• Journal of Radiation Protection and Research
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• v.13 no.2
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• pp.78-87
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• 1988

This article suggests the radionuclides which should be considered more important to the offsite consequence assesment during a nuclear power plant accident. For this purpose, the relative importance to the early health effects of released radionuclides on the major organs during the accident is estimated under the assumption of the same release fraction. The inventories of the 25 elements, 54 nuclides selected in the Reactor Safety Study are calculated by ORIGEN 2 code. The organs of interest in the estimation are G. I. track, bone marrow, thyroid and lung. The result shows the relative potential importance of radionuclides as follows: For G.I. track, Np, Ce, Ru, Y, and Zr are of importance in sequence, Np, I, La, Sr, Ba for bone marrow, I and Te for thyroid, Cm, Ce, Ru, Pu, Zr for lung. In addition to iodine and noble gases, therefore, the potential contribution of those nuclides listed above to the offsite consequences should not be overlooked for some accidents of particular sequence.

• BMB Reports
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• v.33 no.3
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• pp.213-220
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• 2000

A fulminant hepatitis is associated with massive liver cell necrosis and a high mortality rate. But survivors regenerate a normal liver and do not have chronic liver disease. This clinical course suggests that the acutely injured livers release a factor that allows a recovery from chronic hepatitis or cirrhosis. The objective of this study was to isolate and characterize an anti-fibrotic factor from acutely damaged rat livers. The liver cell necrosis was prepared from rat by warm ischemical perfusion and the perfusates were assessed against the growth inhibition of fat-storing cells (FSC). A liver-derived growth inhibitory factor (LDGIF) was purified from ischemically damaged rat livers by chromatographies on Sephacryl S-300, CM Sepharose, hydroxyapatite, and Superose 12. The LDGIF was isolated with an overall purification of 194-fold and 40% recovery. Although LDGIF was identified as the rat liver arginase by Nterminal sequence analysis, LDGIF exists as a monomer and the purified native arginase has a trimer form. Furthermore, LDGIF has a lower enzyme activity on the hydrolysis of L-arginine and a higher inhibitory effect on proliferation of FSC than the normal rat liver arginase. The catalytic activity of LDGIF is ascribed to the monomeric characteristics of the LDGIF. Therefore, the inhibitory action of LDGIF might not be due to the arginine depletion by the catalytic activity of arginase. In conclusion, the presence of the LDGIF could interpret the clinical course that serious fibrosis is not found in the liver of patients recovering from severe hepatic necrosis due to fulminant hepatitis, suggesting that this LDGIF may provide a novel target for the prevention and treatment of hepatic fibrosis.

• BMB Reports
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• v.40 no.6
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• pp.928-935
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• 2007

Three Angelica sinensis polysaccharide fractions (APFs), named APF1, APF2 and APF3, were isolated and purified from Radix A. sinensis and their antioxidant activities were evaluated in isolated mouse peritoneal macrophages by pretreatment with APFs before exposure to 0.2 mM tertbutylhydroperoxide (t-BHP). The results showed that pretreatment of the macrophages with APFs as low as $10{\mu}g$/ml could significantly enhance t-BHP-decreased cell survival, intracellular glutathione (GSH) content and superoxide dismutase (SOD) activity, and also inhibited t-BHP-increased lactate dehydrogenase (LDH) leakage and malondialdehyde (MDA) formation (p < 0.05), and APF3 was the most active fraction, followed by APF2 and APF1 in decreasing order. Furthermore, we found for the first time that the bound-protein in APF3 was associated closely with the protective effects and the polysaccharide inhibited the excess NO release from t-BHP-activated macrophages to protect host cells.

• BMB Reports
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• v.51 no.10
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• pp.508-513
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• 2018

Fibronectin fragments found in the synovial fluid of patients with osteoarthritis (OA) induce the catabolic responses in cartilage. Nuclear high-mobility group protein Box 1 (HMGB1), a damage-associated molecular pattern, is responsible for the regulation of signaling pathways related to cell death and survival in response to various stimuli. In this study, we investigated whether changes induced by 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) in HMGB1 expression influences the pathogenesis of OA via an HMGB1-modulated autophagy signaling pathway. Human articular chondrocytes were enzymatically isolated from articular cartilage. The level of mRNA was measured by quantitative real-time PCR. The expression of proteins was examined by western blot analysis, immnunofluorescence assay, and enzyme-linked immunosorbent assay. Interaction of proteins was evaluated by immunoprecipitation. The HMGB1 level was significantly lower in human OA cartilage than in normal cartilage. Although 29-kDa FN-f significantly reduced the HMGB1 expression at the mRNA and protein levels 6 h after treatment, the cytoplasmic level of HMGB1 was increased in chondrocytes treated with 29-kDa FN-f, which significantly inhibited the interaction of HMGB1 with Beclin-1, increased the interaction of Bcl-2 with Beclin-1, and decreased the levels of Beclin-1 and phosphorylated Bcl-2. In addition, the level of microtubule-associated protein 1 light chain 3-II, an autophagy marker, was down-regulated in chondrocytes treated with 29-kDa FN-f, whereas the effect was antagonized by mTOR knockdown. Furthermore, prolonged treatment with 29-kDa FN-f significantly increased the release of HMGB1 into the culture medium. These results demonstrated that 29-kDa FN-f inhibits chondrocyte autophagy by modulating the HMGB1 signaling pathway.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.39 no.7
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• pp.609-615
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• 2015

In this study, the combustion and exhaust emission characteristics in a gasoline direct injection engine with variations of the bio-ethanol-gasoline blending ratio and the excess air factor were investigated. To investigate the effects of the excess air factor and the bio-ethanol blends with gasoline, combustion characteristics such as the in-cylinder combustion pressure, rate of heat release (ROHR), and the fuel consumption rate were analyzed. The reduction of exhaust emissions such as carbon monoxide (CO), unburned hydrocarbon (HC), and nitrogen oxides ($NO_x$) were compared with those of gasoline fuel with various excess air factors. The results showed that the peak combustion pressure and ROHR of bio-ethanol blends were slightly higher and were increased as bio-ethanol blending ratio is increased. Brake specific fuel consumption increased for a higher bio-ethanol blending ratio. The exhaust emissions decreased as the bio-ethanol blending ratio increased under all experimental conditions. The exhaust emissions of bio-ethanol fuels were lower than those of gasoline.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.36 no.7
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• pp.767-774
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• 2012

A fluidic device (FD) has been adopted in the safety injection tanks (SITs) of APR1400. A flow control mechanism of the FD was used to vary the flow regime in the vortex chamber corresponding to the SITs water level. The flow regime in the vortex chamber has a different pressure loss from low to high in accordance with the SITs water level. Nitrogen at the top of the SIT could be released owing to inertia of discharge flow when changing from a high flow rate to a low flow rate. This phenomenon is important to design improvement perspective because it can affect the performance of the FD. This paper shows a result of a preliminary numerical study to obtain the transient data related to air release in the flow turn-down period using a two-fluid free-surface model provided from ANSYS CFX 13.0. In conclusion, there is no significant effect on the performance of the FD, though a small quantity of air is released during the flow turn-down period.

• KSCE Journal of Civil and Environmental Engineering Research
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• v.32 no.6A
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• pp.411-418
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• 2012

In this study, behavior of unpatched and patched cylindrical shells with through-wall cracks has been estimated using numerical experiments, and patching effect of them has been investigated according to various patching parameters. To show credibility of numerical models considered, two ways such as h- and p-methods have been adopted. Also, domain integral method and virtual crack extension method have been considered to calculate energy release rates based on linear elastic fracture mechanics. For examples, the unpatched cylindrical shells with circumferential cracks under remote tension have firstly been analyzed to show the validity of finite element modeling with h-method or p-method, and then the results have been compared with literature values published. Next, the sensitive analysis of patch repaired problems in terms of thickness of patch and adhesive, shear modulus of adhesive, composite material type of patch, crack length, etc. has been carried out.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.804-809
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• 2003

Kagam-bojungikgitang is the water extracts prepared from Ginseng Radix, Astragali Radix. Angelicae gigantis Radix, Astractylodis Rhizoma alba, Aurantii nobilis Pericarpium, Glycyrrhizae Radix, Artemisiae iwayomogii Herba, and Scutellariae Radix. This is a modified prescription of Bojungikgitang, which has been used for the treatment of indigestion, and immunological disease in oriental countries. In this study, the effects of Kagam-bojungikgitang and Bojungikgitang on the production of prostaglandin E₂ (PGE₂) and the expression of cyclooxygenase-2 (COX-2) were examined using RAW 264.7 macrophages activated with lipopolysaccharide (LPS). Both prescriptions dose-dependently reduced the release of PGE2 and expression of COX-2 caused by stimulation of LPS without cytotoxic effect. Kagam-bojungikgitang's inhibitory effects were better than Bojungikgitang in PGE2 production and COX-2 expression. Moreover, Kagam-bojungikgitang also attenuated markedly the production of tumor necrosis factor (TNF)-α, and IL-6 than Bojungikgitang in LPS-stimulated RAW 264.7 macrophages. These results suggest that Kagam-bojungikgitang decreases PGE2 and pro-inflammatory cytokine production in macrophages and these properties may contribute to the anti-inflammatory activity of Kagam-bojungikgitang.

• Toxicological Research
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• v.26 no.1
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• pp.37-46
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• 2010

This study aimed to elucidate anti-inflammatory activities from extracts of Asterina pectinifera on nitric oxide (NO) production, TNF-${\alpha}$ and IL-6 release in lipopolysaccharide (LPS)-stimulated murine macrophage cell, RAW264.7. We prepared the methanolic extracts (60-MAP, 70-MAP, 80-MAP and 90-MAP), aqueous extract (W-AP) and functional bioactive compound fraction (He-AP and EA-AP) from Asterina pectinifera according to extract method. The 60-MAP, 70-MAP, 80-MAP, 90-MAP and W-AP were significantly suppressed LPS-induced production NO, TNF-${\alpha}$ and IL-6 secretion in a concentration-dependent manner (P < 0.05). Especially, 80-MAP by extracted 80% methanol had the strongest activity in reduction of inflammatory mediators among these extracts. Indeed, to identify active fraction, which contained potential bioactive compounds, from 80-MAP of Asterina pectinifera, we tested anti-inflammatory activity of the He-AP or the EA-AP. The He-AP was next extracted from 80-MAP and the EA-AP were extracted from the other methanol layer except the He-AP. The EA-AP demonstrated a strong anti-inflammatory effect through its ability to reduce NO production and it also inhibited the production of proinflammatory cytokines such as IL-6 and TNF-${\alpha}$ at low concentration. These results suggested that the methanolic extract from Asterina pectinifera had the potential inhibitory effects on the production of these inflammatory mediators.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.383-389
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• 2017

Dexmedetomidine is an ${\alpha}2$-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of $1{\mu}g/kg$ load dose, followed by $0.05{\mu}g/kg/min$ infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-$1{\beta}$, interleukin-6 and tumor nevrosis factor-${\alpha}$ as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-${\kappa}Bp65$, inhibitor of ${\kappa}B{\alpha}$ and phosphorylated of ${\kappa}B{\alpha}$ in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-${\kappa}B$ pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.