioxidant substance, and may reduce the risk of neurodegenerative disease.

• IMMUNE NETWORK
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• v.21 no.5
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• pp.36.1-36.16
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• 2021

Peroxiredoxins (Prxs) are ubiquitously expressed peroxidases that reduce hydrogen peroxide or alkyl peroxide production in cells. Prxs are released from cells in response to various stress conditions, and they function as damage-associated molecular pattern molecules. However, the secretory mechanism of Prxs and their roles have not been elucidated. Thus, we aimed to determine whether inflammasome activation is a secretory mechanism of Prxs and subsequently identify the effect of the secreted Prxs on activation of the classical complement pathway. Using J774A.1, a murine macrophage cell line, we demonstrated that NLRP3 inflammasome activation induces Prx1, Prx2, Prx5, and Prx6 secretion in a caspase-1 dependent manner. Using HEK293T cells with a transfection system, we revealed that the release of Prx1 and Prx2 relies on gasdermin-D (GSDMD)-mediated secretion. Next, we confirmed the binding of both Prx1 and Prx2 to C1q; however, only Prx2 could induce the C1q-mediated classical complement pathway activation. Collectively, our results suggest that inflammasome activation is a secretory mechanism of Prxs and that GSDMD is a mediator of their secretion. Moreover, secreted Prx1 and Prx2 bind with C1q, but only Prx2 mediates the classical complement pathway activation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.53-61
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• 1988

The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.

• Resources Recycling
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• v.17 no.6
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• pp.62-67
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• 2008

Oil shale is a sedimentary rock that contains organic compounds called kerogen that are released as petroleum-like liquids by retorting. In order to evalute oil shale as alternative oil resources, the physical properties of oil shale samples from US and Russia were investigated and Fischer assays were carried out. Thermogravimetric analysis shows that thermal degradation of oil shale consisted of two stage processes, with hydrocarbon release from kerogen followed by $CO_2$ release by carbonate decomposition. Organic compounds in oil shale have an high hydrogen/carbon ratio, and therefore liquid hydrocarbons could be obtained easily. Shale oil yields from Russian and US oil shales by Fischer assay were 12.7% and 18.5%, respectively. The density and boiling point of shale oils are higher than that of Middle East crude oil, indicating that further upgrading processes are necessary for refinery. On the other hands, sulfur contents are relatively low, and the amounts of Vanadium and Nickel are extremely small in shale oil. It was found that paraffins were rich in US shale oil while main components of Russian shale oil were oxygenated hydrocarbons.

• Proceedings of the Korea Society for Energy Engineering kosee Conference
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• 2003.11a
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• pp.51-55
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• 2003

The thermal behavior of NiFe$_2$O$_4$ prepared by a solid-state reaction was investigated for H$_2$ generation by the thermochemical cycle. The reduction of NiFe$_2$O$_4$ started from 800 $^{\circ}C$, and the weight loss was 0.2-0.3 wt％ up to 1000 $^{\circ}C$. At this reaction, NiFe$_2$O$_4$ was reduced by release of oxygen bonded with the Fe$^3$ion in the B site of NiFe$_2$O$_4$. In the $H_2O$ decomposition reaction, H$_2$ was generated by oxidation of reduced NiFe$_2$O$_4$. The crystal structure of NiFe$_2$O$_4$ for redox reaction maintained spinel structure. Then, NiFe$_2$O$_4$ is excellent material in the thermochemical cyclic reaction due to release oxygen at low temperature for the reduction reaction and produce H$_2$ maintaining crystal structure for redox reaction.

• Journal of Life Science
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• v.20 no.7
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• pp.1121-1126
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• 2010

The oxidative stress induced by reactive oxygen species (ROS) may play an important role in the pathogenesis of neurodegenerative diseases. In this study, we investigated the neuroprotective effects of methanolic extracts of Prunella Spica (PSE) against $H_2O_2$-induced oxidative stress in PC12 cells. The cells exposed to $H_2O_2$-induced oxidative stress were treated with various concentrations of PSE; this treatment resulted in the induction of a dose-dependent protective effect, which was evidenced by the results of MTT reduction assay, lactate dehydrogenase (LDH) release assay, morphological assay, and colony-formation assay. Interestingly, we also observed reduction of apoptotic bodies in the Hoechst staining and flow cytometric analysis. These data show that apoptosis was significantly suppressed in the PC12 cells that were exposed to $H_2O_2$-induced oxidative stress and treated with PSE. These results suggest that Prunella Spica could be a new potential protective agent against $H_2O_2$-induced oxidative stress.

• Korean Journal of Soil Science and Fertilizer
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• v.17 no.2
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• pp.101-107
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• 1984

The suitable paddy soil for application of rice straw under well to moderately well drained soil, the yield and yield components were pronounced more than poorly drained soil. Based on laboratory experiment, application of rice straw promoted the decrease of oxidation-reduction potential in well to moderately well drained soil. This results seems to be enhanced the release of some mineral nutrients such as calcium, potassium, silicon, and increases of availability of soil phosphorus. This explains reason why soil condition became more favorable for the increases of mineral nutrient in rice plant. On the contrary, poorly drained soils, became readily reduced even without application or rice straw, when soil wat submerged. Application of rice straw did not promoted the decrease of oxidation-reduction potential as much as in well drained soil. It was suggested that in this type of soil series, the release of mineral nutrients and the additional increase of available soil phosphorus did not proceed well. It was also suggested that the retardation of root development owing to accumulation of toxic substances such as organic acid, hydrogen sulfide or some other reducing substances formed by the application of rice straw in poorly drained soil series might be considered. In fact, the effect of rice straw on the yield of brown rice became lower.

• Toxicological Research
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• v.35 no.1
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• pp.45-63
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• 2019

In view of the growing industrial use of Bacterial cellulose (BC), and taking into account that it might become airborne and be inhaled after industrial processing, assessing its potential pulmonary toxic effects assumes high relevance. In this work, the murine model was used to assess the effects of exposure to respirable BC nanofibrils (nBC), obtained by disintegration of BC produced by Komagataeibacter hansenii. Murine bone marrow-derived macrophages ($BMM{\Phi}$) were treated with different doses of nBC (0.02 and 0.2 mg/mL, respectively 1 and $10{\mu}g$ of fibrils) in absence or presence of 0.2% Carboxymethyl Cellulose (nBCMC). Furthermore, mice were instilled intratracheally with nBC or nBCMC at different concentrations and at different time-points and analyzed up to 6 months after treatments. Microcrystaline $Avicel-plus^{(R)}$ CM 2159, a plant-derived cellulose, was used for comparison. Markers of cellular damage (lactate dehydrogenase release and total protein) and oxidative stress (hydrogen peroxidase, reduced glutathione, lipid peroxidation and glutathione peroxidase activity) as well presence of inflammatory cells were evaluated in brochoalveolar lavage (BAL) fluids. Histological analysis of lungs, heart and liver tissues was also performed. BAL analysis showed that exposure to nBCMC or CMC did not induce major alterations in the assessed markers of cell damage, oxidative stress or inflammatory cell numbers in BAL fluid over time, even following cumulative treatments. $Avicel-plus^{(R)}$ CM 2159 significantly increased LDH release, detected 3 months after 4 weekly administrations. However, histological results revealed a chronic inflammatory response and tissue alterations, being hypertrophy of pulmonary arteries (observed 3 months after nBCMC treatment) of particular concern. These histological alterations remained after 6 months in animals treated with nBC, possibly due to foreign body reaction and the organism's inability to remove the fibers. Overall, despite being a safe and biocompatible biomaterial, BC-derived nanofibrils inhalation may lead to lung pathology and pose significant health risks.